Acvc Handbook HM

2022 edition
Prof. Josep Masip

MD, PhD, FESC
Handbook of
Acute
CardioVascular
Monitoring
Quick access to most relevant practical
information on haemodynamic
and general monitoring in acute
cardiovascular care
GENERAL APPROACH
Prof. Josep Masip, MD, PhD, FESC

Intensive Care Department, Consorci Sanitari Integral ,
University of Barcelona, Spain
In daily practice, doctors and nurses are regularly considering how to early identify and treat
patients potentially severe. The information obtained through direct physical examination,
together with the measurement of body temperature and blood pressure, usually allows an
immediate bedside approach, but often becomes insufficient, and other tools are required
to facilitate a better control of the patient's conditions.
Thus, the first step is to have basic monitoring, which includes continuous electrocardio-
gram with heart rate and rhythm, oxygen saturation by pulse-oximetry, respiratory rate and
automatic non-invasive measurement of blood pressure. This basic monitoring allows the
management of the majority of patients in most scenarios. However, in cases with a greater
degree of severity and complexity, additional resources are required to achieve a more pre-
cise control of the patient, including the assessment of the most appropriate treatment and
the response to it. It is in this context where having a handbook on haemodynamic monito-
ring emerges as a necessity tool to guide clinicians to face these complex clinical scenarios.
Designed as a pocket format, this handbook is essentially structured into four parts, with
28 chapters covering most of the aspects related to monitoring, not only haemodynamics.
The first part offers a general overview of what is essential to monitoring. The second part
addresses the main monitoring techniques. The third part, probably the most important,
covers the principal clinical scenarios that usually require monitoring. Finally, the fourth part
shows an overview of what will be the future, complemented with an appendix containing
practical scales, scores, calculations and algorithms.
Each chapter has key messages, recommended readings and a precise body text, illustrated
with numerous tables and figures, which allows a rapid and easy reading. Unfortunately, due
to the limitations of the format, some neurocritical and surgical-anesthetics techniques and
scenarios have not been covered in this edition.
The book has counted with the participation of 54 authors among the best experts in the
world on each topic. The first edition will be in pdf format, but further editions will be printed
and in electronic format as app, allowing to include videos and interactive questions and to
set up a learning program. This initiative emerged from the board of the Acute Cardiovascular
Care Association of the European Society of Cardiology. Although initially it was targeted
to intensive cardiovascular physicians, this handbook would be useful for sure to any health
professional managing complex critical patients.
III TABLE OF CONTENT
GENERAL APPROACH P.2

Prof. J. Masip
PART I - OVERVIEW OF HAEMODYNAMIC MONITORING

1 - CRUCIAL PARAMETERS AND SYSTEMS
FOR MONITORING IN THE ICU P.7
Prof. M.R. Pinsky, Prof. M. Hravnak
2 - INDICATIONS FOR HAEMODYNAMIC MONITORING P.15

Prof. J-L. Vincent
PART II - TECHNIQUES FOR HAEMODYNAMIC MONITORING

1 - INVASIVE HAEMODYNAMIC MONITORING P.23
Prof. A. Rudiger, Dr. J. Stuby, Dr. P. Jorge Pérez, Dr. B. Darias-Delbey
2 - NON-INVASIVE HAEMODYNAMIC MONITORING P.41

Prof. J. Masip, Prof. C. Muëller, Prof. E. Gayat, Dr. J. Joachim, Prof. D. Zahger,
Dr. K. Orvin, Dr. J. Mesquida, Dr. E. Cortés, X. García Nogales, Prof. S. Price,
Prof. J. Čelutkienė, Dr. G. Balčiūnaitė, Dr. D. Zakarkaitė, Assoc. Prof. E. Platz,
Prof. R.M. Vicho
3 - PRELOAD RESPONSIVENESS P.125

Prof. J-L. Teboul, Dr. R. Shi, Prof. X. Monnet
PART III - SPECIFIC CLINICAL SCENARIOS

1 - GENERAL APPROACH TO SHOCK STATES P.145
Prof. A. Mebazaa, Dr. M. Arrigo, Dr. J. Hermes-Laufer
2 - ACUTE LEFT VENTRICULAR FAILURE P.154

Prof. J. Masip, Prof. Dr. U. Zeymer, Prof. Dr. H. Thiele
3 - RIGHT VENTRICULAR FAILURE P.173

Prof. A. Vieillard-Baron
4 - ACUTE MITRAL REGURGITATION AND

VENTRICULAR SEPTAL RUPTURE P.179
Dr. O. Chioncel, Dr. L. Antohi, Prof. V. Iliescu
TABLE OF CONTENT IV
5 - CARDIAC TAMPONADE AND CONSTRICTION P.197

Prof. E. Bonnefoy-Cudraz, Dr. T. Bochaton
6 - SEPTIC SHOCK P.204

Prof. D. De Backer
7 - HYPOVOLEMIC SHOCK P.218

Ass. Prof. A. Sionis, Dr. A. Ariza-Solé, Ass. Prof. J. Bañeras
8 - INTRA-ABDOMINAL HYPERTENSION P.225

Dr. E. Amestoy, Prof. Dr. M. L.N.G. Malbrain
9 - HAEMODYNAMICS DURING MECHANICAL VENTILATION P.235

Ass. Prof. C.L. Alviar, Assoc. Prof. S. Van Diepen
10 - HAEMODYNAMICS DURING MECHANICAL CIRCULATORY SUPPORT P.250

Prof. P. Vranckx
11 - CARDIAC ARREST AND POST-CARDIAC ARREST P.260

Prof. C. Hassager , Prof. J. Eifer Møller, Dr. J. Kjærgaard
THE FUTURE
1 - HAEMODYNAMIC MONITORING IN THE FUTURE P.267
Prof. M. Cecconi, Dr. A. Messina, Dr. F. Collino
APPENDIX
1 - ADJUNCTIVE TABLES, FIGURES AND SCORES P.277
Prof. Dr. F. Chacón-Lozsán, Assoc. Prof. K. Czerwińska-Jelonkiewicz
ABBREVIATIONS P.303
REFERENCES AND COPYRIGHT ACKNOWLEDGMENTS P.309
NOTES P.333
V
PART I
OVERVIEW OF
HAEMODYNAMIC
MONITORING
1 - CRUCIAL PARAMETERS AND SYSTEMS
FOR MONITORING IN THE ICU P.7
Prof. M.R. Pinsky, Prof. M. Hravnak
2 - INDICATIONS FOR HAEMODYNAMIC MONITORING P.15

Prof. J-L. Vincent
I.1
1 - CRUCIAL PARAMETERS AND

P.7 SYSTEMS FOR MONITORING IN THE ICU
Prof. Michael R. Pinsky, MD, FCCP, MCCM

Department of Critical Care Medicine
School of Medicine, University of Pittsburgh, Pittsburgh, PA USA
Prof. Marilyn Hravnak, RN, PhD, FAAN, MCCM

Department of Tertiary Care Nursing
School of Nursing, University of Pittsburgh, Pittsburgh, PA USA
Key messages
Haemodynamic monitoring is not one measure or monitor, but an array of
monitors that may be non-invasive, invasive, report their data intermittently
or continuously or create a fused parameter
The goals of monitoring vary with the condition, but include the early identi-
fication of cardiorespiratory insufficiency, aid in diagnosis of the insufficiency
etiology, guide titration of therapies, and identify when stability has recurred
In general, continuous monitoring measures, by describing trends and compi-
latory individual monitoring devices, are more informative than intermittent
and/or redundant measures
Monitoring will only improve patient outcomes when coupled to an actionable
therapy that itself improves outcomes
Thus, systems of monitoring and alerts need to be linked to selection of
effective treatment options
I.1
P.8
Introduction
Haemodynamic monitoring comprises a broad array of monitoring devices and analyses.

The physiologic data can be collected non-invasively or require intravascular catheteri-
zation. It can be collected and reported intermittently or continuously. The data can also
be viewed as physiologic waveforms or as discreate numeric values, and derived diffused
parameters can be displayed to be even more informative as to physiologic state. Table 1
lists the various monitoring parameters and devices that are available to supply that
information at the bedside.
I.1
Table 1 - List of various haemodynamic monitoring devices and

P.9 their associated parameters.
Monitor Invasive Intermittent

Physiologic measures
(brand name) or NI or Continuous
Heart rate, rhythm, ischemia,
Electrocardiogram
Non-invasive Continuous dynamic changes in stroke
(various)
volume
Capnography Continuous
Non-invasive etCO2, CO
(various) Intermittent
Automated blood
Non-invasive Intermittent SBP, DBP, MAP
pressure (Dynamat)
Pulse oximetry
Non-invasive Continuous SpO2, haemoglobin
(various)
Oximetry
plethysmographic den- Non-invasive Continuous PVI
sity waveform (Masimo)
Contractility, volume res-
ponsiveness (inferior vena cava
Transthoracic
diameter changes), volume sta-
echocardiography Non-invasive Intermittent
tus, tamponade, cor pulmonale,
(various)
valve function, fractional area
of contraction, VTI, CO
Finger
plethysmographic SBP, DPB, MAP, pulse rate,
Non-invasive Continuous
density waveform PPV, CO, SVV
(CNAP & Clearsight)
Arterial
Invasive Continuous SBP, DBP, MAP, PPV
catheterization
Arterial pulse contour
SPB, DBP, MAP, PPV, CO
analysis (PiCCO, LiDCO, Invasive Continuous
and SVV
FloTrac, MostCare)
Central venous Continuous/
Invasive CVP, ScvO2, PvCO2
catheterization Intermittent
Pulmonary artery CVP, ScvO2, PvCO2, PAP, SvO2,
Continuous/
catheterization Invasive CO, SVR, PVR, pulmonary artery
Intermittent
(Swan-Ganz catheter) occlusion pressure
Indicator dilution
Continuous/ CO, extravascular lung water,
cardiac output Invasive
Intermittent global cardiac volume
(PiCCO, Vigilio)
Esophageal doppler
Invasive Continuous VTI, stroke distance, FTc
(CardiaQ)
Contractility, volume responsive-
ness (superior vena caval
Transesophageal
diameter changes), volume sta-
echocardiography Invasive Intermittent
tus, tamponade, cor pulmonale,
(various)
valve function, fractional area of
contraction, VTI, CO
I.1
P.10
1.1 - Goals of haemodynamic monitoring
Although the goals of monitoring vary with the clinical scenario, usually monitoring is per-
formed to identify cardiorespiratory insufficiency and its presumed etiology, while hopefully
doing so early enough to minimize tissue hypoperfusion and end organ injury. Once identified,
monitoring is used to titrate therapies, such as bolus fluid and vasoactive drug infusions, and
to identify when stability has recurred. Importantly, haemodynamic monitoring on its own,
no matter how insightful its data will only be associated with improved patient outcomes if
used to guide therapies which themselves improve outcome. Thus, haemodynamic monito-
ring must be considered within the overall disease management spectrum and will be most
effective if simple treatments rapidly revise insufficiency, as is the case with fluid infusion in
hypovolemia or supplement oxygen for mild hypoxemic respiratory failure. Whereas it will be
less effective when the diagnosis of disease is questionable and when the goals of therapy
are unclear such as in the treatment of septic shock.
1.2 - Haemodynamic monitoring landscape

The routine measure of haemodynamic data is central to patient diagnosis. Routine measures
of heart rate, respiratory rate, temperature and blood pressure (by sphygmomanometer)
reflect the basic vital signs reported on all patients. However, any form of haemodynamic
monitoring can be acquired non-invasively or via invasive catheters usually placed intravas-
cularly, but also others. Commonly urinary catheters are placed to monitoring urine output
but also measure intra-abdominal pressure. Patients with potential intracranial processes
can have placed both intracranial catheters and sensor, though outside the scope of this
chapter. Similarly, the collected data can be displayed and reported intermittently or conti-
nuously. And the display rate for intermittent measures can span sampling frequencies of
once daily to as short as every 20 seconds. Continuous data display has the added advantage
of allowing richer featurization and trend monitoring. To the extent that data can be accura-
tely collected and continuously-displayed non-invasively, that method should be the default.
Presently, the invasive monitoring options, as listed above, require central venous, arterial
or pulmonary arterial catheterization. Each approach carries its own list of complications
and advantages. Central venous pressure can be used as a surrogate of right ventricular
reserve and, if it increases rapidly during fluid resuscitation, should be a stopping rule for that
infusion. However, central venous pressure poorly identifies either volume responsiveness
or blood volume. Mean arterial pressure is the input pressure to most tissues excepting the
heart, wherein diastolic pressure defines better the cardiac arterial input pressure. Systemic
I.1
P.11
systolic arterial pressure is a function of stroke volume, contractility and arterial resistance,
whereas diastolic pressure follows arterial vasomotor tone. Pulse pressure approximates
left ventricular stroke volume and the pulse pressure variation and stroke volume variation
during positive-pressure breathings quantifies the body’s ability to increase cardiac output if
venous return increases, known as volume responsiveness, while the ratio of pulse pressure
variation to stroke volume variation defined central arterial tone, called dynamic arterial
elastance. Recent advances in finger cuff plethysmography has permitted the continuous
display of the arterial pressure waveform non-invasively and the calculation of cardiac out-
put and both pulse pressure variation and stroke volume variation at the bedside. Thus, the
haemodynamic monitoring options available to the bedside clinician are evolving over time
and focus more now on continuous non-invasive monitoring options. Finally, pulse oximetry
plethysmography waveform analysis trends arterial pulse pressure variations, making the
bedside assessment of volume responsiveness readily available. Watch this space, since
the most novel advances in haemodynamic monitoring are occurring in the area of dynamic
continuous and non-invasive approaches to monitoring, and their integration into the overall
healthcare information network.
1.3 - Fused parameters and monitoring systems
As an aid to clinical decision making, haemodynamic monitoring is often used as a simple

alert wherein specific measured values exceed some threshold values, such as heart rate,
systolic blood pressure or SpO2. However, such population-based threshold alerts may to
too insensitive to accurately identify cardio-respiratory insufficiency early on. To improve
their predictive value, trend analysis of haemodynamic variables over time, or development
of derived parameters from existing variable displayed that have specific physiologic signi-
ficance can be displayed. For example, a falling SpO2 coupled with an increasing respiratory
rate suggests impending acute hypoxemic respiratory failure. The treatment of this abnor-
mal profile is less clear but may include improved tracheal secretion clearance, recruitment
maneuverers, supplemental inhaled oxygen, or non-invasive ventilation and continuous posi-
tive airway pressure. Similarly, dynamic parameters from the arterial pressure waveform
including diastolic, systolic and mean arterial pressure, pulse pressure and pulse pressure
variation, all give different but informative information. Examples of derived and fused parame-
ters that are informative of physiologic state are shown in Table 2.
I.1
P.12
Finally, since haemodynamic monitoring needs to have an actionable efferent limb to be use-
ful, bedside and hospital-based information systems utilizing these real-time haemodynamic
monitoring data and linked to the patient’s specific demographics represents the final layer
of support. This information gathering and processing systems linked to clinical decision sup-
port efferent limbs represent the next level of monitoring development and carry with them
the promise of more precise and specific alerts, while targeting specific caregivers across
a larger number of patients. Examples of such system-based approaches in haemodynamic
monitoring decision support structures are summarized in Table 3.
Of note, these predictive analytics vary based on the physiologic circumstance or event that
serves as the predictive endpoint (i.e. any instability, a specific unstable state such as sepsis
or shock, up-transfer, in-hospital mortality, etc.)
Table 2 - Summary of dynamic parameters and methods for functional hae-

modynamic monitoring.
Method Variable Threshold Limitations

Beat-to-beat
PPV Pulse pressure
>13%
SVV or stroke
volume
IVC Cannot be used in spontaneously breathing
Diameter >12%
Diameter patient, cardiac arrhythmias, low tidal
IJV volume/lung compliance. May be false
Diameter >18% positive in right heart failure
Diameter
Tidal
volume Delta PPV >3%
challenge
Cannot be used in spontaneously breathing
SVC
Diameter >36% patient, low tidal volume/lung compliance,
Diameter and requires TEE
Requires direct measurement of cardiac
PLR Test Cardiac output >10% output, may be affected by intra-abdominal
hypertension
Cannot be used in non-mechanically
EEO Test Cardiac output >5% ventilated patient or in patients who cannot
tolerate a 15s respiratory hold
Cannot be used to predict the change in
Eadyn PPV/SVV <1
MAP to inotropes
I.1
Titre ligne 1
P.13 Sous-titre ligne 1
Table 3 - Fused parameter critical illness scoring systems
System Timing Outcome Source Intent
General illness scoring systems
In-hospital Worst values: bedside Group severity of

APACHE IV Within 24h
death assessment + EHR illness
In-hospital Worst values: bedside Group severity of

SAPS 3 Within 24h
death assessment + EHR illness
In-hospital Bedside assessment Probability of

MPMO-III Within 1h
death + EHR in-hospital mortality
Organ dysfunction scores
In-hospital Bedside assessment Severity of organ

LODS Within 24h
death + EHR dysfunction
First Organ Bedside assessment Severity of organ

MODS
measure dysfunction + EHR dysfunction
Bedside assessment
SOFA Daily None Identify risk of death
+ EHR
qSOFA As needed None Bedside assessment Identify risk of sepsis
Early warning scores
VS as ICU
MEWS Bedside assessment Identify at risk
needed admission
Cardiac
VS as
CART arrest in Bedside assessment Identify arrest at risk
needed
48h
Death,
VS as arrest or Ward based escalation
NEWS Bedside assessment
needed ICU admit of care
in 24h
Need for
Rothman Bedside assessment
Continuous escalation Identify instability
Index + EHR
of care
I.1
Titre ligne 1
Sous-titre ligne 1 P.14
Variables Variable selection
34 Machine learning regression

1.4 - Summary
Haemodynamic monitoring is a very large

Unknown Logistic regression
umbrella covering a vast array of invasive
and non-invasive devices that give both pri-
6 organ
Expert opinion mary and derived variables which often allow
systems
for insightful monitoring of cardiorespiratory
6 Expert opinion insufficiency. Their use is highly wedded to
a solid understanding of cardiopulmonary
3 Machine learning regression physiology and the pathophysiologic signa-
tures of disease and the warning or reassuring
signs of deterioration and recovery, respec-
tively. A monitor will not save a life or prevent
6 Expert opinion untoward events, a skilled clinician will, but
monitoring can help.
Multiple Logistic regression

I.2
2 - INDICATIONS
P.15 FOR HAEMODYNAMIC MONITORING
Prof. Jean-Louis Vincent, MD, PhD, FCCM, FCCP

Department of Intensive Care, Erasme Hospital,
Université libre de Bruxelles, Brussels, Belgium
Key messages
Different patients will require different degrees and types of haemodynamic
monitoring and choices should be based on individual patient factors as well
as local device availability
Indications for haemodynamic monitoring can be considered as preventive
(or pre-emptive) diagnostic and therapeutic
Haemodynamic monitoring alone cannot improve outcomes but obtained
values need to be correctly interpreted and an effective therapy applied
Monitoring of individual variables is usually insufficient to provide an accurate
picture of an individual’s haemodynamic status. Multi-variable monitoring is
needed to optimally guide haemodynamic management
I.2
P.16
Introduction
The word ‘monitor’ is derived from the Latin word "monere", meaning "to warn".
Haemodynamic monitoring, of whatever type, provides the physician with an indication
of a patient's haemodynamic status. When monitored variables fall outside “normal”
ranges, this offers a warning that further assessment or a change in treatment may be
necessary. All critically ill patients need some form of haemodynamic monitoring, but
the degree and frequency of monitoring will vary according to their underlying condition
and ongoing status. In the acute stages of critical illness when haemodynamic variables
change rapidly and patients are requiring vasopressor or inotropic therapy, continuous
advanced, often invasive, monitoring will be necessary. Once the patient’s haemodynamic
status has improved and vasoactive agents weaned, less invasive and less continuous
monitoring may be adequate. Importantly, monitoring on its own is not a treatment and
there is no evidence that any form of monitoring improves outcomes. Only when the
measured variable is correctly interpreted and an effective therapy applied as a result
(the Measure, Interpret, Apply (MIA) rule) can monitoring be effective. Moreover, moni-
toring of individual variables is usually insufficient to provide an accurate picture of an
individual’s haemodynamic status and the combination of several variables is needed to
optimally guide haemodynamic management.
Here we will briefly consider some of the key indications for and roles of haemodynamic
monitoring in the critically ill patient population.
I.2
P.17
2.1 - Indications for haemodynamic monitoring
2.1.1 - Preemptive monitoring
Monitoring of at-risk patients can help identify a problem before it arises, enabling preven-
tive action to be taken. On the general floor, monitoring is generally limited to intermittent
measurements of simple physiologic variables, e.g., heart rate and blood pressure. Clearly,
it is not practical, affordable or necessary for all hospitalized patients to receive full, inva-
sive haemodynamic monitoring and decisions on how much and what type of monitoring is
necessary should be made on an individual patient basis, taking into account multiple fac-
tors including age, comorbid conditions, present diagnosis, clinical status and reason for
hospitalization. The key issue is how best to define the at-risk patient and to adapt moni-
toring choices accordingly. In the perioperative setting, "at risk" is generally considered to
indicate a higher risk of death and is often a subjective concept dependent on the presence
of a variety of conditions, including the complexity and likely duration of the surgical proce-
dure, the degree of urgency, the patient’s clinical status and comorbid burden, and older
age. Attempts have been made to create more objective scores of risk and in the operative
setting, the American Society of Anesthesiologists classification (ASA) grading scale is the
most widely used. As simple non-invasive systems become more widely available and more
accurate, preemptive monitoring will be used more extensively.
2.1.2 - Diagnostic monitoring
When a particular haemodynamic problem is already present, for example circulatory shock,
some types of monitoring can help elucidate underlying pathophysiological processes, to
diagnose particular conditions or to differentiate between several possible diagnoses, and
to help select appropriate initial therapy. For example, haemodynamic monitoring can help
distinguish between the four key types of shock - hypovolemic, distributive, cardiogenic and
obstructive. In distributive shock, cardiac output is usually elevated, compared to other forms
of shock. Central venous pressure is generally low in hypovolemic shock, but usually high in
cardiogenic and obstructive shock. In massive pulmonary embolism, pulmonary artery pres-
sure is increased and right-sided heart cavities are dilated. In cardiac tamponade, another
form of obstructive shock, right and left ventricles are small and intracardiac pressures are
high. Echography is particularly apt for initial evaluation as not only can it provide non-inva-
sive estimates of cardiac output and flow, but also important physical diagnostic information.
Nevertheless, echography is limited in that it cannot provide continuous values and requires
some training. In more complex cases, some form of invasive monitoring will be required.
I.2
P.18
2.1.3 - Monitoring to guide management
Monitoring is perhaps most widely used to guide treatment decisions and ongoing patient
management, notably in terms of intravenous fluids and vasoactive agents. Appropriate
monitoring can help determine whether preload, cardiac function (with inotropic agents)
or afterload should be modulated to improve tissue perfusion. Increasingly we are able to
monitor multiple haemodynamic variables on an almost continuous basis enabling trends
in values to be followed, supporting the need to increase or decrease treatment according
to the direction in which values are moving. Dynamic measures of fluid responsiveness or
the haemodynamic response to repeated fluid challenges can help guide ongoing fluid admi-
nistration, preventing the risks associated with both excess and insufficient fluid. Again, no
single variable is adequate to guide patient management and the combined evaluation of
several measures -multi-variable monitoring- is needed. For example, targeting a single MAP
value of 65 mmHg in all patients with shock may be beneficial in many, but this target could
be inadequately low in patients with pre-existing chronic hypertension or atherosclerosis
and unnecessarily high in fit, younger patients. Combining monitoring of MAP with measures
of organ dysfunction and tissue perfusion will help tailor haemodynamic therapy to each
individual situation. In the surgical setting, measurement of pre-operative "normal" values
of cardiac output or oxygen delivery in each patient may provide a useful guide to optimal
perioperative targets in that patient rather than relying on population-based estimates as
is currently the case.
2.2 - Different aspects of haemodynamic monitoring
There are many different settings where haemodynamic monitoring will be indicated but I will
divide these into two key areas, although clearly there is some overlap and the two comple-
ment each other: cardiac, where the heart is the prime concern and monitoring acts to help
assess cardiac function, and non-cardiac, where other organs are the focus of our monito-
ring, with the heart used as a pump to prevent or limit organ failure.
I.2
Titre ligne 1
2.2.1 - Cardiac aspects
Assessment of cardiac function can include multiple variables, but notably cardiac output,
for which various techniques -invasive, less-invasive, and non-invasive- are available. These
will be elaborated on in detail in other chapters. Knowing the exact cardiac output may not
help much, but the relationship between stroke volume and cardiac filling can inform better
about cardiac function (Figure 1). This application of the Frank-Starling function curve can
be evaluated by various monitoring systems.
Figure 1 - The relationship between stroke volume and cardiac filling.
The optimal method for each patient will depend on the underlying reason for monitoring car-
diac output. For example, in patients with circulatory shock associated with right ventricular
dysfunction, pulmonary artery hypertension or ARDS, invasive monitoring using indicator
dilution methods is indicated. In patients undergoing cardiac surgery, transesophageal echo-
cardiography is recommended although more invasive thermodilution methods may be needed
in some high risk patients. Pulse wave analysis techniques, such as stroke volume and pulse
pressure variation, are useful for assessment of fluid responsiveness in sedated patients.
I.2
P.20
2.2.2 - Non-cardiac aspects
The aim of haemodynamic resuscitation is to ensure adequate oxygen transport to the

tissues and thus limit the development of organ dysfunction. Although cardiac output is a
key determinant of oxygen delivery, whether or not a specific cardiac output is adequate
for the patient being monitored is dependent on multiple other factors (Figure 2). Cardiac
output cannot therefore be interpreted in isolation but requires assessment of other fac-
tors, including tissue perfusion and oxygenation. Blood lactate levels reflect altered cellular
metabolism and are associated with worse outcomes. Although blood lactate levels change
too slowly to be used to guide acute changes in vasoactive agents or fluids, persistently
raised blood lactate concentrations suggest that oxygen delivery is inadequate and that an
alternative diagnosis or therapy should be considered. Mixed (or central) venous oxygen
saturation (S(c)vO2) can also provide a valuable indication of an imbalance between oxygen
delivery and consumption (Figure 3). Although treatment targeting a specific S(c)vO2 value
in all patients is not associated with improved outcomes, in cases of persistent shock, S(c)
vO2 monitoring, perhaps combined with the veno-arterial PCO2 gradient (VAPCO2), can help
interpret the adequacy of oxygen delivery in septic shock.
Figure 2 - Factors influencing the interpretation of cardiac output.
From Vincent et al. Crit Care 2011;15: 229 (under a Creative Commons Attribution 4.0 International License).
I.2
P.21
Figure 3 - Interpretation of mixed venous oxygen saturation

Panel A: low ScvO2 - Panel B: high SvO2
2.3 - Conclusion
Many haemodynamic variables can be measured and monitored using different monitoring
devices, with an increasing move towards less invasive approaches. The type of monitoring
required will vary between patients, and in the same patient as their haemodynamic status
improves or worsens. As such, haemodynamic monitoring choices should be individualized
and reassessed during the course of disease.
PART II
TECHNIQUES FOR
HAEMODYNAMIC
MONITORING
1 - INVASIVE HAEMODYNAMIC MONITORING P.23
Prof. A. Rudiger, Dr. J. Stuby, Dr. P. Jorge Pérez,
Dr. B. Darias-Delbey
2 - NON-INVASIVE HAEMODYNAMIC MONITORING P.41

Prof. J. Masip, Prof. C. Muëller, Prof. E. Gayat, Dr. J. Joachim,
Prof. D. Zahger, Dr. K. Orvin, Dr. J. Mesquida, Dr. E. Cortés,
X. García Nogales, Prof. S. Price, Prof. J. Čelutkienė,
Dr. G. Balčiūnaitė, Dr. D. Zakarkaitė, Assoc. Prof. E. Platz,
Prof. R.M. Vicho
3 - PRELOAD RESPONSIVENESS P.125

Prof. J-L. Teboul, Dr. R. Shi, Prof. X. Monnet
II.1
1 -INVASIVE
P.23 HAEMODYNAMIC MONITORING
1.1 - Intravascular access
Prof. Alain Rudiger, MD, FESC

Department of Medicine, Spital Limmattal, Schlieren, Switzerland
Dr. Johann Stuby, MD

Department of Medicine, Spital Limmattal, Schlieren, Switzerland
Key messages
Ultrasound guidance increases safety and efficiency and is therefore sug-

gested as the method of choice for any kind of vascular cannulation
Central venous catheters allow the assessment of CVP and ScvO2, surro-
gates of volume status and CO
Peripheral arterial catheters are used for continuous monitoring of blood
pressure in patients with haemodynamic instability and allow the perfor-
mance of ABGA
The PAC enables the gold standard measurement of cardiac output and
remains frequently used for assessment of patients with severe heart fai-
lure, cardiogenic shock and pulmonary hypertension
The PiCCO catheter is an alternative to measure stroke volume and cardiac
output. It enables the measurement of a wide array of parameters of pre-
load, lung function and cardiac performance
II.1
P.24
Introduction
Vascular access is a basic procedure in patients with AHF and allows the withdrawal of
blood for laboratory analysis, the measurements of physiologic parameters (Table 1) and
the administration of drugs. Traditional techniques to assist the cannulations of veins
(peripheral venous access, central venous access, pulmonary artery catheter) and arteries
are location of anatomic landmarks and palpation of the vessels. An alternative approach
is the utilisation of an ultrasound device.
II.1
P.25
1.1.1 - Ultrasound guidance
Ultrasound guidance increases safety and efficiency of vascular access procedures and is
therefore suggested as the method of choice for any kind of vascular cannulation. It can
increase the success rate, shorten the time of the procedure, reduce the number of puncture
attempts and minimize complications. Furthermore, it can be useful to detect immediate
and life-threatening complications of punctuations, such as inadvertent arterial puncture,
bleeding, or pneumothorax.
1.1.2 - Venous access
Peripheral venous access

Peripheral venous accesses are a simple and inexpensive way for short-term intravenous
therapy. Typical locations of insertion are veins of hand or forearm. Short cannulas with a
large diameter are best for the rapid infusion of large volumes of fluids, for example in the
case of bleeding. The problem with the administration of short-acting vasoactive drugs is that
an obstruction of the canular or the vein (e.g. by arm displacement) can lead to unintended
haemodynamic alterations. The incidence of local (thrombophlebitis) and systemic (blood
stream infection) complications associated with peripheral venous catheters is low (Table 2).
Central venous access

A central venous access is required for the safe and continuous administration of short-acting
positive inotropic drugs, vasopressors or vasodilators. It also allows the administration of
substances that commonly irritate peripheral veins, such as intravenous potassium supple-
mentation. Furthermore, it allows haemodynamic monitoring and frequent blood sampling.
Central venous accesses can be divided in PICC and centrally inserted catheters. For periphe-
ral insertion, commonly used veins include the cephalic, basilic and brachial veins. Centrally
inserted catheters are preferably located in the internal jugular vein. Alternatives are the
subclavian and femoral veins. Complications include arterial puncture, hematoma, nerve
injury and infections. Centrally inserted catheters carry the additional risk of pneumotho-
rax and hemothorax (Table 2).
Central venous catheters allow the measurement of CVP and ScvO2. While decreased CVP (nor-
mal range of 5-7mmHg) may indicate hypovolemia, CVP increases in patients with hypervolemia,
right heart failure or pericardial tamponade. ScvO2 is often used as a surrogate for SvO2, the
percentage of saturated Hb in the pulmonary artery. Decreased values are a sensitive marker of
reduced CO, but SvO2 also falls in cases of hypoxemia, anemia and increased oxygen expenditure.
II.1
P.26
Pulmonary artery catheter

The PAC, also known as Swan-Ganz catheter, has long been the cornerstone for haemo-
dynamic monitoring of critically ill patients. Despite the controversy about its safety and
efficacy, it remains frequently used for the assessment of patients with severe HF, CS and
pulmonary hypertension.
PACs are inserted in the jugular, subclavian or femoral vein and then advanced towards the
pulmonary vasculature using waveforms to track the catheters tip.
Next to complications similar to central catheter placement (pneumothorax and hemothorax,

infection, air embolism), the Swan-Ganz catheter can lead to arrhythmias, valve injury, myo-
cardium perforation and pulmonary artery rupture (Table 2). Further potential risk includes
erroneous measurement of haemodynamic parameter and the misinterpretation of results.
Insertion of a PACs allows the measurements of CVP, RA pressure, RV pressure, MPAP, pul-
monary artery occlusion or wedge pressure and SvO2. PCWP gives an indirect assessment
of left sided filling pressures. It increases in HF and can therefore help to differentiate from
other shock forms. Reduced CO leads to a decreased mixed venous oxygen saturation due
to a prolonged transit time of blood in the periphery. A sudden SvO2 increase of ≥5% in
the right-sided heart chambers during the insertion of the PAC indicates the presence of
a ventricular septum defect. The various saturations allow the calculation of the degree of
left-to-right shunting (Qp/Qs, pulmonary-systemic shunt ratio). Importantly, PAC enables
the gold standard measurement of CO and its derived parameters, such as oxygen delivery,
cardiac power or pulmonary vascular resistance.
1.1.3 - Arterial access
Peripheral arterial access

Peripheral arterial catheters are routinely used for continuous monitoring of BP in patients with
haemodynamic instability, which facilitates the titration of vasoactive medication. The morpho-
logy of the curve gives information on underlying cardiovascular disorders: A flat increase of the
upstroke curve suggests an impaired contractility, a small area under the arterial curve a low
SV, a big difference between systolic and diastolic pressure (PP) aortic valve insufficiency, and
a low diastolic pressure can be a sign of vasoplegia. In patients with respiratory insufficiency,
information about the gas exchange can be obtained by performing an ABG analysis, in parti-
cular by measuring the partial pressures of arterial oxygen and arterial carbon dioxide. ABG
machines usually also provide other valuable parameters such as potassium or lactate levels.
II.1
P.27
Peripheral arterial lines are inserted into the radial, or femoral artery and, in selected patients,
in the brachial or axillary artery. Radial access is frequently chosen due to the dual arterial
supply of the hand (radial and ulnar artery), easy access and low complication rate.
Possible complications of arterial access include occlusion of the artery, vascular dissec-
tions, formation of pseudoaneurysm, bleeding and infection (Table 2).
1.1.4 - PiCCO catheters
The PiCCO catheter is an alternative to the PAC to measure stroke volume and cardiac
output. It requires the placement of an arterial line and a central venous catheter. CO mea-
surements derived by PiCCO catheter correlate with values obtained by PAC. When the
insertion of a 5 French catheter into the femoral artery is contraindicated (e.g. after femo-
ral artery surgery), a smaller 4 French catheter can be inserted in the brachial artery. By
combining trans-cardiopulmonary thermodilution with pulse contour analysis, a wide array
of parameters of preload (GEDV, SVV), lung function (EVLW) and cardiac performance (CFI,
GEF) can be assessed. Low CFI and GEF identify cardiac dysfunction in patients with acute
heart failure. The complications of PiCCO catheter correspond to those of the insertion of
an arterial line and of a central venous catheter. Arrhythmia, in particular atrial fibrillation,
makes parameters of the pulse contour analysis such as SVV invalid.
Table 1 - Useful haemodynamic parameters derived from vascular lines
Vascular access Parameters Interpretation
Peripheral venous Lactate concentration If lactate >2mmol/l, perform arterial mea-

catheter in venous blood surement and look for (cardiogenic) shock
SvO2 If SvO2 <60% look for (cardiogenic) shock
Central venous
catheter A low CVP may indicate hypovolemia
CVP A rising / high CVP may indicate fluid over-
load, RV failure or pericardial tamponade
II.1
P.28
A MPAP >25mmHg indicates pulmonary

MPAP
hypertension
A low PAOP may indicate hypovolemia

PAOP, wedge pressure A PAOP >20mmHg may lead to hydrostatic
pulmonary edema
DPAP – PAOP (norm <7mmHg) or MPAP –

PAOP (norm <14mmHg)
Trans-pulmonary
Normal values indicate post-capillary pul-
pressure
monary hypertension, elevated values
pre-capillary pulmonary hypertension
A CI <2.2l/min/m2 indicates low cardiac out-

put. In combination with organ dysfunction
CI
Pulmonary artery and/or hyperlactatemia, it indicates car-
catheter diogenic shock
DO2 = CO x CaO2 x 10
(CaO2 = (Hb x 1.39 x

SaO2) + (PaO2 x 0.003))
A low cardiac power is associated with poor

CP = CO x MAP/451
prognosis
PVR = 80 x (MPAP
– PAOP)/CO
Degree of left to right shunting (calculation

Qp/Qs
with the Fick principle)
II.1
P.29
MAP
An impaired pressure acceleration indicates

low contractility
Pulse curve
Irregular curves occur in arrhythmia, parti-
cularly atrial fibrillation
A high SVV predicts an increase in stroke

SVV
volume in response to a fluid bolus
If lactate >2mmol/l, look for (cardiogenic)

Arterial lines Lactate
shock
Information on insufficient oxygenation and

pO2, pCO2, SaO2
ventilation, e.g., in pulmonary edema
GEDV = ITTV – PTV =

A low GEDV indicates low preload
CO x (MTt – DSt)
EVLW = ITTV – ITBV Values >10 indicate pulmonary edema
CFI = (CO/GEDV) x 103 A CFI < 4.5/l indicates cardiac dysfunction

II.1
P.30
Table 2 - Risks of vascular access
Vascular access Risks Risk rates
Infection
Peripheral venous access (rate per 1000 0.2 to 0.7
catheter-days)
Infection Internal jugular vein 8.6

(rate per 1000 Subclavian vein 4
Central venous catheter
catheter-days) Femoral vein 15.3
(including sheath for pulmonary
artery catheter)
Pneumothorax <0.1 to 3.1%
Injury (%)
Arterial puncture 0.5 to 6.25%
Infection Similar to central venous lines
Vascular injury
Injury Right heart perforation
Tricuspid valve lesion
Arrhythmia
Misinterpretation of
results
Radial artery 0.1 to 0.4%

Femoral artery 0.8 to 2.2%
Infection Radial 0.72%
Femoral artery 0.78%
Arterial line
Axillary artery 2.24%
Vascular injury
Injury
Limb ischemia 0.09 - 0.20 %
II.1
P.31
Figure 1 - Ultrasound Guidance for Vascular Access

In panel A, the ultrasound probe is aligned parallel to the vessel (longitudinal axis, "in-plane"). This brings the advantage
of visualizing the entire shaft of the needle, including the tip. In panel B the ultrasound probe is placed perpendicular to
the vessel (short axis , "out-of-plane"). This brings the risk that the depth of the needle is underestimated, as the depicted
structure may be shaft and not tip.
From Moore CL, Copel JA. Point-of-Care Ultrasonography. New England Journal of Medicine. 2011;364(8):749-57.
II.1
1.2 - Essential invasive and less-invasive

calibrated techniques (PAC or two catheters) P.32
Dr. Pablo Jorge Pérez, MD

Acute Cardiovascular Care Unit,
Canary Islands University Hospital, Tenerife, Spain
Dr. Beneharo Darias-Delbey, MD

Cardiovascular Anesthesiology, and Reanimation,
Canary Islands University Hospital, Tenerife, Spain
Key messages
Haemodynamic monitoring in the cardiovascular critical care setting should be

personalized and patient-centered in order to make appropriate therapeutic
decisions. Haemodynamic monitoring may help in optimize cardiovascular sys-
tem according to three main goals: Identifying the haemodynamic alteration,
essentially the type of shock / Selecting the best therapeutic intervention /
Evaluating response to therapy
The choice of the appropriate haemodynamic monitoring may differ depen-
ding on the phase and complexity of the scenario, the response to the initial
therapy, and also the expertise of the therapeutic team
In cardiovascular haemodynamically unstable patients, calibrated devices
such as PAC or PWA are preferred
Calibrated PWA have been demonstrated reliable in critically ill patients
PAC still plays a key role but users must be aware in the interpretation and
patient-selection, and be familiar with the pitfalls, risk of misinterpretation
and potential complications
Transpulmonary thermodilution devices should be reserved for patients with
shock and acute respiratory distress syndrome while PAC should be reserved
for patients with refractory shock and right ventricular dysfunction
II.1
P.33
Introduction
Haemodynamic monitoring plays a key role in critical care and perioperative management
of the cardiovascular patient. Over the last years haemodynamic monitoring techniques
have evolved from intermittent toward continuous and real-time measurements, from
invasive toward less-invasive approaches and also differ in terms of number and nature of
the provided haemodynamic variables without losing accuracy and precision. The acquired
knowledge allows a better case-selection in an environment where patients are increa-
singly complex.
Advanced haemodynamic monitoring is recommended to be used in patients with shock

who do not respond to the initial therapy and/or in complex conditions. The choice of
the appropriate haemodynamic monitoring may differ depending on the type, phase and
complexity of shock, and the response to the initial therapy. Transpulmonary thermodi-
lution devices should be reserved for patients with shock and acute respiratory distress
syndrome while PAC should be reserved for patients with refractory shock and right
ventricular dysfunction.
II.1
P.34
1.2.1 - Techniques with calibrated CO
Pulmonary artery flow-directed catheter

PACs have been used for haemodynamic monitoring in cardiac, medical, and surgical ICUs
since the 1970s and still remains the gold standard for measuring CO. The use of PACs has
decreased after the advent of new reliable less invasive techniques, the lack of evidence of
benefit in some studies and the complications associated with its routine use in the last years.
In the recent years, first evaluation of cardiogenic shock patient suggests the combination
of cardiac and lung ultrasound, lactate quantification, and haemodynamic parameters such
as CVP, ScvO2 and CO to guide the initial shock resuscitation.
In the setting of profound circulatory shock or refractory to the initial treatment, especially
those with RV dysfunction, ARDS, high-risk patients undergoing cardiac surgery, or com-
plex circulatory conditions, PAC is the prefer option. In this setting, knowing PAP, PAOP,
oxygenation parameters, or estimation of pulmonary vascular resistance, might be useful
for identifying the main disorders and for therapeutic decision-making.
The PAC provides information on important haemodynamic variables (RAP, PAP, PAOP and
CO. Tissue perfusion variables like SvO2, oxygen utilization, oxygen delivery, oxygen extrac-
tion and PvCO2). CO can be measured intermittently according to the thermodilution principle
after cold bolus injections. Continuous PAC monitoring also provide PVR and RV volumes
estimation.
PAC provides real-time monitoring of CO allowing to track short-term changes in CO com-

paring with discontinuous CO measurement. The major limitations are related to invasive
technique and vascular access complications.
PAC is typically placed at the bedside usually through the internal jugular vein. Between
11 cm and 15 cm, the balloon is inflated and the catheter advanced. PAC should always be
fully inflated during catheter advancement, and fully deflated during catheter withdrawal.
II.1
P.35
Figure 1 - PAC curve monitoring

RA pressure wave forms: “a,” occurs during RA systole; “c” wave: tricuspid valve into RA during RV isovolumic systole; “v,”
occurs during the end of RV systole. In atrial fibrillation, “a” waves are absent; “x” atrial relaxation; “y” descent, occurs
during RV rapid filling.
Wedge position can be verified by withdrawing blood with the balloon inflated for determi-
nation of oxygen saturation. If the catheter is in proper wedge position, withdrawn blood will
be “arterialized” with an oxygen saturation of 95% or higher. There may be considerable
inaccuracy in proper measurement of PCWP.
II.1
P.36
Table 1 - PAC, tips and tricks
Reasonable approach and safety use of PAC Results
Appropriate patient selection and clinical scenario Greater benefit
Understand potential pitfalls and complications Safety and higher benefit
Optimize procedural insertion by experienced staff Safety
Safety and lower

Use as long as necessary
infection-risk
Increases accuracy and

Correlate with other parameters (Lactate; SvO2, ultrasound) goal-directed therapies
selection
Greater benefit and

Follow trends, not absolute parameters
accuracy
Expertise in handling and interpreting haemodynamic monitoring Greater benefit, higher

data efficiency
Research and analyze your results Future improvement
TPTD and cPWA
by Temperature: PiCCO and VOLUME-VIEW
by Lithium injection: LiDCO
cPWA devices allow to calculate SV and CO beat by beat, through the analysis of the sys-
tolic portion of the arterial wave, but requires assuming certain parameters of the arterial
system, such as compliance or impedance. These systems assume the premise that there
is a proportional and predictable relationship between the BP and the SV. However, in those
situations in which the assumed parameters change, as in circulatory shock, this relationship
is no longer proportional and loses reliability. Calibrated systems, both by TPTD, such as
PiCCO or VolumeView systems, or by indicator substances, such as the LiDCO system, using
lithium, allow a reliable assessment of CO in critically ill patients, in which the pressure-vo-
lume that determines a PA for a given SV is altered.
II.1
P.37
Device calibration
The TPTD is based on the Stewart-Hamilton principle for CO measurement. Cold saline soil
(15 ml at 8 degrees) is injected through a central venous access and blood temperature is
measured in the femoral artery.
TPLD is based on lithium-bolus injection through a central or peripheral venous access, which
by means of an ion-selective electrode placed in an arterial, central or peripheral catheter,
allows the indicator concentration-time curve assessment. The Nernst equation relates the
voltage across the membrane to the plasma lithium concentration.
Initial calibration is mandatory and frequent recalibrations are often needed, especially when
clinical conditions change. The quality of the pulse wave signal determines the reliability of
the SV measurement, since the damping modifies the waveform, and thus the estimation
of the SV.
cPWA haemodynamic parameters

In addition to the parameters can be obtained with uncalibrated PWA systems (Continuous
CO, Stroke volume variation (SVV) o Pulse Pressure Variation (PPV), the cPWA system can
measure:
Intermittent CO
EVLWI: Normal Value: < 10 ml/kg. It is a quantitative index of the amount of fluid in
the lung parenchyma
PVPI: Normal value 1-3. It is obtained from the ratio between EVLW and pulmonary
blood volume, and is a useful test for the differential diagnosis of hydrostatic pulmonary
edema (2-2.5) and pulmonary edema by increased permeability (inflammatory) (>3)
GEDVI: Normal value: 680-800 ml/m2. It is a reliable parameter to estimate the

cardiac preload
ITBVI, Normal value: 850-1000 ml/m2: It is obtained from GEDVI plus pulmonary
blood volume and it is a cardiac preload parameter
CFI: Normal value 4.5-6.5 min-1. It is the ratio of CO to GEDVI, and allow cardiac
contractility estimation
II.1
Table 2 - Advantages and limitations of the invasive P.38

haemodynamic monitoring techniques
Advantages Limitations
1. Require periodic external calibration

and it must be exhaustive (injection
volume, circuit leaks control, fluid tempe-
1. Reliable method for critically ill
rature, infusion rate).
patients.
2. In addition to central venous access,
2. Does not need PA catheterization,
requires percutaneous central arterial
avoiding the risk of PA rupture, pulmo-
access (femoral artery).
nary embolism and other complications.
3. The cannulation of a femoral artery can
3. TPTD mainly measures left heart
be contraindicated in patients with severe
TPTD output.
peripheral vascular disease.
4. Successive measurements can be
4. Femoral artery cannulation may
obtained without significant interference
increase risk of infection.
from recirculated indicator.
5. Can be distorted with thermal varia-
5. Continuous measurement of BP, CO,
tions, intracardiac shunt or extrarenal
PPV and SVV.
depuration techniques.
6. It can assess GEDV, ELVWI and PVPI
6. It cannot measure mixed venous
oxygen saturation, PA pressures, or PA
occlusion pressure.
1. Require periodic external calibration,

and it must be exhaustive (injection
volume, circuit leaks control, fluid tempe-
rature, infusion rate).
2. Limited in patients who are receiving
lithium therapy.
3. It cannot measure mixed venous
oxygen saturation, PA pressures, or PA
1. Reliable method for critical ill patients.
occlusion pressure.
2. It does not need a central vascular
4. The number of measurements over
TPLD access.
a short period is limited because of a
3. Continuous measurement of BP, CO,
potential accumulation of lithium
PPV and SVV.
5. Patients in the first trimester of pre-
gnancy and patients who are < 40 kg in
weight are contraindicated
6. Certain muscle relaxant can produce
inaccurate measurement.
7. Can be distorted by thermal variations,
intracardiac shunt or extrarenal depura-
tion techniques.
II.1
P.39
1.2.2 -Practical approach of these techniques
Table 3 - Device comparaison
Reliability in ICU
Device Invasiveness
patients
Pulmonary artery catheter Yes High
Transpulmonary thermodilution system Yes High
Uncalibrated arterial pulse contour analysis Yes Low
Noninvasive arterial pulse contour analysis No Low
Echocardiography No High
Esophageal Doppler Low/no Low
Figure 2 - Algorithm for haemodynamic monitoring
FIRST HEMODYNAMIC ARDS

ASSESSMENT RV dysfunction
(early approach) Early profound shock
SHOCK Refractory shock
(any type of Arterial catheter
shock) Echocardiography and LUS
CVP Responsive to
Lactate goal-directed
PacO2-PvCO2 ratio therapies
II.1
P.40
Provide more
Real-time CO Frequent
Set up variables than
monitoring calibration
CO
++ - +++ +
+ +++ +++ +++
++ +++ + +++
+++ +++ + ++
+
+++ + ++
(user dependent)
++ +++ + +
PAC:
-Semicontinuous or continuous CO
measurement
-PAP/PCWP
-PVR
-SvO2
ADVANCED -RV volumes
HEMODYNAMIC
NO MONITORING
Transpulmonary dilution devices:
-Intermitent (Calibration) or Continuous CO
measurement
YES Considered -SVV/PVV
uncalibrated PWA
*Thermodilution : ELWI, GEDV, PVPI, CFI
II.2
2 -NON-INVASIVE
P.41 HAEMODYNAMIC MONITORING
2.1 - Basic essential non-invasive monitoring

Intensive Care Department, Consorci Sanitari Integral,
Prof. Christian Muëller, MD, PhD, FESC

Cardiovascular Research Institute Basel,
Department of Cardiology, University Hospital, Switzerland
Physical examination often provides essential insights regarding the haemodynamic and
cardiorespiratory condition of a patient. It is therefore also the first step when facing critical
patients. Inspection of the conscious state, the respiratory rate and the depth of respira-
tions, respiratory distress, cyanosis of the lips and/or extremities, icteric sclera, the colour
of the skin, the filling of the jugular veins, oedemas or livedo reticularis, provide valuable
information. Palpation may allow to assess pulse pressure, the skin temperature and peri-
pheral capillary refilling, as simple surrogates for the quality of the peripheral circulation. It
may also allow to detect some painful, hot or oedematous zones of the body as expression
of inflammation or congestion. Auscultation will provide additional clues by assessing heart
rhythm, valvular dysfunction, pericardial rub, bowel sounds, as well as signs of pulmonary
congestion, consolidation, hypoventilation, bronchospasm or pleural effusion.
Monitoring devices, most of them portable, provide more objective, quantitative, continuous,
and reproduceable assessment of several vital parameters. Basic, standard or essential
non-invasive monitoring parameters provided by these devices are:
Continuous (automatic) Intermittent (automatic)

- ECG (at least one lead) to visualize heart
rhythm and QRS form
- Heart rate
- Blood pressure non-invasively
- Oxygen saturation by pulse-oximetry (SpO2),
usually showing pulse pressure curve
- RR
II.2
P.42
This basic equipment allows a close control of the patients’ condition in the majority of sce-
narios and can be implemented in less than one minute. Therefore, most bedside monitor
devices are equipped with these parameters (Figure 1).
Figure 1. Example of basic non-invasive monitoring
The data displayed in the majority of commercially available monitoring devices has been
demonstrated to be accurate and reliable, though the measurement of RR is less consistent
when is based on chest respiratory movements, but improves when is based on specific airway
sensors. Alternatively, these devices can be complemented with the manual registry of:
Body temperature
Urinary output
Insertion of a urinary catheter to enable the monitoring of urinary output is often the first
semi-invasive measure to assess renal function as a surrogate for the perfusion of critical
organs. These seven items may be considered the essential basic non-invasive monitoring in
clinical practice. It is important to highlight that in many critically ill patients, this essential
basic non-invasive monitoring is sufficient. Although new technology has been developed
to registry continuously BP and other haemodynamic parameters from plethysmography
or other methods, their higher cost and less validation have limited their extension as first
line basic monitoring.
II.2
P.43
In cases of more severe clinical presentation, like initial phases of shock or severe respiratory
failure, the basic non-invasive monitoring should be extended to minimally invasive haemo-
dynamic monitoring, just with the insertion of an arterial and/or a central venous catheter.
These catheters provide the following continuous parameters:
Invasive BP measurement
Central venous pressure
The addition of these parameters allows a more accurate control of the haemodynamic
state and also provides the possibility to obtain direct blood samples for analysis and calcu-
lations (i.e. ScvO2 or PaCO2-PvCO2). CVP was initially measured intermittently in "cmH2O"
by connecting the end of a central venous catheter to a water column, but currently, it is
measured in "mmHg" through electrical transducers. Indeed, these two catheters (central
venous and arterial line) are often complemented with some other non-invasive or minimally
invasive techniques to measure CO and fluid distribution (non-calibrated pulse-pressure, dop-
pler devices, bioimpedance, etc.) providing a better approach to the haemodynamic state.
Likewise, echocardiography, and more recently, LUS and other ultrasound techniques, have
emerged as essential tools in the management of critical patients, allowing non-continuous
haemodynamic calculations, but more limited by the expertise of the operator. All of these
non-invasive techniques are deeply covered in the next chapters of this handbook.
In intensive care units, however, there are patients that require advanced invasive haemodyna-
mic monitoring with the direct measurement of intracavitary pressures, CO by thermodilution
and derived calculations, fluid distribution, systemic flow or body oxygenation indices. This
information is usually obtained with PAC catheters or calibrated pulse contour analysis, which
have been broadly validated. This invasive monitoring approach is often complemented with
the study of microcirculation and organ perfusion with different devices.
In recent years many applications, programs and electronic devices, have been implemented
through telemetry, mobile interface, and other online internet connexions, to provide remote
information about several physiological parameters like BP, HR, body weight, SpO2, level of
exercise, and even, in patients wearing pacemaker-ICD, some cardiovascular intrathoracic
pressures. In subacute conditions, these technologies, managed directly by the patients,
are changing the paradigm of monitoring in a more personalised and interactive way, being
extremely useful to anticipate complications or further decompensations of several diseases.
II.2
2.2 - Assessment of cardiac output

and perfusion P.44
2.2.1 -Minimally invasive (non-calibrated) assessment of CO
Prof. Etienne Gayat, MD, PhD

Department of Anesthesiology and Critical Care,
Hôpital Lariboisière, AP-HP Nord, Paris, France
Dr. Jona Joachim, MD

Department of Anesthesiology and Critical Care,
Hôpital Lariboisière, AP-HP Nord, Paris, France
Key messages
Three methods are currently available to obtain minimally invasive assess-

ment of cardiac output: the partial CO2-rebreathing analysis, the pulse wave
analysis and the transesophageal Doppler
All those methods have the main advantage to be less invasive than PAC.
The level of validation of those minimally invasive assessment is heterogeneous.
The major limitation of those method is the lack of validation in the most
severely ill patients.
II.2
P.45
Introduction
Three methods are currently available to obtain minimally invasive assessment of CO:
the partial CO2-rebreathing analysis, the pulse wave analysis and the transesophageal
Doppler. The Table 1 describes the physiological background supporting the use of these
three minimally invasive methods of measure of CO.
II.2
P.46
Partial CO2-rebreathing
The principle, advantages and limits of this method are described in Table 1. This system is
using a CO2 rebreathing system that allows to estimate CvCO2. CaCO2 can be approximated
by the change in EtCO2 during the rebreathing. Then, using the Fick’s principle, the CO can
be estimated. Only one commercially available device using this method is available (NICO
System, Novametrix Medical Systems). NICO has been validated against thermodilution
using PAC and esophageal Doppler with mixed results. The highest level of validation was
observed in cardiac surgery.
PWA
Calculating SV from the contour of the arterial pressure curve was first described by Otto
Frank in 1899. Since then, several algorithms have been proposed to determine CO based on
determination of systolic area by analysis of the contour of the pulse wave (Table 1). In most
cases, these signals are obtained from an arterial line. Table 2 is summarizing the principles
algorithms: some make a comparison with a closed hydraulic or electric circuit, such as the
Windkessel concept, while others analyse the area under the systolic portion of the arterial
pressure waveform. More recently, an additional algorithm has described, the PRAM, which
is based on a statistical analysis of pulse waveform characteristics combined with biome-
tric parameters, and an estimate of regional aortic compliance for each patient. Algorithm
validity has been verified in a variety of patients and circumstances, but performance could
be compromised in the presence of haemodynamic instability, cardiac arrhythmias, or other
factors that disturb the arterial pressure waveform, particularly during vasopressor use. To
increase the reliability of PWA, some commercial systems have calibrated their algorithms
(Figure 1). The methods used to calibrate can be thermodilution, lithium-dilution (addressed
in other chapters) or transesophageal Doppler.
II.2
P.47
Table 1 - Measurement principle, advantages and limitations

of the 3 main minimally invasive methods of CO measurement
Principles Method of measure
Partial CO2-rebreathing
PWA
Transesophageal Doppler
II.2
P.48
Explanation Advantages and limits
This method applies Ficks' principle, using

expired carbon dioxide (CO2) concentration.
Advantages:
Venous CO2 (VCO2) can be calculated from the
- Continuous assessment of CO
difference between inspired and expired gases.
- Less invasive than pulmonary artery catheter
The system used an extra loop of ventilatory
Limits:
circuit to create a transient partial CO2 rebrea-
- Need for endotracheal intubation and
thing, thus increasing the etCO2. The CO is
artificial ventilation
estimated from the ratio between the variation
- Affected by pulmonary shunt level
of VCO2 and of etCO2 during the rebreathing
period.
Advantages:
- Less invasive than PAC
PWA is based on the hypothesis that the wave-
- Continuous assessment of CO
form of BP is directly related to the variation in
Limits:
the SV. SV is proportional to the area under the
- Limitation with vasopressors use and
systolic portion (Asys) and inversely proportio-
severely unstable patients
nal to impedance (Z(t)).
- Impact of aortic valvular disease and of
severe cardiac arrythmia
Advantages:
- No need for arterial or central line
Using a probe inserted into the esophagus, - Continuous assessment of CO
blood velocity is measured in the descending - Still valid in case of cardiac arrythmia
aorta. The VTI is measured using continuous Limits:
wave Doppler. The diameter (D) of the des- - Instability of the signal
cending aorta is estimated using patients' - Need training to use properly
anthropometric data. Finally, the SV is extrapo- - Estimation of the SV based on assumptions
lated from the volume in the descending aorta. (fixed aortic diameter and fixed repartition
of flow between supra-aortic trunks and
descending aorta
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P.49
Transesophageal Doppler
The principle, advantages and limits of this method are described in Table 1. Using Doppler
to estimate stroke volume consists in measuring the blood velocity through a hole whose
diameter can be measured or estimated. Then, the VTI is the distance travelled by the blood
column during systole. As soon as the diameter by which this column passes is known, the
area can be estimated. The VTI multiplied by this area gives the volume of blood circulating.
Dedicated devices have been developed, allowing continuous CO monitoring using this method.
Small ultrasound probe inserted into the esophagus through the nose or mouth to measure
blood velocity in the descending aorta have been developed. Two major assumptions are
underlying CO estimation using this technique:
The repartition of the blood flow between supra-aortic trunks and the descending aorta
The diameter of the aorta is not measured but estimated based on anthropometric
data and is fixed
Of note, SV could also be measured using TEE according to the same principle. During TEE,
based on the deep transgastric incidence, velocity inside the LVOT can be measured using
Doppler, as the diameter of the LVOT. Although TEE offers the possibility to detect anato-
mical abnormalities, to assess volume status, myocardial contractility and other functional
parameters, this is not a continuous monitoring solution.
Table 2 - Different Name of the algorithm Formulae

algorithm of pulse
Windkessel K1x(SAP-DAP)xHR
wave analysis to
estimated stroke Windkessel with RC decay K2x(MAPxHR/60)xln(SAP/DAP)
volume
Liljestrand-Zander K3x[(SAP-DAP)xHR]/(SAP+DAP)
Asys: area under the systolic
2
arterial pressure curve; Pressure root-mean-square K4x (SBP-MAP) xHR
Tsys: duration of systole
(estimated as 30% of cardiac Herd K5x(MAP-DBP)
cycle time);
k: calibration factor; Systolic area K6xHRxAsys
T: duration of cardiac cycle
(T √HR/60);
Systolic area with correction K7xHRxAsysx(1+Ts/Td)
Tdia: duration of diastole
Systolic area with corrected K8xHRx(163+HR - 0.48xMAP)
(Tdia = T – Tsys);
impedance xAsys
II.2
P.50
Figure 1 - Different devices using pulse wave analysis to estimate SV

Of note, FloTrac/Vigeleo (Edwards Lifesciences) is not calibrated, is based on Windkessel algorithm and doesn’t require
anthropometric data. MostCare (VYTEC Health, Padova, Italy) is based on the PRAM and uses anthropometric data of the
patients to set up its estimation.
The calibrated devices include CombiQ™ (DeltexMedical, Chichester, Sussex, UK), LiDCOplus (LiDCO, Cambridge, UK) and
PiCCO (Pulsion Medical System, Munich, Germany). The calibration using PiCCO is based on transpulmonary thermodilution
and requires both central venous and arterial lines. The calibration using LiDCO is less invasive and it only requires an
arterial line and a peripheral venous line.
ARTERIAL CONTOUR ANALYSIS DEVICES
UNCALIBRATED CALIBRATED
FloTrac/VigeleoTM Using
Using Using
transesophageal
thermodilution lithium-dilution
Doppler
MostCareTM
PiCCOTM LiDCOplusTM CombiQTM

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2.2.2 -Full Non-invasive assessment of CO
Dr. Katia Orvin, MD

Department of Cardiology, Rabin Medical Center, Petach Tikva,
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Prof. Doron Zahger, MD, FESC

Department of Cardiology, Soroka Medical Center,
Faculty of Health Sciences, Ben Gurion University
of the Negev, Beer-Sheva, Israel
Key messages
Critical patients require close haemodynamic and CO monitoring in order

to frequently evaluate their status and to titrate treatment in the intensive
care unit settings
Invasive haemodynamic monitoring is considered the gold standard, but is
associated with inherent iatrogenic complications
Non-invasive monitoring offers a safer approach but with uncertain accuracy
and precision particularly in critically ill intensive care unit patients
In the past few years, the options for non-invasive monitoring including conti-
nuous CO measurement, have increased and improved, with several available
alternatives suitable for cardiac intensive care units
Further studies are required in order to evaluate the accuracy of the avai-
lable non invasive monitors, especially in case of complex and diverse cardiac
critical patients
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P.52
Introduction
Critical patients require close haemodynamic monitoring in order to frequently evaluate

their status and to titrate treatment, including correct dosing of fluids, inotropes or vasoac-
tive drugs . CO is believed to be one of the most important haemodynamic parameters in
both the perioperative and ICU settings.
Invasive haemodynamic monitoring is considered the gold standard, but is associated

with inherent iatrogenic complications, particularly for esophageal probes and pulmo-
nary arterial catheters. As such, non-invasive monitoring offers a safer approach, and
has the clear advantage of being associated with less hurdles and more convenient for
repeat measurements. With new devices capable of continuous CO measurements, there
is growing interest in the trending capabilities of these latest devices. However, the per-
formance of non-invasive devices for CO monitoring remains uncertain, particularly in
critically ill ICU patients due to uncertain accuracy, precision, and step-response change.
In the past few years, the options for non-invasive monitoring have increased and impro-
ved, with several available alternatives for CO measurements suitable for cardiac ICUs.
This chapter will provide an overview of the current commercially available devices for
non-invasive continuous CO measurement.
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P.53
Bioimpedance
Bioelectrical impedance analysis is the collective term that describes the non-invasive method
of measuring the electrical body responses to the introduction of a low-level, alternating
current. This technology relies on the fact that the impedance of the thorax (i.e. the resis-
tance to electrical current) is dependent on the amount of fluid in the thoracic compartment.
Therefore, fluctuations in the electrical resistance of the thorax are assumed to reflect
fluctuations of intrathoracic blood volume . CO is then computed based on mathematical
equations under the assumption that thoracic impedance changes over time are proportional
to the stroke volume. Due to advances in this technology, it is now possible to have detailed
and comprehensive data analysis in the critical care environment.
This has led to the production of several devices that all use slightly modified algorithms
based on the principle explained above: NCCOM (Bomed Medical, Irvine, CA, USA), ICG
(Philips Medical Systems, Andover, MA, USA), NICOMON (Larsen and Toubro Ltd., Mumbai,
India), BioZ (Cardiodynamics, San Diego, CA, USA), NICCOMO (MEDIS, Limenau, Germany),
AESCULON/ ICON (Osypka Cardiotronic, Berlin, Germany), and PHYSIOFLOW (Manatec
Biomedical, Paris, France).
The NCCOM, one of the first non-invasive monitors in the market, eliminates the effect of
respiration from thoracic impedance as a function of time, to provide a signal that indicates
the continuous changes of the pulsatile thoracic impedance; which is then processed to
signals indicative of ventricular ejection time, and the maximum rate of change of pulsa-
tile thoracic impedance, which is used to calculate stroke volume according to an improved
systolic upstroke equation.
In the Impedance Cardiography-ICG monitor, two voltage electrodes are placed on the neck
and two on the chest. Changes in the impedance of the thoracic fluid are measured and a
sophisticated algorithm is used to calculate a total of 12 haemodynamic parameters.
The Impedance plethysmograph NICOMON was originally described for measurement of blood
flow and uses the same principle as the above mentioned Philips ICG device to monitor CO.
The BioZ measures the change in impedance by introducing a high frequency (60 kHz
Minimum), low amplitude (4.0 mA rms Maximum) alternating electrical current through
the thorax between a pair of sensors placed on the neck, and another pair placed in the
mid-axillary line at the xiphoid process level, eliminating the possibility of interference with
bioelectrical activity of the heart and the brain.
II.2
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NICCOMO measures heart rate and blood pressure and utilizes a noninvasive physiological
adaptive signal algorithm ('plug and play') which requires no calibration. A study by Waker
and Jonas, compared this new ICG algorithm with the reference method of lithium dilution
(LIDCOM); The percent error for this new method was found to be unacceptable, sugges-
ting that this ICG algorithm does not have the required accuracy on which haemodynamic
management decisions can be confidently made in critically ill patients. Further studies are
needed to validate this algorithm.
AESCULON and ICON uses EC and four skin sensors placed on the neck and left thorax for
the non-invasive determination of SV, CO, and other haemodynamic parameters. Because of
the similar setup, EC is often confused with the traditional bioimpedance technology, most
commonly known as ICG. Even though both methods use sensors placed on the thorax, tra-
ditional bioimpedance or ICG methods rely on the periodical volumetric changes in the aorta
to determine SV and CO, while EC relies on the increase in conductivity to the orientation
change of red blood cells to determine the velocity of the blood flow. A recent meta-analysis
which assessed the accuracy and precision of EC showed high mean percentage error and
inter-study heterogeneity, therefore making this method unreliable for absolute CO values.
PHYSIOFLOW measures impedance changes in response to high frequency (75kHz) and low
amperage (1.8mA) electrical current transmitted via electrodes on the thorax. It was proven
non-inferior to thermodilution and superior to the standard IGC Philips monitor mentioned
above15. Nevertheless, it was shown not to be in agreement with CO measured by doppler
echocardiography in critically ill patients. However, it may be reliable for estimating changes
in CO during haemodynamic load challenge.
Although easy to use, the concept of bioimpedance does have important limitations. Impedance
is influenced by all changes in thoracic fluid composition, such as pulmonary oedema and
pleural effusions; changes in systemic vascular resistance will influence the volume changes
in the aorta and will therefore interfere with CO measurements. Furthermore, bioimpedance
is highly sensitive to electrode positioning and electrical noise, which is abundant in cardiac
ICU (monitoring devices) and may disrupt the signal1. Studies have consistently demonstrated
bioimpedance to be less accurate than thermodilution and doppler-based techniques when
measuring CO in surgical and critically ill patients; but, this method might provide insight
into CO in isolated points of time, and be of further help in monitoring the critically ill. At pre-
sent, bioimpedance is not generally accepted as accurate enough to estimate CO in the ICU.
II.2
P.55
Whole Body Impedance

Whole body impedance has been used for thirty years for estimation of body cell mass and
total body water. It uses the same principles of thoracic bioimpedance analysis, but is applied
to the whole body and is less accurate than localized thoracic impedance for monitoring
haemodynamic parameter1.
The NICaS system (NImedical, Petach Tikva, Israel) utilizes bipolar electrodes at the wrist
and at the ankle and provides real-time data on various parameters of a patient’s cardiovas-
cular-renal function as well as body water; the system is highly responsive to fluid changes
and is an effective non-invasive method for fluid management. The data is graphically dis-
played such that short-term mortality risk, and volume status can be quantified. Agreement
between NICaS CO and thermodilution CO was found to be within the boundaries of the FDA
guidelines of bio-equivalence. It was also found to be efficient in various perioperative and
cardiovascular settings.
Bioreactance
The CHEETAH-NICOM by Cheetah Medical is a device that uses a technique called Bioreactance
based on the principle of thoracic electrical bioimpedance. To improve the signal-to-noise
ratio, Cheetah not only measures changes in voltage amplitude, but rather phase-shifts in
the alternating current which depends almost exclusively on pulsatile flow and, therefore,
should be more closely related to aortic blood flow and, thus, cardiac output.
A small number of studies implied that bioreactance has a theoretical advantage over bioim-
pedance. A validation study which compared this method to pulmonary artery catheter
derived continuous thermodilution showed that it has similar monitoring capabilities post
cardiac surgery. More recently, a study by Cheung and colleagues, revealed that the NICOM
device is a safe, convenient, and reliable way of continuous non-invasive CO and cardiac
index monitoring, as well as for following changes in CO during off-pump coronary artery
bypass surgery. However, there are concerns about the its accuracy during low-flow states
and during electro-cauterization.
The endotracheal cardiac output monitor-the ECOM system uses electrodes that are located
on a cuff of an endotracheal tube, therefore close to the ascending aorta, so that the impact
of analogous signals from other cardiac structures are minimized. Compared to pulmonary
artery catheter thermodilution, the ECOM system underestimates changes in CO in posto-
perative cardiac surgical patients; however, it was considered clinically acceptable and may
be as efficient as invasive pulmonary arterial pressure monitoring to track CO changes.
II.2
P.56
Photoplethysmography
PPG is a simple optical technique that can be used to detect blood volume changes in the
microvascular bed and is often used to make non-invasive measurements at the skin surface.
The PPG waveform resembles that of the arterial blood pressure, but instead of pressure it
is related to the volume changes in the measurement site.
Figure 1 - Examples of monitors configuration

II.2
P.57
The ClearSight monitor device (Edwards Lifesciences, Irvine, CA, USA; previousl y known as
Nexfin by BMEYE B.V. Amsterdam, the Netherlands) allows for continuous blood pressure
and CO monitoring based on finger arterial pressure pulse contour analysis. The finger cuff
method provides a reasonable estimate of CO and blood pressure, but a number of studies
claim it does not meet the criteria for clinical interchangeability with currently used inva-
sive devices.
The CNAP/VERIFY technology (by CNSystems Medizintechnik, Graz, Austria), uses the same
technique of photoplethysmography as Clearsight. However, in order to correct for changes
in vasomotor activity, the CNAP device uses a different algorithm which continuously ana-
lyses the shape of the waveform and can distinguish between changes in blood volume due
to changes in blood pressure or due to changes in arterial diameter. To our best knowledge,
the only validation study (pilot retrospective study) showed that CO determination is fea-
sible in critically ill patients.
The T-LINE system (TL-300 by Tensys Medical Inc.San Diego, CA, USA) is a relatively new
non-invasive method based on pulse contour analysis using a technique called applanation
tonometry. A pressure sensor is placed upon the patient’s radial artery. A newly developed
auto-calibrating algorithm uses the arterial wave to estimate cardiac output. The physiologi-
cal parameters used are gender, age, height, body weight, systolic arterial pressure, diastolic
arterial pressure, mean arterial pressure, pulse pressure, beat-to-beat interval, maximal slope
within systole and systolic area under the curve. A validation study to pulmonary artery
thermodilution showed reasonable accuracy however, it's capability to accurately measure
cardiac output needs more validation.
Pulse wave velocity

The PWTT is the time required for a pulse pressure wave to travel between two points and
it can be estimated from the time interval between the development of the R-wave on the
electrocardiogram and its peripheral detection. PWTT is inversely proportional to velocity
and as such, PWV is a surrogate measure of vascular properties in general, and a simple,
non-invasive way of measuring arterial stifness.
Estimated continuous cardiac output-EsCCO ( by Nihon Koden, Tokyo, Japan) designed to

estimate CO with an algorithm that continuously produces estimates based on patient's
characteristics and measurements of electrocardiography, peripheral saturation and non-in-
vasive measured blood pressure. With these measurements, a PWTT can be determined and
in combination with the heart rate EsCCO is able to estimate the CO. A major limitation of
II.2
P.58
this system is the calibration. A reference CO value is required at the start of the measure-
ment from pulmonary catheter. Calibration approach based on patient demographic data and
cardiovascular variables including HR, pulse pressure, and pulse wave transit time was des-
cribed, this approach is not well validated. Nevertheless, it may be appropriate for use during
gradual decline from pulmonary invasive measurements; although, at present, there are no
data about the reliability of calibration after discontinuation of invasive measurement of CO2.
Transthoracic echocardiography
TTE can be used to estimate CO in several ways. The most frequently recommended method
involves measuring the blood flow velocity (using doppler) at the LVOT and thus obtaining the
SV. Since the area of the LVOT does not change significantly over time, it is sufficient to follow
short-term changes in VTI to assess changes in SV. Although it cannot provide continuous
haemodynamic data, it is the best bedside method to assess cardiac function repeatedly.
Echocardiography is now recommended as the first non-invasive evaluation of the patient

in circulatory failure and was shown to be reliable in critically ill patients.
Conclusions
The ideal non-invasive method for CO monitoring should be easy to use and well validated
in a wide variety of clinical settings, including critically ill patients with cardiac and non-
cardiac conditions. There is a large and interesting spectrum of non-invasive devices using
different technologies in the cardiac ICU, all having their advantages and disadvantages.
At present there are insufficient data regarding the correlation of any of the devices with
gold standard validated techniques to measure CO in critically ill patients and decompensa-
ted HF. Nevertheless, there is definitely a need for less invasive devices since non-invasive
haemodynamic monitoring technologies can provide the clinician with useful information
that can help decision-making and modify treatment strategies of the critically ill patient.
II.2
Table 1 - Strength and limitations of full non-invasive
monitoring
P.59 vs SG: compared to Swan Ganz catheter;
Fluid
Technique Study CO CI SV vs SG
Volume
Bioimpedance
37
NCCOM + + + + +
38
ICG 9 + + + + +
39
NICOMON 10 + + + + +
40
BioZ 8 + + + + +
NICCOMO 12 + + + - -
ICON 14 + + + + -
16
PHYSIOFLOW + + + - -
17
NICAS 22 + + + + +
Thoracic Bioreactance
25
CHEETHA- NICOM + - + + -
2
Photoplethysmography
2
ECOM + + + + -
30
ClearSight 31 + - + - -
CNAP/VERIFY + - + - -
T-LINE + - - - -
Pulse wave velocity
EsCCO 30 + + + + -
TTE 41 + + + + +
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P.60
Valid in
Limitations
Critical
- High HR, Pacemaker, MV, chest tubes
+ Aortic Insufficiency, high hypertension, extreme BMI, Septic Shock and IABP
+ Shows higher CO values in AMI patients
- Only if good ECG and ICG. Not for pacemaker, septic shock or cardiac surgery
- COPD, major abdominal or cardiac surgery
- Thoracic fluid
- Anaemia
+ Suboptimal quality signal, IABP, high vascular resistance, arterial line
- Changes in thoracic fluid and vascular resistance or sudden CO changes
Thoracic fluid and high vascular resistance, cardiac surgery.

+
Poor in patients non-intubated
- Low CO, finger oedema, hypothermia or high vascular resistance
Unstable haemodynamic or hyperdynamic.

-
Insufficient studies
- Insufficient studies
- A reference CO is initially required
+ Small study, excluding patients with arrhythmia

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2.2.3 -Microcirculation: direct and indirect evaluation
Dr. Jaume Mesquida, MD, PhD

Critical Care Department, Parc Taulí Hospital Universitari,
Sabadell, Spain
Dr. Edgar Cortés, MD

Intensive Care Department, Hospital Moisès Broggi,
Consorci Sanitari Integral, Sant Joan Despí, Barcelona, Spain
Xaime García Nogales, MD

Intensive Care Department, Hospital Moisès Broggi,
Consorci Sanitari Integral, Sant Joan Despí, Spain
Key messages
The microcirculation is the final site for oxygen delivery to the cells
The current whole-body approach is of limited utility in order to infer the

microcirculatory status
Monitoring the microcirculation at the bedside is already feasible
Alterations in the microcirculation have prognostic value, independently of

systemic haemodynamics
The ability to manipulate the microcirculation is, to date, restricted to inter-
ventions aiming at increasing global flow and pressure
Randomized controlled trials assessing the impact of targeting the micro-
circulation in critically ill patients is mandatory before the implementation
of these technologies into clinical practice
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Introduction
The microcirculation, as a whole, comprises functional units of vessels of diameter < 100-
150 µm, namely arterioles, capillaries, and venules, and is considered the largest organ
in the body. Since, amongst other functions, the microcirculatory network is critical to
deliver oxygen to the cells, no haemodynamic evaluation would be complete without a
proper microcirculatory evaluation. In daily practice, this evaluation has been inferred from
global haemodynamic and metabolic parameters. Notably, the microcirculation might be
abnormal despite normalization of macrocirculatory parameters, such as MAP, CO and/
or ScvO2 and therefore, the quest for adequate monitoring of the microcirculation has
been a priority in critical care research for the past decades.
To date, in addition to clinical evaluation of capillary perfusion, several technologies are

available to monitor the microcirculation (Table 1). These technologies can be classified
in two main groups: those allowing the direct visualization of the microvessel network
(direct methods); and those evaluating tissue metabolism as a surrogate of microcircu-
latory blood flow (indirect methods).
II.2
Table 1 - Principal techniques available for monitoring

P.63 the microcirculation
Bedside Measured
Advantages Limitations
technique variable
Direct evaluation
Qualitative
No technological
evaluation;
Clinical Regional peripheral device required;
Limited use for
Examination perfusion Easy and rapid
shock monitoring
applicability
and titrating therapy
Microcirculatory blood
Gold Standard Technical issues for
flow; high-quality videos
acquisition;
Semi-quantitative
Videomicroscopy Vascular density; evaluation; No immediate
availability of micro-
Heterogeneity of Potential use for bed-
circulatory video
perfusion side monitoring and
analysis
titrating therapy
Indirect evaluation
Gastric tonometry
has been abandoned,
Quantitative
Mucosal due to technical
evaluation;
issues interfering its
CO2 derived Tissue CO2 Potential use for bed-
measurements;
measurements side assessment of
Fewer evidence on
flow adequacy
sublingual optic
capnometry
Quantitative Measurement
Tissue pO2
evaluation; variability
+ Oxygen Challenge
Potential use for bed- (Value derived from
Tissue O2 tension Test (dynamic test to
side assessment of a mixture of arte-
assess adequacy of
convective O2 trans- rioles, capillaries and
DO2)
port adequacy venules)
Quantitative StO2 measurements

Tissue O2 saturation evaluation; altered by edema/fat
(StO2) In addition to moni- tissue;
+ Vascular Occlusion tor regional flow Technology diversity
NIRS Test (dynamic test adequacy, potential (high variations in
to assess O2 local use for assessing sensed areas);
consumption and local metabolic sta- Off-line processing
endothelial function) tus, and endothelial for dynamic parame-
dysfunction ters calculation
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One of the main issues of debate has been which vascular bed to choose for microcirculatory
monitoring purposes. According to the pathophysiological response to alterations in the sys-
temic circulation, regional organ perfusion can be classified into two main categories: organs
with efficient blood flow autoregulation, and organs with very limited blood flow autoregu-
lation (Figure 1). Some strongly protected organs, with very efficient autoregulation, are
the brain, the heart and the kidneys. On the other hand, areas such as the skeletal muscle,
the splanchnic territory, or the skin have limited autoregulatory performance. Therefore, in
situations where the systemic circulation is altered, although global compensatory mecha-
nisms, such as increased sympathetic activation, might be able to maintain normal blood
pressure values, blood flow will be diverted towards "vital" organs, resulting in hypoperfusion
of less protected areas. This is the basis for monitoring "non-vital" areas when assessing
the microcirculation in critical illness.
Figure 1 - Territories of the body according to their autoregulatory

performance.
Organs with efficient autoregulation will be able to maintain local blood flow despite systemic alterations in flow/pressure.
Conversely, in territories with limited autoregulation, global compensatory mechanisms, namely sympathetic activation,
will predominate. The final result will be blood flow diversion from "non-vital" areas to "vital" areas, generating local
hypoperfusion even with apparently normal systemic haemodynamics.
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Direct methods for evaluating the microcirculation

Clinical examination
Classical evaluation of peripheral perfusion includes clinical signs such as skin appearance
and temperature. In order to overcome a qualitative approach, some quantitative tools have
been proposed, mainly the capillary refill time, the mottling score, and the central-to-toe
temperature gradient (Figure 2). CRT consists in classifying peripheral perfusion into nor-
mal or abnormal according to its response to local compression. It is measured by applying
a gradual direct pressure to the ventral side of the third phalanx of the index finger with a
glass microscope slide, until the skin is blank. Once this degree of pressure is achieved, it
must be maintained for 10 seconds and, afterwards, released. A time greater than 3 seconds
to recover the normal skin color will be considered abnormal. The mottling score is based
on the mottling extension, defined as a patchy skin discoloration, around the knees of the
patient. The score is ranked from 0 (no mottling) to 5 (extensive mottling area reaching the
fold of the groin) (Figure 2).
Videomicroscopy
Several handheld microscopes allowing bedside direct visualization of the microcirculation
have been developed since the late 1990s. Although the technologies show slight variations,
they share their basic principle. Briefly, a light source is placed on a surface of the body, the
light emitted is reflected by the deeper layers of the tissue, and ultimately this reflected
light is sensed by the device, obtaining a final image of trans-illumination of the superficial
layers of the tissue. Since the selected wavelength is absorbed by the hemoglobin of the red
blood cells, the image acquired appears as black-grey bodies (absorbed light), forming ves-
sels, over a white backscreen (reflected light) (Figure 2). Of note, the technique can only be
applied on tissue surfaces covered by thin epithelial layers, such as the sublingual mucosa,
which is the most largely explored area in critically ill patients.
Although qualitative evaluation has been largely used, quantitative evaluation would be
required for a more precise characterization of the microcirculatory status. Accordingly,
several scoring systems have been proposed. To describe entirely the microcirculatory alte-
rations, the combination of variables informing of convective blood flow, diffusive capacity,
and heterogeneity is mandatory (Table 2). Regrettably, to date, the analysis needs to be
performed off-line and manually, remaining highly time consuming, and representing a limit
for its introduction into clinical practice. Nevertheless, due to its direct visualization of the
vascular network, videomicroscopy is considered the gold standard technique for the assess-
ment of the microcirculation.
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Table 2 - Main parameters used to quantify the microcirculatory status
Bedside Values of
Parameter Interpretation
technique interest
Direct evaluation
CRT (seconds) > 3 sec Peripheral hypoperfusion
Clinical Graded scale: 0 (no From normal peripheral

Examination mottling) to 5 (extensive perfusion (0) to severe
Mottling score
mottling, reaching the fold peripheral hypoperfu-
of the groin) sion (5)
Grid-based score (3
horizontal and 3 verti-
Proportion of
cal equidistant lines).
perfused small Convective blood flow
Percentage of perfused
vessels (%)
vessels per total number
of vessel crossings
< 2.6
Video- Grid-based score per qua-
microscopy drant (mean of 4):
MFI (AU) 0 = no flow; Altered diffusive capacity
1 = intermittent flow;
2 = sluggish flow;
3 = normal flow
Coefficient of variation of
Heterogeneity Microvascular
MFI:
index (AU) heterogeneity
(highest/lowest)/mean
Indirect evaluation
Mucosal
CO2 gap (tissue -
CO2 derived > 20 mmHg Regional hypoperfusion
arterial) (mmHg)
measurements
tPO2 (mmHg) < 30 mmHg Tissue hypoxia

Tissue O2
tension OCT (delta tPO2)
< 40 mmHg Inadequate global flow
(mmHg)
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Bedside Values of
Parameter Interpretation
technique interest
< 75% (thenar site, using
StO2 (%) Peripheral hypoperfusion
15mm sensors)
DeO2 (%/min) Local metabolic rate

NIRS High variability depending
ReO2 (%/min, or Local vascular response
on the site and the probe
%/sec)) to ischemia
size of the technology
(lack of standardization) Local vascular response
AUCH (AU)
to ischemia
Indirect methods for evaluating the microcirculation

Mucosal PCO2 measurements
Although the technology has presently almost disappeared, tissue partial pressure of PCO2
monitoring appeared as a key factor for regional and microcirculatory evaluation in the
critically ill patient. The rationale of the technology relies on the principle that tissue CO2
depends on three factors: tissue CO2 production, blood flow to the tissue (responsible for
CO2 removal), and arterial CO2 content. In stable respiratory conditions (constant arterial
CO2), tissue CO2 would reflect the balance between local CO2 production and removal. The
gradient between tissue and arterial PCO2 values, namely the PCO2 gap, has been proposed
as a hypoperfusion marker, with better performance than tissue pH or tissue PCO2 alone.
Gastric tonometry was the most used method for evaluating the microcirculatory status,
with extremely significant results. However, due to several technical concerns, gastric tono-
metry has been progressively abandoned. Following the principle of measuring PCO2 on body
mucosae, other surfaces have been explored, and sublingual optic capnometry has revealed
an excellent correlation with gastric PCO2, showing similar behavior in different shock condi-
tions. Moreover, an inverse correlation between sublingual PCO2 and the density of perfused
capillaries, assessed by videomicroscopy, has been confirmed, strengthening the physiolo-
gical value of sublingual CO2 measurement as a surrogate of tissue perfusion. Surprisingly,
this non-invasive technique is now delimited to experimental studies.
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Tissue O2 tension
tPO2 reflects the partial pressure of oxygen in the interstitial space of a sampled volume of tissue
(approximately 0.5 mm3). It represents the balance between local oxygen delivery and consump-
tion. Initial technologies for tPO2 determination used Clark electrodes, but newer techniques
use dynamic luminescence oxygen-sensing optodes, allowing more reliable determinations
of low tPO2 values. The technology accurately measures tissue PO2 when it is homogenously
distributed, but it is not consistent in conditions of PO2 heterogeneity, as it is sensitive to the
highest PO2 in the sampled volume.
Clark electrodes have been used in animal models in several organs, but in patients the evidence
is limited, and the electrodes' insertion has been explored in small studies in the muscle or the
subcutaneous compartment. The appearance of luminescence techniques, due to its non-inva-
sive nature, has allowed a broader use in patients, and transcutaneous tPO2 has shown some
promising results. There is disparity in the site analyzed, but according to preceding positive
results, some authors promote monitoring the upper torso, below the clavicle, in a non-bony
area, in order to standardize the technique.
In addition, a provocative test has been proposed, consisting in increasing the inspired oxygen
concentration, the so-called OCT. The test explores the ability of the circulation to transport
high partial pressures of oxygen to the tissues. The downstream increase in tPO2 after a rise
in arterial PO2 would reflect a normal ability of the circulation to transport high partial pres-
sures of oxygen. Conversely, a poor rise in tPO2 would correspond to an insufficient blood flow.
NIRS
NIRS technology consists in the measurement of the attenuation of light in the near-infrared
spectrum (700-1000nm wavelenghts) in a tissue. The main chromophore for the NIRS light is
hemoglobin, with specific behavior of oxy- and deoxyhemoglobin for slight variations of the
wavelength. Hence, using different wavelengths at a time, the technology allows the calculation
of the overall oxygen saturation of the hemoglobin comprised in the microvascular network
(vessels < 100μm) of the sensed area. Amongst other applications, in critical care the technology
has been used mainly to monitor StO2 of the skeletal muscle non-invasively. Although several
locations have been explored, the forearm and the thenar eminence seem to be the most highly
accepted sites, due to the possibility of performing a provocative ischemic maneuver. As results
of the so-called VOT, the resulting dynamic StO2 parameters will inform on the local metabolic
status (deoxygenation slope) and the vascular reactivity (reoxygenation slope and hyperemic
response) (Table 2). The discriminatory power of dynamic StO2 parameters for detecting micro-
circulatory disturbances in different scenarios has proven superior to the steady state StO2.
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Some other existing techniques might also provide information on the microcirculatory sta-
tus, either directly or indirectly. For instance, LDF, a technology that uses Doppler shifts of
visible and infrared light to measure microvascular blood flow. LDF has several limitations
for its clinical use, including excessive variability, and the lack of absolute blood flow values,
which confines its value to monitor trends. Another available technology is Microdialysis,
a system that allows quantification of energy-related metabolites (mainly lactate and piru-
vate) in the interstitial space by using a thin catheter that mimics a capillary. Although it
has demonstrated prognostic value in brain injury, there is limited evidence on its utility
as a haemodynamic monitoring tool. Finally, in the recent years, a new marker of periphe-
ral perfusion derived from the photoelectric plethysmographic pulse-oximetry signal has
been proposed. It is built from the pulsatile and non-pulsatile signal of the pulse-oximeter,
and has proven useful in order to identify abnormal peripheral perfusion associated with
vasoconstriction. Despite some evidence on its prognostic value, the parameter needs fur-
ther validation in different scenarios.
Figure 2 - Peripheral sites, and key technologies for assessing the

microcirculation
Direct methods for assessing the microcirculation are mainly semi-quantitative, as compared to indirect methods, which
allow a continuous quantitative monitoring. In addition, tPO2 and StO2 can be tested with provocative interventions, such as
the OCT and the VOT.
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Clinical utility of microcirculatory variables

Prognostic value
To date, every single technology has demonstrated its prognostic value in almost every cli-
nical scenario. But probably the most relevant feature is that microcirculatory parameters,
either direct or indirect, have proven their performance in outcome prediction independently
of macrocirculatory variables. The fact that the microcirculatory status cannot be properly
inferred from global flow or metabolic variables is the main reason for the quest of incorpo-
rating these technologies in the toolbox of haemodynamic monitoring.
Targeting the microcirculation

Despite all the evidence generated in the past three decades, very few authors have explored
the incorporation of microcirculatory parameters in a resuscitation protocol. In the early
1990s, Gutierrez and colleagues demonstrated a positive impact on survival in a mixed
population of critical patients when targeting gastric mucosal pH in the process of haemo-
dynamic resuscitation. Fifteen years later, in a small trial in septic shock patients, Yu and
coworkers demonstrated reductions in mortality when using a transcutaneous tPO2-driven
resuscitation protocol, as compared to a protocol targeting global DO2 and SvO2. Recently, the
ANDROMEDA-SHOCK trial, a large multicenter trial, compared two strategies, one using lactate
and another using CRT for guiding the resuscitation process of septic patients. Although no
significant differences in mortality were found, a strong tendency towards a positive impact
on survival in the CRT group was observed, with significant reductions in fluid administration
in the initial resuscitation, as compared to the lactate group.
Although these results are promising, randomized controlled trials assessing the impact of
targeting the microcirculation in critically ill patients are needed before these technologies
can be implemented into clinical practice.
Manipulation of the microcirculation

Probably the last frontier for the incorporation of the microcirculation in the resuscitation
process is the limited ability for its manipulation beyond the optimization of systemic hae-
modynamics. The combination of fluids, vasopressors and inotropic drugs is the cornerstone
of the haemodynamic resuscitation process in critical care. These therapies are delivered
in an attempt to increase global blood flow, but this might not be equal to recruiting the
microcirculation, and macrocirculatory benefits might not be always coupled to microcircu-
latory improvement. This is especially relevant in septic shock, due to the heterogeneous
nature of microcirculatory alterations, but might also be applicable to other conditions with
increased inflammatory response, such as pancreatitis, major surgeries, burns, or trauma
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patients. Several studies have demonstrated a lack of correlation between macrocirculatory

and microcirculatory changes as results of fluid administration, or dobutamine infusion, a
phenomenon that has been conceptually defined as loss of haemodynamic coherence. This
loss of haemodynamic coherence might be explained by four underlying mechanisms:
Heterogeneous perfusion of the microcirculation, as in septic shock
Hemodilution, resulting in a loss of red blood cell filled capillaries
Congestion of the microcirculatory network, as results of increased venous pressures,

producing stasis of the red blood cells
Tissue edema, caused by capillary leak, that increases the diffusion distance between
capillaries and tissue cells
These alterations are clinically significant, also in terms of morbidity and mortality, and
their identification will be mandatory in order to properly guide haemodynamic resuscita-
tion interventions.
In addition to the effect of manipulating pressure and global flow, some other treatments
have exhibited a positive impact on the microcirculation. These therapeutic interventions
include the administration of hydrocortisone, activated protein C, red blood cell transfu-
sions, and perfusion of vasodilatory drugs. But when incorporated in resuscitation protocols,
almost each one of these therapies has generated controversial results. Of note, none of the
large trials analyzing the inclusion of these treatments paid attention on microcirculatory
performance. So, lack of patient's selection might account for some of the negative results.
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2.3.1 -Echocardiography: LV function and filling pressures
Prof. Susanna Price, MD, PhD, FESC

Adult Intensive Care Unit, Royal Brompton Hospital,
London, UK
Key messages
Understand the indication for the echo study
Ensure all confounding factors are noted (inotropes, ventilation, acid-base

status)
Estimate LV contractility using standard parameters (EF, long axis function)
and measure LVOT VTI
Where LVOT VTI is low, but LV function appears good, exclude RV failure,
MR/VSD
Where trans-mitral Doppler is not as expected, other causes should be
excluded
Lung US should be used to confirm/exclude pulmonary oedema by the pre-
sence/absence of bilateral homogeneous B-line pattern
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Introduction
Echocardiography is one of the most powerful diagnostic and monitoring tools available
to the modern intensivist. Although the most frequent documented indication for echo-
cardiography in the acute setting, assessment of LV function remains one of the most
challenging. Every acute/critical care intervention may alter echocardiographic findings,
most critically ill patients have been excluded from trials, and normal values in this setting
are largely unknown. Each parameter must be interpreted in the context of the pharma-
cological and mechanical support (ventilatory or circulatory), loading conditions, arterial
blood gas analysis, and always in the context of right ventricular function. Repeated studies
may be required to determine the response (beneficial or otherwise) to interventions. A
high level of expertise is required in order to undertake echocardiography in the critical
care/acute setting, and where findings are unexpected, or do not explain the patient’s
clinical condition, a second opinion should be sought.
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LV systolic function
LV contractility is complex, and comprises numerous motion vectors related to the sum
effects of myocyte contraction and their orientation within the layers of the myocardium:
Radial myocardial thickening
Longitudinal myocardial contraction
Rotational, circumferential vectors
Additional “wringing” differential, between the base and apex of the heart
Figure 1 - LV contractility
A schematic representing the different movements of the myocardium that make up contractility
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Global assessment
Assessment of LV systolic function, although seemingly simple, is therefore one of the most
complex, with echocardiography only recently being able to interrogate true contractility of
the myocardium using advanced techniques (strain/strain rate imaging, velocity of circumfe-
rential fibre shortening, 3D echo). In daily clinical practice, echocardiography assessment
of global LV systolic function uses changes in LV cavity dimension as a substitute for LV
systolic function assessment, using techniques that assess:
Cavity size (Parasternal long axis view, M-mode or 2D)
Wall thickness (any changes represent long-standing disease)
Changes in cavity dimensions between systole and diastole (fractional shortening

ejection fraction)
A number of potential pitfalls exist:
Reliance on assumptions regarding LV geometry and function: do not use if there are
regional wall motion abnormalities
Minor degrees of off-axis measurement result in significant measurement changes
They do not measure myocardial contractility, but rather changes in cavity dimensions
They are highly inotrope, activation and load-dependent
They have not been validated in the critically ill

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Figure 2 - Abnormalities of LV wall motion

The different abnormalities that may be seen are shown in this schematic. Each area of the myocardium visualized should
be considered and reported in this context. Extremes are very useful: in terms of dimensions and wall thickness to delineate
long-standing disease, and in terms of ejection fraction/fractional shortening should be appropriate to the clinical context
(i.e. a ‘normal’ ejection fraction in a young patient with sepsis and receiving inotropes and pressors is very abnormal).
NORMAL
DYSKINETIC HYPOKINETIC AKINETIC HYPERKINETIC
Regional Wall motion abnormalities

Detection of regional wall motion abnormalities is as defined in standard cardiology practice,
remembering that the rate of infusion of any inotropic agent may mean that in effect the study
is a stress echocardiogram. Remember additional to ischaemia, causes in the ICU include:
Takotsubo cardiomyopathy
Non-ischaemic DCM
Myocarditis/peri-myocarditis
Activation abnormalities
RWMA on MCS
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Figure 3 - Assessment of LV long axis function

A schematic shows an optimal apical 4 chamber view with red arrows demonstrating cursor position for obtaining
M-mode across the mitral lateral annulus (MAPSE) and tricuspid anulus (TAPSE). The lower part of the figure shows the
corresponding M-mode in a normal patient.
OS: onset of systole; OL: lnset of lengthening; A2: aortic component of the second heart sound;
Long axis function

Using basic M-mode, it is possible to assess longitudinal function of the basal LV (MAPSE).
The principles are exactly the same as those for TAPSE. As the insertion moves relative to
the M-mode, the longitudinal excursion can be demonstrated on the M-mode display. It has
components of magnitude as well as timing. Normal values correspond relatively well with
ejection fraction and are as follows:
Parameter Range Table 1 - Parameters measured from MAPSE

q-OS: timing of q wave onset to onset of systole; msec: milliseconds;
Amplitude (mm)
Abnormalities in MAPSE relate to:
Lateral 15-20
Septal 12-17 Onset (bundle branch block, dyssynchrony)

Posterior 15-20 Magnitude (ischaemia, reduced EF)
Timing (msec) Velocity (ischaemia, reduced EF)
q-OS 80-90
Duration (ischaemia)
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MAPSE is useful as it does not rely upon high quality images, and it is impossible to ove-
restimate excursion (only underestimate if not well aligned). An additional advantage is
that as the longitudinal fibres are endocardial, and coronary arteries are epicardial, abnor-
malities related to myocardial ischaemia occur earlier than those seen using 2D imaging
(as post-ejection shortening), and as with 2D imaging can be mapped to the corresponding
likely culprit coronary artery.
Ventricular asynchrony
The tIVT is an easy and highly reproducible measurement that reflects the degree of ventri-
cular asynchrony. It has a negative correlation with CO, and, under normal conditions,
shortens in response to stress (physiological/ pharmacological), but may be prolonged in
case of ischaemia, conduction abnormalities, or even related to prolonged systole on the
right in case of pulmonary hypertension. Monitoring changes therefore provides the oppor-
tunity to intervene to improve CO, and may suggest the need for electrical correction in
order to improve clinical outcome.
Figure 4 - Calculation of total

isovolumetric time
Upper figure shows PW at the LVOT, the duration of which

gives the ‘LVOT filling time’
Lower figure shows CW across the mitral valve, with the

time between MR giving the mitral filling time.
Calculation:
Total ejection time = ET x heart rate (measured from
LVOT)
Total filling time = FT x heart rate (measured from trans-

mitral Doppler)
Total isovolumic time = 60-(ET + FT) sec/min

Abnormal is >15sec/min
Prolongation of tIVT should prompt a search for the
underlying cause, and to maximise CO by demonstrating a
reduction in tIVT after intervention.
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Filling pressures
Absolute values cannot be measured, but relative values estimated using a number of diffe-
rent parameters, generally in combination, and in the context of the ejection fraction:
Table 2 - Parameters used in evaluating left-sided filling pressures
View &
Parameter Relevant values Notes
technique
Normal: 70+12msec;
Transmitral Abnormal diastolic function: Relatively independent of
IVRT filling (PW >110msec; inotropic status;
Doppler) Restrictive physiology: IVRT Not widely used.
<60msec
Normal: E/A 0.75-1.4; Age and filling dependent;

Transmitral Abnormal diastolic function: Not possible to assess in AF/
E/A filling (PW E/A< 0.7 ; flutter;
Doppler) Restrictive physiology: E/A Changes with ischaemia/
>1.5-2 incoordination.
Normal: EDT: 160-240msec;

E decele- Weak negative correlation
Transmitral Abnormal diastolic function:
with PCWP (r=0.54);
ratio, time filling (PW EDT >240msec;
Sensitivity 86%, Specificity
(EDT) Doppler) Restrictive physiology:
59%.
EDT<160msec
<10 normal; 10-15: need other measures;

>15 elevated LAP (septal or More accurate in patients
Transmitral
average); with reduced EF;
filling (PW
E/e' >12 elevated LAP (lateral); Not validated in: MiV disease,
Doppler) plus
+PV <8 (lateral) predicts AF, pacing;
TDI
PCWP <18mmHg (sensitivity No good correlation with pul-
83%, specificity 88%) monary oedema.
If S/D > 0.65 in presence of

Pulmonary
PW Doppler normal E/A and EF, LAP unli- Varies with age.
vein S/D kely to be elevated
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View &
Parameter Relevant values Notes
technique
Sensitivity 97%, Specificity

Calculate LAP by:
96%;
LAP = 53,236-[0.301-PV-
Good correlation with PCWP:
Pulmonary DT]+[0.000484 (PV-DT)2]
PW Doppler r=-0.89;
vein DT Confounding variables: HR,
PV-DT <160msec correlates
CO, Age, IPPV, LV compliance/
with PCWP >18mmHg
afterload/relaxation.
Colour
M-mode
Colour across MiV,
<50cm/sec may indicate dias-
M-mod measure
tolic disease; Image quality with TTE may
from MiV
e +PV: E/Vp <1.7 predicts PCWP preclude use;
annulus to
propagation <18mmHg (sensitivity 80%, Relatively low sensitivity.
4cm into
specificity 100%)
velocity LV, slope of
first aliasing
velocity
Cardiac output measurement

Can be used to estimate the stroke volume from the left and right heart, by measurement
of the relevant outflow tract cross-sectional area (calculated from the LVOT diameter) and
VTI or stroke distance, measured using PW Doppler. This is usually measured from the left
heart (LVOT and aortic VTI), but can also be done from the right.
Stroke volume = LVOT area x quantity of blood passing through the LVOT. This is measured
from two views using two different echo modalities
Average velocity: measured from the 5 chambers view, the PW sample volume is
placed in the LVOT, 5mm proximal to the aortic valve. The brightest portion of the
spectral tracing represents the velocity of the majority of blood cells (modal velocity)
Cross sectional area: diameter measured from the PLAX view
Multiply the VTI by the calculated LVOT area = Stroke volume

Stroke volume x heart rate = Cardiac output
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Figure 5 - PW Doppler for

measurement of VTI or cal-
culation of stroke volume
A clear Doppler envelope is acquired from
a well-aligned apical 5-chamber view. This
can then be traced for the VTI, or used to
calculate the SV.
If serial measurements of SV
are made, the LVOT area cal-
culated can be reused, but take
care to obtain equivalent Apical
5Ch images for your PW Doppler
each time.
Serial measures may be used in VTI in response to interventions but great care must be
taken for equivalent views. In patients receiving MCS, a VTI of >10 is associated with a grea-
ter chance of successful weaning.
Table 3 - Predicted values at rest and stress for cardiac output in a normal heart
A number of assumptions are made: (1) flow is laminar; (2) the dimensions of the LVOT do not change during systole the
findings should be compared with previous studies. All should be taken in context of changes; (3) the LVOT is circular; (4)
the sample volume is at the same position as the LVOT is measured; (5) the stroke volume does not change significantly
beat-to-beat
Challenges present where the images are suboptimal, as any error in measurement of LVOT will result in a squared error in
stroke volume calculation. Irregular rhythm (ie. atrial fibrillation) will result in very different values – averaging 10-13 has
been suggested. Where subaortic velocities are high (left ventricular outflow tract obstruction/very high cardiac output
states) this technique cannot be used.
Exercise (physiological stress?)

Rest
in a normal heart
Stroke volume 70-110ml 80-130ml
Cardiac output 5-8.5L/min 10-17L/min
Cardiac index >2.5L/min/m2 >5L/min/m2

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Sequence for evaluation of LV systolic function, filling pressures and cardiac output. Where
possible comparisons should be made with previous studies. All must be taken into context
of loading conditions, inotropy and ventilation. If necessary, comparisons can be made at
rest and on stress (pharmacological/physiological).
Figure 6 - Algorithm for undertaking basic critical care echocardiography
Acute/critical care echo checklist - Age

- Inotropes/pressors
- Arrhythmia
- Coagulation (if TOE)
- Acid-base status
Step 1
Estimate LV contractility
and stroke distance Disproportionalety good
LV with low VTI:
?RV dysfunction
?MR
?VSD
Step 2 ?Electromechanical
Is transmitral Doppler as dyssynchrny
expected?
NO Cause for abnormal
YES transmitral filling:
?LV restriction
?Conduction disease
Step 3 ?Ischaemia (post-
Is LAP/LVEDP low/normal ejection shortening)
NO
Step 4
Evidence of pulmonary
oedema on LUS?
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2.3.2 -Echocardiography: RV function and systemic venous pressures
Prof. Jelena Čelutkienė, MD, PhD, FESC

Clinic of Cardiac and Vascular Diseases,
Institute of Clinical Medicine, Faculty of Medicine,
Vilnius University, Vilnius, Lithuania
Dr. Giedrė Balčiūnaitė, MD

Dr. Diana Zakarkaitė, M.D, PhD

Key messages
RV function is an important determinant of cardiac output and a major pre-

dictor of patient clinical course and outcome
In a patient with RV failure repeated echocardiographic assessment is usually
necessary to monitor course of a disease and response to therapy
RV abnormalities most frequently arise due to pressure overload, volume
overload, primary myocardial injury, or a combination of these mechanisms
RV dilatation, hypertrophy, and signs of pulmonary hypertension are typical
for the case of pressure overload. Significant tricuspid regurgitation most
frequently causes volume overload with concomitant RV dilatation
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Primary RV myocardial dysfunction most often occurs due to RV ischemia,

cardiomyopathies or systemic/toxic damage
The main reasons of significant tricuspid regurgitation include RV remo-
delling due to increased afterload, dilatation of tricuspid annulus in case of
atrial fibrillation and primary valvular abnormalities
In an acute setting bedside echocardiography allows an instant non-invasive
monitoring of right heart condition and assists in correct diagnosis and opti-
mal management choices
Introduction
The Main Considerations in the Evaluation of RV structure and function are to determine
whether the chief underlying process affecting RV is a pressure overload, volume overload,
or a primary myocardial damage, because the clinical course and therapeutic approach
in these 3 situations differ significantly (Figure 1).
This classification is useful from a clinical perspective, although in real life different patho-
logical processes frequently coexist in various degrees. A stepwise approach in assessing
RV function will lead to a correct diagnosis and management of RV failure. Frequently uti-
lized parameters and reference values of RV dilatation (Step 1), chamber pressures (Step
2), volume load (Step 3) and RV systolic function (Step 4) are graphically represented on
pages. In addition, an estimation of pulmonary vascular resistance is shown.
In the setting of acutely increased afterload the RV responds by increasing its end –dias-
tolic volume. RV dilatation with compensatory hypertrophy may be observed in chronic
pulmonary hypertension of pre- or postcapillary origin.
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Figure 1 - Stepwise approach in assessing main mechanisms of RV dysfunction
RV size ?
Normal/mild dilatation Moderate/severe dilatation
NO Signs of PH ? Significant TR ?
YES YES NO
Pressure Pressure/volume Volume

overload overload overload
YES RV systolic dysfunction ? YES
Secondary myocardial dysfunction
Primary myocardial damage

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Step 1: RV dimensions
Refer to figure 2A
A visual assessment in multiple views, including standard and atypical, should be used
to monitor RV geometry and degree of enlargement
Visual assessment of RV size is acceptable and sometimes sufficient in critical conditions
It is recommended that visual inspection of right chambers be supported by quantitative

measurements of RV diameters, RV and RA areas
Linear and planar measurements of RV and RA should be made in standard parasternal,

apical and subcostal views
The size of right chambers as sensitive to haemodynamic load
Figure 2A - Visual assessment of RV size

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Step 1B: RV dimensions

Refer to figure 2B
Linear and planar measurements of RV and RA should be made in standard parasternal,

apical and subcostal views
The size of right chambers are sensitive to haemodynamic load
Figure 2B - Normal RV measurements

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Step 2A: RV pressure overload

Refer to figure 3
Absence of RV pressure overload does not exclude pulmonary embolism
Presence of pulmonary hypertension in combination with systolic septal shift is

indicative of RV pressure overload
Significant dilatation and dysfunction of RV with an evidence of RV hypertrophy

suggests chronic pressure overload
If “McConnell’s” or “60/60” sign is present in a patient with PH, acute pulmonary

embolism should be suspected
PA pressure should be reported and interpreted in respect to systemic blood pressure
Figure 3 - RV pressure overload

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Step 2B: Estimation of RA pressure

Refer to figure 4
In assessing of IVC collapsibility the sniff is preferred instead of a normal inspiration

to cause quick decrease of intrathoracic pressure and sufficient collapse by sudden
emptying of blood from the IVC
The lower is the SFF in hepatic veins, the higher is the RA pressure
SFF is proved useful in patients on ventilators; averaging 5 or more beats is

recommended
Figure 4 - Estimation of RA pressure

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Step 2C: Estimation of PVR in WU

Refer to figure 5
Non-invasive estimation of PVR is possible using routine Doppler measurements
Figure 5 - Estimation of PVR

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Step 3: RV volume overload

Refer to figure 6
The most frequent cause of RV volume overload is a significant tricuspid regurgitation

and intracardiac left to right shunts
Mechanism of TR:
- secondary to RV remodeling, most often related to RV afterload or primary myocardial
damage
- secondary to RA and TV annulus dilatation, usually associated with long-standing
atrial fibrillation
- primary valvular abnormality (infective endocarditis, jatrogenic, chordae rupture,
Ebstein anomaly, carcinoid syndrome)
Signs of hyperaemia of the hepatic veins and systolic flow reversal are additional
markers of RV volume overload
Volume overload typically causes diastolic septum flattening, whereas combined

pressure and volume overload is characterized by systolo-diastolic septal flattening
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Figure 6 - RV volume overload

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Step 4: RV systolic dysfunction

Refer to figure 7A
An initial visual assessment of RV wall motion and RV areas change should be

accompanied by measurement of quantitative markers
The recruitment of septum to maintain RV stroke volume, or paradoxical septal motion,

is helpful to recognize RV systolic dysfunction
Motion of the TV annulus is affected by prior cardiac surgery, therefore TAPSE and
S’ are less useful in this population
Systolic function, measured by TAPSE, S’ and FAC may be overestimated, in case of

volume overload
Tissue-Doppler derived IVRT is close to zero in a healthy right ventricle
Refer to figure 7B
RV outflow tract VTI is a surrogate marker of RV output and can be applied for
repeated haemodynamic assessment
RV longitudinal strain is angle-independent measure and has the potential to detect

early and regional myocardial impairment, when conventional echocardiographic
parameters remain within normal limits
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Figure 7 - RV systolic dysfunction
B
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2.3.3 - Lung ultrasound
Assoc. Prof. Elke Platz, MD, MS, FESC, FACEP

Cardiovascular Division, Brigham and Women’s Hospital,
Harvard Medical School, Boston, USA
Key messages
Ultrasound of the lungs and pleural space is a useful tool in the detection
and quantification of pulmonary congestion in patients with known or sus-
pected HF.
LUS can be performed with most types of ultrasound equipment, ranging
from high-end ultrasound systems to pocket-size devices.
The main finding of pulmonary congestion on lung ultrasound are so called
"B-lines", which are vertical, hyperechoic lines that arise from the pleural
line and move back-and-forth with respiration.
If multiple B-lines are visualized in several areas (zones) of the chest, pul-
monary congestion should be considered.
The differential diagnosis for multiple B-lines includes interstitial lung disease,
acute respiratory distress syndrome, pneumonitis, and pulmonary contusions.
Pleural effusions can be identified laterally on each hemithorax as anechoic
spaces above the diaphragm.
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Introduction
While echocardiography traditionally plays an important role in the diagnosis and mana-
gement of patients with known or suspected HF, ultrasound of the lungs and pleural space
has more recently been identified as a useful tool in the detection and quantification of
pulmonary congestion in these patients. The main focus of this chapter is the utility of
sonographic findings of pulmonary congestion, in addition to a brief overview of other
LUS findings that could lead to alternative diagnoses in patients with acute dyspnea and/
or hypoxia.
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Technical considerations
LUS can be performed with either standard ultrasound equipment or pocket devices with
different transducers, depending on the condition in question. An overview of relevant tech-
nical aspects is provided in Table 1.
Table 1 - Overview of lung and pleural ultrasound techniques in patients with

known or suspected heart failure
Pulmonary Pleural
Pneumothorax
congestion effusions
Ultrasound
High-end, portable or pocket device
system
Linear
Transducer type Phased array or curvilinear (Phased array or
curvilinear)
Imaging depth ~18 cm Variable (~20 cm) Variable (~10 cm)
Anterior and late- Lateral chest at level

Anterior chest, both
Scan areas ral chest, both of diaphragm, both
hemithoraces
hemithoraces hemithoraces
Number of areas
(zones) on each (2 to) 4 1 At least 1
hemithorax
Patient
Sitting or supine
positioning
Anechoic fluid col-

Multiple bilateral lection above the
Ultrasound B-lines (hyperechoic, diaphragm; loss of Absence of lung sliding
findings vertical lines arising mirror image artifact; along the pleural line
from the pleural line) visualization of tho-
racic spine
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Normal lung
Normal lung tissue does not typically lend itself to sonographic imaging due to high impedance
differences between air and surrounding tissue. In contrast to other ultrasound techniques,
e.g. imaging of the heart, LUS relies on the identification or absence of certain imaging
findings, often artefacts, rather than the display of actual anatomic structures. For the per-
formance of a LUS examination the appropriate transducer (Table 1) is positioned in sagittal
orientation (perpendicular to ribs) in one intercostal space for imaging of the lung or pleural
space in one of several areas (zones) of the chest. Normal findings on LUS include a back-and-
forth movement along the pleural line (Figure 1), which is also called "lung sliding". Other
normal findings that can be seen in some patients are reverberations artefacts between the
pleural surface and the chest wall, which appear as equally spaced, horizontal lines on the
ultrasound screen and are called "A-lines" (Figure 1).
Figure 1 Normal appearance of lung on ultrasound

Left panel without labels ; Right panel with labels.
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Pulmonary congestion
Diagnosis
What are B-lines: For the detection of pulmonary congestion, the presence and number of
vertical "B-lines" (Figure 2) on LUS are assessed. These hyperechoic reverberation artefacts,
when present, provide a graded measure of extra-vascular lung water with high inter-rater
reproducibility after as little as 30 minutes of training. They are thought to stem from fluid
filled or otherwise thickened interstitial and alveolar spaces in the lungs. B-lines arise from
the pleural line, extend to the far field of the ultrasound screen and move back and forth
during respiration.
Where to scan: Several different imaging protocols have been described, ranging from 4 to
28 chest zones examined. The most commonly used imaging protocol involves the sono-
graphic assessment of 8 anterior and lateral zones (4 on each hemithorax) (Figure 3). An
abbreviated protocol employing 6 zones (3 on each hemithorax) has also been reported to
demonstrate high diagnostic accuracy for the detection of pulmonary edema in patients with
undifferentiated dyspnea presenting to the Emergency Department. LUS can be performed
with the patient sitting or supine, however, for serial examinations, patient positioning and
ultrasound clip length (if videos are interpreted off-line) should be kept constant since both
may impact the number of B-lines visualized. For off-line B-line quantification, ~6 second
video clips should be recorded for each zone.
Figure 2 - Example of B-lines on lung ultrasound

Right panel without labels; Left panel with labels.
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How to count B-lines: Several B-line quantification methods have been reported that are
either count or score based. All of these methods quantify the maximum number of B-lines
in one intercostal space per chest zone (in a single imaging frame). Count based methods
sum the number of B-lines across all zones, whereas score-based methods consider one
zone as positive if at least 3 B-lines are visualized in one intercostal space. The presence of
≥3 B-lines in ≥2 zones on each hemithorax should be considered diagnostic for pulmonary
edema in the appropriate clinical context (see "Differential diagnosis" below).
Figure 3 - 8-zone imaging protocol for lung ultrasound
Adapted from Platz E. et al. Eur J Heart Fail. 2017 Sep;19 (9): 1154-1163
Monitoring
LUS may represent a useful tool in the monitoring of patients with either acute or chronic HF,
allowing for serial assessment of changes in pulmonary congestion in response to therapy.
Prior research demonstrated that the number of B-lines decreases rapidly after hemodialysis
in patients with end-stage renal disease. Similarly, during a hospitalization for acute HF, the
number of B-lines declines significantly with treatment in as little as 24 hours. In addition,
early data suggest that in patients who were recently hospitalized for acute HF serial exami-
nations with LUS in the outpatient setting may be a feasible strategy to tailor decongestive
therapy based on LUS findings. While these data are encouraging, further research is nee-
ded to gain a better understanding of B-line cut-off values and the patients that are most
likely to benefit in clinical practice, should this technique prove to be useful in larger trials.
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Prognosis
Both hospitalized and ambulatory patients with a greater degree of (residual) pulmonary
congestion, as indicated by a higher number of B-lines at the time of discharge or clinic visit,
are at greater risk for subsequent HF hospitalizations or death, independent of ejection frac-
tion. Specifically, the presence of ≥3 B-lines on 5 or 8-zone LUS by pocket ultrasound has
been associated with an up to 4-fold increase in 6-month HF hospitalizations or death in
ambulatory HF patients. More than 80% of HF patients in the highest B-line number group
had no abnormal findings on lung auscultation. Similarly, the presence of ≥7 B-lines total on
4-zone LUS with standard echocardiographic equipment at the time of hospital discharge
identified acute HF patients at a 3-fold risk of 90-day HF hospitalization or death. These
findings suggest that LUS may identify subclinical pulmonary congestion in HF patients, and
those at greater risk for subsequent adverse events. Larger, randomized clinical trials are
needed to examine whether tailoring therapeutic strategies to reduce the number of B-lines
on LUS can improve outcomes in patients with HF.
Pleural effusions
In addition to the assessment of pulmonary congestion by B-lines, the presence of pleu-
ral effusions may be examined laterally at the level of the diaphragm. If there is a pleural
effusion, the normally visible mirror image artefact caused by the diaphragm is absent and
instead an anechoic fluid collection can be visualized above the diaphragm. The presence
of a pleural effusion usually allows for visualization of the thoracic spine. Pleural effusions
can also be seen on standard echocardiographic views (e.g. the parasternal long axis view)
and should be differentiated from pericardial effusions. Pleural effusions on ultrasound can
be detected in up to 70% of patients with acute HF. Although they may be clinically relevant
in individual patients, their diagnostic and prognostic importance in acute HF is currently
less clear than that of B-lines.
Pneumothorax and other findings

As dyspnea is one of the most common symptoms of acute HF, but non-specific, alterna-
tive diagnoses, such as a pneumothorax, should be considered. LUS can be used to detect
a pneumothorax with higher sensitivity than supine chest x-ray. The main finding on LUS
that rules out a pneumothorax in the examined area is the presence of "lung sliding" (hori-
zontal movement of the pleural line with respiration). Absent lung sliding should raise the
concern for a pneumothorax. In some cases of pneumothorax, a "lung point" can also be
seen. The lung point marks the border of a pneumothorax and demonstrates lung sliding
adjacent to absent lung sliding in the same intercostal space. Patients can be examined either
in supine or sitting position. As air typically collects anteriorly and on the highest point of
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the chest, one or several intercostal spaces of the upper anterior chest, in or medial to the
midclavicular line, should be examined. It is important to understand, that the presence of
a pneumothorax can only be excluded in those areas of the chest in which lung sliding is
present, i.e. patients could still have a pneumothorax in other areas of the chest. Other fin-
dings that can be detected with LUS include pulmonary consolidations, which can be seen
in pneumonia, for instance. Consolidations may demonstrate variable echogenicity and have
more of a solid-organ-like appearance on ultrasound.
Differential diagnosis of lung ultrasound findings

While LUS can be an extremely helpful tool in the assessment of patients with known or
suspected HF, it is important to keep in mind that LUS remains one piece of the diagnostic
puzzle. The results of this – and any other test – should not be considered in isolation but
rather in the context of the patient’s history, physical examination and other investigations.
For example, patients with predominant right-sided HF may not demonstrate any pulmonary
congestion and others (e.g. those with interstitial lung disease) may demonstrate B-lines
for reasons other than pulmonary congestion. A summary of differential diagnoses of LUS
findings is provided in Table 2.
Table 2 - Differential diagnosis of lung ultrasound findings
Pulmonary Pleural Pneumo-

congestion effusions thorax
Anechoic fluid col-

lection above the
Absence of lung
Ultrasound diaphragm; loss of
Multiple B-lines sliding along the
findings mirror image artifact;
pleural line
visualization of thoracic
spine
Interstitial lung disease/

Examples of other Hemothorax, Apnea, right main
pulmonary fibrosis,
chylothorax; stem intubation,
conditions with ARDS, pneumonitis
Empyema (complex fluid adhesions, large
these findings (including Covid-19),
collection) blebs
pulmonary contusions
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2.3.4 - Other uses of ultrasound as a clinical tool
Prof. Raul M. Vicho, MD, PhD, FESC

Servicio de Cuidados Criticos Hospital Quironsalud Rotger,
Palma de Mallorca, España
Key messages
The use of ultrasound as a guide and complement the clinical assessment

is recommended
In critical patients a more accurate and early diagnosis with this tool impro-
ves the prognosis.
This chapter is focused on the use of the different modalities of ultrasound
as a tool, in the patient with acute renal injury, hypercapnic respiratory fai-
lure, acute cognitive impairment and acute abdomen.
Introduction
In critical care units the use of ultrasound techniques by the physicians who are directly
attending the patients has been mainly focused and restricted to the heart, the abdomen,
main vessels, and more recently, the lungs. However, in the last years it has significantly
expanded the use of this technique to several other organs and clinical settings. This chap-
ter is focused on these new scenarios, like the use of ultrasounds to assess the diaphragm
function, renal flow, intracranial pressure and vessels, acute abdomen and gastric content.
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Renal doppler ultrasound applied to the critically ill patient

The use of renal ultrasound may lead to a lower use of vasoactive drugs and a better adjust-
ment of volume and diuretics, with lower rate of RRT.
Window and acquisition technique

Probe in upper lower orientation (mark up or down) from posterior axillary line to thoracic
level is lowered to abdomen (Figure 1). It is a lateromedial projection and the image obtained
is as follows: in the right-side abdomen, close to the probe, there is the liver and then, far-
thest from the transducer, the kidney in its longitudinal axis. In the left-side abdomen, close
to the probe there is the spleen and then the kidney also in its longitudinal axis.
Figure 1 - (Left) Renal ultrasound window image in critics;

(Right) Probe position
Indications
The first step is to establish an anatomical assessment:
Diagnosis of a patient with acute pyelonephritis (Figure 2)
Hydronephrosis especially in a situation of sepsis of urinary origin (Figure 2)
Chronic renal failure and the consequent atrophy and decrease in both the length
and thickness of the renal cortex (Figure 3)
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Figure 2 - (Left) Acute non-obstructive pyelonephritis;

(Right)Hydronephrosis
Figure 3 - Renal atrophy

in chronic renal failure
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After the anatomical overview, it should be used doppler ultrasounds at the level of the renal
cortex to assess perfusion and, above all, to confirm or rule out consolidated tubular damage.
This measurement is carried out by applying color doppler and identifying arcuate or inter-
lobar arteries, the volume of sample on one of them is followed and with this a time-speed
spectral doppler curve is achieved. The analysis of this curve involves obtaining the systolic
peak velocity (SysVel) and the diastolic peak velocity (DiasVel) as well as the relationship
between them through the RI. The RI is SysVel-DiasVel / DiasVel and the normal value is
<0.75. It implies that there is still no tubular lesion of haemodynamic origin, the renal cor-
tex in its most peripheral vessels is still perfused by compensatory mechanisms, and there
is no tubular damage. When the DiasVel decreases it implies a decrease in diastolic flow at
this level and reflects a loss of vasotonic compensatory mechanisms with the consequent
progressive necrosis of renal tubular cells. If the diuresis is decreased and there is ARF with
an RI <0.75, it indicates pre-renal failure, before ischemic tubular necrosis. However, if there
is an ARF with RI> 0.75, there is already an ischemic tubular lesion. When RI value is close
to 1, the need for RRT in the next few hours is very high (Figure 4). RI has also been used
to monitoring acute or chronic renal graft rejection in transplanted patients.
Figure 4 - (Left) Renal Doppler of normal interlobar arteries ;

(Right) Ischemic tubular necrosis
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Diaphragmatic ultrasound
The diaphragm is the most important muscle of breathing. All respiratory dysfunctions of origin
or with a ventilatory component affect its structure, movement or thickening. Its assessment
by dynamic image is basic and there is already enough evidence to use it at the bedside with
the POCUS philosophy. The US study of the diaphragm applied to clinical settings where there
is, or may exist, ventilatory insufficiency, should be carried out assessing:
Size
Thickening
Excursion
Window and acquisition techniques

To assess the diaphragmatic excursion, it is carried out through the post-inferior window in
the upper lower orientation but with the echocardiographic sectorial probe or the convex of
the abdomen (Figure 5A). Because this study requires a greater depth, therefore, these less
frequently used probes are used. In addition to the upper and lower placement of the brand,
its focus, instead of transverse, will be directed towards the patient's neck. In this way, the
echo sector of the screen places the hyperechogenic image that is on the roof of the liver
(the right hemidiaphragm) or the spleen (left hemidiaphragm) quite facing the probe and,
when analyzing the displacement in M mode, the result will have high performance (Figure
5A and 5B). Its normal value is >40mm in women and >50mm in men at deep inspiration.
Lower values may suggest ventilatory insufficiency.
To assess the size and the diaphragmatic excursion, the high frequency probe in the upper
lower orientation (the apposition zone) will be used, which will be the axillary posteroinfe-
rior region of each side according to the hemidiaphragm to be studied (Figure 6A). Only 2D
mode will apply. Once the diaphragm is visible, the thickening fraction is calculated which is
a ratio of difference in thickness in the respiratory cycle, which must be greater than 30%
under normal conditions. The distance from pleura to peritoneum is the diaphragm (Figure
6B) and it is measured on inspiration (DI) and expiration (DE) and the thickening fraction is
the calculation that derive from them:
Thickening fraction= (DI- DE)/DE

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The diaphragmatic thickness in expiration (DE) under normal condition in the apposition
zone is 3-4 mm.
During the weaning from mechanical ventilation, a diaphragmatic excursion >25mm and a
thickening fraction >30–36%, increase the likelihood of success of the spontaneous brea-
thing trial. Conversely, in patients with decompensated chronic ventilatory insufficiency, the
diaphragm excursion may be less than 5 mm.
Indications for diaphragm US
To guide the weaning of Invasive or Non-Invasive Mechanical Ventilation
To indicate Invasive or non-Invasive Mechanical Ventilation
To assess diaphragmatic atrophy in patients in controlled modalities of ventilation
To assess the component of ventilatory insufficiency that leads to hypoxemia
To diagnose a phrenic paralysis in a hemidiaphragm
To rule out phrenic paralysis in the contralateral hemidiaphragm next to the anaesthe-
sia performing a staging block, which is sometimes complicated by phrenic paralysis
and thus avoid apnoea if it occurs
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Figure 5A - (Left) Scheme of the posteroinferior axillary window sectorial probe

(Right) Line cursor cutting the diaphragm at the liver (top) and M-mode image obtained (bottom), allowing to measure the
height
INTERMAMMARY LINE
Figure 5B - Diaphragm excursion M

mode ultrasound during inspiration
Measuring the height
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Figure 6A - (Left) Apposition zone with high frequency flat craniocaudal mark
probe (blue arrow) ; (Right) Ultrasound image showing from top to bottom in order: pleura-dia-
phragm-peritoneum lines
INTERMAMMARY LINE
PLEURA
PERITONEUM DIAPHRAGM
Figure 6B - Reduced diaphragm thickening (1.3mm) in a patient with

muscular dystrophy
PLEURAL
LAYER
DIAPHRAGM PERITONEAL
LAYER
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Transcranial ultrasound in critics

Optic nerve sheath
A two-dimensional study with a high-frequency flat probe from the orbit allows to assess the
width of the optic nerve sheath, which correlates with the ICP. It has the same pathophysio-
logical significance as papillary oedema valued by ophthalmoscopy-fundus. The flow of the
MCA with a sectorial probe may also be analysed
Window acquisition and technique

With a high frequency flat probe located above the eyelid transversely, near the roof of the
orbit, hypoechoic tubular image is obtained behind the eyeball (Figure 7). A width greater
than 5.9 mm at a level of 3 mm after the retina, indicates an ICP> 20 mmHg.
Transcranial echo-doppler
Window acquisition and technique
The sectorial probe is placed transversely in a temporary window (mark in the anterior or
posterior position) (Figure 8). 2D mode is initially used and colour doppler is added to find
the Willis polygon. Depending on the depth, an artery is soundproofed. A doppler curve with
SysVel and DiasVel is obtained that will be positive in all arteries except in the ACA, as it is
the only flow that moves away from the transducer. The mVel and the PulsI are calculations
that derive from them:
mVel cm/sec = (Peak SysVel + 2 x End DiasVel) / 3
PulsI = Peak SysVel- End DiasVel/ mVel

(Normal: 0.6- 1.2)
Table 1 shows the normal mVel values and the depth at which they are acquired. It is also
interesting to remember that CPP depends on the result of two balanced opposing forces:
the ICP or CVP pushing the blood out of the cranium and the MAP pushing into.
CPP = MAP-ICP (or CVP whichever is greater)

(Normal CPP > 60 mmHg)
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Figure 7 - (Left) Probe position for optic nerve sheath analysis ; (Right)
Nerve optic sheath width of 7.6mm at 3 mm behind the retina indicating an intracranial pressure > 20mmHg
3MM
Figure 8 - Temporal transcranial ultrasound windows to Willis polygon

with sectorial probe (blue arrow) anterior mark.
Cerebral arteries doppler color ultrasound of the Willis polygon’s
TEMPORAL WINDOW
BACK FRONT
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Table 1 - Normal values of velocity and depth of each artery of the Willis
polygon from the temporal window
Mean velocity Probe distance

Artery Window
(cm/s) (mm)
MCA 55 50 Temporal
ICA 40 65 Temporal
ACA -50 70 Temporal
PCA 40 65 Temporal
Indications for transcranial US
Intracranial hypertension: In addition to the width of nerve sheath >5.9mm, the confir-
mation is possible by obtaining the flow of the MCA and estimating the PulsI. The
Bellner equation is applied: ICP = 10.93 x PulsI- 1.28. The value is pathological above
12 mmHg (figure 9)
Assessment of self-regulation: IAS = Average velocity MCA/CPP. Normal value is < 1
Vasospasm in SAH: The LI is a relationship with the average velocity of the extracra-
nial carotid artery to obviate hyperdynamic states. In the vasospasm, LI is > 3. Table 2
shows mean velocities that suggest radiological and clinical vasospasm
To rule out phrenic paralysis in the contralateral hemidiaphragm next to the anaesthe-
sia performing a staging block, which is sometimes complicated by phrenic paralysis
and thus avoid apnoea if it occurs
Hyperaemia: In hyperdynamic state (high CO) the arterial velocity is increased and the LI is <3
Encephalic death: Crucial in the diagnosis and maintenance of the organ donor. In
cases of brain death, in the middle cerebral artery there is no diastolic flow or is
reversed in diastole (Figure 10)
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Figure 9 - Doppler example of the middle cerebral artery

Example of intracranial hypertension
Figure 10 - Doppler registries of encephalic death (red circles).

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Table 2 - Mean velocity values for radiological cerebral arterial vasospasm
Mild-moderate spasm Severe spasm

Cerebral
mVel (cm/sec) ≥ mVel (cm/s) ≥ Window
Artery
Size reduction: 25-50% Size reduction >50%
Middle 120 200 Temporal
Internal
80 130 Temporal
Carotid
Anterior >50% basal o >50 cm/s/24h 170 Temporal
Posterior 80 130 Temporal
Basilar 80 130 Transforaminal
Abdominal ultrasound in critics

POCUS may be considered a fast approach to many critical intra-abdominal complications.
It may be useful in abdominal trauma, abdominal pain (cholecystitis, intestinal obstruction,
gastrointestinal perforation, suspected rupture of abdominal aorta, retroperitoneal assess-
ment), appropriate placement of central venous catheter, preoperative gastric evaluation,
pre-invasive procedures that involve sedation, nasogastric tube placement, abdominal com-
partment syndrome and intra-abdominal hypertension.
Main techniques and Indications

Fast abdominal ultrasound in trauma
The purpose of the e-fast is to detect free fluid collection in terms of hemoperitoneum,
hemopericardium, and its extension pneumothorax and/or haemothorax, with a high accu-
racy. The main advantages of this technique are: quick, non-invasive, innocuous, at bedside,
non-interrupting resuscitation, may be made by the same attending physician, shortens the
time to surgery and/or other therapeutic decisions, and reproducible in the follow-up. The
limitations are poor images (i.e. obesity, subcutaneous emphysema).
The following sequence should be performed: Firstly, the abdominal probe or the sectorial
echocardiography probe in abdomen mode is used. The patient, if possible, will be placed
supine using several windows (Figure 11). Probably, the best performing window for detec-
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ting intraperitoneal free fluid is the right hypochondrium, in the hepatorenal space called
Morrison's space (Figure 12), a very posterior fold of the peritoneal cavity, where the negative
predictive value for absence of free fluid is close to 100%. To diagnose or rule out free fluid
from the suprapubic window (Douglas sack bottom), the bladder rectum space in men, and
the uterovesical space in women, are seen as areas where small amounts of intraperitoneal
pathological fluid can accumulate early. However, the bladder must be full to see de Douglas
sack bottom. The sub-xyphoid window (Figure 13) explores the presence of hemopericar-
dium. In addition, pneumothorax should be ruled out by placing the probe perpendicular to
the ribs in the middle clavicular line, exploring the sliding presence or absence in 2D, and/
or image of “beach and sand” or code of bars in M mode (Figure 14). Furthermore, in the
thoracic posteroinferior axillary window (Figure 15), the presence and quantity of pleural
fluid, which in the case of trauma, it will mainly be haemothorax. The approximate amount
of pleural fluid can be assessed at that level through the formula of Balik et al., considering
the pleural effusion as mild, moderate or severe:
Pleural effusion volume (millilitres)= distance lung to diaphragm in millimetre x 20
The time needed to perform an echo abdominal fast should be less than 3 minutes.
Figure 11 - E-fast ultrasound windows

THORACIC ANTERIOR
INTERMAMMARY LINE
THORACIC RIGHT THORACIC LEFT
POSTEROINFERIOR POSTEROINFERIOR
AXILLARY LINE AXILLARY LINE
RIGHT HYPOCHONDRIUM LEFT

HYPOCHONDRIUM
SUBXPHOID
SUPRAPUBIC
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Figure 12 - Right hypochondrial window posterior axillary line

5-10 cm under intermammary line level. Morrison space. Morrison / Fast positive
INTERMAMMARY LINE
Figure 13 - (Left) Subxiphoid window ; (Right) Pericardial effusion from

subxiphoid window
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Figure 14 - (Left) Four windows each hemithorax ; (Right) Lung ultrasound

pneumothorax
Windows number 1 for rule out or rule in pneumothorax; Pleural line is less echogenic and has no sliding
Figure 15 - (Left) Posteroinferior axillary thoracic window In supine decubitus, with

the probe under 5-10 cm of the intermammary line (blue arrow) near bed ; (Right) Pleural effusion at
that level. Balik formula distance in millimeters from lung to diaphragm (red line)
INTERMAMMARY LINE
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Acute abdominal pain

The performance of abdominal ultrasound focused on this syndrome is around 45% for
changes in therapeutic decisions, mainly assessing the presence of intraperitoneal free fluid,
or as an introduction to another test, or the operating room. The e-fast does not replace a
regulated abdominal echo. The best performance could be in the following scenarios:
Acute cholecystitis: It is a simple exploration, with a very short learning curve. It is

the fourth cause of infection in critical patients. In the elderly, alithiasic cholecysti-
tis is prevalent and may occur, especially initially, without fever and in poor general
condition or shock. (Figure 16). The main findings of cholecystitis are: Gallbladder
wall greater than 3 mm / Gallbladder dilated > 10 cm in its major axis and >5 cm in its
short axis / The ultrasound Murphy sign, at the point where the gallbladder is seen,
has a sensitivity and specificity close to 80% / Peri-vesicular fluid in advanced cli-
nic situation (20%).
Intestinal obstruction: The following questions are intended to be answered with

POCUS: Is there an obstruction? Is it mechanical or functional? Where is the obstruc-
tion? How does conservative treatment evolve? The diagnostic performance of the
intestinal obstruction assessed by ultrasound has a sensitivity of 88% and a speci-
ficity of 100%. Intestinal obstruction, involves anechoic/hypoechoic tubular images
due to the accumulation of fluid due to ileus/mechanical obstruction. In jejunum, the
diameters will be greater than 25 mm and greater than 15 mm in the ileum. In the
jejunal level, there are linear images that are not found in the ileal dilations (Figure
17). When there is a colonic obstruction, the intestinal loop is larger than 50 mm. You
can also see an intestinal wall that is greater than 3 mm. If it is a mechanical obstruc-
tion, peristalsis will be increased and if it is not mechanical (paralytic ileus), peristalsis
will be abolished. The anterior abdominal windows, may not be seen because of air,
giving some artefact images, similar to thoracic echo pattern A. To visualize dilated
loops with liquid content, the flanks and iliac fossae should be further explored and
the transducer should be positioned with lateral inclined approach.
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Contained abdominal aortic rupture: It is another cause of acute abdominal pain,

where an early suspicion and diagnosis is crucial. The window for assessing possible
abdominal aortic rupture is in the epigastrium, with the probe placed or transverse
or longitudinal. If the probe is placed transversely, a transverse image of the aorta is
seen and the presence of a rupture contained in the hypoechogenic image (Figure 18)
surrounding the vascular structure. When the analysis is performed with the probe
placed longitudinally, the abdominal aorta will be seen along its long axis. The risk
of rupture is important with a short axis calibre of the aorta > 5 cm. If the patient is
not very obese, the sensitivity and specificity to assess the calibre of the abdominal
aorta, and diagnose or rule out an acute abdominal aortic pathology is nearly 100%.
Figure 16 - Image suggestive of

cholecystitis
Thickened wall (> 3 mm) with oedema
Figure 17 - (Left) Jejunal dilation

(36mm); (Right) Ileal dilation
(52mm)
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Figure 18 - Abdominal aortic

aneurysm with external
hypoechogenic image (blue arrow)
of contained rupture
Retroperitoneal ultrasound assessment

It is an important clinical scenario because
there are many procedures currently per-
formed through the femoral vascular bundle
(electrophysiological studies, cardiac cathe-
terization, interventional neuroradiology,
insertion of devices such as intra-aortic
balloon pump, extracorporeal oxygenation
systems, prosthetic valves with percutaneous access, etc.). These procedures are often
performed in patients with vasculopathy treated with antiplatelet or anticoagulants. The
rupture of the vascular bundle has a non-negligible frequency and will imply a haemorrhage
that will progress to the retroperitoneal space causing abdominal distension and pain with
non-irritative characteristics (usually less intense). The hematoma may cause shock and/
or compartment syndrome. It may be identified when the level of the retroperitoneal hema-
toma is upper to the pelvis (renal level). In this case, the space between the kidney and the
spine is visualized in the right or left hypochondrial window (Figure 19).
Figure 19 - (Left) Retroperitoneal hematoma at renal level detected by

ultrasounds in the right posterior hypochondrial window ;
(Right) Abdominal CT scan (white arrow)
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Correct insertion of central venous catheter

The right atrium and superior vena cava can be seen through subxiphoid window (Figure
20). After the injection of 5 ml of agitated saline solution, check if the right atrium is rep-
lenished before 2 seconds. With this procedure a chest X-ray is not necessary.
Figure 20 - SVC and right atrial filling with saline serum
SVC
Intra-abdominal hypertension
In situations of intra-abdominal hypertension or when there is an established abdominal
compartment syndrome, ultrasound allows to study causes or treatment:
Detection of dilated bowel loops as mentioned before
Assessment of gastric size and the possibility to insert a nasogastric tube, while
monitoring its appropriate function
To guide the evacuation of a collection
A parallel echocardiographic study can be done to assess the collapse of the IVC, espe-
cially if there are clinical data of positive fluid balance and anasarca. It is an important
tool and guide when performing depletive or resuscitation treatment, when IVC col-
lapse is less than 50% in spontaneous ventilation or 18% - 22% under mechanical
Ventilation. A negative fluid balance decreases hypervolemia and intra-abdominal
hypertension
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Gastric ultrasound assessment

Although it is an abdominal US study, this approach deserves a specific section because of
its practical utility, even in the daily practice of an Anaesthesia or Critical Care departments.
Window and acquisition technique

At the subxiphoid level, with the abdominal probe or the echocardiography probe placed
perpendicular and longitudinal to the epigastrium. With this gastric antrum window, peris-
taltic movements will be displayed in a circular way. When the stomach is empty, the image
will be a hypoechogenic impeller that will surround a more hyperechogenic structure that
is the constricted mucosa: “bull´s-eye” sign (Figure 21). When there is liquid content, the
image will be hypoechoic, close to anechoic. If the stomach is full of solid content, “frost
sign” is displayed (Figure 22). When the stomach is full and, therefore, enlarged, the gastric
body is also visible in the upper abdominal level, in the middle axillary line with the probe
placed upper to lower, in the same window where the splenorenal space, but with a slightly
closer visualization.
Indications
The assessment of the size and content of the stomach is useful for:
Avoid bronchoaspiration at the time of airway management in anaesthesia (most

common cause of death in relation to anaesthesia)
To diagnose gastroplegia
To guide correct insertions of nasogastric tube
Monitoring enteral nutrition tolerance
Assessment of gastric involvement in an ileus or mechanical obstruction

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Figure 21 - Ultrasound view of the gastric antrum with a longitudinally

placed (craniocaudal) probe in a subxiphoid window
LEFT LIVER LOBE
GASTRIC ANTRUM
SUPERIOR
MESENTERIC
ARTERY
PANCREAS
Figure 22 - (Left) Stomach full of liquid; (Right) Empty stomach

II.3
P.125 3 -PRELOAD RESPONSIVENESS
Prof. Jean-Louis Teboul, MD, PhD

Professor of Therapeutics and Critical Care Medicine,
Service de médecine intensive-réanimation, Bicetre hospital,
AP-HP. Université, Paris-Saclay, Le Kremlin-Bicetre, France
Dr. Rui Shi, MD

AP-HP / Université, Paris-Saclay, Le Kremlin-Bicetre, France
Prof. Xavier Monnet, MD, PhD

Professor of Critical Care Medicine,
AP-HP / Université, Paris-Saclay, Le Kremlin-Bicetre, France
Key messages
Dynamic tests rather than static indices are appropriate to assess preload
responsiveness
Preload responsiveness should only be assessed when patients present signs
of haemodynamic instability and/or of tissue hypoperfusion and when hypo-
volemia is not evident
Presence of preload responsiveness does not mean that fluid administration
is mandatory. Individualized fluid management should be applied
Application of the preload responsiveness concept helps guiding fluid admi-
nistration and fluid removal, and identifying the cardiac origin of failure of
weaning from mechanical ventilation
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Introduction
Preload responsiveness is defined as the increase in stroke volume or cardiac output

following an increase in cardiac preload. Fluid administration results in an increase in
left ventricular stroke volume (fluid responsiveness) if both ventricles are preload res-
ponsive. It is logical to state that fluid responsiveness is equivalent to biventricular preload
responsiveness.
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3.1 - Physiological principles
In most patients with acute circulatory failure, fluid administration is a first-line therapy
aimed at increasing cardiac output, according to the Frank-Starling’s relationship (Figure 1),
and ultimately oxygen delivery. However, after the initial resuscitation phase, the decision
to give fluid should be weighted depending on the expected benefits and risks. Indeed, fluid
overload has been shown to worsen critically ill patient’s outcome, especially in cases of
ARDS, sepsis, and acute kidney injury, and half of the patients are no longer fluid-responsive
after the initial phase of shock. Therefore, testing preload responsiveness is essential in this
setting, to identify patients who will benefit from fluid administration.
Several tests and indices have been developed to assess preload responsiveness. This chap-
ter aims at providing a comprehensive overview of physiological principles, interpretation
and clinical applications of these tests (Tables 1 and 2).
Figure 1 - Frank-Starling curve

The slope of the Frank-Starling curve depends on the ventricular systolic function. One given value of preload can be
associated with preload responsiveness as well as preload unresponsiveness. By contrast, dynamic preload challenges
induced by mechanical ventilation or provoked by passive leg raising, end-expiratory occlusion or “mini” fluid challenge,
allow detection of preload responsiveness by observing the resulting effects on stroke volume.
STROKE
VOLUME
Normal ventricular
systolic function
Significant response
Poor ventricular
No response systolic function
Preload challenge: - Mechanical ventilation CARDIAC

- EEO test PRELOAD
- PLR test
- «Mini» fluid challenge
Reprinted with permission from Monnet et al.
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Table 1 - The reported predictive performance of preload responsiveness

indices or tests
AUROC Threshold
Parameter Sensitivity Specificity
(95%CI) value (%)
Static
CVP 0.55(0.48-0.62) NR NR NR
LVEDA 0.64(0.53-0.74) NR NR NR
Dynamic
Mini-FC 0.91(0.85-0.97) 0.82 0.83 5
SVV 0.84 (0.78–0.88) 0.82 0.86 12
PPV 0.94 (0.91–0.95) 0.88 0.89 12
VIVC 0.75 (NR) 0.79 0.70 12-46
PLR 0.95 (0.93–0.97) 0.85 0.91 10
EEO 0.96 ( 0.92–1.00) 0.86 0.91 5

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Table 2 - Summary of available indices or tests to assess preload

responsiveness
Indices or tests Equations
Fluid challenge
Mini fluid challenge

=(COmax-CObase)/CObase *100%
PLR
PPV =(PPmax-PPmin)/[(PPmax+PPmin)/2]*100%
SVV =(SVmax-SVmin)/[(SVmax+SVmin)/2]*100%
= PPVTV8-PPVTV6
Tidal volume challenge
=SVVTV8-SVVTV6
=[(DIVCmax on inspiration-DIVCmin on expiration)/DIVCmin on

DIIVC
expiration]*100%
=[(DSVCmax on expiration-DSVCmin on inspiration)/DSVCmax on

CISVC
expiration]*100%
EEO =(COmax-CObase)/CObase *100%
=[(COmax EEO - CObase)/CObase *100%] +[CObase- COmin EIO)/

EEO+EIO
CObase *100%]
max: maximal value during the test; min: minimal value during the test
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Main advantages Main limitations
Golden standard Risk of fluid overload especially when repeated
Less volume of fluid used Requires precise cardiac output monitoring
Intra-abdominal hypertension, compressive

Reversible and no drop of fluid infused
stockings, head trauma, hip or spine injury
Spontaneous breathing, low tidal volume, low

No need for cardiac output monitoring lung compliance, cardiac arrhythmia, intra-ab-
dominal hyper-tension
Accurate in regular rhythm and regular TV Spontaneous breathing, low tidal volume, low
ventilation; be measured invasively and lung compliance, cardiac arrhythmia, intra-ab-
non-invasively dominal hypertension
Useful in case of low tidal volume Spontaneous breathing, cardiac arrhythmia
Spontaneous breathing, low tidal volume, low

Non-invasive cardiac output monitoring lung compliance, poor echogenicity and mode-
rate accuracy
Spontaneous breathing, low tidal volume,

Non-invasive cardiac output monitoring low lung compliance, poor echogenicity and
contra-indications to transesophageal Doppler
Too marked spontaneous breathing activity

Easy to perform in ventilated patients
impeding the 15 seconds test
Too marked spontaneous breathing acti-

Easy to perform in ventilated patients and
vity impeding the 15 seconds test and poor
monitored by a non-invasive method
echogenicity
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3.2 - Static indices of preload
Even though it has been well demonstrated that static indices of preload are not adequate
to guide fluid resuscitation, they are still used by many intensivists. The rationale for using
static indices of cardiac preload is that a low cardiac preload, rather than a higher one, may
predict a significant increase in stroke volume after fluid administration according to the
Frank-Starling mechanism. Nevertheless, there is not only one Frank-Starling curve, but a
family of curves depending on the cardiac contractility so that except for extreme values
of cardiac preload markers, a given value of preload may be associated with preload res-
ponsiveness as well as preload unresponsiveness (Figure 1).
Among the static markers of preload, CVP has been historically the most commonly used.
However, for the reasons mentioned above, even if CVP is an indicator of cardiac preload, it
is not a marker of preload responsiveness (Figure 1). In this regard, the current Surviving
Sepsis Campaign guidelines no longer recommend the use of CVP to guide fluid resuscitation
in septic patients. Nonetheless, although CVP is not able to assess preload responsiveness,
it is still useful in the management of critically ill patients.
Analogously, other static indices of preload including either pressure (such as pulmonary
artery occlusion pressure) or volume/surface (such as right and left ventricular end-diastolic
volumes/surfaces or inferior/superior vena cava diameters) share most of the limitations of
CVP to assess preload responsiveness.
3.3 - Dynamic indices and tests of preload

responsiveness
3.3.1 - Fluid challenge
Fluid challenge is the most direct way to detect preload responsiveness. Conventional fluid
challenge is performed by an infusion of a fluid bolus (300-500 mL) during a short period of
time. Fluid responsiveness is defined as an increase of at least 15% in cardiac output after the
fluid infusion. However, fluid challenge is not really a test, but rather a treatment. Since this
fluid administration is not reversible, repeated fluid challenges will inevitably increase the risk
of fluid overload and hemodilution, thus impairing tissue oxygenation in critically ill patients.
In order to limit such deleterious consequences, smaller volumes of fluid have been proposed.
A mini-fluid challenge of 100 mL colloid infused over 1 minute has been shown to predict fluid
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responsiveness, with a diagnostic threshold of 10%, and more recently some authors sug-
gested the administration of a bolus of only 50 mL (“micro-fluid challenge”) over 10 seconds.
A meta-analysis has shown that a mini-fluid challenge of 100 mL has a good performance to
predict fluid responsiveness. The pooled AUROC was 0.91 (0.85-0.97) with a sensitivity of
0.82 and specificity of 0.83. Nevertheless, performing a mini or even a micro-fluid challenge
requires precise and real-time cardiac output monitoring, such as the pulse contour analysis
method, which is capable to track the fast and small changes in cardiac output.
3.3.2 - Passive leg raising
The PLR test, which mimics the haemodynamic effects of an about 300 mL challenge of blood,
is a well-established manoeuvre to predict fluid responsiveness. This postural manoeuvre mobi-
lizes the blood from the lower extremities and the splanchnic circulation toward the intrathoracic
component. Importantly, since no fluid is administered, this blood mobilization is completely rever-
sible and thus does not carry the risk of pulmonary edema. Numerous studies have consistently
shown that PLR is a reliable test to predict fluid responsiveness in critically ill patients.
In order to be properly performed and, thus, to be reliable, five rules should be followed (Figure 2) :
The patient should be placed in semi-recumbent position (45 degrees) at baseline
The haemodynamic effects of the manoeuvre should be assessed by a direct mea-

surement of CO. An increase in CO ≥10% from baseline allows one to define the
patient as “preload responder”. Changes in BP cannot be used to detect the effects
of the PLR test
The CO monitoring should be assessed in real-time as the haemodynamic effects of

PLR are transient and in general maximal between 30 to 60 seconds after its start
The return of the CO value to the baseline should be verified at the end of the test,
once the patient has returned to the initial position
The test should be performed by passively raising the patient’s legs and lowering
the trunk to the horizontal position using the automatic position adjustment of the
bed. Besides, during the one-minute test, one should not touch the patient to prevent
discomfort, pain, awakening, etc. Before the test, inform the patient and suction
bronchial secretions
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Figure 2 - Five rules to follow for performing passive leg raising
5
3 Assess PLR effects by Re-assess CO in the
directly measuring CO (not semi-recumbent position
with blood pressure only) (should return to baseline)
2 Use the bed adjustement Volume

and avoid touching the expansion
patient (pain, awakening)
1 Check that the 4

Use a real-time
trunk is at 45° measurement of CO
The major advantage of the PLR test is that it can be performed in almost all patients, inclu-
ding those with spontaneous breathing, AF, low lung compliance and any TdV.
Nonetheless, the two major limitations of the PLR test are intra-abdominal hypertension
that may impede venous return and compression stockings. Besides, head trauma, hip, legs
or lumbar spine injury, as well as deep venous thrombosis, are contraindications to PLR. In
patients in prone position, Trendelenburg manoeuvre may be an alternative to PLR.
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3.3.3 - Heart-lung interaction indices
Most of the dynamic indices or tests of preload responsiveness rely on the heart-lung inte-
ractions in ventilated patients. The physiological principle is based on the changes in preload
conditions during the respiratory cycle induced by the positive pressure ventilation. Briefly,
the overall effect of mechanical ventilation is a decrease in left ventricular stroke volume
at the end of expiration and an increase at the end of inspiration. So, the larger the changes
in stroke volume during the respiratory cycle, the more likely the patient has biventricular
preload responsiveness, and thus is fluid responsive.
Pulse pressure variation and stroke volume variation

The pulse pressure, defined as the difference between the systolic and diastolic pressure,
is positively related to the left ventricular stroke volume and is negatively related to the
aortic compliance. As aortic compliance is assumed to remain unchanged during mecha-
nical ventilation, the changes in stroke volume induced by mechanical ventilation could be
detected by the changes in pulse pressure, also called PPV. The latter is calculated as the
difference between the maximal and minimal pulse pressures values over the respiratory
cycle, divided by the mean of the two values, and expressed as a percentage. In practice, PPV
is directly obtained from the peripheral arterial pressure wave using an arterial catheter, or
indirectly estimated by the volume-clamp method. The estimation of the SVV obtained by
using pulse pressure contour analysis or by using the volume-clamp devices, relies on the
same principle (Table 2).
Derived values of the VTI of the flow in the left ventricular outflow tract obtained with
echocardiography, or of the aortic blood flow obtained with esophageal Doppler, or of the
amplitude of the plethysmographic signal have been proposed as non-invasive indices to
predict fluid responsiveness in patients receiving mechanical ventilation. The diagnostic
threshold of PPV, SVV, and derived values to predict fluid responsiveness is about 12-13%.
When PPV and SVV values are within a “grey zone” ranging from 9% to 12-13%, the inter-
pretation of results should be cautious.
Nevertheless, some limitations of PPV and SVV should be taken into account for the clini-
cal decision-making.
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PPV, SVV and derived dynamic indices cannot be used in case of spontaneous brea-
thing activity and cardiac arrhythmias
Low tidal volume ventilation and/or low lung compliance might induce false negatives
of PPV and SVV, due to relatively small changes in intrathoracic pressure. By contrast,
in such cases, a value >12-13% is highly suggestive of preload responsiveness
Intra-abdominal hypertension could result in falses positives of PPV and SVV
Under some other conditions such as open-chest (false negatives), high-frequency

ventilation (false negatives), and severe right ventricular failure (false positives), the
interpretation of PPV and SVV is also limited
The limitations of PPV and SVV (Figure 3) should be always kept in mind since
patients are usually not deeply sedated for long periods, low tidal volume ventilation
is often used, and cardiac arrhythmias are common in critically ill patients. However,
in the operating room setting, the limitations of PPV and SVV are less frequently
encountered. Thus, the place of PPV and SVV is important in the fluid management
of patients undergoing surgery
Figure 3 - Conditions where pulse pressure variation and stroke volume

variation are less reliable

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Tidal volume challenge

Recently, a novel test called “tidal volume challenge” was proposed to overcome the limi-
tations of PPV and SVV in the case of low tidal volume (6 mL/kg) ventilation. This test is
performed by transiently increasing tidal volume from 6 to 8 mL/kg for one minute. An
increase in the absolute value of PPV (ΔPPV) ≥3.5% or SVV (ΔSVV) ≥2.5% can reliably pre-
dict fluid responsiveness during low tidal volume ventilation.
Respiratory variation of vena cava diameter

During positive pressure ventilation, the increase in intrathoracic pressure during insuffla-
tion may impede venous return. Therefore, the variation of the diameter of both the superior
and inferior vena cava may be influenced by this mechanism. In particular, the SVC (purely
intrathoracic) collapses during inspiration and enlarge during expiration, whereas the IVC
(purely abdominal) dilates at the end of insufflation and then will be compressed at the end
of expiration. The effects related to the changes in intrathoracic and intra-abdominal pres-
sures are magnified in the case of hypovolemia. Accordingly, the greater the distensibility of
IVC and the greater the collapsibility of SVC, the more likely the patient is fluid responsive.
The DIIVC is calculated as the difference between the maximum diameter on inspiration
and minimum diameter on expiration, divided by the minimum diameter on expiration, and
expressed as a percentage. In parallel, the CISVC could be calculated as the difference between
the maximum diameter on expiration and minimum diameter on inspiration, divided by the
maximum diameter on expiration.
Measurement of DIIVC can be obtained with transthoracic echocardiography, whereas CISVC

measurement requires transesophageal echocardiography. Nonetheless, the threshold of
DIIVC for predicting fluid responsiveness varies largely according to different studies, ranging
from 8% to 46% with moderate accuracy of pooled AUROC of 0.75 according to a recent
meta-analysis. The CISVC seems to have a better predict performance with the diagnostic
threshold ranging from 21% to 37%. Nevertheless, in a study including a large number of
mechanically ventilated patients, the AUROC of CIsvc was only 0.75, a result, which can partly
be explained by a high number of patients receiving low tidal volume ventilation.
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The major advantage of DIIVC and CISVC is that the method to obtained them is non invasive
and can be used when no other advanced monitoring devices are available. However, CISVC
evaluation through transesophageal Doppler requires a skilled operator to be performed
and is in practice, difficult to be repeated many times a day. Also, DIIVC or CISVC share some
of the limitations of PPV and SVV, such as spontaneous breathing activity, low tidal volume,
low compliance, and high intra-abdominal pressure.
The end-expiratory occlusion test

The mechanism on which relies the EEO test to assess preload responsiveness is the inter-
ruption of mechanical ventilation at end-expiration. By preventing the cyclic decrease in
venous return during insufflation, the test allows both the ventricles to receive a larger
amount of blood which may increase cardiac output in the case of preload responsiveness.
In practice, as for the PLR test, some rules should be followed when performing the EEO test.
After a period of stability, EEO should be started and maintained for at least 15 s.
The haemodynamic effects of EEO should be assessed by direct measurement of car-

diac output. The maximal change in cardiac output compared to baseline appears in
the last seconds of the test. An increase in cardiac output ≥5% from baseline allows
one to define the patient as a “preload responder” (Figure 4).
A real-time and continuous cardiac output monitoring device is required.
The return of the cardiac output value to the baseline should be verified after the test.
The EEO test could also be performed in patients with mild spontaneous respiratory
activity provided that an expiratory hold can be maintained.
The EEO test is easy to perform at the bedside and is valid even in patients with arrhythmias
or low respiratory system compliance. Obviously, the test cannot be performed in patients
without mechanical ventilation and in those with intense spontaneous breathing activity.
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Since the least significant change of VTI of the left ventricular outflow tract at echocardio-
graphy is 10%, this method might not be precise enough to track the changes in cardiac
output induced by the EEO test. To overcome this issue, the combination of the absolute
percentage changes in VTI of a 15s EEO test and a 15s end-inspiratory occlusion (EIO) test
has been proposed. The diagnostic threshold increased to 13%, which is compatible with the
precision of echocardiography.
Figure 4 - Performing the end-expiratory occlusion test in the right way
EEO must
Perform EEO like be at least Can be inspiratory
The EIO must also be
when measuring 15" long efforts if they do
at least 15" long
intrinsic PEEP not interrupt EEo
Baseline EEO Baseline EIO Baseline Fluid infusion
Measure CO
value during a
period of stability Check patient’s
Use a precise stability before
and real time infusing fluid
CO monitoring
Reprinted with permission from Gavelli et al.

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Other tests
Other tests based on heart-lung interaction have emerged over the past years. However,
given the less available evidence, more research focusing on their validity and applicability
is necessary. In neurosurgery patients ventilated with a low tidal volume, the magnitude of
the decrease in cardiac output induced by increasing the level of PEEP was shown to predict
fluid responsiveness better than PPV and SVV. In patients with septic shock, the absence of
a decrease in MAP during an elevation of PEEP from 10 to 20 cmH2O was shown to predict
fluid responsiveness.
In patients ventilated with low tidal volume during surgery, a decrease in cardiac output
during a LRM was shown to predict fluid responsiveness. However, interpretation of this
dynamic test in patients with ARDS should be cautious, since in those patients with low
lung compliance, LRM results in a marked increase in transpulmonary pressure rather than
a marked increase in intrathoracic pressure. Thus, the LRM can increase markedly the right
ventricular afterload and thus the decrease in cardiac output during the test could be a false
positive of fluid responsiveness.
In non-ARDS patients receiving pressure support ventilation, the response of blood pressure
to three consecutive sigh maneuvers at different airway pressures has also been proposed
to predict fluid responsiveness.
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3.4 - Clinical application of the preload

responsiveness concept
3.4.1 - To guide fluid resuscitation in the early phase of shock
Even though assessing preload responsiveness is recommended in acute circulatory failure

patients, it should be applied in a reasonable way. One should keep in mind that preload
responsiveness is a physiological condition, so that the presence of preload responsiveness
does not mean the fluid administration is mandatory. The question of knowing whether
the patient is preload responsive or not only makes sense in the case of circulatory failure,
when fluid administration is aimed at increasing cardiac output to increase tissue oxygen
delivery. In this regard, it is futile to use any of these tests in patients with evident hypovo-
lemia, such as early phases of septic shock, since patients must be preload responsive and
life-saving fluid bolus must be urgently administered. In this case, an individualized fluid
strategy, should be applied. A fluid infusion rate of around 10 mL/kg within the first hour of
resuscitation (e.g. from 30 to 60 minutes) is reasonable. However, a higher rate should be
considered in cases of evident fluid losses, abdominal sepsis, mottling, increased capillary
refill time, while a lower rate of infusion should be considered if signs of pulmonary edema
appear during fluid infusion or in the case of severe ARDS.
After the initial phase of resuscitation, the decision of continuing fluid administration relies
on three prerequisites:
Persistence of haemodynamic instability or peripheral hypoperfusion (mottled skin,

hypotension, oliguria or anuria, hyperlactatemia…)
Presence of fluid responsiveness
Limited risks of fluid overload (Figure 5)

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Figure 5 - The algorithmic approach to the use of the preload responsiveness

concept in mechanically ventilated patients at the bedside
Ventilated patients with acute circulatory failure
NO YES
Ventilated patients with fluid overload in Initial phase of hypovolemic of

the late phase of shock management septic shock
NO YES NO YES
Test fluid Test fluid Do not test fluid Fluid

responsiveness to responsiveness responsiveness administration
guide fluid removal Adapt the rate
of infusion
- PPV/SVV - The clinical
- Tidal volume challenge tolerance
- Respiratory variations of IVC/SVC - The clinical
diameter context
- End-expiratory occlusion test
-Passive leg raising
-Mini-fluid challenge If shock persists,
Consider other
NO Depending on the limitations of YES test fluid
therapies
each test responsiveness
Assess benefit/risk ratio of

Benefit<Risk Benefit>Risk
continuing fluid administration
Reconsider fluid administration

Adapted with permission from Jozwiak et al.
When the risks are judged to be greater than the benefits, especially in patients with ARDS,
other therapies such as cardio-vascular agents should be considered even in the case of pre-
load responsiveness. In such patients, the transpulmonary thermodilution technique could
be helpful to guide the fluid management, since it allows the measurement of the EVLW and
the PVPI. Both are independent predictors of mortality and allows one to estimate the risk
of fluid administration in patients with ARDS.
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Assessing preload responsiveness is also important when considering to stop fluid infusion.
In this regard, the decision should be made according to either the disappearance of hae-
modynamic instability or the appearance of preload unresponsiveness or the presence of
high risk of fluid overload (value of EVLW and PVPI).
3.4.2 - To guide fluid removal in cases of fluid overload
It is now well established that fluid overload may increase morbidity and mortality in critically
ill patients. In patients with ARDS and/or during the de-resuscitation phase of septic shock,
fluid removal by ultrafiltration has been suggested. However, a too aggressive fluid removal
could induce hypovolemia, which may cause haemodynamic deterioration and organ hypo-
perfusion. In this context, testing preload responsiveness may help the physician to guide
fluid removal. In this regard, the presence of preload responsiveness assessed by a PLR test
before starting ultrafiltration during renal replacement therapy has been shown to reliably
predict the occurrence of intradialytic hypotension.
3.4.3 - To guide weaning from mechanical ventilation
WiPO is one of the most common causes of weaning failure. During weaning, occurrence of
marked decreased intrathoracic pressure, increased adrenergic tone, hypoxemia, hyper-
capnia and increased work of breathing may result in increased right and left ventricular
preload and afterload, leading to WiPO. One study showed that WiPO is associated with the
presence of preload unresponsiveness (negative PLR test) before the SBT. Another study
reported that a fluid removal treatment, changing preload unresponsiveness to responsive-
ness, increased the rate of successful SBTs.
3.5 - Conclusion
Assessment of preload responsiveness is crucial in every step of fluid management of cri-

tically ill patients. Dynamic tests rather than static indices should be used for assessing
preload responsiveness. Nevertheless, knowing both the indications and limitations of each
test is essential when interpreting results and making clinical decisions.
P.143
PART III
SPECIFIC CLINICAL
SCENARIOS
1 - GENERAL APPROACH TO SHOCK STATES P.145

Prof. A. Mebazaa, Dr. M. Arrigo, Dr. J. Hermes-Laufer

Prof. J. Masip, Prof. Dr. U. Zeymer, Prod. Dr. H. Thiele
3 - RIGHT VENTRICULAR FAILURE P.173

Prof. A. Vieillard-Baron
4 - ACUTE MR AND VSR P.179

Dr. O. Chioncel, Dr. L. Antohi, Prof.V. Iliescu
5 - CARDIAC TAMPONADE AND CONSTRICTION P.197

Prof. E. Bonnefoy-Cudraz, Dr. T. Bochaton

Prof. D. De Backer

Ass. Prof. A. Sionis, Dr. A. Ariza-Solé, Ass. Prof. J. Bañeras
8 - INTRA-ABDOMINAL HYPERTENSION P.225

Dr. E.Amestoy, Prof. Dr. M. L.N.G. Malbrain
9 - HAEMODYNAMICS DURING MECHANICAL

VENTILATION P.235
Ass. Prof. C.L. Alviar, Assoc. Prof. S. Van Diepen
10 - HAEMODYNAMICS DURING MECHANICAL

CIRCULATORY SUPPORT P.250
Prof. P. Vranckx
11 - CARDIAC ARREST AND POST-CARDIAC ARREST P.260

Prof. C. Hassager , Prof. J. Eifer Møller, Dr. J. Kjærgaard
III.1
1 - GENERAL APPROACH
P.145 TO SHOCK STATES
Dr. Mattia Arrigo, MD

Department of Internal Medicine, Triemli Hospital Zurich /
University of Zurich, Zurich, Switzerland
Dr. Julia Hermes-Laufer, MD

Department of Cardiology, University Hospital Zurich,
Zurich, Switzerland
Prof. Alexandre Mebazaa, MD, PhD, FESC

Department of Anesthesiology and Critical Care Medicine,
St. Louis and Lariboisière University Hospitals, Paris, France
Key messages
Recognize shock states by detecting signs of hypoperfusion: hypotension,
altered mental status, cold periphery, skin mottling, reduced urine output <
0.5ml/kg/h, elevated blood lactate levels >2mmol/l
Identify the form of shock clinically and with the help of echocardiography:
distributive, hypovolemic, cardiogenic, obstructive
Perform adequate monitoring in all shock patients and evaluate advanced
haemodynamic monitoring, including cardiac output in selected patients
Mandatory use of echocardiography or other tools to estimate stroke volume,
assess fluid responsiveness and/or effect of cardiovascular agents
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Introduction
This chapter aims at providing practical guidance on how to approach a patient in shock.
The proposed algorithms, values, and targets are primarily for educational purposes and
need to be personalized for each patient.
III.1
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1.1 - Definition and forms of shock
Shock is an acute circulatory failure with global organ dysfunction due to inadequate cellular
oxygen utilization related to insufficient oxygen delivery. Cellular dysoxia associated with
liver dysfunction leads to increased blood lactate levels.
Shock is usually classified in 4 distinct forms: distributive, hypovolemic, cardiogenic and

obstructive. (Figure 1)
Figure 1 - Shock forms and their prevalence
HYPOVOLEMIC
16%
DISTRIBUTIVE
CARDIOGENIC
66%
16%
OBSTRUCTIVE
2%
The hallmark of distributive shock is a disproportionate vasodilation/vasoplegia, mostly

due to sepsis or systemic inflammation. The hallmark of hypovolemic shock is an insuffi-
cient intravascular volume (e.g. fluid or blood loss). Cardiogenic shock is caused by severe
cardiac dysfunction (e.g., ACS). Obstructive shock is an umbrella of different mechanical
obstructions leading to reduced cardiac filling of the left ventricle (e.g., pericardial tampo-
nade, pulmonary embolism).
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1.2 - Determinants of oxygen delivery
Shock is an acute circulatory failure causing insufficient oxygen delivery for tissue demands.
Oxygen delivery to the peripheral tissues is determined by the cardiac output and the blood
oxygen content. While the latter is influenced by the Hb concentration, the oxygen binding
of Hb and the SaO2 of the blood, CO is the product of HR and SV. The two items are interde-
pendent since high HR may reduce SV. The SV is mostly influenced by cardiac preload,
afterload and myocardial contractility. Regional differences in oxygen delivery may be caused
by regional perfusion (dys-) regulation mechanisms and different metabolic processes.
Figure 2 - Major determinants of oxygen delivery
1.3 - Signs and markers of inadequate tissue perfusion
In case of hypotension (i.e. mostly MAP < 65 mmHg), it is crucial to detect the presence or
not of signs of tissue hypoperfusion such as alterations of mental status (e.g., confusion,
disorientation, delirium), cold periphery (i.e. cold, clammy skin, mottling, prolonged capillary
refill time > 2 seconds), reduced hourly urine output of less than 0.5 ml/kg/h. For that rea-
son, urine output should be monitored hourly. Decreased SVcO2 (i.e.< 70%) usually indicates
hypoperfusion but is often difficult to put into clinical context and can be falsely elevated in
case of distributive shock (the most common type of shock) or excessive vasopressor the-
rapy. Elevated blood lactate levels (i.e.>2 mmol/l) may indicate hypoperfusion but are usually
of less value in the initial phase of shock.
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Figure 3 - Clinical findings

indicating peripheral
hypoperfusion
1.4 - Standard monitoring
Patients with circulatory shock require appropriate monitoring of vital functions. Minimal
monitoring includes:
Basic monitoring including pulse-oximetry (SpO2)
Invasive BP monitoring
Monitoring of urine output, preferably hourly by indwelling catheter
Serial blood lactate levels
In case of vasopressor therapy: central venous access for CVP and ScvO2, if indicated
Assessment of the cardiac function is recommended in presence of circulatory shock,

except when an extra-cardiac cause is obviously present (e.g. hypovolemia/hemorrhage).
Echocardiography provides a complete assessment of cardiac (and great vessels) function
but requires appropriate training and is a tool to diagnose rather than monitor cardiovascu-
lar function. In selected cases, continuous monitoring of CO is recommended, particularly
when the form of shock is mixed, or the cause cannot be identified, when the shock state is
refractory to initial treatment, or associated with other critical conditions, or when shock is
related to severe RVF. CO can be measured continuously by different devices (see dedicated
chapter of this Handbook), mainly PAC, LiDCO, PiCCO, FloTrac and several other methods.
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P.150
1.5 - Assessment of fluid status and fluid responsiveness
The assessment of fluid status and fluid responsiveness is a crucial step when approaching
a patient with circulatory shock. Indeed, in the majority of shock forms (e.g., distributive,
hypovolemic), fluid administration may improve haemodynamics (at least in the initial phase
of treatment), while fluid overload might have detrimental effects after the initial resuscita-
tion or in other forms of shock (e.g., cardiogenic).
The first assessment of the fluid status is clinical with a physical examination searching for
signs of congestion (S3 gallop, pulmonary crackles or pleural effusion, elevated JVP, positive
hepato-jugular reflux, hepatomegaly, peripheral edema, ascites) or visible signs of hypo-
volemia. Imaging studies like chest X-ray, lung and/or abdominal US and CT scans should
also be taken into consideration and checked for signs of congestion or bleeding stigmata.
Laboratory studies should include electrolytes, kidney function, Hb, and natriuretic peptides.
If the first clinical assessment does not provide clear evidence of the fluid status, additio-
nal information may be derived from a focused ultrasound of the inferior vena cava, which
reflects RA pressure. A small (i.e., < 15 mm) or collapsed IVC is compatible with normo- or
hypovolemia, an IVC diameter of more than 25 mm with reduced collapsibility suggests hyper-
volemia. Caveat: The interpretation of IVC diameter is impaired in patients on MV. (Table 1)
Table 1 - Assessment of volume status through Inferior Vena Cava
Findings compatible with...
hypovolemia hypervolemia
IVC diameter <15mm IVC diameter >25mm
IVC collapsibility > 50% No/little IVC collapsibility
III.1
P.151
1.6 - Evaluation of fluid responsiveness
Fluid responsiveness is defined as the ability to increase SV (and, ultimately, CO) by increasing
cardiac preload. Fluid responsiveness can be assessed by echocardiography by estimating
SV before and after the application of a fluid bolus of 250-500 ml.
Stroke volume can be measured by echocardiography using this formula:

SV = left-ventricular outflow tract velocity time integral (LVOT-VTI) x LVOT Area
From a practical point of view and to reduce errors due to inaccurate measurement of the
LVOT diameter/area, fluid responsiveness is assessed by evaluation changes in LVOT-VTI.
After the application of a fluid bolus of 250-500ml, an increase of the LVOT-VTI of 12-15%
shows fluid responsiveness and should encourage the careful further application of fluid
with regular follow-up assessments. Passive leg raise test can also be performed to assess
fluid responsiveness. However, in awake patients, sudden lifting of the legs in a conscious
patient may however lead to sympathetic activation, which may contribute to an increase
in SV or BP, falsely mimicking fluid responsiveness (Table 2).
Table 2 - Findings indicating fluid responsiveness after a fluid challenge of

250-500 ml or passive leg raise test
Yes No
VTI increase > 12-15% VTI increase < 8-10%

III.1
P.152
Figure 4 - Determinants of stroke volume and its estimation by

echocardiography
SV is influenced by LV preload, LV afterload, and LV contractility and is the product of LVOT-

VTI and LVOT area. LVOT-VTI can be easily measured from an apical 5-chambers view using
a PW Doppler sample in the LVOT and is highly reproducible. The LVOT area is calculated
from the LVOT diameter and is frequently inaccurate. In clinical practice, just LVOT VTI is
used to assess fluid responsiveness.
III.1
P.153
1.7 - Diagnostic and therapeutic approach to shock
Patients presenting with hypotension or with haemodynamic instability should be evaluated

for the presence of circulatory shock. In the absence of symptoms or signs of hypoperfusion,
the diagnosis of shock should be revised and regularly reassessed. In presence of shock, we
recommend the use of a vasopressor to stabilize MAP during the diagnostic process and
treatment optimization. Causes of increased oxygen demand such as pain, agitation, and
fever, should be evaluated and treated, as well as factors contributing to the impaired oxygen
content of the blood, such as anemia and hypoxemia. Next, fluid responsiveness should be
tested by using echocardiography to demonstrate improved SV volume after fluid adminis-
tration. Finally, the type of shock is assessed, and the specific cause investigated.
Figure 5 - Diagnostic and therapeutic approach to shock

III.2
2.1 - Acute pulmonary edema and

Acute decompensated HF

Intensive Care Department, Consorci Sanitari Integral,
Key messages
CS and ACPE are severe forms of ALVF that usually require intensive hae-
modynamic monitoring
ACPE is characterized by acute respiratory distress and respiratory failure
Close BCM is essential in the first hours of ACPE, being RR, SpO2 and BP
the most important parameters to control
Early identification of signs of treatment failure is crucial in order to proceed
to endotracheal intubation and/or give additional treatments
Once recovered from the very acute phase, ACPE patients should be
managed as other non-severe forms of ALVF
Non-severe forms of ALVF usually do not need BCM, but require different
levels of monitoring across the hospitalization, being BP, diuresis and renal
function probably the most important. New alternative parameters have
been developed in this setting
After the discharge, there are numerous devices and technological applica-
tions for remote haemodynamic and clinical monitoring
III.2
P.155
Introduction
Patients with ALVF can be classified on admission presentation into two large groups:
severe presentation [CS and ACPE] and non-severe forms (all other scenarios). All the
patients have elevated pulmonary capillary pressure (pulmonary congestion) and some
of them, mainly those with CS, also have hypoperfusion [reduced CO]. CS is addressed
in part III.1.
III.2
P.156
2.1.1 - Acute Cardiogenic Pulmonary Edema (ACPE)
This ALVF syndrome is mainly characterized by significant respiratory distress and respi-
ratory failure. The increase in LV diastolic or left atrial pressure is transmitted retrogradely
to the capillaries leading to transvascular fluid filtration to the interstitial space and finally
flooding of the alveoli. This hydrostatic mechanism should be differentiated from “non-car-
diogenic” pulmonary edema, commonly seen in sepsis, in which the inflammatory response
alters the permeability of the capillary membrane. CI and LVSV index are depressed or at
the limit, while systemic and pulmonary resistances are usually augmented. RVSVI may be
greater than LVSVI precipitating an imbalance in the lung circulation.
BCM is essential in ACPE, being BP, SpO2 and RR the most relevant (Figure 2).
Patients experience severe dyspnea with orthopnea. Criteria for the diagnosis at bedside
and subsequent confirmatory tests are shown in Figure 2. They mostly tend to present
hypertension that requires a specific approach. Some of them may show a very rapid pre-
sentation, commonly termed “flash ACPE”, without previous accumulation of fluids (often
with preserved LV systolic function), in whom vasodilators are crucial and the use of diure-
tics should be more restrictive.
Likewise, NIV is crucial in these scenarios by decreasing and shortening the acute respira-
tory failure, avoiding intubation in many cases, with no clear impact on hospital mortality.
There are several parameters for monitoring the response to NIV (Table 1). Because most
patients overcome the critical phase in 2-4 hours, intensive monitoring should be restricted
to this critical time, paying special attention to signs of treatment failure. After the reso-
lution of the acute phase, patients should be managed as other cases of non-severe-ALVF.
III.2
P.157
Figure 1 - Monitoring ACPE
AHF
Cardiogenic shock
Non-severe AHF
Acute RV failure
Monitoring Management
Standard
Continuous
Monitoring SpO2
Upright position
Respiratory rate
Venous line
ACUTE BP
NIV- Oxygen
PULMONARY Heart rate
IV- Furosemide
ECG
EDEMA
HYPERTENSION NI- BP/ 2-5 min IV- Vasodilators
Airway pressure
Adjust device
ADAPTATION Tidal Volume
Tune ventilator
TO NIV Leakage
Sedation
Synchrony
Inotropes?
pH, CO2 RRT
POOR
Mental state HFNC?
RESOLUTION Urinary output Intubation?
RECOVERY
III.2
P.158
Figure 2 - Diagnosis of ACPE

Respiratory distress: increase in the work of breathing (WOB) and tachypnea; Respiratory failure is mainly hypoxemia
AHF
INITIAL BEDSIDE ASSESSMENT
↑ WOB RESPIRATORY DISTRESS

ORTHOPNEA
CRACKLES - S3
Spo2<90% RESPIRATORY FAILURE
ACUTE PULMONARY EDEMA
CONFIRMATION
↑ BNP/Pro BNP
↑ PCWP/EVLW
III.2
P.159
Table 1 - Main parameters to monitoring in ACPE
Signs Of Treatment Failure

Initial Assessment
In The First Hours
Basic monitoring
No reduction in respiratory rate

BP-HR-SpO2-RR-Temp-ECG rhythm Persistently low or decreasing SpO2
Hypotension
Patient
No decrease in dyspnea
Degree of dyspnea
Signs of fatigue
Accessory muscle use
Neurological impairment
Level of consciousness
Agitation despite sedation
Comfort with the interface
Intolerance to NIV
Collaboration
Underlying disease impairment
Ventilator and NIV circuit
Tidal volume (>4mL/Kg: 6–7 mL/Kg) Insufficient Tidal volume - low Vol/min
Minute ventilation Persistent significant asynchrony
Asynchrony Excessive air leakage or Pressure unreached
Air leakage volume (<0,4L/s or <25L/min) Increasing auto-PEEP
Gas exchange
No improvement or impairment in pH or
Arterial gases: pH, PaO2, PaCO2, Bicarb, SaO2
oxygenation (SpO2, SaO2 or PaO2/FIO2)
or Venous gases: pH, Bicarbonate, SvO2
Increasing carbon dioxide
III.2
P.160
2.1.2 - Non-severe forms of ALVF
This group involves cases with ALVF who do not have severe presentation. Although the
vast majority of these patients also complain of dyspnea, less than half show some degree
of ARF which is usually mild. These patients generally do not require intensive or conti-
nuous monitoring (Table 2). If HR or SpO2 are not initially out of range, BP and diuresis
probably are the main parameters to be monitored, initially frequently (varying from every
30 min to 4h for BP, depending on initial values and the response to treatment) in order to
actively adjust IV diuretic and other drugs, and at longer intervals thereafter (every 8-24
h, depending on the clinical state). More than half of the patients, manly those with chronic
HF and depressed LV function, also show elevate PAP, as well as elevated CVP and dilated
IVC and edemas, often with third space (pleural effusion, ascites, etc.). In addition to moni-
toring classical physiological and analytical parameters shown in Table 2, there are other
parameters, mostly noninvasive and haemodynamic, which can be used in the management
of these syndromes (Table 3).
III.2
P.161 Table 2 - Main test and timing of monitoring in non-severe

forms of ALVF
Factors of decompensation may require specific monitoring like in infections: leucocyte, cultures, procalcitonin, C-reactive
protein (CPR), etc. ; in Acute Coronary Syndromes: serial ECG, troponin, coagulation; in Arrhythmias: HR and ECG are crucial.
Standard parameters
On arrival First 24-48 hours In-hospital stay
Signs and symptoms Signs and symptoms Signs and symptoms
BP BP/2-4h BP/8h
HR-SpO2-RR HR-SpO2-RR/4h (1)

HR-SpO2-RR/8h
ECG rhythm ECG rhythm ECG rhythm(1)
Echocardiography(2) Echocardiography
Lung ultrasound Lung ultrasound at discharge?
X-Ray Film score Coronary angiography(3) Cardiac MRI(4)
Temperature Temperature/8h Temperature/8h
Body weight Body weight Body weight/24h
Urinary output/6h
Diuresis/8h
Urinary sodium after 2h
Daily and cumulated fluid

24h fluid balance
balance
Hemogram, Glycemia, RF,

Iron status, electrolytes, VBG, RF, electrolytes, other(5) RF, electrolytes/24h
other
Troponin Troponin
BNP / NT-ProBNP BNP/NT-ProBNP at discharge
ECG 12 leads ECG 12 leads ECG 12 leads(1)
Factors of decompensation Factors of decompensation
(1)
These parameters may require different timetable of monitoring according to the severity of presentation, the initial
values and the resources available (i.e. Telemetry, Observation unit, etc.) - (2) Echocardiography should be performed in the
first hours in “de novo” and in haemodynamically unstable patients. - (3) In suspected acute coronary syndromes. - (4) In
myocarditis or the novo cases with unclear etiology. - (5) Other parameters should be monitored according to initial values.
III.2
Table 3 - Alternative monitoring parameters in AHF P.162
Technique Parameter Abnormal value in AHF
Right venous
Central venous pressure >10-12cmH2O
catheterization
Presence and number of ≥3 B-Lines in 2 chest zones on

Lung ultrasound
B lines each hemithorax
Elevated LV filling pressure

E/A>2
or
Two-dimensional E/A 0.8-2 E/E’>15 or
Echocardiography + two of PTRV>2.8
flow and tissue doppler
these: LA-Vol>28ml/m2
Elevated RV filling pressures

IVC>21cm and collapse <15-50%
Biphasic pattern
Doppler renal Intrarenal venous flux
Monophasic pattern
Stroke Volume Index 33-45mL/m2

(1) <15%
Pulse finger photo-plethys- Stroke Volume Variation
mographic volume Cardiac index <2.2 l/min/m2
calculation
Systemic Vascular
<700 or >1500 dynes/sec/cm2
Resistance
Bioimpedance
Body composition Hyperhydration
(standard or vector analysis)
(1)
to predict fluid responsiveness.
2.1.3 - Chronic HF monitoring
Chronic HF patients with decompensated AHF present haemodynamic changes starting

1-3 weeks before admission. New technology has been developed in order to detect these
changes in the pre-symptomatic phase, allowing the introduction of therapeutic adjust-
ments. Several implanted devices, generally connected by bluetooth/wireless and measuring
pulmonary artery pressure, left atrial pressure or RV, have been validated in clinical trials
(COMPASS, CHAMPION, HOMEOSTASIS) (Table 4). In addition, some implanted devices like
pacemakers, ICD or resynchronization therapy are also able to measure haemodynamic
parameters. Finally, the interaction between personal smartphones and wearable or implanted
devices are currently extending worldwide the possibility of monitoring to all scenarios.
III.2
P.163 Table 4 - Monitoring chronic heart failure patients
Main parameter Device
RV systolic / diastolic pressures

Chronicle, Medtronic,
ePAD (RV pressure at maximal
Minneapolis, MN, USA(1)
RV dP/dT)
Heart POD, St Jude,

Implanted Minneapolis, MN, US(2)
Left atrial pressure V-LAP Vectorious Medical
haemodynamic
Technologies, Tel Aviv
monitoring devices Israel)
CardioMEMS, Atlanta, GA,

Pulmonary artery pressure
US(3)
RV pulsatile load (Ea) Pulmonary
Cordella, Endotronix,
artery elastance
Illinois, US
Data derived from other HR and HR variability

From Pacemakers, ICD
Intrathoracic impedance
implanted devices: PM, or Resynchronization
Atrial/ventricular arrhythmias
ICD, CRT-P, CRT-D systems
Percentage pacing
Medication adherence Raisin System, Proteus

(automated pill boxes) Biomedical, CA, US
Home testing and monitoring

point of care biomarkers
Wearables measuring:
Body weight
Physical activity
Other wireless or remote Blood pressure
control SpO2
Phone Voice analysis
Aortic pressure tracings(4)

LVEF from carotid artery
waveform(5)
Other interactive mobile

applications
(1,2,3)
Main trials analysing devices: COMPASS HF Study; HOMEOSTASIS Study and CHAMPION study, respectively;
(4)
waveform analytical methods quantifying ventricular-vascular coupling); (5) Iphone camera
III.2
2.2 - Cardiogenic shock P.164
Prof. Dr. Uwe Zeymer, MD, FESC

Klinikum Ludwigshafen und Institut für Herzinfarktforschung,
Ludwigshafen, Germany
Prof. Dr. Holger Thiele, MD, FESC

Heart Center Leipzig at University of Leipzig,
Department of Internal Medicine/Cardiology, Leipzig, Germany
Key messages
Cardiogenic shock has heterogeneous severity
Cardiogenic shock severity grading can be done by several scores
SCAI shock score has a grading from A – at risk, B – beginning, C – classical;

D – deteriorating; E – extremis
Monitoring haemodynamics and also laboratory markers in cardiogenic shock
is important
Monitoring is particularly important for patients with mechanical circula-
tory support
III.2
P.165
Introduction
CS caused by LV failure is the most frequent cause of death in patients hospitalized for
AMI. Mortality in patients with CS ranges from 30-80%, mostly related to the severity of
shock (Table 1). Other causes of CS due to LV failure include the following:
a) Chronic HF (established etiology) with decompensation
b) AHF first presentation: chronic ischemic or dilated cardiomyopathy, myocarditis, brady-
or tachyarrhythmias, decompensated valvular disease, Takotsubo syndrome, pregnancy
associated heart disease (peripartum cardiomyopathy, coronary artery dissection).
III.2
P.166
2.2.1 - Definition of cardiogenic shock
CS is defined as the inability of the heart, in most patients as a result of impairment of its
pumping function, to deliver blood to the organs to meet their metabolic demands. The
clinical definition of persistent CS includes poor CO and evidence of tissue hypoxia in the
presence of adequate intravascular volume. The criteria for infarct-related CS most often
used are given in Table 1.
Table 1 - Cardiogenic shock definition

2.2.2 - States of cardiogenic
SBP <90 mmHg for >30 min or need for vasopressors shock
to maintain SBP >90 mmHg during systole or Just recently the new SCAI definition
MAP 30 mmHg lower than baseline. of CS including 5 states has been pro-
Severe reduction in CI : posed which is listed in Table 2.
<1.8 l/min/m2 without support or
<2.0 to 2.2 l/min/m2 with support 2.2.3 - Monitoring of cardioge-
nic shock
Adequate or elevated filling pressure:
LV end diastolic pressure >18 mmHg, or
RA pressure >10-15 mmHg Patients with CS should be moni-
tored in order to differentiate causes
Tissue hypoperfusion indicated by one of the
of haemodynamic instability, enable
following:
a) Altered mental status monitoring of the response to any the-
b) Cold, clammy skin and extremities rapeutic intervention and determine
c) Oliguria with urine output <30 ml/h if the need for MCS may be indicated.
d) Arterial lactate >2.0 mmol/l The exact level and type of monitoring
will depend upon the local facilities,
and the clinical context of the patient. In patients managed with advanced MCS, additional
monitoring will be necessary including perfusionists if available. Calculation of cardiac power,
with monitoring of CO, can assist in prognostication, especially in unclear haemodynamic
situations, in differential diagnosis of the cause of shock and in cases with worsening hae-
modynamics or increasing requirement for vasopressors or inotropes. Table 3 summarizes
the recommendations for monitoring in patients with CS.
III.2
P.167
Table 2 - Stages of cardiogenic shock severity
Stage Clinical signs or symptoms
At risk. A patient who is not currently Normal JVP

experiencing signs or symptoms of Lung sounds clear
A CS, but is at risk for its development, Warm and well perfused
such as large AMI of chronic severely • Strong distal pulses
impaired LV function. • Normal mentation
Pre
Elevated JVP
Beginning CS. A patient who has clini- Rales in lung fields
B cal evidence of relative hypotension or Warm and well perfused
tachycardia without hypoperfusion. • Strong distal pulses
• Normal mentation
May Include Any of:

Looks unwell
Classic CS. A patient who manifests
Panicked, ashen, mottled, dusky
with hypoperfusion that requires
Volume overload
intervention (inotrope, pressor or
Extensive rales
C MCS, including ECMO) beyond volume
Killip class 3 or 4
resuscitation to restore perfusion.
NIV or MV
These patients typically present with
Established
Cold, clammy
relative hypotension.
Acute alteration in mental status
Urine output <30 mL/h
Deteriorating/doom. A patient who is

similar to category C but are getting
D Any of stage C
worse, showing failure to respond to
initial interventions.
Extremis. A patient who is experien-

Near pulselessness
cing cardiac arrest with ongoing CPR
E Cardiac collapse
and/or ECMO, being supported by mul-
MV
tiple interventions.
III.2
P.168
Normotensive (SBP ≥100 mmHg or normal for

pt.)
Normal labs
If haemodynamics done
• Normal renal function
• CI ≥2.5 l/min/m2
• Normal lactic acid
• CVP <10 mmHg
• PA saturation ≥65%
SBP <90 mmHg or MAP <60 mmHg or

Normal lactate
>30 mmHg drop from baseline
Minimal renal function
Pulse ≥100 bpm
impairment
• CI ≥2.2 l/min/m2
Elevated BNP
• Pulmonary SaO2 ≥65%
May Include any of:

SBP <90 or MAP <60 or >30 mmHg drop from
May Include Any of:
baseline and drugs/device used to maintain BP
Lactate ≥2mmol/L
above these targets
Creatinine doubling or
Haemodynamics
>50% drop in GFR
• CI <2.2 l/min/m2
Altered liver function
• PCWP >15mmHg
tests
• CVP/PCWP ≥0.8
Elevated BNP
• PAPI <1.85
• cardiac power output ≤0.6 W
Any of Stage C and:

Any of Stage C and:
Requiring multiple pressors or addition of MCS
Deteriorating
to maintain perfusion
“Trying to die” No SBP without resuscitation

CPR (A-modifier) PEA or refractory VT/VF
pH ≤7.2 Hypotension despite maximal support
III.2
P.169
Table 3 - Recommended monitoring parameters in shock
Monitoring
Frequency Comment/Rationale
Parameter
Non-Invasive Monitoring
High risk and incidence of arrhythmias, ventilator

ECG-telemetry, SpO2, RR Continuously
failure and/or pulmonary edema
Invasive Monitoring
Consider continuing until full haemodynamic stabi-

Arterial BP monitoring Continuously
lization has been achieved for 12-24 hours
A central line is required for delivery of vasoactive

medications.
Single point in time CVP measurements may be
CVP Continuously
unreliable measures of fluid status, but longitudi-
nal CVP trends may provide information on trends
in fluid status
Trends in Scv02 in patients with a central line can

ScvO2 Every 4 h
be used to monitor trends in CO
Urine output along with serum creatinine moni-

Urine output Every hour toring are markers of renal perfusion and acute
kidney injury
Selected use, Consider using early in the treatment course in

PAC or minimal invasive
mandatory in patients not responsive to initial therapy, or in
CO monitoring
MCS cases of diagnostic or therapeutic uncertainty
2.2.4 - Considerations of haemodynamic monitoring on mechanical circula-

tory support devices
Patients with MCS devices are usually in more advanced state of CS. Therefore, intense moni-
toring is necessary in such patients. Figure 1 depicts the effect of different MCS devices on
pressure-volume loops in CS. However, pressure-volume loops are not clinical standard and
may more help to understand the differential effect of these devices. In clinical practice,
other monitoring parameters are more important.
III.2
P.170
In addition, to Table 3 the focus should be on preventing limb ischemia because of the large
bore cannula used for MCS and also bleeding, hemolysis complications and infections are
of relevance to be prevented and/or to be discovered as early as possible to prevent more
severe complications. In addition, each device has specific requirements to be monitored
which would be beyond the scope of this handbook. However, in particular venoarterial
extracorporeal membrane oxygenation (va-ECMO) requires a specific monitoring for possible
venting indications and/or changes in device settings.
Specifically, the following parameters need to be monitored as shown in Table 4:
Figure 1 - Pressure-volume loops of different MCS devices

x-axis: LV volume; y-axis: LV pressure
In red the effect of the different devices on pressure volume loops is shown.
a) The IABP has a very moderate effect with left shifting of the left ventricular volumes and no effect on left ventricular
pressure.
b) pLVAD provide a left shifting of the pressure volume loops and increase in left ventricular pressure.
c) Venoarterial (va)-ECMO leads to increase in left ventricular pressure but also has a narrowing and negative effects on left
ventricular volumes.
d) The combination of va-ECMO with pLVAD partially reverts the negative effects of va-ECMO with positive left shifting of
left ventricular volumes by left ventricular venting.
III.2
P.171
Table 4 - Recommended monitoring parameters in MCS
Monitoring
Parameter
Limb ischemia
Pulse-oximetry on toe of High risk of limb ischemia with TandemHeart,

Continuously
arterial puncture site Impella, ECMO.
Once daily.
Doppler ultrasound of dis- High risk of limb ischemia with TandemHeart,
If ischemia
tal arteries Impella, ECMO.
more often
Alternatively: NIRS on toe High risk of limb ischemia with TandemHeart,

Continuously
of arterial puncture site Impella, ECMO.
High risk of limb ischemia, bleeding and possible

Cannula and puncture site
Every 8 h cannula dislocation with TandemHeart, Impella,
inspection
ECMO.
Possible venting parameters for va-ECMO
Possible volume overload and development of

Echo: opening of aortic
Every 8 h LV thrombus formation. If no opening, consider
valve
venting.
Echo: LV outflow tract–

Possible volume overload and development of LV
velocity time integral Every 8 h
thrombus formation. If <10 cm, consider venting.
<10 cm
Echo: Significant increase

Possible volume overload and development of LV
in diameters and volume Every 8 h
thrombus. If significant increase, consider venting.
of the LV
Device Monitoring
See specific settings for Important to detect possible malfunctioning, insuf-

Continuously
the different devices. ficient support or dislocation o devices.
III.2
P.172
Monitoring
Parameter
Invasive Monitoring
In particular for ECMO use the right arm to detect

possible Harlequin-syndrome, which would require
a possible different cannulation.
Arterial BP monitoring Continuously
Arterial waveform pulsatility is an important mar-
ker for possible venting. If no pulsatility, consider
venting.
To differentiate between cardiac or septic shock,

PAC or non-invasive CO especially in patients with TandemHeart, Impella
Every 4 h
monitoring and ECMO or in cases of diagnostic or therapeutic
uncertainty
Laboratory Investigations
Complete blood counts Every 12-24 h High bleeding risk and complement activation.
Hemolysis is frequent in particular with Impella

Hemolysis parameters Every 12-24 h
device
Lactate clearance is a marker of resolving endor-

gan hypoperfusion and lack of clearance is
Lactate Every 1-4 h
associated with a higher risk of mortality. In parti-
cular for MCS this is of paramount importance.
Every 4-6 h
Coagulation laboratories High bleeding risk and complement activation.
for MCS
Low oxygen saturation or high CO2 may require

Arterial blood gas
Every 1 h changes in ventilation parameters or change in
analysis
VA-ECMO settings.
III.3
P.173
3 - RIGHT VENTRICULAR FAILURE
Prof. Antoine Vieillard-Baron, MD, PhD

Head of the Surgical and Medical ICU University Hospital
Ambroise, APHPB, Boulogne-Billancourt, France
Key messages
RV failure is the association of a clinical situation at risk with signs of sys-
temic congestion and systemic hypoperfusion
Diagnosis is done when CVP>8 mmHg and RV is dilated at echocardiography
Monitoring should include at least CVP, echocardiography and biomarkers

(BNP, creatinine, bilirubin, transaminases)
Core of management is fluid restriction (and even fluid removal), nore-
pinephrine when BP is low and adapted respiratory strategy
III.3
P.174
Introduction
Since many years, it appears obvious to physicians that the RV function plays a crucial
role in critically-ill patients. RV injury has been indeed reported in many different situa-
tions as sepsis and septic shock, ARDS, acute pulmonary embolism, acute chest syndrome
in patients with sickle cell disease, inferior wall AMI, HF with preserved or reduced EF,
COPD, and, of course. pulmonary artery hypertension (Table 1). In many of these situa-
tions, RV failure is an independent predictor of mortality. Detecting RV failure is then of
huge importance. Besides, it may modify haemodynamic and respiratory management.
A point of caution has to be especially done about fluid management since patients with
RV failure are usually unresponsive to fluids and fluids have been even reported to be
deleterious in experimental studies.
III.3
P.175
3.1 - Definition and characterization of RV failure
Due to its specific physiology and pathophysiology as well as the paucity of clinically avai-
lable data at the opposite of the left ventricle, definition of RV failure required to be clarified.
During a long time, confusion was done between RV systolic dysfunction, i.e. remodeling
of the RV potentially leading to an impairment in its systolic function, and RV failure (i.e. a
syndrome with well-characterized clinical consequences). Three recent statements in the
field recently gave the same definition of RV failure, mainly physiologically based. Briefly,
RV failure is defined as a syndrome which associates systemic hypoperfusion (tachycardia,
cyanosis, skin mottling, reduced capillary refill, low BP...) with systemic congestion (increased
CVP, hepatojugular reflux, tricuspid regurgitation murmur, pericardial effusion and when
chronic, lower limb swelling, ascites and hepato/splenomegaly). Laboratory investigations
may confirm the systemic hypoperfusion showing acute renal failure and increased serum
lactate. Systemic congestion may be confirmed by markers of hepatic congestion (transa-
minitis, hyperbilirubinemia), renal congestion (acute renal failure) and increased BNP. To
summarize, besides biomarkers and clinical signs, RV failure is diagnosed by the association
of a situation at risk, a significantly dilated right ventricle and an elevated CVP (Figure 1).
While RV dilatation may be accurately diagnosed by CT-scan, critical care echocardiography
is much more suitable for at the bedside in the critically-ill patients.
Table 1 - Potential causes of RV failure with their respective incidence
Situations at risk Expected incidence of RV failure*

Sepsis and septic shock ≈ 30-40%
ARDS ≈ 20-25%
Pulmonary embolism ≈ 20-25%
Acute chest syndrome in sickle cell disease ≈ 20-25%
Inferior wall myocardial infarction ≈ 30%
HF with preserved EF ≈ 20%
Pulmonary arterial Hypertension 100% at end-stage
* Most studies only reported RV dilatation without any information about CVP value and signs of congestion and many were
mainly based on alterations of echo parameters of RV systolic function. Then, these incidences have to be understood as
the maximal ones that could be observed in the different situations at risk. Finally, such incidences obviously depend on the
severity of the disease.
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3.2 - Monitoring of RV failure
Monitoring may especially associate markers of systemic congestion and of RV size.

Among patients with ADHF, those with higher CVP at admission, or who did not achieve
a CVP<8mmHg after treatment, were more likely to develop worsening of renal failure by
venous congestion. It is then reasonable to recommend monitoring CVP and to consider that
a CVP>8 mmHg is a good marker of systemic congestion (Figure 2, panel A). At the bedside,
critical care echocardiography is perfectly suitable to detect significant RV dilatation: a ratio
between the end-diastolic area of the RV and the LV above 0.6 is very suggestive of such
dilatation (Figure 2, panel B). Among all the echo signs that may be detected in a patient
with RV failure, a paradoxical septal motion is interesting as it suggests to physician that the
mechanism of failure is a pressure overload and pulmonary hypertension (Figure 2, panel C).
Figure 1 - RV function. from risk to failure
At risk -Pulmonary embolism - Inferior wall MI

- ARDS - Acute chest syndrome
- Acute exacerbation of - PAH
COPD - Fluid overload
RV remodeling - Low EF (MRI, PAC) - Low S’ velocity (echo)

(+/- systolic - Low FAC (echo) - Altered RV strain (echo)
dysfunction) - Low TAPSE (echo)
ECHO Systemic hypoperfusion

Significant RV dilatation tachycardia, low BP,
(echo, CT-scan) cyanosis, skin mottling,
raised capillary refill time
Systemic congestion
RVF Raised CVP, BNP,
transaminitis,
hyperbilirubinemia, HJR
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Figure 2 - Typical pattern of RV failure
3.3 - Management
A summary is given in the figure 3. Management is based on 3 points:
A restrictive approach of fluids requirement
A respiratory strategy, especially if patient requires positive pressure ventilation,

which is to limit airway pressure (PEEP, plateau pressure), hypoxemia and hypercapnia.
An haemodynamic strategy based on infusion of norepinephrine in case of low BP to

restore the coronary perfusion pressure and then support the RV
In some particular situations, other more specific treatments may be considered (fibrinoly-
sis in pulmonary embolism, prone position in ARDS, diuretics in HF, inhaled nitric oxide in
severe pulmonary hypertension).
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Figure 3 - Management of RV failure
- Norepinephrine infusion
Hemodynamic - Levosimendan?
strategy - Fluids restriction
- Hemofiltration?
- Fibrinolysis
Specific - Prone position
RV Failure strategy - Diuretics
- iNO, PDESI, PGI2...
- Limit PEEP
- Limit plateau pressure
Respiratory - Correct hypoxemia
strategy - Avoid significant
hypercapnia
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4 - ACUTE MITRAL REGURGITATION

AND VENTRICULAR SEPTAL RUPTURE
Dr. Ovidiu Chioncel, MD, PhD, FHFA

Prof of Cardiology. University of Medicine Carol Davila,
Bucharest / Emergency Institute for Cardiovascular Diseases
“C.C.Iliescu” Bucharest, Romania
Dr. Laura Antohi, MD

University of Medicine Carol Davila, Bucharest / Emergency
Institute for Cardiovascular Diseases “C.C.Iliescu” Bucharest,
Romania
Prof. Vlad Iliescu, PhD

Prof of Cardiac Surgery at University of Medicine Carol Davila,
Bucharest, Romania / Emergency Institute for Cardiovascular
Diseases “C.C.Iliescu” Bucharest, Romania
III.4
4.1 - Acute Mitral Regurgitation P.180
Key messages
Early identification of mechanical complications post AMI is crucial
Intensity of monitoring in acute MR will depend on severity of clinical

presentation
Acute MR may occur in different clinical settings/scenario
Echocardiography is of paramount importance for assessing aetiology, type,

severity and mechanism of MR
In acute MR, the aims of monitoring include: assessing the severity of MR,
monitoring the cause of MR, monitoring the impact of acute MR on car-
dio-respiratory status and monitoring the response to the therapies
Emergent cardiac surgery is required in patients with ruptured papillary

muscle or in those with severe acute MR and cardiogenic shock
Introduction
In the acute settings, the majority of causes of acute mitral regurgitation (MR) present
as an acute, de novo event, when the cause of MR and MR are concomitant, but can also
occur in patients with chronic MR, when regurgitant severity is exacerbated by factors
such as coronary ischemia, sepsis, endocarditis, high BP. In other instances, the acute
MR is the result of worsening of a previous mild to moderate functional MR, in patients
with dysfunctional LV. The pathophysiology responsible for cardiac adaptation in these
three entities looks different and may be responsible for different clinical presentations
and haemodynamics (Figure 1).
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Figure 1 - Mitral Regurgitation phenotypes

A. Acute MR. The pulmonary circulation is overloaded (chest X ray), but a normal LV compliance limits the increase in
end-diastolic volume (Echo). The LV response to acute MR includes an increase in preload, a decrease in afterload, an
increased EF, and a variably decreased SV. B. Chronic MR a large compliant ventricle that is well suited to deliver a large SV
and preload reserve is re-established. C. LV dilation, elevated LV diastolic pressure, increased systolic wall stress, and an
EF<50%. It can be difficult to establish whether the primary problem is that of MR causing LV dilatation and dysfunction or a
cardiomyopathic process leading to secondary (ie, “functional”) MR.
A B
Acute severe primary MR in setting of posterior Acute severe primary MR in setting of endocarditis in
papillary muscle rupture patients with Barlow disease and previous moderate MR
PAC: Very high PCWP and LVEDP. Low CI and PAC: Normal or mildly increased PCWP and LVEDP CI and
stroke volume; large v wave. stroke volume are normal; large v wave.
Chest X ray: Severe pulmonary congestion with Chest X ray: Severe pulmonary congestion with
alveolar edema but normal CT index. interstitial edema and high CT index.
Echo: Normal LV and LA dimension LVEF is normal, Echo: LV and LA are dilated. LVEF is normal or mildly
dp/dt is normal. reduced, dp/dt is normal.
C
Acute severe functional MR in patient with ischemic
cardiomyopathy and recent posterior MI
PAC: Increased PCWP and LVEDP. Low CI and stroke
volume; large v wave.
Chest X ray: Severe pulmonary congestion with
interstitial edema and high CT index.
Echo: LV and LA are dilated. LVEF is severely reduced,
dp/dt is decreased.
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Chronic MR affords time for the ventricle to dilate to accommodate the regurgitant volume.
This adaptation maintains forward stroke volume (SV) and cardiac output (CO) despite the
regurgitant volume. Correspondingly, LV end-diastolic pressure remains normal unless there
is coexistent pathology that impairs diastolic function. Even in the presence of the precipi-
tants that worsen severity of MR, these patients may tolerate better an additional volume
overload. In acute MR, the LV is not able to adequately compensate for the regurgitant
volume, and excessive backward blood flow impairs forward SV. Compensatory tachycardia
may preserve CO initially, but eventually hypotension, organ failure, and other evidence of
cardiogenic shock will develop. PCWP increases abruptly and pulmonary oedema develops.
Acute MR may result from either “organic” or “functional” causes. Organic causes are those
that result in permanent structural disruption of the valve, such as leaflet perforation or,
MiV prosthesis dehiscence from endocarditis, chordal rupture in myxomatous valve disease,
or papillary muscle rupture due to myocardial infarction. Functional MR results from abnor-
malities of the LV, such as cardiomyopathies in which the papillary muscles are laterally
displaced, or acute ischemia, in which an akinetic wall segment and papillary muscle impair
mitral valve closure. The distinction between organic and functional causes is an important
one because the treatment of organic causes requires surgical repair, whereas functional
causes may improve with treatment of the underlying myocardial ischemia, infarction, or
cardiomyopathy.
4.1.1 - Monitoring in acute MR depending on clinical scenario
Patients with acute MR with AHF present in ED with different clinical scenario, including a
broad spectrum of clinical presentations varying from mild-moderate symptoms to CS, and
including diverse aetiologies such as, AMI, endocarditis, prosthetic valve thrombosis. Initial
clinical assessment should include stability of vital signs, severity of symptoms and identifi-
cation of the potentially life-threatening cause leading to AHF (Figure 2). Initial evaluation
and continued non-invasive monitoring of the patient’s vital cardiorespiratory functions,
including basic monitoring (SpO2, BP, HR, RR, continuous ECG) and urine output instituted
within minutes, is essential to evaluate whether ventilation, peripheral perfusion, oxygena-
tion, HR and BP are adequate. Patients with acute MR should be closely monitored during
hospitalization (Figure 2). The intensity of monitoring will depend on severity of clinical
presentation, the response to medical therapies and the cause leading to acute MR.
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Figure 2 - Acute MR: diagnostic, monitoring and treatment algorithms
Classification Functional MR Organic MR
Rupture of PM
Ischemic MR, Rupture of chordae
Etiology
Non-ischemic MR Endocarditis
PV dysfunction
Large coaptation defect/valve

morphology
Dense triangular CW signal
Large flow convergence zone
EROA>20mm2
Severity Vena contracta >8mm EROA>40mm2
Rvol>30ml/beat
Systolic PV flow reversal
E wave >1.5m/sec
VTI Mitral/VTI Aortic >1.4
Large "v" wave
IV vasodilators/diuretics CV catheter
Arterial hypotension Arterial line
Refractory hypotension/hypoperfusion/therapeu- PAC

tic uncertainity/biV dysfunction
Stabilization IMV
Hypoxaemia (PaO2<60mmHg), hypercapnia
(PaCO2>50mmHg) and acidosis (pH<7.35)
MCSs
Refractory to initial terapies including high doses
of inotropes/vasopressors
Medical therapies
MV surgery at moment of revascularization
Treatment Isolated MV surgery when surgical risk is low
Percutaneous MV edge-to edge repair
MV surgery
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In-hospital monitoring
Clinical:
BP, HR, T0, RR, SpO2 Consider NVI if RR>25/min and SpO2<90%
S/S of congestion
S/S of hypoperfusion
ECG: continuous ECG monitoring>48h

Biology: Troponine, renal function, Na, K, AST, ALT, Lactate
ECHO: initial-FoCUS including lung ultrasound
ECHO: assessing etiology, mechanism and severity of MR; guiding the response to therapies
CVP, ScVO2
MAP, pressure curve, ABG analysis (pH, PaO2, PaCO2)
CI, SVR, CPO, PCWP, "V" wave
Tidal volumes, Assynchrony, Air leakage

ABG analysis (pHn PaO2, PaCO2)
LUS
ECHO: LV and RV dimensions, Ao-VTI,

AoV opening, EF
PAC: CI, PCWP
Biology: Lactate End organ function tests (creatinine, AST, ALT)
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P.185
E/e' should not be used in monitoring LAP of patients with decompensated heart failure with
depressed systolic function several studies have shown that these parameters do not predict
LAPs or guide management in this clinical setting. On the basis of available evidence, the use
of echocardiography for monitoring purposes is justified when changes have occurred, such
as an increase in LAP from normal to abnormal (an increase in E/E' ratio from <8 to >13 in the
setting of normal systolic function). It can be used for continuous monitoring in settings in
which LVIDD, RV FAC, or PA systolic pressure are being re-evaluated in weaning protocols.
In both of these settings, it is important to note what degree of change must occur before
one can say the given change is beyond the interobserver variability of the measurement.
In the specific areas of IVC collapsibility index, E/ A, and PA systolic pressure changes, we
have added categorical changes (on the basis of guidelines) that should be used when gui-
ding management. These categorical changes are well within the published data regarding
coefficient of variation and interobserver variability of the monitoring parameter.
Figure 3 - Echocardiographic criteria for MR severity; correlation with right

catheterisation data
MV closure MV opening
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The ESC guidelines recommend the insertion of an arterial line in patients with AHF and
clinical evidence of CS. The arterial line allows for repetitive sampling of ABG, providing
important information on oxygenation (PaO2), ventilation (PaCO2), acid - base balance, elec-
trolytes and lactate levels. The continuous measurement of arterial pressure allows for the
appropriate titration of vasoactive medication, if needed. Respiratory variations of invasive
arterial pressure might indicate, among others, RV failure or pericardial tamponade.
Urgent coronary angiography needs to be performed to identify coronary anatomy, as conco-

mitant revascularization during mitral valve surgery is associated with improved short-term
and long-term outcomes. Right heart catheterization has limited use in the diagnosis of
acute MR, but can be useful in differentiating it from VSR. The PCWP tracings from pulmo-
nary artery may show large V waves or giant “C-V” wave, which is the hallmark of acute MR
the wedge pressure tracing (Figure 3). However, this finding is not pathognomonic since it
may be seen in others conditions, such as VSR and massive LV failure. Acute MR can atte-
nuate or obliterate the X descent (LA relaxation). The giant V wave of acute MR may be
transmitted retrogradely into the pulmonary artery. This yields a biphasic pulmonary artery
systolic waveform composed of the pulmonary artery systolic wave, followed shortly by the
V wave. A large V leads the mean PCWP to overestimate the LV end diastolic pressure, and
for the best estimate of the LV end diastolic filling pressure in the presence of a large V
wave, PCWP should be measured at a single time point (end diastole). The CO is decreased
and CS is frequently present. The aortic SBP is usually low, and the aortic pulse pressure is
usually narrow, reflecting a decreased LV forward SV. The degree of MR is sensitive to LV
afterload. Afterload reduction with nitroglycerin or nitroprusside can significantly reduce
the amount of MR and the amplitude of the PCWP V wave. IABP and Impella in acute MR
decrease afterload, resulting in less MR and more forward flow from the LV into the aorta.
IABP should continue for at least 24 h following surgery, in addition to the supportive pos-
toperative care that will be required for these patients with multiorgan dysfunction.
IMV and NIV should be used as necessary. While IMV is considered in the setting of CS,
severe ACPE and cardiopulmonary arrest deterioration of consciousness due to acute and
persistent respiratory insufficiency, NIV is adequate and effective in most episodes of stand-
alone ACPE or pulmonary congestion.
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4.2 - Ventricular Septal Rupture
Key messages
Early identification of post MI VSR in ED is critical, since it may avoid intense

DAPT regimen and bleeding risk associated to surgery
Clinical presentation depends on size, location and pulmonary and systemic
vascular resistance
The intensity of monitoring depends on clinical presentation and the size
of the defect
Echocardiography is of crucial importance for the diagnosis and monitoring
of VSR patients
Monitoring of the RV dimensions and function, coupled with monitoring of
Pulmonary Hypertension and Tricuspid Regurgitation represent key elements
for the indication, and type and timing of cardiac surgery
Close haemodynamic monitoring is required at least 48-72h post intervention

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Introduction
The incidence of the acute ventricular septal rupture (VSR) has been estimated between
0.5% and 2% of all myocardial infarctions However, the mortality is still high, with 60–70%
of patients dying within the first 2 weeks, and less than 10% survive after 3 months. The
acute rupture occurs 3–7 days after a huge transmural infarction, with the weakening of
the septal wall, but the median time for rupture occurrence decreased below 24 h with
the use of thrombolysis. Late rupture is rare, but possible (as long as 2 weeks). Anterior
infarctions are more likely to cause apical defects and inferior or infero-lateral infarctions
are more likely to cause basal defects at the junction of the septum and the posterior
wall. The rupture may vary in size from mm to cm. This determines the magnitude of left-
to-right shunting, influencing the clinical presentation (from mild symptoms to CS), and the
likelihood of survival. Classification of the defect includes three types: type I ruptures show
an abrupt tear in the wall of normal thickness, and is associated with acute infarcts <24 h
(more common in apical VSR); in type II, the infarcted myocardium erodes before the rup-
ture, and is covered by thrombus, clinically with a sub-acute presentation (more common
in posterior VSR); type III shows perforation of an aneurysm grown after infarct healing
associated to older infarcts. VSR results in a left-to-right shunt with diversion of blood flow
towards pulmonary circulation. The immediate effect of VSR is shunting of blood from the
left to the right ventricle. Systemic vasoconstriction in response to peripheral hypotension
and hypoperfusion worsens the shunt. The magnitude of this shunt is determined by the
left- and right-sided pressures, as well as the size of the defect, which in turn determines
the extent of haemodynamic compromise. The degree of shunting, or shunt fraction (Qp/
Qs), is determined by the relative vascular resistances in the systemic and pulmonary
beds. As a consequence of shunting of a large volume RV and in pulmonary circulation,
RV is overloaded, LV stroke volume is decreased and low CO and CS shock may occur.
Whereas LV dysfunction is related to the extent of the AMI, RV dysfunction is related to
the volume overload produced by the intraventricular shunt as well as the initial infarct.
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4.2.1 Monitoring in VSR
Patients with acute VSR may present in ED with diverse clinical presentations varying from
mild symptoms to CS. Initial clinical assessment should include stability of vital signs, severity
of symptoms and clinical identification of the VSR. Initial evaluation should be concomitant
to the establishment of a continuous basic non-invasive monitoring to assess patient’s vital
cardiorespiratory functions. Patients with VSR should be closely monitored during hospita-
lization. The intensity of monitoring will depend on severity of clinical presentation, and the
magnitude of the shunt (Figure 2).
Ideally, VSR would be diagnosed prior to PCI to minimize the associated risks of surgical
bleeding after the administration of dual-antiplatelet therapy. All patients who develop hae-
modynamic compromise during AMI should have an immediate echocardiography to identify
the possibility of the mechanical complications. A FoCUS echo protocol may rapidly identify
the VSR. Particularly, subcostal images (less prone to poor acoustic windows due to respi-
ratory distress) may allow detection of VSR (Figure 1). However, when a VSR is suspected,
a systematic echo study is mandatory.
Figure 1 - Echocardiographic assessment of the ventricular septal rupture

in subcostal views
A large inter-ventricular gradient is noted (93mmHg).
A: Basal septum VSR; B: Inter-ventricular gradient by CW-Doppler.
A B
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Patients with haemodynamic stability, do not generally require intensive or continuous moni-
toring. If RR or SpO2 are initially in the normal range, BP and diuresis probably are the main
parameters to be monitored, initially frequently (varying from every 30 min to 4h for BP,
depending on initial values and the response to treatment) in order to actively adjust IV
diuretic and other drugs, and at longer intervals thereafter (every 8-24 h, depending on the
clinical state (Figure 2). For patients presenting with haemodynamic instability, especially
for those with large rupture, a high intensity and complexity of monitoring is required. In
addition, RRT with hemodialysis, nasogastric feeding, and prolonged ventilator support often
required in these patients.
Figure 2 - Acute VSR: diagnostic, monitoring and treatment algorithms
Conservative
Hemodynamic stable
Percutaneous closure
-Clinical: with small VSR
when suitable anatomy:
BP,HR, T0, RR, SpO2 CVC-CVP, ScVO2
small apical VSR without
Consider NVI if RR>25/min and Arterial line-MAP, pressure curve,
valve Involvement
SpO2<90% ABG analysis (pH, PaO2, PaCo2)
Biology: Lactate, end organ
Delayed,elective
S/S of congestion and function tests (creatinine, AST,
ALT), coagulopathy surgery
hypoperfusion, systolic murmur
Close monitoring and
-ECG: 12 lead-site of AMI
Hemodynamic stable Afterload reduction with
continuous ECG monitoring>48h
with large VSR IV vasodilators/inodilators
-Biology: Troponine, renal
CVC-CVP, ScVO2
function, Na,K,AST, ALT, lactate
Arterial line-MAP, pressure curve,
-ECHO initial: detecting Delayed surgery>7days
ABG analysis (pH, PaO2, PaCo2)
mechanical complication:VSR Close monitoring and
Biology: Lactate, End organ
Avoid upfront DAPT Afterload reduction with
function tests (creatinine, AST,
-ECHO: IV vasodilators/inodilators
ALT), Coagulopathy
*identification of LV entry site IABP+/-VA ECMO
Waiting on IABP or VA ECMO
and RV exit site, size of deffect
*assessing LV and RV function, Hemodynamic Immediate surgery
MiV involvement, TR, PHT unstable Continue post op>48h
*other cardiac abonormalities CVC-CVP, ScVO2 IABP+/-VA ECMO
(e.g. LV aneurysm, free wall Arterial line-MAP, pressure curve, Percutaneous closure
rupture, AoR) ABG analysis (pH, PaO2, PaCo2) -when suitable anatomy:
-Coronary angiography+/-LV PAC-CI, SVR, CPO, PCWP small apical VSR without
angiography IABP+/-VA ECMO (depending on valve Involvement
RV dysfuntion) -severe comorbidities
-continue IABP,VA ECMO >48h
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Patients presenting with VSR are often in extremis, secondary to ACPE. Management of
these patients usually requires ventilatory support. NIV or IMV with intubation should be
used as necessary. IMV is considered when there is a severe deterioration of consciousness
due to acute and persistent respiratory insufficiency.
Patients with severe AHF and non-responsive or refractory to pharmacological therapies

aimed to afterload reduction, require MCS (IABP, Impella or VA-ECMO). In patients with severe
RV dysfunction, VA-ECMO is preferred, since it may assist an overloaded RV. Patients require
complex monitoring measures in order to assess the efficacy of MCS and to establish the
timing and modality of weaning. These measures include clinical (BP,HR), echocardiography
(LV and RV dimensions, LVOT-VTI), biological (surrogates of hypoperfusion, such as lactate,
ScVO2, and specific markers of end-organ perfusion, creatinine and liver function tests), and
in some cases invasive haemodynamic monitoring (Figure 2).
The optimal management approach varies with the clinical presentation. Medical therapy is
considered to be a support tool of surgery, and is usually managed with the use of pharma-
cologic support with vasodilators (which reduce afterload, thereby decreasing LV pressure
and the left to right shunt), inotropic agents (which may increase CO), diuretics, and IABP. In
patients with CS, death is inevitable in the absence of urgent surgical intervention. Delayed
elective surgical repair is feasible in haemodynamically stable patients or in those with small
VSR. Delayed surgery may be considered when surgical anatomy is complex and there is
concern regarding tissue fragility and the ability to perform definitive repair. Percutaneous
MCS (IABP or VA-ECMO) are implanted in patients waiting for surgery. The level of monitoring
in these patients includes haemodynamic parameters derived from non-invasive and invasive
measurements. In stable but inoperable patients, percutaneous trans-septal closure may be
considered. Patients with severe end-organ failure despite aggressive support may not be
considered for further interventions, and transition to palliative care may be appropriate.
Clinical decisions should be individualized according to clinical status, age, comorbidities
and willings of the patient/family.
Post-surgery, patients should be closely monitored in the ICU, at least 48-72 hours, or till
resolution of haemodynamic compromise. Very often, these patients require PAC to monitor
PCWP and RV function parameters.
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4.2.2 - Main parameters to monitoring in acute MR
Initially, basic non-invasive haemodynamic monitoring should be settled down (Table 2).
Signs and symptoms are quite variable and may include recurrent chest pain and dyspnoea,
but even a precipitous onset of haemodynamic compromise characterised by hypotension
and biventricular failure (often predominantly right-sided failure), up to cardiogenic shock
is possible. At physical examination, a harsh and loud pansystolic murmur at the left lower
sternal border is present in over 90% of cases. A palpable thrill can be detected in up to
50% of patients. All patients who develop haemodynamic compromise during AMI should
be rapidly examined to disclose VSR, although both, murmur and thrill, may be difficult to
detect in patients with a low output state. Other physical exam findings result from aug-
mented right-sided flow, and may include left or right S3 gallop, or tricuspid regurgitation.
Clinical signs of right-sided congestion failure should be monitored daily, in conjunction with
biological and echo data.
ECG shows tachycardia, usually confirms an inferior or anterior AMI. A continuous ECG moni-
toring is required at least 48 h in patients with severe AHF.
Chest radiography demonstrates pulmonary venous congestion There is no need to repeat

chest X-ray, except when want to check position of cardiac catheters.
Blood sample include the whole tests required for an AHF patient (Figure 2/ section 4.1-
Acute Mitral Regurgitation). In the absence of other known confounders, venous lactate >2
mmol/L is marker of tissue hypoperfusion. When the RV is involved, especially in the setting
of an inferior MI, hepatic dysfunction and coagulopathy may also be noted. Liver function
tests and coagulation tests should be obtained daily.
Echocardiography with colour-flow Doppler is the standard for diagnosis, assessing the posi-
tion, the size of VSR and the magnitude of the shunt. When a VSR is suspected, a systematic
echo study is mandatory. First step is defining the position, complexity and size of the VSR
with the site of infarction (anterior versus inferior). Septal ruptures in patients with anterior
MI are generally apical and simple. Conversely, in patients with inferior MI, septal ruptures
involve the basal infero-posterior septum and are often complex. Evaluating the function
and size of both ventricles is of critical importance. For an anterior VSR, it is important
to assess the severity of LV dysfunction, presence of coexisting CAD, suitability of poten-
tial revascularization targets, and anatomy of previous infarctions. For a posterior VSR, an
additional understanding of RV function and the presence of mitral regurgitation is impor-
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tant. For surgical intervention, assessment of right ventricular function is of paramount

importance. A RV basal dimension>42 mm suggests severe RV dysfunction. Also, A TAPSE
<17mm, a peak systolic tissue velocity at the tricuspid annulus (S') <9.5cm/sec, RVFAC<35%
and a RV GLS<20%, are considered indicators of severe RV dysfunction. Also, a RV dp/dt<
400mmHg/sec was associated to an abnormal RV function and can be used for monitoring
purposes. Other indexes, such as Myocardial performance index or Tei index are difficult to
assess on emergency bases.
Assessing RVSP from the tricuspid regurgitant velocity and estimation of right atrial pressure
is an obligatory step of echo protocol. Care should be taken not to include any left-to-right
VSR jet in the measurement of the TR, which could seriously overestimate the RVSP. To
calculate Qp/Qs, the right ventricular stroke volume and left ventricular stroke volume are
derived from four measurements: RVOT diameter, LVOT diameter, a pulsed wave Doppler
VTI of the RVOT, and a pulsed wave Doppler VTI of the LVOT, which are taken from both the
parasternal and apical imaging windows. The equation is SV-RVOT / SV-LVOT (Figure 3). VSR
can coexist with a pseudoaneurysm, when contained free-wall rupture and septal rupture
have both occurred. In these challenging cases, 3D echo can be very useful to delineate the
different pathologies. When image quality is poor, particularly in ventilated patients, TEE may
be required and is a standard component of precardiac surgery work-up. TEE gives impro-
ved visualization of rupture morphology and better delineation of multiple rupture sites.
Agitated saline bubble contrast can be used for diagnosis of VSR. A positive contrast study
is defined by the presence of contrast within the LV within three cardiac cycles. Because LV
pressure is much higher than RV pressure, the presence of a VSR is often characterized by
a "negative" contrast effect, which appears as nonuniform opacification of the RV at the
site of the defect. In patients with acute VSR, daily monitoring of LV size and function is
recommended, as well as monitoring of PHT and TR.
Coronary angiography needs to be performed to identify coronary anatomy. Left ventricu-

lography performed in the LAO projection in a patient with VSR may demonstrate shunting
of contrast from the LV to the RV (Figure 4). Frequently, VSR patients have multivessel
disease and concomitant revascularization of coronary vessels not involved in ruptured
myocardium during VSR surgery may be associated with improved long-term outcomes.
Furthermore, when cardiac surgery is not possible, a step-by-step procedure including PCI
and percutaneous closure of VSR may be considered.
The central venous catheter enables the monitoring CVP and allows the safe and continuous
administration of vasoactive drugs and inotropes in patients with AHF who require inten-
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P.194
sive treatment. CVP should be maintained <10-12 cmH2O, in order to avoid overloading of
the dysfunctional RV. ScvO2 can also be monitored with the central venous catheter. The RA
SaO2 can be artificially decreased if the proximal catheter lumen is adjacent to the coronary
sinus (venous blood flow). The RA SaO2 can be artificially increased if significant TR further
complicates the ventricular septal rupture. Oxygenated blood is shunted across the septal
defect into the RV and then refluxes across the tricuspid valve into the RA.
Figure 3. Echocardiographic and haemodynamic criteria for calculation of

shunt ratio
Qp=pulmonary output; Qs=systemic output;
In panel A (Echo): QS= S x V (LVOT), Qp= S x V (RVOT). In panel B (Haemodynamic): are presented PAC curves in RA, RV
and LV. A high RA and RV pressure are noted. Qs= MVO2/(SaO2-SRAO2); QP= MVO2/SPVO2-SPAO2); Qp/Qs= (SPVO2.SPAO2)/
(SaO2-SRAO2). There is a significant increase in SaO2 (≥ 10%) between RA an PAw
A B
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Figure 4 - Percutaneous closure of an apical VSR

Echocardiography and contrast ventriculography. Instantaneous and simultaneous opacification of LV and RV. Panel A: Echo
of a large apical VSR. RV of normal dimensions. Panel B: LV angiography with simultaneous contrast in both ventricles.
C. Transseptal closure with residual shunt.
B C
III.4
P.196
As in acute MR, the insertion of an arterial line is indicated in patients with AHF and clini-
cal evidence of CS. Right heart catheterization with PAC is reserved for patients with CS or
severe AHF, or for patients with MCS waiting for cardiac surgery. It has limited role in the
diagnosis of VSR, but can be useful in monitoring patients with bi-ventricular dysfunction.
With acute VSR, the mean RA pressure, wedge, and PA pressures are all significantly elevated.
A large and delayed “V” wave is often present in the PCWP tracing. A large “Y” descendent
signifies severe TR. VSR can be confirmed by demonstrating a significant increase (>10% ) in
the SO2 between RA and PA (Figure 3). With acute VSR, the systemic blood flow averages
only one-half to one-fourth of the thermodilution determined CO. Thus, a “normal” thermo-
dilution CO in a patient with VSR usually reflects a severe reduction in systemic blood flow.
In patients without CS, a large RA pressure (>12cmH20) and SVO2>85%, suggests a large
intraventricular shunt and/or severe RV failure. Also, a RA/PCWP ratio>0.5 is an indicator
of RV failure. In patients with large VSR, a RA/PCWP ratio>0.63 suggests the utilization of
VA-ECMO instead of IABP. Although, influenced by preload, RV stroke work index [(mean
PAP-RAP) x SV index] is an established marker of RV function, very useful for monitoring
purposes. PA pulsatility index (PAPs-PAPd/P AD) is a sensitive marker of RV dysfunction
but is waiting prospective validation in large cohorts.
The pulmonary to systemic blood flow ratio provides an estimate of the size of the shunt. The
excess pulmonary blood flow represents the amount of blood passing through the defect.
The shunt ratio can then be calculated by the following formula: Qp/Qs = (SaO2-SvO2)/(SpvO2-
SpaO2) (Figure 3). A Qp/Qs ratio of greater than 2 suggests a large shunt, which is usually
poorly tolerated by patients. Standard PAC reference values need to be interpreted with
caution in patients with a shunt, and other continuous real-time haemodynamic monitoring
tools, such as the LiDCO or PiCCO systems, may be more useful.
After cardiac surgery, 35-60% of VSR patients still have haemodynamic instability. In this
group of patients, continuation of MCS is imperiously required, as well as close monitoring,
including serial echocardiography and PAC. The intensity of monitoring is high in the first
48-72h, or till resolution of the haemodynamic instability. Monitoring data will guide wea-
ning protocols, starting with day 2 post-operative, including step by step de-escalation of
mechanical assistance.
III.5
5 - CARDIAC TAMPONADE
P.197 AND CONSTRICTION
Prof. Eric Bonnefoy-Cudraz,

Intensive Cardiac Care Unit, Université Lyon 1, France
Dr. Thomas Bochaton, MD

Intensive Cardiac Care Unit, Université Lyon 1, France
Key messages
Cardiac tamponade is an increase in pericardial pressure sufficient to seve-
rely restrict filling of heart chambers
Paradoxical pulse, jugular distension, tachycardia and then, hypotension, are
the main haemodynamic clinical parameters monitored during tamponade
Echocardiography documents volume of pericardial effusion, residual size
of cardiac cavities and changes in cardiac haemodynamics: CO, pressure
gradient, ventricular filling rate during breathing
Tamponade is an emergency and its haemodynamic monitoring (clinical and
echocardiographic) aims at defining the best timing of pericardial drainage.
Most often it is immediately
The relationship between volume and pressure in the pericardium has a J
shape with a steep slope. Because pericardiocentesis in tamponade occurs
on the vertical part of the J shape curve, haemodynamic improve dramati-
cally with a small extraction of volume
III.5
P.198
Introduction
Cardiac tamponade is an increase in pericardial pressure sufficient to restrict filling of

the heart chambers. Most often it is caused by intrapericardial fluid accumulation. The
increase of pressure in the intrapericardial space (IPP, normally nil or negative) will reduce
the transmural pressure of heart chambers and their volume. The right atrium with its
thin wall will be the first cardiac cavity to show signs of compression. Tamponade is not
an all-or-nothing but a progressive 3 phases process:
a) During the first phase right cavities' transmural pressure in diastole will remain higher
than IPP. That is done through increase in RA pressure. There is no effect on SV.
b) A second phase is reached when IPP and right cavities pressure equalise (right transmu-
ral pressure is nil) but are lower than the left diastolic pressure (left transmural pressure
still positive). There is a limited impact on stroke volume.
c) The third phase is observed when all diastolic pressures in all cardiac cavities are equal
to the IPP. At this stage, SV is reduced and decrease further with any increase in IPP.
Haemodynamic consequences and clinical severity of a tamponade will depend on the
rate of accumulation, nature of effusion, thickness and compliance of the pericardium,
compliance and basal intracavitary pressure of cardiac cavities and cardiac or pulmonary
associated pathologies.
III.5
P.199
5.1 - Haemodynamic of compensatory response
Cardiac tamponade will induce haemodynamic compromise and ultimately collapse and activate
several compensatory mechanisms mediated by the sympathetic system. All will be used for
diagnosis, risk stratification and monitoring of tamponade. The most immediate is mobilization
of blood from the splanchnic system to increase intracavitary pressures and preserve a filling
capacity. This will be marked by distension of jugular veins. When this first compensatory res-
ponse is insufficient sympathetic activation leads to increase contractility and tachycardia that
compensate for reduction of SV and preserve CO. An increase in peripheral arterial resistance
will maintain organ perfusion pressure. When these compensatory mechanisms are overwhel-
med CO and BP will fall and organ perfusion will suffer. In more progressive cases, urine output
will be a sensitive indicator because of its early susceptibility to increase in venous pressure
and reduction in arterial pressure and CO. Tachycardia and hypotension signal here an imminent
haemodynamic collapse. Note that tamponade does not induce pulmonary oedema despite a
mark rise in LVDP. Possibly this is because transmural pressure falls toward zero and right heart
compression protects the lung from critical level of blood flow.
5.2 - Echocardiography haemodynamic and monitoring
Association of low arterial BP, distended neck veins, tachycardia have few differential
diagnoses beyond tamponade (mainly pulmonary embolism) and require emergent echo-
cardiography. Echocardiography documents all the important monitoring parameters needed
to assess the severity and immediate risk of tamponade: volume of pericardial effusion, resi-
dual size of cardiac cavities over the cardiac cycle, CO, pressure gradient, ventricular filling
rate and their change during breathing.
Volume of the effusion does not imply its haemodynamic repercussion because pericardial
compliance may gradually increase with the effusion. Echocardiographic measurements,
however, reassuring at a given moment, do not prejudge the haemodynamic effect of even
a modest increase in intrapericardial fluid. Haemodynamic collapse can develop rapidly.
2D echocardiographic signs of compression will first be apparent with the RA early in diastole,
when intracavitary volume and pressure is lower. It signals that intrapericardial pressure equals
or exceeds RA pressure and is not specific of tamponade. Compression of the RV will appear later
because compliance of the RV is lower than that of the RA. Its collapse will therefore signal a much
higher intrapericardial pressure. The longer the collapse of the RA the more severe the tamponade.
III.5
P.200
5.3 - Paradoxical pulse and its echocardiographic

equivalent
Because of ventricular interdependence, physiologically, during inspiration, there is an

increase in transmural pressure, venous return and, the volume of the right cavities and,
a reduction of LV SV. This is haemodynamic consequences of inspiration are increased in
tamponade because competition of cardiac cavities for intrapericardial space is increased.
Also, the diastolic gradient between the left atrium (wedge pressure) and the left ventricle
will decrease further.
On a clinical monitoring basis, cardiac tamponade induces a paradoxical pulse. That is defined
as a reduction of at least 10 mmHg of the SBP in inspiration. Note that for the paradoxical
pulse to be apparent some conditions are required: negative pressure in the thorax in ins-
piration (spontaneous breathing), intact septa between ventricle and atria, equalization of
diastolic pressures between all cardiac cavities. Paradoxical pulse will therefore not be pre-
sent in assisted ventilation or when the pericardial effusion is confined to a cardiac cavity.
On an echocardiographic monitoring basis, similar to paradoxical pulse, flow through the tri-
cuspid valve will increase markedly on inspiration and decrease through the mitral valve (and
SV as well). On expiration, flow will increase sharply through the mitral valve and decrease
through the tricuspid valve. A 25% or more variation between inspiration (increasing tri-
cuspid, decreasing transmitral) and expiration (increasing transmitral, decreasing tricuspid)
has good specificity for tamponade.
5.4 - Catheterisation
Haemodynamic monitoring does not request a cardiac catheterization in tamponade. Diastolic

filling pressures are found high and equalized in all cardiac cavities. This pressure equaliza-
tion is not observed if the effusion is localized or if other cardiac disorders modify diastolic
pressure regimes (i.e. LV dysfunction, pulmonary pathology).
On the AP curves, the descent X that corresponds to modifications occurring in systole is

very marked and the Y descent (occurring in diastole) is blunted.
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P.201
5.5 - Haemodynamic effect of pericardiocentesis
In case of cardiac arrest, external cardiac massage is not effective because there is no free
capacity for filling the heart chambers. However, even at this final stage, the evacuation of
a small volume of effusion can restore a satisfactory haemodynamic because the evacua-
tion of the effusion is performed on the vertical part of the J shape volume-pressure curve.
With the evacuation of the effusion, all haemodynamic signs will normalise or disappear.
In the absence of rapid and clear improvement, it is necessary to suspect the puncture of a
vein, of the heart or, of another cavity (pleura). It may also be that the haemodynamic signs
were not caused by the pericardial effusion or that exists another cause for the rigidity of
the pericardium (effusive-constrictive pericarditis).
5.6 - Effusive-constrictive pericarditis
Constriction is uncommon as an emergency. Most of the time the issue arises when discus-
sing the possibility of pericardial constriction versus myocardial restriction in patients with a
history of thoracic radiotherapy or heart surgery and right heart failure. Table 1 summarises
the main haemodynamic differences between the 2 entities.
Effusive-constrictive pericarditis is a slightly less uncommon issue. It is suspected when RA

pressure fails to decrease by more than 50% or below 10 mmHg after pericardiocentesis. It
signals a decreased pericardial compliance and is marked haemodynamically by a transition
from haemodynamic of tamponade to haemodynamic of pericardial constriction (Table 1).
III.5
P.202
Table 1 - Constrictive (pericardium) and restrictive (myocardium) haemody-

namics as assessed with echocardiography and in the cath lab
Constrictive Restrictive
Restrictive pattern, with early diastolic mitral

inflow Doppler velocity (E) greater than late
LV septal shift in inspiration
velocity (A)
Inspiratory decrease in early mitral inflow velo-
Severe bi-atrial enlargement
city (E)
No ventricular septal shift in inspiration
Normal or increased medial and lateral annular
No change in early mitral inflow velocity with
velocities (e')
breathing
Hepatic vein decreased expiratory forward
Decreased medial and lateral annular veloci-
velocities and end diastolic flow reversals in
ties (e')
expiration
Hepatic vein end diastolic flow reversals in
inspiration
Increased venous (RA) pressure with square

root sign
Discordance of LV and RV systolic pressure Square root sign present but parallel changes
with breathing (right increases when left in LV and RV pressure curve areas with
decreases) breathing
Prominent X descent, blunted y descent Prominent y descent, blunted x descent
Equalisation of right and left heart diastolic No discordance between PCWP and LVDP in
pressure inspiration
Disproportionate (as compared to LV) decrease
of PCWP in inspiration
III.5
P.203
Figure 1 - Pressure / Volume curves of the pericardium
INTRAPERICARDIAL
PRESSURE
PRESERVED CO
Cardiac
Jugular output
Tachycardia
distension decreases
All diastolic pres-
sure in all cardiac
cavities are equal
to the IPP. Stroke
volume is reduced
a n d d e c rea ses
further with any
LVEDP
increase in IPP.
RAP
INTRAPERI-
CARDIAL
VOLUME
Right cavities’ transmural IPP and right cavities pressure

pressure in diastole will remain equalise but are lower than
superior to IPP. That is done the left diastolic pressure (left
through Progressive increase transmural pressure still posi-
in RA pressure. No effect on tive). There is a limited impact
stroke volume. on stroke volume.
III.6
Prof. Daniel De Backer, MD, PhD

Intensive Care, Université Libre de Bruxelles, Brussels, Belgium
Key messages
SS is a medical emergency and need to be rapidly recognized. SS management
requires identification and control of the source, and haemodynamic support.
SS is sepsis requiring vasopressors and associated with lactate ≥4 mmol/L
Sepsis is the dysregulated host response to an infection. At sepsis reco-
gnition, 30 ml/kg crystalloids should be administered as soon as possible
Antibiotics should be administered within one hour of hypotension
After initial fluid resuscitation, fluid administration should be guided by dyna-

mic indices of fluid responsiveness
Vasopressors should be administered without delay in case of severe

hypotension or low diastolic pressure
The selection of haemodynamic tools should be based on patient severity,

ideally after performing echocardiography
Balanced crystalloids is the preferred fluid solution for most patients, but
saline may be used in selected patients
Albumin may be administered in SS patients with hypoalbuminemia
Norepinephrine should be the first vasopressor agent. Vasopressin and ter-

lipressin are excellent second line vasopressor agents
Target MAP is 65 mmHg, but higher MAP may be required in selected patients
Inotropic agents are not routinely indicated, and should not be based only
on a decreased ejection fraction at echocardiography. They may be conside-
red in cases of impaired tissue perfusion associated with inadequate cardiac
output related to impaired contractility
III.6
P.205
Introduction
Septic shock is a life-threatening and generalized form of circulatory failure in response

to an infectious process, associated with impaired tissue oxygen utilization. SS is asso-
ciated with a high mortality either directly due to uncontrolled severe circulatory failure
or indirectly thru the protracted organ dysfunction and/or induced immunosuppression.
It requires rapid recognition and treatment of its cause together with supportive therapy
for circulatory failure and for the failing organs.
III.6
P.206
6.1 - Definition-Pathophysiology of septic shock
Sepsis is characterized by a dysregulated response to an infection and SS is its most severe

form, associated with an increased risk of death. The implicated mechanisms are complex
and result from the activation of various pathways including cytokine and chemokine release,
soluble receptors, cell surface markers and others, so that targeted molecular therapy has
usually failed. It results in the activation of various inflammatory but also anti-inflammatory
pathways, so that broad anti-inflammatory agents also failed.
The haemodynamic alterations result from diffuse endothelial dysfunction accompanied by

severe vasoplegia, increased permeability, activation of coagulation and inflammation. It
includes profound hypotension, relative hypovolemia (redistribution of blood from dilation
of venous capacitance veins), absolute hypovolemia (from capillary leak and external losses),
myocardial depression, and impaired microvascular perfusion.
Table 1 - Haemodynamic alterations in SS
Mechanism Consequence Supportive therapy
Decreased vascular tone Hypotension Vasopressor
Hypovolemia Decrease preload

- Relative - Vasopressors
- Absolute - Fluids
Myocardial depression Impaired cardiac output Inotropic agents?
Regional blood flow Inadequate perfusion of Low dose dobutamine??

redistribution splanchnic organs Milrinone??
No specific therapy
Altered microcirculation Impaired tissue perfusion Variable effects of fluids and
vasoactive agents
III.6
P.207
6.2 - Identification of a patient with septic shock
While most cases are often caricatural (i.e. severe hypotension in a patient with perforated
bowel), some cases are more subtle (i.e. patient with normotensive shock or patient with
mixed alterations such as preexisting cardiac failure and pneumonia). Identification should
thus be based on two lines:
1. Does this patient with infection have septic shock;
2. Does this patient in circulatory failure have an infection
as the source/contributor to shock?
Suspicion of infection should be based on history (cough, fever, etc.), clinical examination,
biological signs (white blood cells, CRP, platelets, etc.), and incidental radiological findings.
Importantly, the presence of several criteria of the systemic inflammatory response syn-
drome (SIRS) based on leukocytosis/ leukopenia, fever or hypothermia, tachycardia, and
tachypnea can be used to suspect an infection, but these signs are neither specific (many
patients have SIRS criteria without infection) nor sensitive (15% of patients with sepsis do
not present SIRS criteria).
Organ dysfunction can be multiple Cough, productive sputum,

Clinical
and not restricted to the one usually fever, abdominal complains,
history headache, …
used in organ dysfunction scores
(respiratory, haemodynamic, neu-
Lung crackles, dysuria,
rologic, renal, coagulation, and liver
Clinical signs abdominal pain, meningism,
impairment). purpura….
An easy screening tool outside the - Leukocytosis or leukopenia

Biological - Elevated CRP, PCT or iL-6
ICU environment, is the quick SOFA
signs - Thrombopenia
(qSOFA), with the presence of at - Positive urine analysis
least two of three qSOFA near the
time of diagnosis or suspicion of Radiological Lung infiltrate/condensation,
infection is associated with poor signs pneumoperitoneum
outcome (greater risk of death and/
or prolonged ICU stay).
SIRS criteria Temperature > 38°C or <36°C
Table 2 - Signs used to suspect (3 or more / WBC > 12000 or <4000
an infectious process 2 or more if Respiratory rate >20/min
arrythmia) Heart rate >90/min
III.6
P.208
6.3 - What are the main diagnostic procedures

to perform?
Table 3 - Signs used to suspect organ dysfunction associated with a suspec-

ted or proven infection
- Shock
When facing a patient who may - Altered mental state
Clinical signs
potentially suffer from SS, there - Oliguria
- Jaundice
are three lines of actions to take:
identification of the pathogen(s),
- Elevated creatinine levels
identification of the source, identi- -Impaired oxygenation /
fication of circulatory failure. altered compliance
- Thrombopenia
Biological
Identification is often delayed, - Coagulation abnormalities
signs (DIC)
based on the results of the different
- Elevated bilirubin levels
cultures. Accordingly, it is important - Gut ileus
to obtain very rapidly samples for -Insulin resistance
bacterial analysis.
Blood cultures should be obtained in any single patient just prior antibiotic administration;
when possible urine sampling and sputum should also be obtained but the latter are some-
times delayed (i.e. oliguric patient) so that these are often obtained after initial dose of
antibiotics. According to the suspected source of infection, other samples such as lumbar
puncture or ascites/pleural puncture may also be considered.
Main sources of sepsis are:

Table 4 - Quick SOFA Lungs, Abdomen, Urinary tract, skin, catheters,
(qSOFA) score soft tissues and brain
SBP ≤ 100 mmHg Identification of circulatory failure is based on hypoten-

sion (often present even though non mandatory),
RR ≥ 22/min tachycardia (unspecific but often present) associated with signs
of tissue hypoperfusion (assessed mainly using three clinical
Glasgow Coma Score <15
windows: skin, kidney, brain) and signs of anaerobic metabolism
(hyperlactatemia).
III.6
P.209
Table 5 - Signs of cir- - SBP <90 mmHg

culatory failure Signs of - MBP <65mmHg
impaired central - Vasopressors to maintain
haemodynamics BP above these targets
- Tachycardia
- Skin: prolonged capillary

refill time (>4sec), mottled
Signs of tissue
skin, vasoconstriction
hypoperfusion - Oliguria
- Obnubilation
Biological signs - Lactate > 2 mmol/L
6.4 - Haemodynamic monitoring
The goal of the haemodynamic monitoring to provide information on whether oxygen deli-
very is sufficient to meet oxygen requirements, and when impaired, on the best options to
improve it.
While measurements of CO are often performed, it is very difficult to determine what value
should be reached. Indeed, CO should always be evaluated as a mean to achieve adequate
oxygen delivery for meeting the oxygen requirements of the tissues. Hence instead of discus-
sing whether CO is low or elevated, it is preferred to mention whether CO is adequate or not.
To determine whether CO is adequate, a combination of basic haemodynamic signs (hypoten-

sion and tachycardia), biological signs, and clinical signs of tissue hypoperfusion. A ScvO2
<70% is often considered as an index of inadequate CO. However, as ScvO2 can be increased
due to microvascular shunting associated with impaired microcirculation, other signs such
as increased PvaCO2 should also be considered in case of relatively normal ScvO2.
When CO is considered inadequate, the next step will be to evaluate LV and RV function, and
preload responsiveness. This allows a stepwise therapeutic approach based on the interven-
tion that is the most likely to provide beneficial effects and minimal risks.
III.6
P.210
Table 6 - Goals of haemo- Capillary refill time

Assessment of
dynamic monitoring
tissue perfusion
Mottling score
Cardiac output
Assessment of
Oxygen delivery Hemoglobin
(DO2)
Arterial O2 saturation
Central venous O2 saturation

Assessment of
adequacy of DO2 Veno-arterial gradient PCO2
Assessment of
impaired tissue Lactate
oxygenation
Figure 1 - Interpretation and integration of cardiac output measurements

III.6
P.211
6.5 - Which tools?
Basic haemodynamic tools should be applied as first line. An arterial line is crucial for arte-
rial pressure monitoring in patients requiring vasopressors but also for ABG and lactate
measurements. A central venous access is also required for drug administration and also
provides a unique opportunity to have access to venous blood gases (ScvO2 and veno-ar-
terial differences in PCO2).
In simple cases with rapid favorable evolution, haemodynamic resuscitation can be based
on basic monitoring added with repeated measurements of quantifiable clinical signs (such
as capillary refill time). Echocardiography should be relatively rapidly be obtained in order
to confirm the absence of significant impairment in cardiac function. In these patients, a
minimally invasive CO (i.e. pulse contour analysis) may be helpful as nurse-driven continuous
haemodynamic method able to identify patients who subsequently deviate from the sche-
duled uneventful course.
In more complex cases or in patients not rapidly responding to simple therapies, echocardio-
graphy should be first performed in order to identify the dominant component (hypovolemia /
right heart dysfunction / left heart dysfunction) and then, more invasive CO monitoring
(transpulmonary thermodilution or PAC) should be inserted. The selection between the two
techniques would depend on the presence or not of right heart dysfunction: in presence of
right heart dysfunction the pulmonary artery catheter is preferred as it allows to better fol-
low RV function and afterload. In absence of right heart dysfunction, both techniques are
equivalent and transpulmonary thermodilution is often preferred due to better safety profile
and similar information gained.
6.6 - The main variables
Multiple variables can be measured with haemodynamic monitoring. We here synthetize the
most commonly measured ones, their interest and limitations.
BP: MAP represents the perfusion pressure of most organs and is thus one of the most impor-
tant variables to monitor. Diastolic is also very important as an index of vascular tone, a low
diastolic reflecting a low vascular tone and hence often requirement of vasopressor agents.
III.6
P.212
Table 7 - Invasive arterial line:

Haemodynamic -Arterial BP
monitoring tools -Respiratory variation in pulse pressure
-ABG
Lactate
Basic mini-
mally invasive Central venous line
monitoring - ScvO2
- Veno-arterial difference in PCO2
Continuous 3 lead EKG
Urine output
Capillary refill time

Clinically quanti-
fiable indices Mottling score
Minimally invasive
Cardiac output
Transpulmonary thermodilution
monitoring
Figure 2 - Stepwise
haemodynamic approach
III.6
P.213
CVP is an important but complex variable: it is influenced by intravascular volume,

RV function, and pleuropericardial pressures. A low CVP indicates a low intravascular
volume and good cardiac function, hence often reflects a positive response to fluids
if these are deemed indicated. A high CVP indicates either an elevated intravascu-
lar volume or impaired cardiac function so that fluids are unlikely to have beneficial
effects. Middle range values are more difficult to interpret. Changes in CVP during
interventions are also informative: a marked elevation of CVP during fluid loading
indicates a limited tolerance to fluids, whatever its cause.
CO is a key determinant of oxygen delivery and hence tissue perfusion. While absolute
values of CO (except extremes) are somewhat difficult to interpret, changes in CO are
useful to interpret responses to therapy (including to fluid challenge).
ScvO2 reflects the balance between oxygen consumption and oxygen delivery. A low
ScvO2 reflects an inadequate CO if Hb and SaO2 are within reasonable limits. Changes
in ScvO2 can be used to evaluate changes in CO.
PvaCO2 increases as a consequence of impaired tissue perfusion and/or metabolic
metabolism. An increase in PvaCO2 should be considered as a trigger to increase CO
unless ScvO2 is already elevated, in these conditions it rather suggests microcircula-
tory alterations for which therapeutic interventions are much more limited.
CRT is an easily quantifiable index to tissue perfusion. It may also be altered in cold
environment, and in patients with peripheral arterial disease. CRT is an excellent
guide of haemodynamic resuscitation.
Lactate is an index of anaerobic metabolism. However, it can also be increased under
the influence of inflammatory mediators and stress hormones (including adrenergic
compounds). Changes in lactate levels are very informative of the evolution of the
patient and response to therapy, even though lactate decreases are delayed com-
pared to improvement in tissue perfusion.
Advanced haemodynamic variables (PAC pressures and TPTD derived): PAC-related
variables include the PAP and the PCWP, the latter reflecting the LA pressure. These
pressure measurements are interesting in the context of severe LV or RV failure. In
other conditions, less invasive monitoring techniques provide similar information
with less invasiveness.
III.6
P.214
TPTD-related variables include the global end diastolic volume and extravascular
lung water. These variables are interesting to evaluate cardiac function and seve-
rity of lung edema. The limitation of the volume measurements is that these od not
separate left and right ventricular volumes, so that PAC-related variables are often
preferred in the context of marked RV dysfunction.
6.7 - Targets for resuscitation
There is no single for which a definitive target value can be recommended. These should be
individualized, taking into account the risks of the therapies that need to be engaged to reach
the target values. As an example, a higher MAP may be associated with decreased risk of
requirement of renal replacement therapies but reaching higher MAP values requires higher
doses of vasopressor agents which are associated with higher incidence of adverse events.
Table 8 - Target values for the main haemodynamic variables
Variable Target value Comments
MAP 65 mmHg Higher MAP may be considered in some patients

DAP 40 mmHg
CVP 8-12 mmHg is a commonly reported value, however, one
CVP No real target should target the lowest CVP value associated with an ade-
quate CO
CO No real target Cardiac index: 3-5 L/min.m2 usually
A high ScvO2 may still be associated with impaired tis-
ScvO2 ≥70% sue hypoperfusion. To be combined with PvaCO2 and other
indices of tissue perfusion
PvaCO2 < 6 mmHg
Capillary
≤3 sec
refill time
While reaching normal values is associated with best out-
Lactate <2 mmol/L
come, chasing normal lactate values may lead to
Urine In established renal failure, oliguria may persist despite opti-
>0.5 ml/kg.h
output mization of renal perfusion
III.6
P.215
6.8 - Therapeutic interventions
6.8.1 - Source control and antibiotics
Early appropriate antibiotic coverage allows to minimize the risk of death. Accordingly, ade-
quate antibiotics should be administered within one hour. Higher doses are often required
initially. Source control (catheter removal, surgery, drainage, etc.) is always recommended.
6.8.2 - Fluids
It is recommended to administer 30 ml/kg of crystalloids within one hour of SS recognition.

Further fluid administration should be based on the prediction of fluid dynamic responsive-
ness rather than static measurements of preload, performing a fluid challenge. Pressure
measurements are useful as safety limits not to overcome.
Table 9 - Fluid administration in septic shock patients
At time of septic 30 ml/kg crystalloids within one hour (unless obvious fluid
shock recognition overload)
Further fluid administration

Presence of tissue hypoperfusion that is considered to be poten-
1- Considering that fluids tially responsive to fluids
are the best option The risks associated with fluid administration are limited and
lower that the risks of the alternative therapies
Predict the response to fluid using dynamic variables (respira-
2- Prediction of fluid tory variations in stroke volume or in vena cava size, positive
responsiveness response to a passive leg raising test) rather than using static
variables (filling pressures or ventricular volumes)
Perform a fluid challenge (4 ml/kg of fluids in 15 min, measuring
3- Evaluation of the res-
its impact on CO or surrogates, and ensuring that it does not
ponse to fluids overcome some safety limits (CVP)
The type of fluids is question of intense debate. Crystalloids are the cheapest and most com-
monly used. Balanced crystalloids seem to be associated with less adverse effects than saline
(NaCl 0.9%), except in hypochloremia. Colloids may expand threefold plasma than crystal-
loids, but are much more expensive and may sometimes be associated with adverse events.
Albumin in cases of SS with hypoalbuminemia may be associated with improved outcomes.
Hydroxyethyl starches may increase the risk of AKI and is now banned both by EMA and FDA.
III.6
P.216
6.8.3 - Vasopressors
The timing of initiation of vasopressors is not yet well defined. Some observational data sug-
gest that early vasopressor initiation may be associated with a more limited fluid requirement
and perhaps an improved survival rate. Three types of agents can be used: adrenergic agents,
vasopressin derivatives and angiotensin. Randomized studies have shown that norepinephrine
is the preferred first line vasopressor agent compared to dopamine and even epinephrine,
as associated with less adverse effects and probably improved outcome.
When norepinephrine fails to control blood pressure, non-adrenergic agents should be consi-
dered. Vasopressin derivatives are excellent second line agents. Vasopressin derivatives,
added to norepinephrine, help to increase BP. It is associated with similar survival rates,
less requirements of renal replacement therapy and less atrial fibrillation but more digital
ischemia.
Angiotensin may also be considered showing beneficial renal effect, but may increase tachy-
cardia, thromboembolic events and fungal infections.
Table 10 - Vasopressor agents in septic shock patients
Agent Usual doses Potential adverse effects
First line
Norepinephrine 0.01-1.0 mcg/kg.min Arrythmias, immunosuppression?
Second line
Vasopressin Splanchnic ischemia, digital ischemia, cardiac output

derivatives impairment?
Vasopressin 0.01-0.03 u/min

Terlipressin 20-160 mcg/h
Third line
Angiotensin 20-80 ng/kg/min Tachycardia, thrombotic events, immunosuppression?
Finally, hydrocortisone should be considered in the most severe patients.

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P.217
6.8.4 - Inotropes
Inotropic stimulation may be indicated only when tissue hypoperfusion occurs in response
to an impaired CO related to an impairment in myocardial contractility. Dobutamine remains
the preferred inotropic agent, but is associated with tachycardia and arrhythmias, metabolic
and immunologic effects. Its short half-life allows to stop rapidly. Phosphodiesterase inhibi-
tors and levosimendan may be used, especially in patients previously under beta-blockade
agents. Their main disadvantage is the long half-life, so that when adverse events occur
these are also long lasting.
6.9 - Management in specific situations
SS with congestive HF may be different:
Initial fluid bolus may be more limited than 30 ml/kg. It is essential to predict fluid
responsiveness and to evaluate the response to fluids very early
Tachycardia (even if hindered by beta-blockade) is poorly tolerated.
Patients with CHF are often treated with beta-blockers and angiotensin converting
enzyme inhibitor, which may affect their haemodynamic response to drugs
III.7
Ass. Prof. Alessandro Sionis, MD, FESC

Unitat de Cures Agudes Cardiològiques, Servei de Cardiologia /
Hospital de la Santa Creu i Sant Pau /
Universitat Autònoma de Barcelona, Barcelona, Spain
Dr. Albert Ariza-Solé, MD, PhD

Cardiology Department. Hospital Universitari de Bellvitge /
Universitat de Barcelona / Hospitalet de Llobregat,
Barcelona, Spain
Ass. Prof. Jordi Bañeras, MD, PhD, MSc, M.Ed

Cardiology Department / Hospital Vall d'Hebron /
Universitat Autònoma de Barcelona,
Barcelona, Spain
Key messages
Anamnesis and physical examination are key for differential diagnosis
Treatment is based on support measures (volume reposition and vasopres-

sors) and on correcting the etiology of hypovolemia. Echocardiography is a
valuable tool to orient diagnosis and to guide therapy.
The haemodynamic pattern of hypovolemic shock consists of reduced cardiac
preload and stroke volume together with high systemic vascular resistances.
No routine use for haemodynamic monitoring is recommended but it can be
used in selected cases (e.g. type of shock is uncertain or to guide treatment).
Dynamic parameters (SVV) are useful to predict fluid responsiveness while
static parameters (CVP, PCWP) alone should not be used to guide fluid
resuscitation.
III.7
P.219
Introduction
Severe volume depletion followed by hypovolemic shock can occur in a wide variety of
clinical scenarios. The initial management should be directed to the assessment shock
severity (risk stratification) and stabilizing the patients through the administration of the
required immediate resuscitation therapies. At the same time, prompt recognition of the
underling etiology is of paramount importance in order to deliver the necessary targeted
treatment. For example, while intravenous fluids and vasopressors are the mainstay of
initial treatment of hypovolemic shock, identification of an arterial-site complication will
lead delivery of a specific treatment (e.g. compression or surgical repair).
III.7
P.220
7.1 - Clinical presentation and differential diagnosis
Clinical findings in hypovolemic shock may vary according to the etiology and the presen-
tation phenotype or stage (e.g. pre-shock or refractory shock). Several clinical features are
shared with other type of shock and are thus not specific of hypovolemic shock such as: per-
sistent hypotension, tachycardia, altered mental status (e.g. confusion), cool, clammy skin,
skin mottling, oliguria and metabolic acidosis with elevated lactates. Other more specific
findings include dry skin and mucosae, absent jugular venous pulse and established acute
kidney injury with accompanying electrolyte abnormalities. Careful anamnesis and physical
examination are key for the differential diagnosis. Broadly, causes of hypovolemic shock can
be divided in hemorrhagic and non-hemorrhagic related (Table 1).
Table 1 - Differential diagnosis of hypovolemic shock in acute cardiac care
Aetiology Symptoms and signs Key finding
Haemorrhagic
Perioperative bleeding Overt bleeding Drains, imaging
Previous procedure, antithrombotic
Retroperitoneal bleeding Unexplained volume loss
therapy
Vascular site access Overt bleeding, haematoma Drop in haematocrit or haemoglobin,
complication or swelling imaging
E.g. In the setting of chest tube inser-
Procedure related Acute presentation
tion, pericardiocentesis…
Clinical setting (acute chest
Aortic dissection Imaging
pain)
Non-haemorrhagic
History of vomiting and/or Associated acute kidney injury and

Gastrointestinal losses
diarrhoea electrolyte abnormalities
Associated acute kidney injury and

Renal losses Diuretic treatment
electrolyte abnormalities
Third space losses Right heart failure Anasarca
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P.221
7.2 - Echocardiographic assessment of

hypovolemic shock
Assessment of intravascular volume is the starting point in all types of circulatory failure,
especially in patients with hypovolemic shock. In most cases, clinically insufficient volume is
evident. However, in some patients, echocardiography can help to achieve diagnosis and to
guide therapy. Echocardiography is one of the most single useful tools in this clinical setting.
Non-invasive and rapid to initiate, it can be applied at bedside anytime. At the basic level of
competency, the clinician relies on 2D and M-mode echocardiography only.
Assessing left ventricle systolic size and function is a key point in order to identify the rea-
son for haemodynamic collapse. In patients with hypovolemia, the left ventricle becomes
small. A left ventricle end diastolic area of less than 10 cm2 indicates significant hypovole-
mia. Hyperdynamic left ventricle with normal or higher than normal ejection fraction and
normal myocardial thickening is found. When hypovolemia is severe, 2D views can show
collapse of the left ventricular walls at end-systole (so-called “kissing walls”). In contrast,
when volemia has been corrected fixed bowing of the atrial septum into the right atrium
throughout the cardiac cycle means elevated left atrial pressures, and therefore further
fluid is not necessary. However, is important to note that none of these signs are specific
for intravascular fluid status.
On the other hand, IVC variation has been recognized as a useful parameter for assessing
volume status. Several studies have explored the use of vessel diameter variation in res-
ponse to the respiratory cycle, maximum diameter, and percentage of diameter alteration
to assess right atrial pressure.
Guidelines state that in the spontaneously breathing patient, an IVC diameter >21 mm that
collapses <50 % with a sniff indicates a right atrial pressure >15 mmHg.
In routine critical care, clinical practice changes in IVC are used to assess fluid responsive-
ness rather than pressure equivalents. In spontaneously breathing patients the IVC diameter
is measured in the subcostal view. When the diameter is < 10 mm the patient is likely to res-
pond to fluid. In contrast, when IVC diameter is > 20 mm that is unlikely. Collapse of >50 %
between the diameters of 10-20 mm should result in a trial of fluid. In the patient on fully
supported positive pressure ventilation, the distensibility index (dIVC= (Dmax- Dmin)/Dmin,)
can help to guide fluid therapy. A threshold of 18 % can help to discriminate between res-
ponders and non-responders.
III.7
P.222
The assessment of IVC changes has some pitfalls. The operator should obtain a good longi-
tudinal view with the scan plane parallel to the IVC and the probe tilted in both directions, in
order to to obtain the largest diameter. IVC can move inferiorly during inspiration. Therefore,
two different segments of the vessel can be inadvertently measured using M-mode. It is
recommended to perform 2D measurements, with the highest possible frame rate.
Neither collapse nor distension of the IVC during respiratory ventilation should be used on
patients receiving partial ventilatory support. The clinician can only occasionally confidently
predict fluid responsiveness on the IVC alone. Other factors such as right heart failure,
increased intra-abdominal pressure, or pericardial fluid makes the use of IVC less reliable.
Dynamic techniques can also be used to assess fluid status. As a guide, fluid responsiveness
is determined if there is, on average, a >15 % increase in SV or CO.
Application of a bolus of intravenous fluid has long been used to assess fluid responsive-
ness. It has been suggested that a change in VTI of >10 % after a mini bolus of 100 ml can
predict fluid responsiveness.
On the other hand, during the inspiratory phase of positive pressure ventilation, right
ventricular output is reduced because of a decrease in venous return (increased intratho-
racic pressure). It leads to a decrease in left ventricular output after two to three beats if
both ventricles are volume responsive. A SV variation >10 % is highly predictive of volume
responsiveness.
PLR has been demonstrated to be applicable in both spontaneously breathing and venti-
lated patients. CO is measured using pulsed-wave Doppler. An increase in CO or SV of >12 %
during PLR was highly predictive of fluid responsiveness. A false positive response to PLR
may occur in the presence of increased intra-abdominal pressure.
Finally, in cases of suspected hypovolemic shock due to bleeding, echocardiography can help
to find the source of bleeding. Haemothorax may be an incidental finding and it should not
be misinterpreted as pericardial effusion. The epigastric area should be screened for the
presence of an aortic aneurysm. Key parameters are summarized in Table 2.
III.7
P.223
Table 2 - Echocardiographic signs of hypovolemic shock
Echocardiographic parameter Sign

Higher MAP may be considered in some
LV size and function
patients
IVC <10 mm
IVC diameter
Distensibility index (Dmax- Dmin)/Dmin) >18%
7.3 - Haemodynamic monitoring techniques in

hypovolemic shock
Hypovolemic shock in cardiac intensive care unit, basically in the context of arterial punc-
tures and antiplatelet and anticoagulant drugs in patients with bleeding risk factors, should
be monitored invasively to identify and select the treatment, especially in patients where
more than one type of shock coexists at the same time, and to evaluate the response to
the therapy.
In the case of an isolated hypovolemic shock, a decrease cardiac preload and stroke volume,
and an increase in systemic vascular resistance is the expected pattern. Despite this, one
has to be cautious because it is not uncommon for more than one type of shock to coexist
and haemodynamic profiles result from the combination of several parameters that can be
summative or go in the opposite direction. In addition, the use of circulatory assist devices
requires an excellent management of their parameters to detect hypovolemia, especially since
traditional invasive monitoring is not validated in these cases. Furthermore, we must not for-
get that clinical assessment is helpful to guide and dictate appropriate management therapy.
The routine measurement of CO is recommended only in shock patients that do not respond
to initial treatment. Keep in mind that the measurements of CO, CVP and PCWP sometimes
are not enough to discriminate between different types of shock and both CVP and PCPW,
as static parameters, have been shown to have poor predictive value for predicting fluid
responsiveness.
TPTD techniques include PiCCO® technology (Pulsion Medical Systems - Germany) and
EV1000/volume view technology (Edwards Life sciences - USA). The systolic volume then is
measured beat by beat, using a pulse contour analysis, through a thermistor tipped catheter
inserted into a peripheral artery. SVV >15% may indicate hypovolemia as a dynamic parame-
III.7
P.224
ter of fluid responsiveness, but it should be emphasized that the patient should be sedated,
paralyzed, mechanically ventilated, in sinus rhythm and closed chest, and without severe
pulmonary hypertension or severe right ventricular failure. The Vigileo system (Edwards
Lifescience, Irvine, CA) with arterial pressure waveform analysis device via special blood
flow sensor (FloTrac® Sensor, Edwards Lifesciences, Irvine, CA) also allows measuring the
SVV. The relationship between haemodynamic monitoring system and key parameters for
hypovolemic shock diagnosis are listed in Table 3.
Table 3 - Relationship between haemodynamic monitoring system and key

parameters for hypovolemic shock diagnosis
Device Measured parameter Target

Arterial catheter Continuous blood pressure >65 mmHg
Continuous central venous
Central venous catheter 8-12 mmHg
pressure
Pulmonary capillary wedge
4-12 mmHg
pressure
Swan-Ganz catheter Systemic vascular resistance
1970 - 2390 dynes-sec/cm–5/m2
index
Cardiac output 4.0 - 8.0 L/min
PiCCO® technology Stroke volume variation ≤10%
Vigileo FloTrac® Stroke volume variation ≤10%
In summary, the monitoring systems that can be useful in hypovolemic shock are:
Arterial catheter. It allows to monitor invasive blood pressure measurement, usually

from the radial or femoral artery access.
Central venous pressure measurement, which is obtained from a central venous cathe-
ter, usually from jugular, subclavian, femoral access or from peripherally inserted
central catheter access.
Swan Ganz catheter. It allows to measure directly CVP and PCWP.
PiCCO® technology. The stroke volume is measured beat by beat, using a pulse
contour analysis, through a thermistor tipped catheter inserted into a peripheral
artery. It offers other critical volumetric parameters and organ function parameters.
Vigileo FloTrac®. It analyses the arterial waveform and allows to measure the SVV.
III.8
8 - INTRA-ABDOMINAL
P.225 HYPERTENSION
Dr. Élida Amestoy, MD, PhD

Intensive Care Department, Consorci Sanitari Integral Hospital
Sant Joan Desp Moisès Broggi, Barcelona, Spain
Prof. Dr. Manu L.N.G. Malbrain, MD, PhD

Intensive Care Departement, Universitair Ziekenhuis Brussel
(UZB), Jette / Faculty of Medicine and Pharmacy,
Vrije Universiteit Brussels (VUB), Belgium
Key messages
IAP is the steady-state pressure concealed within the abdominal cavity
expressed in mmHg
The gold standard IAP measurement technique is via the bladder
IAH is defined as a sustained pathological elevation in IAP ≥ 12 mmHg and

it is graded in four categories
AbCS is a sustained IAP > 20 mmHg that is associated with new onset organ
failure (assessed with sequential organ failure assessment, SOFA score)
Elevated IAP plays a major role in the development of multiple system
organ dysfunction and failure as a result of significant hypoperfusion and
the effects are not limited to the intra-abdominal organs alone
Primary IAH/AbCS is a condition associated with injury or disease in the
abdominopelvic region
Secondary IAH or AbCS refers to conditions that do not originate from the
abdominopelvic region, and are frequently associated with damage of the
glycocalyx and/or tight junctions following massive fluid resuscitation
III.8
P.226
Basic monitoring includes an accurate IAP measurement every 4 - 6 h in

patients with at least 2 or more risk factors for IAH or AbCS
Other important clinical parameters are gastric residual volume, urinary
output, abdominal perfusion pressure calculated as MAP minus IAP, body
weight, daily and cumulative fluid balance
Advanced haemodynamic monitoring is required in severe IAH
Medical management comes first and decompressive laparotomy should be

used as last resort in cases other treatment options fail
Introduction
Intra-abdominal hypertension is a relatively frequent medical situation in intensive care

units which can trigger important complications because it plays a major role in the deve-
lopment of multiple system organ dysfunction. Therefore, intra-abdominal pressure should
be considered another first line parameter to be monitored routinely.
III.8
P.227
8.1 - IAH and AbCS definitions
The 2013 the World Society of Abdominal Compartment Syndrome (WSACS, www.wsacs.org)
changed its name to The Abdominal Compartment Society and updated consensus defini-
tions and recommendations on this topic were published.
8.1.1 - Intra-abdominal pressure (IAP)
IAP is the steady-state pressure concealed within the abdominal cavity and the reference
standard for intermittent IAP measurements is via bladder with a maximal instillation volume
of 25 mL of sterile saline (Figure 1, 2). IAP should be expressed in mmHg and measured at
end-expiration in the supine position, after ensuring that abdominal muscle contractions
are absent and with transducer zeroed at the level of midaxillary line. Normal IAP ranges
from sub-atmospheric to zero mmHg, however, IAP is commonly elevated to a range of 5–7
mmHg in critically ill adults.
Figure 1 - IAP measurement
- Supine position
- End-expiration
- Ensuring absent abdominal muscle contraction - IAP expressed in mmHg
- Transducer zeroed at midaxillary line
- Maximal instilation volume 25 mL sterile saline
Manometer
Instilation
volume
Foley catheter Three way

Urimeter
stopcock
III.8
P.228
Figure 2 - IAP measurement with the Foley Manometer LV
- Open the Foley Manometer LV (Holtech

Medical, Denmark) pouch and close the tube
clamp
- Place the urine collection device under the
patient's bladder
- Insert the Foley Manometer between
catheter and drainage device
- Prime the Foley Manometer with 20ml
of sterile saline through its needle-free
injection/sampling port (only once i.e. at
initial set-up)
- Urine sampling from the needle-free port is

facilitated by temporarily opening the red
clamp
- Replace the Foley Manometer whenever the
Foley catheter or the urine collection device
is replaced, or at least every 7 days
- Place the "0 mmHg" mark of the manometer

tube at the midaxillary line at the level of the
iliac crest and elevate the filter vertically above
the patient
- Open the bio-filter clamp, and read IVP when
the meniscus has stabilized after about 10
seconds
- Close clamp after IVP measurement and place
the Foley Manometer in its drainage position
III.8
P.229
8.1.2 - Intra-abdominal hypertension
IAH is a sustained or repeated pathological elevation Table 1 - WSACS grading of IAH

in IAP ≥ 12 mmHg and it’s graded in four categories
(Table 1). AbCS is a sustained increased IAP > 20
IAH grade IAP (mmHg)
mmHg that is associated with new onset organ failure
(Figure 3). IAH is a graded phenomenon while AbCS Grade I 12-15
is an all-or-nothing condition. AbCS is a syndrome and
not a disease and as such it can have many causes or Grade II 16-20
it can be associated with many disease processes. A
polycompartment syndrome is a condition where two Grade III 21-25
or more anatomical compartments have elevated com-
Grade IV 25
partmental pressures.
Figure 3 - Natural course of IAH/AbCS
ORGAN
DYSFUNCTION Normal IAP IAH AbCS
Death
Cardiovascular
Respiratory
Gastrointestinal
Renal
IAP (mmHg)
12 20
III.8
P.230
8.1.3 - Abdominal compliance
Abdominal compliance is a measure of the ease of abdominal expansion, which is determined

by the elasticity of the abdominal wall and diaphragm. It should be expressed as the change
in intra-abdominal volume per change in IAP.
8.2 - Primary and secondary IAH
Primary IAH or AbCS is a condition associated with injury or disease in the abdominopel-
vic region that frequently requires early surgical or interventional radiological intervention.
However, secondary IAH or AbCS refers to conditions that do not originate from the abdo-
minopelvic region, frequently associated with massive fluid resuscitation in patients with
sepsis, capillary leak and other pathological states (Figure 4). This condition could damage
the endothelial glycocalyx layer (negatively charged luminal protein surface of vascular
endothelium) and the tight junction complexes, whose general function is to prevent lea-
kage of transported solutes and water, so they seal the paracellular pathway. If they are
damaged, they contribute to interstitial oedema and then to IAH. This has been referred to
as the GIPS. This mechanism of injury (i.e. increased vascular permeability) is widely reco-
gnized and accepted in the lung and kidneys, where it is classified as ALI and AKI. The same
pathological process occurs in the gut, but this concept is much slower to seep through.
However, the role of the gut as the motor of organ dysfunction syndrome cannot be denied
and difficulties in assessing gut function should not deter us from recognizing that concept.
8.3 - Pathophysiology of IAH
Although the pathophysiologic implications of an elevated IAP have already been presented
in the last century, they have been re-appreciated during the last two decades after scientific
investigation and clinical experience confirmed the detrimental impact of IAH on end-organ
function. Elevated IAP plays a major role in the development of MOF as a consequence of
significant hypoperfusion (Figure 5). The effects of IAH are not limited to the intra-abdo-
minal organs alone but have a direct or indirect impact on every organ system of the body,
causing significant morbidity and mortality.
III.8
P.231
Figure 4 - Primary and secondary IAH/ACS
PRIMARY
- Abdominal surgery
- Hemoperitoneum
- Gastroparesis/ ileus
- Colonic obstruction
- Acute pancreatitis
- Intra-abdominal tumors/ collections
SECONDARY
- Sepsis
- Polytransfusion
- Massive fluid
resuscitation
III.8
P.232
Figure 5 - Pathophysiologic implications of IAH
Pulmonary
- Elevated diaphragm
- Paw Central nervous
- Pleural Pressure
system
- Auto-PEEP
- Functional residual capacity - ICP
- PaCO2 and PaO2 - CPP
- Chest wall compliance - Idiopathic intracranial
- Dinamic and static compliance hypertension in morbid
- Dead-space ventilation obesity
- Atelectasis
- Intrapulmonar shunt
- Difficult weaning Cardiovascular
- Venous return
- Heart rate
Hepatic - Mean arterial pressure
- Hepatic and portal - CVP
blow flow - CO
IAP
- Lactate clearance - SVR
- Glucose metabolism - PAOP
- Mitocondrial function - Intra-thoracic blood
volume index
- Global enddiastolic
blood volume index
GASTROINTESTINAL Renal
- Celiac and mucosal - Renal blow flow
blow flow - GFR
- APP - Urinary output
- Mesenteric vein - Tubular dysfunction
compression - Compression ureters
- Intramucosal pH - Anti-diuretic hormone
- CO2-gap
- Intestinal permeability
- Bacterial translocation
- Success enteral
feeding
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P.233
8.4 - Monitoring IAH and AbCS
Prevention of IAH is essential in patients with risk factors

for IAH or AbCS. When two or more risk factors are pre-
sent, baseline IAP monitoring is mandatory followed by
sequential assessment in case of IAH grade I. The main
monitoring parameter is the IAP, that can be obtained
via trans-bladder measurement (Figure 1, 2) (Table
2). In order to perform a good measurement, pain and
anxiety must be excluded, since voluntary contraction of
the abdominal muscles can interfere with interpretation
of the results. Other basic monitoring tools are gastric Patients with risk
residual volume via nasogastric tube or antral cross-sec- factors for IAH and
tional area (ultrasound) and urinary output. Overzealous AbCS
administration of fluids can cause secondary IAH/AbCS
(endothelial dysfunction), so it is important to measure - Diminished abdominal
body weight and cumulative fluid balance. Abdominal per- wall compliance
fusion pressure is the difference between mean systemic - Increased intra-
arterial pressure and IAP. It more accurately reflects vis- abdominal contents
ceral perfusion. - Increased intra-luminal
contents
More advanced monitoring is needed in case of IAH grade - Capillary leak/fluid
II or higher. It the presence of an arterial line and a central resuscitation
venous catheter, the use of transpulmonary thermodilu-
tion (PiCCO, Getinge or EV1000, Edwards) can provide
additional information on preload, contractility, afterload
and pulmonary edema (Table 2): oxygenation ratio (PaO2/
FiO2), ScvO2, CO (also through echocardiography), SVR, as
well as fluid management status in the different phases
of shock (PPV, GEDVI and EVLWI). Sequential arterial or
venous lactate levels may be helpful. Barometric preload
parameters like CVP or PCWP are erroneously increased
in case of IAH and cannot be used.
Table 2 - Main parameters to monitoring in

IAH/ACS
III.8
P.234
Monitoring Technique Normal values
Trans-bladder
IAP/4h ≤ 12 mmHg
measurement
APP AMP – IAP ≥ 60 mmHg
< 500cc/6h or
Main Gastric residual volume Nasogastric tube
< 1000cc/24h
parameters
Urinary output Foley catheter > 0,5–1 mL/Kg/h
Glomerular filtration rate 60-90 mL/min/1,73m2

Body weight
Cumulative balance fluid
Continuous AP A-line
Lactate Blood analysis < 2 mmol/L
PaO2/FiO2 Arterial gases > 300 mmHg
ScvO2 Central venous catheter > 70%
Transpulmonary
Advanced
CO thermodilution 4-8 L/min
parameters Echocardiography
SVR 800-1200 din·s·cm-5
PPV <13%
Transpulmonary
thermodilution
GEDVI 600-800 mL/m2
EVLWI 3-7 mL/Kg

III.9
9 - HAEMODYNAMICS DURING
P.235 MECHANICAL VENTILATION
Ass. Prof. Carlos L. Alviar, R., MD, FACC

Cardiac and Coronary Care Unit, Bellevue Hospital Center /
The Leon H. Charney Division of Cardiology /
New York University School of Medicine, USA
Assoc. Prof. Sean Van Diepen, MD, MSc, FAHA

Coronary Intensive Care Unit,
Division of Critical Care Medicine and Cardiology /
University of Alberta, Edmonton, Canada
Key messages
The use of MV is increasing in patients with cardiovascular disease admitted
to cardiac intensive care unit CICUs
MV has differential cardiopulmonary physiologic sequalae in patients preload
or afterload dependent cardiovascular states
Routine monitoring of patients with cardiovascular disease undergoing MV
may include SpO2, beside capnography, invasive and non-invasive haemo-
dynamics, and point-of-care ultrasonography.
PEEP imparted by PPMV can affect cardiovascular haemodynamics by trans-
mitting elevated intrathoracic pressures into the cardiac structures which
increases transmural intracardiac pressures.
Point-of care-ultrasound may provide useful information to assess haemo-
dynamic response to PEEP titration
Liberation from MV can be associated with adverse haemodynamic conse-
quences, such as a rise in PCWP.
III.9
P.236
Introduction
Parallels to disease severity, comorbidities and complications, the use of MV in patients

in the CICU is increasing, Recent studies have reported that about 20-25% of patients
in tertiary CICUs undergo MV. This chapter focuses on the cardiopulmonary interactions,
including MV haemodynamic monitoring, and proposes a practical framework for mana-
gement and monitoring.
III.9
P.237
9.1 - Cardiopulmonary interactions:

Basics of heart-lung physiology and
haemodynamic response during PPMV
During spontaneous breathing, inspiration reduces negative intrathoracic (-3 to -8 cmH20 at

end-inspiration). Contraction of the diaphragm and the intercostal muscles creates a pres-
sure gradient between systemic venous blood and the RA, which promotes venous return. In
addition, as intrathoracic pressure drops, afterload to the RV decreases. In the LV, the lower
intrathoracic pressure leads to a decrease in the transmural intracardiac pressure (pressure
across the myocardial wall) and in the pressure on the proximal thoracic aorta. This lowers
intra-cardiac pressures relative to the extrathoracic circulation, creating a state of tran-
siently higher LV afterload (Figure 1A). During PPMV the intrathoracic vessels and cardiac
chambers are compressed leading to a decrease in RV preload, an increase in RV afterload,
and a decrease in LV afterload (Figure 1B).
Figure 1 - Cardiopulmonary interactions during spontaneous breathing and

PPV
A
III.9
P.238
9.2 - Right ventricular dysfunction and PPMV
In patients with preload-dependent conditions, PPMV can be deleterious. By reducing venous

return and preload, CO can decrease. Similarly, an increase RV afterload can further reduce
CO. Examples of preload-dependent conditions include RV failure, constriction, pericardial
tamponade, hypovolemia, or dynamic left ventricular outflow tract obstruction. Monitoring
of these patients can include vital signs, pulse oximetry, and potentially capnography, as an
alternative to blood gases when arterial access is not readily available (Table 1). Invasive
haemodynamic monitoring provides information on trends in filling pressures, PVR, and CO.
POC-echocardiography can also provide information on the underlying etiology of the pre-
load state, biventricular function, morphology and motion of the interventricular septum,
changes in the inferior vena cava diameter as an estimate of preload, as well as Doppler
parameters such as patterns and variation of LVOT and RVOT VTI, degree of valvular regur-
gitation or portal vein pulsatility.
III.9
P.239
9.3 - Left ventricular dysfunction and PPMV
In patients with afterload-dependent conditions, such as LV dysfunction, severe mitral regur-

gitation, hypertensive emergency, diastolic hypertension or cardiogenic shock, PPV can be
beneficial by unloading the LV. It decreases venous return and LV preload, reduces afterload,
and improves mitral leaflet coaptation. Appropriate monitoring of these patients may include
vital signs, invasive haemodynamics which includes temporal trends in CO, PCWP and SVR
(Table 1). Bedside US monitoring informs on LV contractility and regurgitant valvular flow.
9.4 - Monitoring of the patient with cardiovascular

disease undergoing PPMV
9.4.1 - Oxygenation and ventilatory targets
Restoring adequate tissue oxygenation is a key component in the management of patients

with shock or end-organ hypoperfusion; however, oxygen supplementation resulting in
hyperoxia should be avoided given growing body of evidence suggesting potentially data sug-
gesting potential adverse outcomes, and worse neurological outcomes in patients post-cardiac
arrest. Therefore, we suggest targeting normoxemia with a O2 saturation between 92-94%.
Ventilatory targets in patients with cardiovascular disease merit an understanding that

acidosis –regardless of the etiology or type (metabolic or respiratory)- can cause pulmonary
vasoconstriction and therefore increase PVR and RV afterload. Similarly, hypercapnia can
lead to intracranial vasodilation which has a theoretical risk of increasing the risk of cerebral
edema in patients post cardiac arrest. In addition, in patients with shock the presence of
acidosis can interfere with the effects of catecholamines. Monitoring of PCO2 is encouraged
with beside capnography or ABG with a goal PCO2 of 35-45mmHg (Table 1).
III.9
P.240
Table 1 - Monitoring of the patient undergoing mechanical ventilation
Type of Considerations Considerations in

Comments
monitoring in RV failure LV failure
Basic Monitoring
HR, BP (invasive
Goals: Goals:
or non-invasive), Tachycardia, tachypnea
PCO2 40mmHg PCO2 < 40mmHg or
RR, or hyperpnea may impair
ETCO2 35mmHg ETCO2 35mmHg
SpO2, assessment and interpreta-
SPO2 > 92% SPO2 > 92%
Capnography, tion of haemodynamics
PaO2 60-150mmHg PaO2 60-150mmHg
Telemetry, ABG
Invasive haemodynamic Monitoring
Atelectasis or alveo-
RAP
lar overdistension
PAP
from PPV/PEEP can If ↑PVR (>3 Woods units)
PAPi In elevated PCWP
↑ PVR. with normal PCWP
PCWP (>18mmHg), PEEP can
Ensure RA (8-14) <18mmHg, consider pulmo-
CI improve CI
and MAP (>60) nary vasodilators
SVR
before PEEP
PVR
titration
Ultrasound Monitoring
Fluid responsiveness is
considered with IVC diame-
RV, and LV RV function ter change during MV
function Interventricular LV function >12%-40%
Doppler flows septal motion and LVOTI VTI
Valvular morphology MR Echocardiographic
regurgitation RVOT VTI Diastolic parameters calculations:
Portal vein TR IVC diameter PVR = 10 x TRpeak velocity/
pulsatility IVC diameter RVOT VTI + 0.16
CO = LVOT area x VTI x HR

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9.5 - Mechanical ventilation parameters for

monitoring: Safe TdV, Paw, DP and plateau pressures
In patients with ARDS, MV with low tidal volume (TdV) has shown to improve outcomes, par-
ticularly when associated with limited driving pressure (plateau pressure minus PEEP) below
15cmH2O, but this has not been demonstrated in other scenarios like patients with cardio-
vascular disease, even though to have a protective effect against ventilator-associated lung
injury. Plateau pressures, defined as the alveolar pressure measured at end inspiration, are
a reflection of total lung compliance (intrinsic lung and chest wall compliance). Plateau pres-
sures can be elevated in patients with ACPE due to extra-alveolar fluid leading to increased
lung stiffness. They can be assessed by performing an inspiratory pause in the ventilator.
It is reasonable limit plateau pressures to <30cm H2O in the CICU population. In non-ARDS
patients it may be appropriate to use TdV of 8-10cc/kg of IBW limiting driving pressures to
15-20cmH2O (Table 2). Low TdV ventilation can decrease plateau pressure at the potential
expense of causing respiratory acidosis which can increase in PVR.
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Table 2. Recommended mechanical ventilator parameters for monitoring

Ideal body weight calculation: IBW = 50 kg + 2.3 kg for each inch over 5 feet.
Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.
Mechanical
RV failure LV failure
Ventilation Comments
considerations considerations
Parameters
PEEP Adjust FIO2 and PEEP for a

Recommended
TdV Recommended TdV SPO2 > 92%
TdV 8-10cc/Kg of
FIO2 8-10cc/Kg of IBW Adjust RR and TdV for PCO2
IBW
RR 40mmHg
Plateau Keep driving pres- Control dyssynchrony to

Keep driving pressure
Pressure sure between ensure accurate estimation
between 15-20cmH2O
Driving pressure 15-20cmH2O of intracardiac pressures
High PEEP For assessment of fluid

>5-15cmH2O can be responsiveness by IVC and
beneficial: PPV avoid dyssynchrony
- If PCWP >18mmHg and use TdV >8cc
Patient- Recommended - If severe MR If concomitant ARDS (which
ventilator PEEP 3-5cmH2O. To is rare in the CICU popu-
interactions achieve target PaO2, lation), use TdV of 6-8cc/
(ventilator use FiO2 first then Use PEEP with cau- Kg of IBW. Use appropriate
synchrony) PEEP tion in: NMB and prone positioning.
- Biventricular failure Limit permissive hyper-
- Concurrent hypovo- capnia in post-cardiac
lemia, constriction or arrest for cerebral vasodila-
tamponade tion and edema
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9.6 - Auto-PEEP monitoring and impact on

haemodynamics
Auto-PEEP is the pressure at the end of expiration that occurs due to incomplete exhalation,
typically seen in patients with obstructive lung physiology. Monitoring for and treating auto-
PEEP can prevent haemodynamic instability. Auto-PEEP can be detected by evaluating the
pressure/time and flow/time curves in the mechanical ventilator, and it can be quantified by
performing an expiratory pause (Figure 2).
Figure 2. AutoPEEP detection in the pressure/ time and volume/time curves

in the mechanical ventilator
Ineffective triggering (red arrows) failing to initiate a breath due to superimposed autoPEEP. Dashed green circles:
expiratory pressure does not return to baseline because of autoPEEP. Detection and quantification of autoPEEP by an
expiratory hold (black arrow)
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P.244
High auto-PEEP causes a precipitous rise in intrathoracic pressure and can potentially lead
to haemodynamic collapse through the mechanisms described above (decrease preload,
increase RV afterload, decrease LV afterload). Auto-PEEP can be treated by improving airway
resistance (e.g. bronchodilators), decreasing respiratory rate, increasing exhalation time,
and/or adjusting inspiratory flow dynamics in the ventilator.
9.7 - NI haemodynamic monitoring during positive

pressure ventilation
The accuracy of non-invasive haemodynamic monitoring in patients undergoing PPMV impro-

ves in fully sedated patients, in sinus rhythm or with minimal RR variation.
POC-US is also useful (Table 1). For instance, in patients with preload-dependent conditions,
PEEP can be up-titrated while monitoring C and right heart haemodynamics (e.g. TV veloci-
ties, RVTO VTI, septal motion), while in patients with afterload-dependent conditions, PEEP
can be up-titrated while monitoring LV diameter, MR severity and CO by LVOT VTI. Of note,
low TdV ventilation can preclude the assessment of fluid responsiveness manoeuvres through
changes in IVC diameter or by PPV. As such, it is advisable to adjust to at least 8-12ml/kg
of IBW, when performing these manoeuvres.
9.8 - Invasive haemodynamic monitoring during

spontaneous breathing and during positive pressure
ventilation
The interaction between TdV, driving pressures, PEEP and plateau pressure effects cardiac
chambers and intrathoracic ascending aorta, leading to the changes (Figure 1). In order to
minimize the influence of intrathoracic pressure, invasive haemodynamic assessment should
be performed at the end of expiration when intrathoracic pressures are closest to atmos-
pheric during both spontaneous breathing and PPMV (Figure 3). In patients with significant
respiratory distress, significant swings in intrathoracic pressure can occur directly influen-
cing intracardiac pressures (Figure 4).
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Figure 3 - Assessment of intracardiac pressures

According to the respiratory cycle during spontaneous breathing (A) and PPMV (B).
Note that measurements are always performed at end-expiration, when intrathoracic pressure is closest to zero.
B
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Figure 4 - Relationship between PCWP and intrathoracic pressure

In patients with normal lungs (A) and
with conditions increasing intrathoracic
pressure, such as COPD, obesity or
chest wall deformities (B). The increased
intrathoracic pressure account for an
increase in PCWP. Panel C illustrates
patient efforts during PPMV, seen as
negative deflection in the pressure wave
(yellow arrows) that counteracts the effect
of PPMV by negative intrathoracic effort
from active inspiration.
A
C
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When evaluating waveforms in patients with preload dependent conditions (e.g. hypovo-
lemia), alveolar pressure can exceed PCWP causing the haemodynamic pressure wave to
lose a clearly discernible A and/or V waves, similar to when pulmonary artery catheters are
positioned with tips located in the West zone 1 or 2. In these scenarios, filling pressures (LA
or PCWP) can be overestimated. However, when this clinical scenario is corrected (e.g. fluid
resuscitation), the A and V waves become more easily identifiable as the PCWP overcomes
alveolar pressure, (similar to having the pulmonary catheter tip in west Zone 3).
Even appropriate with timed to haemodynamic measurement at end expiration, it is impor-

tant to assess for patient’s own respiratory efforts during data acquisition. Accordingly, data
interpretation may be confounded by patient-ventilator interactions, often dictated by patient
synchrony with the ventilator, work of breathing, as well as by the presence of pulmonary
disease. For instance, Figure 4C shows how active breathing may counteract the effects of
PPV. In this setting, placing a hand in the thorax or abdomen to examine if there is active
inspiration, as well as assessing the pressure/time curve to look for negative deflections, can
be helpful. If this is the case, a practical approach to identify end-expiration is to look at the
longest phase of the respiratory cycle, which typically corresponds to the expiratory phase.
PEEP (total PEEP, auto-PEEP and set PEEP, Figure 2) will also be transmitted and has the
potential to increase transmural intracardiac pressures and alter haemodynamic interpre-
tations, mainly with PEEP>10cm H2O, wherein intracardiac pressures can be overestimated.
Similarly, PEEP can blunt the transmission of pressure from the LA to the tip of the PA
catheter interfering with haemodynamic assessment (Figure 5).
Figure 5 - Effect of PEEP

on filling pressures
By direct transmission, PEEP will
increase transmural intracavitary
pressure in a non-linear, non-predictable
way. Similarly, alveolar pressure
can affect the measurement by the
pressure transducer located in the tip
of the catheter by affecting pressure
transmission in the fluid column.
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Figure 6 - Intracardiac and intrathoracic pressures

Before (left) and after (right) liberation from mechanical ventilation. Note the abrupt increase in filling pressures and swings
in intrathoracic pressure, which can increase left ventricular afterload from increase negative intrathoracic pressure.
In addition, the effect of PEEP on filling pressures is non-linear and unpredictable, because
PEEP is not homogeneously distributed in lung parenchyma affecting heart chambers.
Consequently, it is not appropriate to simply subtract PEEP from PCWP. It is also not advi-
sable to discontinue PEEP to make measurements.
Patients undergoing MV who have significant desynchrony can have significant swings in
intrathoracic pressure (>10-15mmHg). This can often occur in cases of severe respiratory
distress, anxiety, pain, agitation or in patients receiving intermittent MV or PSV with subop-
timal ventilator support. In these situations, large excursions of intrathoracic pressure get
transmitted to the PAC, leading to an overestimation of the transmural intracardiac pres-
sures, especially when incomplete exhalation occurs, generating auto-PEEP and increased
intrathoracic pressures (Figure 4B). In such cases, first: try to improve synchrony with appro-
priate sedation, management of pain and anxiety, and optimization of respiratory support
(providing higher level of PSV or switching from PSV or intermittent MV to a control mode);
and second, administer neuromuscular blockers. Alternatively, an esophageal balloon can
provide a surrogate of intrathoracic pressure, which can then be subtracted from the intra-
cardiac pressure measurement. An esophageal balloon can also be used in patients where
non-compliance of the chest wall can affect intrathoracic pressure, such as in severe obesity,
intra-abdominal hypertension or severe chest wall deformities.
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9.9 - Haemodynamic monitoring during liberation

from mechanical ventilation
Given the potential favourable effects of PPV on preload and LV afterload in patient with
cardiovascular disease, particularly with reduced LV function, discontinuing PPMV can lead
to adverse haemodynamic shifts. In these situations, liberation from PPMV, particularly
PEEP withdrawal, can lead to abrupt raise in filling pressures and LV afterload, increasing
the risk for ventilator weaning-induced pulmonary edema (Figure 6). This can manifest as
abrupt elevations in PCWP during liberation from MV. A strategy to mitigate these effects
includes extubating from low PPV/PEEP settings, pre- treatment with vasodilators such as
ACE/ARNI or intravenous nitrates, extubation to NIV with subsequent gradual weaning of
the ventilator support, and delaying the weaning of inotropic agents 12-24 hours after a
successful extubation (Table 3).
Table 3 - Weaning strategies
Pathophysiologic mechanism Interventions
Inotropic, vasopressors, vasodilators

Impaired LV function
Extubation to NIV
Vasodilators
Elevated afterload
Extubation to NIV
Percutaneous coronary intervention, antianginal
Myocardial ischemia
therapy
Vasodilators, diuretics
Mitral regurgitation
Extubation to NIV
Volume overload (positive accumu- Diuretics (BNP-tailored improve extubation rates)
lated fluid balance) Extubation to NIV
III.10
10 - HAEMODYNAMICS DURING
MECHANICAL CIRCULATORY SUPPORT P.250
Prof. Pascal Vranckx, MD, MBA, PhD, FESC

Cardiology (interventional) and Critical Care Medicine
Medical director Cardiac Intensive Care Unit
Hartcentrum Hasselt, Stadsomvaart 11, B-3500 Hasselt, Belgium
Prof. Daniel Burkhoff, MD, PhD

Director, Heart Failure, Haemodynamics and Mechanical
Circulatory Support Research, Cardiovascular Research
Foundation, 1700 Broadway, New York, NY 10019
Key messages
pMCS devices never operate in a vacuum and individual patients characte-
ristics must be considered when assessing their performance, including the
degree of residual LV function, right sided factors (i.e. RV systolic and dias-
tolic function, and pulmonary vascular resistance), baroreceptor activation
and its impact on vascular resistance, metabolic factors and concomitant
medication use (i.e. vasoactive drugs)
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P.251
Introduction
Each device acts through a different mechanism and, to different degrees, to unload the
heart, increase blood pressure, cardiac output and systemic perfusion, while reducing
myocardial work and oxygen consumption.
Modalities of blood flow generation distinguish themselves in terms of the insertion tech-
nique (i.e. surgical vs. percutaneous), the sites where blood is withdrawn and returned to
the body, flow capacities, and pumping mechanisms (Figure1).
The interactions between the heart, the vasculature and the device are complex.
Understanding the pathophysiology of haemodynamic changes during disease and pMCS
is critical for proper monitoring, troubleshooting, and assessment of device performance.
Furthermore, haemodynamic changes and severity of heart failure and cardiogenic shock
may also be crucial for appropriate device selection for RV or LV support and also pos-
sible support with respect to oxygenation.
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P.252
Figure 1 - Features of different devices for mechanical circulatory support

IABP, Impella®, veno-arterial ECLS (extracorporeal life support), TandemHeart™, iVAC 2L
Impella
IABP 2.5, CP, 5.0 Tandemheart ECLS iVAC2L
Heat
Pneu- exchanger
matic Motor
Membrane Pneumatic
pump to axial
Centri- oxygenator pump
pump
fugal
pump Centrigual
pump
10.1 - Understanding left ventricular mechanics:

The Pressure Volume Loop
The normal pressure-volume loop is bound by the ESPVR and the EDPVR (Figure 2).
The ESPVR is reasonably linear, with a slope Ees and the volume-axis intercept (V0). The
ESPVR shifts with changes in contractility. EDPVR is non-linear and defines the passive dias-
tolic properties of the ventricle. Ventricular compliance is determined by the inverse of the
slope of EDPVR; the EDPVR slope increases with increased filling pressures and therefore
compliance decreases with increased filling pressures.
Effective Ea is the slope of the line extending from the EDV point on the volume axis through
the end-systolic pressure–volume point of the loop. The slope of the Ea line depends on TPR
and HR, and its position depends on EDV.
The actual position and shape of the pressure-volume loop in health and disease depends
on ventricular contractility, preload and afterload.
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P.253
Figure 2 - Pressure volume loop

Decreased inotropy Increased inotropy
A: Point 1 represents aortic valve closure
and the onset of isovolumic relaxation. A
Point 2 represents mitral valve opening Increased Decreased
and the onset of the diastolic filling TPR TPR
period. Point 3 represents mitral valve
closure and the onset of isovolumic
contraction. Point 4 represents aortic
valve opening and the onset of systolic
ejection.
Decreased Increased
preload preload
B: Total mechanical work of the left B

ventricle is composed of SW and potential
energy (PE). The PVA is the sum of the
SW and PE and represents the total
mechanical work of the heart per beat.
Myocardial oxygen consumption (MVO2) is
directly correlated with PVA.
A significant effort has been devoted to developing real-time, interactive simulations of the
cardiovascular system to be used as educational tools, for exploring basic haemodynamic
principles in health and disease and for predicting the effects of MCS for heart failure (fur-
ther reading see www.harvi.online).
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10.2 - Left ventricular mechanics and percutaneous

mechanical circulatory support
The haemodynamics of pMCS devices are known to us predominately from computer simu-
lations (“in silico” models), and in vivo animal studies.
Current pMCS devices can be characterized by one of three different circuit configurations:
pumping from the right atrium to the systemic artery (e.g. veno-arterial extra corporeal
membrane oxygenation, VA-ECMO); pumping from the LA to the systemic artery (e.g.
the TandemHeart, LivaNova London, UK); or pumping from the LV to the systemic artery
(Impella, Abiomed, Danvers, MA, USA, and PulseCath iVAC2L, PulseCath BV, Amsterdam,
The Netherlands). Circuit configurations of the systems are different and peak flow rates
achievable range between 2.0 and 7.0 l/min (Table 1).
We can use PV loops to illustrate the effects of the different forms of pMCS.
10.2.1 - Right atrium-to-systemic artery circulatory support
Percutaneous VA-ECMO, especially at higher flow rates, may cause LV distension, significant
increases in LA-pressure and in some cases pulmonary congestion/oedema. Specifically, it
is the increased afterload pressure in the setting of compromised LV-contractility that can
result in blood accumulation in the LV and increases LVEDP, LA pressures, and PCWP. In
the most extreme of cases, the aortic valve may remain closed, resulting in stasis in the LV
chamber and in the aortic root. Regardless, the PV loop becomes narrower, taller and shifts
rightward and upward along the EDPVR.
Non-surgical venting can be obtained by atrial septostomy, a 7 Fr pigtail catheter in the LV

connected to the venous limb of the ECMO circuit or by insertion of an additional pVAD with
LV unloading properties (e.g., microaxial flow pump, Impella, Abiomed, Danvers, MA, USA).
10.2.2 - Left atrium-to-systemic arterial support
Given that the blood is taken from the LA with the LA-to-systemic arterial support (i.e.,
TandemHeart support), PCWP and LVEDP will decrease. However, as with other forms of
support, the net impact of this approach is strongly dependent on residual LV function (Ees,
contractility) and the afterload (TPR, arterial pressure).
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10.2.3 - Left ventricle-to-aorta circulator support
With percutaneous LV-to-Aorta axial support (e.g., Impella) flow comes in different configu-
rations offering theoretically up to 5.5 l/min of continuous flow independent of the phase
of the cardiac cycle. This results in a loss of normal isovolumetric periods and the standard
pressure-volume-loop is converted from its traditional trapezoidal to a triangular shape. In
contrast to the earlier discussed systems, removal of the blood flow with the Impella is not
dependent of the ejection through the aortic valve, and with increased pump flow (depending
on configuration and speed), the LV becomes increasingly unloaded (shift of the curve leftward
and downward), with decreased PCWP and LVEDP. In this case, a closed aortic valve is not pro-
blematic since stasis of blood in the LV and the aorta is prevented by flow through the device.
Table 1
Tandem-
IABP Impella ECLS iVAC2L
heart
1 up to 5L/min 2.5 up to 3-7L/min

Cardiac
<0.5L/min Impella 2.5, 5L/min (cannula 2.2L/min
flow CP, Impella5 (cannula size) size)
Aortic counter-
Mechanism LV to Ao LA to Ao RA to Ao LV to Ao
pulsation
Maximal
Up to
support Weeks 7 days 14 days Weeks
24hours
duration
14-19Fr
13-14Fr 15-19Fr
Arterial
Sheat size 7-8Fr Impella 5.0: Arterial 18Fr
18-21Fr
21Fr 21Fr Venous
Venous
Aortic
LV thrombus, disease, AI,
PAD, sepsis,
AI, Mechanical VSD, AI, Left Mechanical
Contra- neurologic
aortic valve, Atrial throm- PAD aortic valve,
indications disorder, AAA,
TIA/stroke, bus, DIC, PAD LV thrombus,
AI
PAD VSD, TIA/
stroke
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P.256
Figure 3
The negative impact of veno-arterial ECMO on PV loop curves with a flow dependent increase in LVEDP and associated
increase in effective Ea. An associated flow-dependent decrease in LV stroke volume (SV) is depicted in the PV loops and is
represented by the width of the PV loop as the volume difference between end-systolic and end-diastolic volumes.
Modified and adapted with permission from Burkhoff et al.

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P.257
Figure 4
Flow-dependent changes in pressure–
volume loops with LA-Ao pump-ing,
showing reducing end-diastolic
pressures, increasing end-systolic
volume, and decreas-ing LV stroke
volume.
Modified and adapted with permission

from Burkhoff et al.
Figure 5
Flow-dependent changes of the
pressure-volume loop with LV-to-aortic
pumping. The loop becomes triangular
and shifts progressively leftward
(indicating increasing degrees of LV
unloading).
Modified and adapted with permission

from Burkhoff et al.
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P.258
10.3 - Invasive haemodynamic monitoring and

Based on pulmonary artery catheter measurements, useful information on right atrial, pul-
monary artery and PCWP, mixed venous oxygenation, CO can be obtained and this also allows
calculation of cardiac index, systemic vascular resistance, pulmonary vascular resistance,
and pulmonary artery pulsatility index [PAPi = (PA systolic - PA diastolic) / RA mean, where
PA pulmonary artery pressure and RA is mean right atrial pressure]. There is a multitude
of different haemodynamic variables associated with impaired outcome in RV dysfunction
which may also help in device selection.
10.3.1 - Right heart catheterisation
Right heart catheterization additionally offers information regarding fluid status and right
heart filling pressures, adequacy of oxygen delivery, and the degree of pulmonary vascular
resistance.
10.3.2 - Pulse contour analysis
Various methods capable of deriving CO from the analysis of arterial pulse wave (PCM) are
available for clinical use. These are based on minimally-invasive or non-invasive techniques
and allow beat-by-beat CO estimates. Pulse contour analysis method may be limited by the
absence of pulsatility.
10.3.3 - Thermodilution
Methods based on ‘cold’ pulmonary thermodilution as well as systems for continuous “hot”
thermodilution are theoretically suitable in patients assisted with pVAD but are unreliable
techniques for patients on RVAD due to ‘cold or hot’ indicator loss bypassed by the pump from
the right heart sections. Similar limitations exist for systems based on transpulmonary ther-
modilution, which cannot be applied to any patient on mechanical circulatory support (RVAD,
LVAD or BiVAD) since indicator loss would happen in both the right and left heart sections.
PRAM does not require any thermodilution calibration and could be a reliable CO-monitoring
technique applicable to either left, right or biventricular mechanical support.
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P.259
10.4 - Echocardiography monitoring and

Echocardiography is considered as the procedure of choice for the evaluation of cardiac per-
formance and to gather other critical information both in the pre, intra and postoperative
phases following MCS implementation.
Transthoracic and transesophageal echocardiography provides important information concer-

ning anatomic contraindications for implantation (e.g., intraventricular or atrial thrombus,
septal or free wall rupture, etc).
Echocardiography can be important for correct positioning of the device, evaluation of ade-
quacy of left ventricular filling and right ventricular function and documenting improvement
of left ventricle performance.
Echo-Doppler-based methods can be used to calculate the flow velocity and volume and
hence systemic blood flow. Unfortunately, due to intrinsic nature, echocardiography cannot
be considered a bedside continuous monitoring system.
In a small cohort, cardiogenic shock patients who tolerated a full ECMO weaning trial and
had aortic VTI ≥10 cm, LVEF >20-25%, and TDSa (lateral mitral annulus peak systolic velo-
city) ≥6 cm/s at minimal ECMO flow were all successfully weaned.
III.11
11 - CARDIAC ARREST AND

POST-CARDIAC ARREST P.260
Prof. Christian Hassager, MD, DMSc, FESC

Department of Cardiology Rigshospitalet, Copenhagen, Denmark
Prof. Jacob Eifer Møller, MD, PhD, DMSc

Department of Cardiology, Odense University Hospital,
Odense, Denmark
Dr. Jesper Kjærgaard, Consultant, MD, PhD, DMSc, FESC

Department of cardiology, Rigshospitalet, Copenhagen, Denmark
Key messages
Initial monitoring during CPR focusses on cardiac rhythm, palpable pulse
and end-tidal CO2 measurements
Important prognostic markers that may aid in the decision to upscale CPR
to eCPR include: Peri-arrest factors (age, witnessed arrest, initial cardiac
rhythm, duration of prehospital CPR, no-flow time, etc.), end-tidal CO2 and
echocardiographic evaluation
Key monitoring after ROSC include cardiac rhythm and HR by telemetry, core tem-
perature (during TTM), respiratory parameters, invasive BP, diuresis and P-lactate
Treatment goals are not different from other intensive care patients
Monitor P-lactate
Always consider fluid before vasopressors and inotropes – cardiac arrest

patients often need a positive fluid balance in the first 24-72 hours
Remember close surveillance of cardiac biomarkers and ECG for later
diagnostic evaluation
Patients on eCPR are very fragile and need close monitoring ideally including
PAC. Remember arterial line in the right arm with frequent ABG gas evalua-
tions and at least, daily echocardiographies and X-rays. Evaluate peripheral
circulation frequently too
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P.261
Introduction
Cardiac arrest is the most extreme medical emergency. Survival with a good neurological
recovery require an immediate diagnosis and good basic life support. Initial shockable
rhythm is common but will often have deteriorated to a non-shockable rhythm before a
defibrillator can be applied. Basic life support supplies the organs with some oxygen but
quick restoration of a spontaneous circulation (by defibrillation if the rhythm is shockable)
is essential for a good outcome. These patients are frequently comatose, minutes to hours
after ROSC, and they most often need specialized ICU care and cardiac interventions in
the following days to restore myocardial function and minimize neurological injury.
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P.262
11.1 - Initial monitoring during CPR until stable ROSC
Monitoring during initial CPR is of minor importance compared to focusing on good quality
basic life support. Focus on giving high quality CPR (chest compressions: 100–120/minutes,
depth of 5–6 cm and full recoil between each compression. If possible, add two rescue breaths
every 30 compressions (30:2 compression: ventilation ratio)), while getting a clear picture
of the history. At this phase, the most important monitoring is time, a palpable pulse during
the CPR, and assessing cardiac rhythm every 2 minutes. Consider reversible factors such
as hypoxia, hypovolemia, hyperkalaemia, hypothermia as well as tension pneumothorax,
cardiac tamponade, toxic and thromboembolic diseases. A quick (10 seconds) echocardio-
graphic evaluation is often helpful.
If ROSC is not achieved within 10-15 minutes, eCPR should be considered in younger previously
healthy subjects. Many simple prognostic factors may aid in determining candidacy for eCPR:
Age < 65 yrs, no known comorbidity, witnessed arrest with immediate basic life support, ini-
tial shockable rhythm, suspected cardiac cause of arrest, and possibility to provide eCPR
within 60-90 minutes from CA, are prerequisites for initializing this therapy. End-tidal CO2 is
a measure of how well the chest compressions support the circulation. A very low value (<1.3
kPa) suggest, that the body is not sufficiently circulated despite the chest compressions and
therefore may preclude upscale to eCPR. A high ETCO2 should raise suspicion of poor ventila-
tion with high pCO2. Plasma pH and lactate upon arrival at the hospital also have prognostic
information, but all patients with prolonged chest compression exceeding 60 min are expec-
ted to have very high p-lactate and reduced pH. Patients that are considered to be candidates
for eCPR without ROSC should be routed directly to cardiac catheterization laboratory for
evaluation and establishment of mechanical circulatory support with fluoroscopic guidance.
Table 1 - Monitoring during CPR
Record timing
Check palpable pulse and, if possible, end-tidal CO2 during
Recording during CPR CPR
When possible, perform a fast (10 seconds) echocardiography
Check heart rhythm every 2 minutes
4 H: Hypoxia, Hypovolemia, Hyperkalaemia, Hypothermia
Consider cause for the
4 T: Tension pneumothorax, cardiac Tamponade, Toxic and
cardiac arrest
Thromboembolic disorders
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P.263
11.2 - Evaluation at ROSC
An ECG must be obtained as soon as possible after ROSC is achieved to assess myocardial
ischemia and underlying cardiac rhythm. The patient should be routed directly to a cardiac
catheter laboratory if the ECG indicates STEMI or severe ischemia. Otherwise, direct trans-
port to an ICU may be considered – but a new ECG should be obtained and evaluated shortly
after arrival to the ICU. In addition, general other diagnostic procedures must be done swif-
tly including ABG, lactate, chest x-ray, an echocardiographic examination and often a CT of
the brain. Further rapid investigations may be necessary depending on the presumed cause
of the CA. Close attention to standard continuous monitoring, including circulatory and res-
piratory functions, is of course of utmost importance in these, often comatose, patients.
Prognostic factors should be documented.
Table 2 - Evaluation at ROSC
ECG and telemetry

Signs of STEMI or severe ischemia on ECG results in immediate transfer for coronary angiography
and potentially PCI (or CABG)
Echocardiography study
Blood samples (ABG, lactate, standard biochemistry and biomarkers of myocardial injury)
Chest X-ray
CT scan of the brain, if obvious cause of CA is lacking
Further exams depend on initial findings, clinical course and previous illnesses-comorbidities.
11.3 - Monitoring during TTM
TTM is indicated in comatose survivors of CA with a suspected cardiac cause, especially

in patients with shockable primary rhythm. TTM should be initialized as soon as possible
after hospital arrival. Core temperature is therefore a key parameter to monitor. It should
be kept constant for 24 hours at either 33°C or 36°C and thereafter increased to normal
body temperature at a rate of ≤0.5°C / hour. TTM may result in increased diuresis, shivering,
bradycardia, hyperglycaemia and electrolyte changes and requires intubation, ventilation
and sedation. Careful monitoring of many parameters is therefore needed during the first
36 hours at the ICU including sedation level, respiratory, circulatory, renal and biochemical
parameters. Suggested goals for some of these parameters are given in Table 3.
III.11
P.264
Table 3 - Suggested goals during TTM
RASS -4 and no shivering, temperature constant

Central nervous system
(33°C or 36°C)
Respiratory PaO2 9.3-12 kPa, SaO2 93-98%, PaCO2 5.0-6.5 kPa
Circulatory MAP 65-100 mmHg, HR 30-100, CVP 5-10 mmHg
Abdominal Aspiration volume form an intestinal tube < 200 ml
Diuresis > 1 ml/kg/hour and positive fluid balanc

Renal
(+ 1-2 litres) first 24 hrs
Haematocrit: 28-35%,
B-Glucose: 6-10 mM/L,
Biochemistry Lactate: decreasing to < 2mM/L,
Potassium: 4-4.5mM/L,
Calcium 1.15-1.35mM/L
11.4 - Additional monitoring during eCPR
Patients on eCPR are very fragile. On top of the above advanced haemodynamic monito-
ring with at PAC if possible, at least daily echocardiographic evaluation, and chest X ray is
a must. An important focus here is to find signs of increased LA pressure and an enlarged
noncontracting LV, indicating the need for a procedure that unloads the LV. Frequent blood
samples for ABG should be drawn from an arterial cannula, preferentially placed in the right
arm, in order to detect deoxygenated blood flow through the heart (Harlequin phenomena) as
early as possible. Furthermore, the coagulation must be frequently and carefully evaluated
and anticoagulation is mandatory for MCS. Finally, the perfusion of the leg where the arte-
rial canula is placed must be protected by using a reperfusion circuit inserted into femoral
artery distal to ECMO cannula, and the perfusion monitored closely both clinically and by
surface temperature measurements, often guided by near-infrared spectroscopy (INVOS).
III.11
P.265
Table 4 - Additional monitoring during eCPR
Pulmonary arterial catheter PCWP<15 mmHg; RA or CVP 8-12 mmHg
Echocardiography Opening of the aortic valve, no ballooning of the LV
Chest X ray Consolidation, congestion
Equal surface temperature, frequent clinical

Lower extremities
evaluation
Corresponding to local protocols regarding full

Coagulation parameters
heparinization
11.5 - Monitoring after TTM
The monitoring initiated during the TTM continues post TTM until the patient is stable.
Sedation should be tapered completely after normal temperature has been reached. If the
patient wakes up, extubation may be performed as general ICU guidelines. Evaluation of
cerebral function follows if the patient remains unresponsive. This includes, on top of serial
detailed neurological assessments, an EEG and in some patients a SSEP examination once
sedation is discontinued (typically at least 24 hours without any sedation or opioids is
required). Imaging of the brain (CT or MRI) is also appropriate, if not previously performed.
Finally, biochemical markers of brain damage (i.e. P-neuron specific enolase, NSE) should be
obtained at 48 hours after the cardiac arrest to aid prognostication. Central temperature
is monitored not only during TTM, but also in the days to follow, and fever above 38.5°C
should be avoided if possible.
THE FUTURE
1 - HAEMODYNAMIC MONITORING IN THE FUTURE P.267

Prof. M. Cecconi, Dr. A. Messina, Dr. F. Collino
1 - HAEMODYNAMIC MONITORING
P.267 IN THE FUTURE
Prof. Maurizio Cecconi, MD, FRCA, FFICM, MD(Res)

Humanista clinical and research center IRCCS,
Rozzano, Milano, Italy
Dr. Antonio Messina,

Department of Anesthesiology and Intensive Care , Humanitas
Research Hospital / Assistant Professor, Humanitas University
Dr. Francesca Collino, MD

Department of Anaesthesia, Intensive care and Emergency
'Città della salute e della Scienza', University Hospital, Turin, Italy
Key messages
Digital innovations are revolutionizing healthcare, providing new tools in the
field of haemodynamic monitoring of critically ill patient
The availability of large amounts of data is critical for the development and
effective implementation of predictive models
Developed decades ago outside of health care, the machine-learning pro-
cess has seen an exponential increase in growth and sophistication also in
medicine
Machine-learning process is currently driving the research forward the deve-
lopment of predictive models and AI, which can assist the physician in the
decision-making process at the bedside, in both in surgical and critically ill
patients
P.268
Introduction
At the bedside, the decision-making process may be currently compared to pendulum

swinging between the adherence to pathways indicated in the international guidelines and
the adaptation of predefined clinical strategy to the single patient (the so-called “pre-
cision medicine”). However, on the one hand, the support available from the literature
could be limited or subject to interpretation because of the paucity of definitive evidence
and, on the other hand, the perception of the short-them efficacy of a therapy may be
inaccurate in predicting the effect on the final outcome of the patient. This is especially
true for haemodynamic monitoring. In fact, it is not the choice of a haemodynamic device
itself [from the pulmonary catheter to more recent and less invasive devices providing
“macro” (i.e. cardiac output) or “micro” (i.e. tissue oxygen saturation) numbers] that can
change the outcome of critically ill patients, but the optimization of strategies and the-
rapies, guided by the obtained numbers.
From the very beginning, medicine had always relied on technology and, nowadays, digital
innovations are revolutionizing healthcare, providing new tools in the field of haemody-
namic monitoring of critically ill patient.
P.269
1.1 - From Macro to Micro:

advances in bedside echocardiography,
cardiac output and microcirculation monitoring
The challenge of shock management is to optimize the heart preload, contractility and afterload.
This process is crucial to avoid the detrimental effects of over or under-resuscitation. Clinical
examination is a cornerstone in shock but is known to be inaccurate in assess the real cardiac
output and intravascular volume status. For these reasons, shock management is guided by
adding bedside quantitative and qualitative evaluation of cardiovascular system function. In
critically ill patients the role of the echocardiography has gained in popularity and is now consi-
dered as part of an integrate approach to the haemodynamically unstable patient, customizing
the therapy at the bedside and reassessing the effects of the strategies adopted. If clinical exa-
mination and critical care echocardiography are considered cornerstones during the phase of
diagnosis and immediate resuscitation of a haemodynamically unstable patient, a more quan-
titative approach may be needed during the stay in an ICU. In this setting, monitoring together
macro and microcirculation is of pivotal importance to appropriately target the therapy. In
fact, the oxygen delivery is often affected by dissociation between these two compartments,
defined as a “loss of haemodynamic coherence”. The progression of the shock is associated
with mitochondrial dysfunction and deregulated cell-signaling pathways, which lead to multiple
organ damage and failure and, eventually, to untreatable haemodynamic instability and death.
1.1.1 - Advances in echocardiography
For decades, however, the echocardiography assessment has been performed with cumbersome
devices, limiting the applicability of this technique at the bedside. However, the miniaturization
of medical devices has boosted the echocardiography as part of the daily clinical assessment of
patient, being useful not only for cardiologists but also for trained intensivists and anesthesiolo-
gists, inside and outside ICUs. The design of pocket-sized equipment continues to evolve. Recently,
mobile application–based ultrasound systems have emerged wherein a smartphone or tablet can
turn into a handheld ultrasound simply by plugging in a transducer or connecting wirelessly. In the
near future new miniaturized cardiac ultrasound systems, would allow 3-dimensional real-time
volumetric imaging on a portable scale for point-of-care diagnostic applications. Another recent
advance in the use of bedside echocardiography is of interest. In fact, it was recently developed
of a mini-invasive, miniaturized, disposable, 2D monoplane trans-esophageal probe (ImaCor-USA)
of 5.5 mm diameter, dedicated for continuous long term haemodynamic and cardiac function
monitoring. The system provides three primary cross-sectional views of the heart, i.e. short axis
trans-gastric, mid-esophageal four chambers and superior vena cava views (Table 1).
P.270
1.1.2 - Advances in cardiac output monitoring
The evolution of pulse contour algorithms, allowing the computation of stroke volume and
cardiac output from an arterial blood pressure curve, is constant. The reliability in provi-
ding accurate measurements mainly depends on the quality of the pressure signal and on
changes in vascular tone. New advances in this setting allow to record the arterial pressure
noninvasively, from finger arteries with the volume clamp method, from the radial artery by
applanation tonometry and soon from a brachial cuff by hydraulic coupling. Moreover, some
downloadable applications, not still approved for clinical use, allow to capture the arterial
pressure waveform from any bedside monitor by a cell phone camera, and to compute hae-
modynamic parameters (Table 1).
1.1.2 - Advances in cardiac output monitoring
Monitoring microcirculation is still challenging. Metabolic sensors are also evolving and
electronic tattoos or biostamps are currently under development. Recent advances are not
still routinely available at the bedside. However, the microvascular alterations during sepsis
(such as a reduced functional capillary density) are strong predictors of outcome in criti-
cally ill patients. Small hand-held video-microscopes to evaluate the mucosa of the mouth
have been recently tested. This microscope (based on the orthogonal polarization spectral
imaging) produces excellent images of the sublingual microcirculation, which could be consi-
dered as mirror of the microcirculation status.
In this context, a new monitoring technology (Eirus – Maquet Germany) for continuous and
simultaneous measurement of lactate and glucose at the patient’s bed-side, has been recently
introduced into clinical use and could be potentially useful in the assessment of lactates pro-
duction and clearance, to titrate the therapy during septic shock (Table 1).
Titre ligne 1
Table 1 - Bedside haemodynamic tools
Haemodynamic tool Actual use Future advances

Pocket-sized equipment.
Critical care Miniaturized, disposable,
Echocardiography echocardiography for daily monoplane trans-esophageal
clinical assessment of patient probe.
Wirelessly connected probes
Record the arterial pressure
Cardiac output calculated
Cardiac output management noninvasively.
from arterial blood pres-
to optimize haemodynamics Record transmitted to pocket
sure curve analysis
monitors
Orthogonal polarization spectral
images
Microcirculation Optimization between oxygen
Continuous and simultaneous mea-
monitoring delivery and consumption.
surement of lactate and glucose
levels
P.272
1.2 - Connectivity, AI-powered predictive

models and machine learning process
On a relatively short-term basis the connectivity allowing the communication between diffe-
rent monitoring systems is an expected transformation. The advantages of cross-checking
monitoring information coming from different sources may be potentially related to the of
decrease false alarms or to provide additional diagnostic information. Moreover, beside these
safety advantages, connectivity is the first step to data integration, which is crucial to develop
predictive analytics. These are statistical methods (i.e. predictive modelling, machine learning,
data mining) evaluating current and historical data to create predictive models about the future.
1.2.1 - Clinical application of AI
The availability of large amounts of data is critical for the development and effective implemen-
tation of predictive models. These data are derived from pharmacy and medical statements,
and include diagnosis codes, demographic data and laboratory results of millions of patients
(Figure 1). One of the first clinical applications of this new technology in the haemodynamic field
is related to the treatment of sepsis. This is a life-threating and time-dependent syndrome, which
is mainly faced with a prompt management of the source associated to intravenous fluids and
vasopressors administration. This bundles of the Surviving Sepsis Campaign aim at methodically
approaching the majority of those patients laying into the core of bell-shaped gaussian pattern
of presentation of the disease. However, in this setting, the individual response to a predefined
panel of treatment may be affected by septic cardiomyopathy, which is a common and variable
feature of sepsis-related cardiovascular failure. The development of predictive models in septic
patients including (also) the monitoring of the haemodynamic pattern of response to fluids and
vasopressors administration is a captivating and very recent approach to this problem. In 2018,
Komorowski et al. developed a reinforcement learning AI Clinician by means of a computational
model in which a virtual agent learns from trial-and-error an optimized set of rules (i.e. the policy
of the AI) that amplifies an expected feedback. The AI “knowledge” is based on the analysis of
an amount of patient data that certainly exceeds by many-fold the life-time experience of human
clinicians and the “treatment” suggested by the analysis of a multitude of treatment decisions.
The more the clinical human decision was coherent to the AI decision, the lower was the morality,
whereas the discrepancy between medical prescription of vasopressors and fluids administration
(both the reduction of excess) and the AI policy was associated with increasing mortality rates,
in a dose-dependent relationship. The authors conclude that computational models can provide
an adjunctive tool to optimize clinical decisions, which could exceed the target of short-term
resuscitation goals and could instead track trajectories toward longer-term survival.
Titre ligne 1
1.2.2 - Machine learning process
Big data and data science gradually permeate most aspects of the clinical and research fields,
and physicians should become familiar with the potentials and limits of these approaches.
Big data can be defined as digital data that are generated in high volume and high variety
and that accumulate at high velocity, resulting in datasets too large for traditional data-pro-
cessing systems. These data are the parameters usually registered each day at the patient's
bedside (i.e. HR, BP, CO…), but they also may be genetic, historical, family information. The
purpose of the data science is to find a computational and statistical tool to make predictions
based on data. Starting from this point of view, scientists develop the machine learning: a
field of study that focuses on how computers learn from data and the development of algo-
rithms that make this learning possible.
Figure 1 - Decision-making process at the bedside.

The “classic” patient-physician relationship is based on pivotal issues: the knowledge of the evidence-based medicine
and the clinical expertise of the physician represent the barycenter of a medical proposal based on the trust and ethical
responsibility, respecting also the patient’s needs. This complex and variable relationship could be supported, in the future,
by the AI and machine-learning systems by tracking trajectories toward longer-term outcomes. The “AI experience” (Big
Data analysis and Data Science) is based on the analysis of a huge amount of data, that overcome life-time experience of
human clinicians.
P.274
The key distinction between traditional approaches and machine learning is that in machine
learning the machine learns from examples (i.e. the datasets), rather than being programmed
with rules. Machine learning starts with a task definition that specifies inputs (or features) and
corresponding outputs (or labels). An example could be to find a model to predict hypotension
in septic patients looking at the shape of the radial artery pressure curves. Using algorithms
for learning from observations, computers determine how to perform the mapping from fea-
tures to labels in order to create a model that will precisely describe the data set. At this
point the task can be performed correctly with new, never-seen-before inputs (Figure 2).
Figure 2 - A simplified example of a machine learning process.

In the first column the dataset is graphically represented. (Notice that the data are randomly divided into 2 subsets: the
training data and the testing data). In the third column the machine training itself continuously in order to obtain the most
precise model as possible to describe the data set of the training data. When finally the machine finds the best fit, the model
is tested with a new pool of data coming from the same macro subset of the training data: the testing data (fourth column).
If the model appropriately represents the testing data population, it will be ready for clinical application.
The machine learning process

Big data Task definition Training a model Testing a model
Digial data from EHR. From the training
They are randomly data the machine The model is
Create a model to
divided into two determins a model evaluated with the
describe the data set
subset : training data that better describes testing data
and testing data the sub set
y = ax2+bx+c
y = mx+q
y = ex
y = ...
Which one ?
Titre ligne 1
A key difference between human learning and machine learning is that humans can learn
to make general and complex associations from small amounts of data, moreover humans
can face “never seen before clinical scenarios”. A machine learning model must be trained
with billions of patient’s data, stored in the Electronic Health Records (EHRs) and if the
model will meet new data sufficiently different from those of the data set, the machine
may fail the task. To be always efficient data sets must be always implemented and
managed by experts, so that the machines can update models quickly. Moreover, models
should be update with new literature evidence on the bases of the local resources.
Even if the challenge seems to be not easy, the accelerating creation of vast amounts of
health care data, may potentially change the nature of medical care. The relationship
patient-doctor will remain the cornerstone of any therapeutic path, but it could potentially
be enhanced by additional insights from machine-learning.
4.1.3 - Conclusions
Medicine and technological progress have been always linked, raising expectations and
concerns, both related to the potential effects of the application of new insights. In the
future, the clinical practice will be supported by medical devices communicating and inte-
grating clinical, physiologic and biological information received on real time by the patient.
This huge amount of data could be used to build predictive models necessary to predict
adverse events, prevent medical errors, propose the most rationale therapy for each single
patient. The challenge of a medicine supported by both driven-data system and clinicians
is fascinating and ambitious
APPENDIX
1 - ADJUNCTIVE TABLES, FIGURES

AND SCORES P.277
Prof. Dr. F. Chacón-Lozsán,
Assoc. Prof. K. Czerwińska-Jelonkiewicz
1 - ADJUNCTIVE TABLES,
P.277 FIGURES AND SCORES
Prof. Dr. Francisco ChacÓn-Lozsán, MD, M.Ed

Critical Care Medicine
Intensive Care unit, Péterfy Sándor Hospital-Budapest
Assoc. Prof. Katarzyna Czerwińska-Jelonkiewicz, MD, PhD

Intensive Therapy Unit, Harefield Hospital, Royal Brompton and
Harefield Hospital NHS Foundation Trust, London UK
1.1 - Basic haemodynamic calculator
As was discussed along this Handbook, critical patients require an advanced knowledge in
haemodynamics and haemodynamic monitoring. However, in low-income countries and in
less complex medical environment than an ICU, calibrated equipment for haemodynamic
monitoring is frequently unavailable.
On the basis of available medical literature, we created a basic haemodynamic calculator,

which may become a useful tool for an easy and fast assessment of many essential haemo-
dynamic parameters of patient in acute circulatory or ventilator event (Figure 1).
This calculator allows for the estimation of preload, afterload, preload responsiveness and
oxygenation parameters using only the basic parameters such as blood pressure, ventilator
parameters, blood gases results and CVP. All the equations for data obtained were previously
tested and were proved to have good correlation with invasive and calibrated equipment’s
in several studies.
This app was made thinking in those scenarios where there’s no haemodynamic monitors
like low income countries/centers, emergency departments or pre-hospital settings. It is
important to point out that this calculator does not replace the calibrated and gold standard
methods for haemodynamic monitoring, but is a tool for a fast haemodynamic assessment
at the acute onset before the most appropriate and accurate method can be used.
It was developed as a first line assessment and for initial management with patients in acute
distress and sudden deterioration, before these patients receives advanced help.
P.278
Figure 1 - Basic haemodynamic calculator interface.

The haemodynamic calculater allows you to input basic haemodynamic parameters obtained by basic monitoring and
echocardiography and obtain more complex data related to preload, afterload, preload responsivenes and cardiac function
P.279
1.2 - Relevant scores
1.2.1 - Haemodynamics
Table 1 - Shock classification

Types of shock states according to haemodynamic and clinical parameters
Hypovolemic Cardiogenic
N/ /N/
Small cardiac chambers, Dilated chambers,

preserved contractility impaired contractility
Cold and pale skin and

Cold extremities, dyspnea,
Modified from: Pinsky M, Teboul J, Vincent
extremities,
peripheral edema, jugular
J (Eds). Haemodynamic monitoring (2019) Tachycardia and vein distention
Lessons from the ICU. doi:10.1007/978-3- tachypnea
319-69269-2
P.280
Low DO2 (shock)
Diagnostic
tools
Low CO High CO
Obstructive Dristributive
Filling
/N pressure
End-Diastolic
( in PE) /N volumes
Systemic vascu-
lar resistance
Mean arterial
pressure
SvO2
Tamponade: pericardial effusion, small ventricles.

Tension pneumothorax: small cardiac chambers: Normal Echocardiography
PE: small LV compressed by dilated RV
Mottled skin,
Jugular vein distention, dyspnea, tachypnea, tachycardia,
Clinical signs
tachycardia. elevated or reduced
temperature
P.281
Table 2 -Shock stages classification
Physical exam /
Stage Description
bedside findings
A patient who is not currently experiencing Normal JVP

signs or symptoms of CS, but is at risk for its Lung sounds clear
A development. These patients may include those Warm and well perfused
At risk with large acute myocardial infarction or prior • Strong distal pulses
infarction acute and/or acute on chronic heart • Normal mentation
failure symptoms.
A patient who has clinical evidence of Elevated JVP

relative hypotension or tachycardia without Rales in lung fields
B
hypoperfusion. Warm and well perfused
Beginning CS • Strong distal pulses
• Normal mentation
A patient that manifests with hypoperfusion May Include Any of:

that requires intervention (inotrope, pressor or Looks unwell
mechanical support, including ECMO) beyond Panicked
volume resuscitation to restore perfusion. Ashen, mottled, dusky
These patients typically present with relative Volume overload
hypotension. Extensive rales
C
Killip class 3 or 4
Classic CS BiPap or mechanical
ventilation
Cold, clammy
Acute alteration in mental
status
Urine output <30 mL/h
D A patient that is similar to category C but are Any of stage C

getting worse. They have failure to respond to
Deteriorating/
initial interventions.
doom
A patient that is experiencing cardiac arrest Near Pulselessness

E with ongoing CPR and/or ECMO, being supported Cardiac collapse
Extremis by multiple interventions. Mechanical ventilation
Defibrillator used
Modified from: Baran DA, et al. This document was endorsed by the American College of Cardiology (ACC), the American
Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April
2019. Catheter Cardiovasc Interv. 2019;94:29–37.
P.282
Biochemical
Haemodynamics
markers
Normal labs Normotensive (SBP>=100 or normal for pt.)

• Normal renal function If haemodynamics done
• Normal lactic acid • cardiac index >=2.5
• CVP <10
• PA sat >=65%
Normal lactate SBP <90 or MAP <60 or >30 mmHg drop from
Minimal renal function Baseline Pulse >=100
impairment If haemodynamics done
Elevated BNP • cardiac index >=2.2
• PA sat >=65%
May Include Any of: May Include Any of:

Lactate >=2 SBP <90 or MAP <60 or
Creatinine doubling >30 mmHg drop from
or >50% drop in GFR baseline and drugs/device
Increased LFTs used to maintain BP above
these targets
Haemodynamics
• cardiac index <2.2
• PCWP >15
• RAP/PCWP >=0.8
• PAPI <1.85
• cardiac power output =<0.6
Any of Stage C and: Any of Stage C and:

Deteriorating Requiring multiple pressors or addition of
mechanical circulatory support devices
to maintain perfusion
“Trying to die” No SBP without resuscitation

CPR (A-modifier) PEA or refractory VT/VF
pH =<7.2 Hypotension despite maximal support
Lactate >=5
P.283
Figure 2 -Forrester haemodynamic classification

P.284
1.2.2 - Mechanical circulatory support
Table 3 -INTERMACS score
Time Frame for

Level Description Haemodynamic Status
Intervention
Persistent hypotension despite
Critical cardiogenic
rapidly escalating inotropic support
1 shock, "crash and Within hours
and eventually IABP, and critical
burn"
organ hypoperfusion
Intravenous inotropic support with

Progressive decline
acceptable values of blood pressure
2 on inotropic support, Within days
and continuing deterioration in nutri-
"sliding on inotropes"
tion, renal function, or fluid retention
Stability reached with mild to

moderate doses of inotropes but
Stable but inotrope
demonstrating failure to wean from Elective over
3 dependent,
them because of hypotension, worse- weeks to months
"dependent stability"
ning symptoms, or progressive renal
dysfunction
Possible weaning of inotropes but

Resting symptoms, Elective over
4 experiencing recurrent relapses,
"frequent flyer" weeks to months
usually fluid retention
Severe limited tolerance for acti- Variable urgency,

Exertion intolerant, vity, comfortable at rest with some dependent on
5
housebound volume overload and often with nutrition and organ
some renal dysfunction function
Variable urgency,
Less severe limited tolerance for
Exertion limited, dependent on
6 activity and lack of volume overload,
"walking wounded" nutrition and organ
fatigue easily
function
Advanced NYHA Patient without current or recent

Not currently
7 III "symptoms, unstable fluid balance, NYHA class
indicated
placeholder" II or III
Adapted from Peura JL, et al. Circulation. 2012;126:2648-2667. DOI: 10.1161/CIR.0b013e3182769a54

P.285
Table 4 - Risk of RV failure after LV mechanical circulatory support device

implantation
Indication of MCSD Destination therapy
Sex Female
Intra-aortic balloon pump and vasopressor requirement

Pre-implantation support
Respiratory: invasive ventilatory support
Hepatic: ALT ≥ 80 UI/L, bilirubin > 2.0 mg/dL

Renal: serum creatinine ≥2.3 g/dl
History of kidney replacement therapy
Organ dysfunction
Nutritional: albumin ≤3.0 g/dL
Coagulation: platelets < 120,000
Others: increased BNP. PCR. Procalcitonin
Right ventricular diastolic diameter > 35 mm. FAC < 30%.

Right ventricular dysfunction
Right atrium > 50 mm
CVP ≥ 15 mmHg or CVP/PCP ≥ 0.63._

Right ventricular work index ≤ 300 mmHg/ml/m2;
Haemodynamic measures
Low pulmonary artery pressures, low cardiac index or
increased pulmonary vascular resistance
Non-ischemic cardiomyopathy, reoperation, important TI,

Others
history of PTE
Modified from: Argiriou M, et al. Right heart failure post left ventricular assist device implantation. J Thorac Dis. 2014 Mar;6
Suppl 1:S52-9. doi: 10.3978/j.issn.2072-1439.2013.10.26.
Table 5 - Pre-/post-implantation peri-operative MCS TTE/ TOE
‘‘red-flag’’ findings P.286
“red-flag” – high risk finding that may contribute to contraindication, failure in MCS implantation,
complications or failure in circulatory support by MCS devices
Pre-implantation peri-operative TTE/TOE ‘‘red-flag’’ findings

Goals: confirm previous echocardiography (TTE or TEE) findings; detect unexpected abnormal
findings before and after LVAD implantation
Small LV size, particularly with increased LV trabeculation

Left ventricle and intra- LV thrombus
ventricular septum LV apical aneurysm
Ventricular septa defects
RV dilatation
Right ventricle
RV systolic dysfunction
Atrial, interatrial sep- Left atrial appendage thrombus

tum, Inferior vena cava PFO /ASD
Any prosthetic valve, especially mechanical MiV, AV

Valvular abnormalities > mild AR, ≥ moderate MS, ≥ moderate TR or
> mild TS, > mild PS, ≥ moderate PR
Any congenital heart disease

Aortic pathology: aortic dissection, atheroma, coarctation
Other
Mobile mass lesion
Other shunts: patent ductus arteriosus intrapulmonary
Post-implantation Perioperative TOE

Goals: monitor for intracardiac air; rule out shunt; confirm device and native heart function
Small LV (over-pumping or RV failure), right-to-left septal shift;

Left ventricle
Large LV (obstructed or inadequate pump flows)
Abnormal flow pattern/high/low velocities, especially after sternal

Inflow-cannula
closure
Right ventricle Signs of RV dysfunction
Interatrial septum PFO/ASD
Aortic/ triscupid valve > mild AR, ≥ moderate TR
Outflow graft-to-aorta Kinked appearance/turbulent

anastomosis flow/velocity >2 m/sec, particularly after sternal closure
Adopted from Stainback RF, et al. J Am Soc Echocardiogr 2015;28:853-909.

P.287 Table 6 - Right ventricle function optimization on mechanical
circulatory support
Modified from: Silvia Moreira Ayub-Ferreira. Arq Bras Cardiol. 2018; 111(1):4-12. DOI: 10.5935/abc.20180126.
P.288
1.2.3 - Arrhythmias haemodynamic
Figure 3 - ECG ischemic localization chart

P.289
Table 7 - Classification
Rhythm ECG Associations
Sinus bradycardia • HR: <60 • Some aerobic athletes, during sleep,

• Rhythm: regular carotid sinus massage, vansalva
• P: normal maneuver, hypothermia, vagal
• PR: normal stimulation
• QRS: normal • Drugs: beta blockers
Sinus tachycardia • HR: 101-200 • Exercise, pain, fever, hypotension,

• Rhythm: regular hypovolemia, anemia, hypoxia,
• P: normal hypoglycemia, heart failure,
• PR: normal hyperthyroidism, fear, anxiety
• QRS: normal • Drugs: atropine, caffeine, theophylline,
hydralazine, beta agonists
Supraventricular • HR: 150-220 • Emotional stress, deep inspiration,

tachycardia • Rhythm: regular/slightly tobacco, caffeine, overexertion
irregular • Rheumatic heart disease, digital
• P: hidden in T wave toxicity, cor purmonale, coronary artery
• PR: normal disease
• QRS: normal
Atrial flutter • HR: atrial 200-250. • Coronary artery disease, mitral

Ventricular can variate. valve disorders, pulmonary embolism,
• Rhythm: regular atrial and cor pulmonae, cardiomyopathy,
regular ventricular hyperthydoidism
• P: none, F waves • Drugs: digoxin, quinidine, epinephrine.
• PR: not
• QRS: normal
Atrial fibrillation • HR: not regular Coronary artery disease, rheumatic

• Rhythm: regular heart disease, heart failure, pericarditis,
• P: normal alcohol intoxication, stress, caffeine,
• PR: normal thyrotoxicosis, electrolytes imbalance,
• QRS: normal acidosis
1° AV Block • HR: normal • Myocardial infarction, fever, coronary

• Rhythm: regular artery disease, vagal stimulation,
• P: normal hyperthyroidism
• PR: >0,2sec • Drugs: digoxin, beta blockers,
• QRS: normal flecainide, calcium channel blockers
P.290
Treatment Example
• Atropine if symptomatic
• Pacemaker (read ESC guidelines)
• Reduce beta blockers dose
• Treat the underlying cause

• If stable: vagal maneuvers, beta blockers
• Vagal stimulation.
Drugs: Adenosine, amiodarone, calcium
channel blocker
• Cardioversion
• Radio frequency catheter ablation (see ESC
guidelines)
• Cardioversion if unstable
• Drugs: amiodarone, propafenone, flecainide
guidelines)
• Cardioversion if unstable
• Correct possible metabolic disturbance
• Drugs: amiodarone, beta blockers, digoxin,
calcium channel blockers
guidelines)
• No specific treatment
• Monitor changes
• Threat possible cause
P.291
Rhythm ECG Associations
2° AV block type • HR: Atrial normal/ • Digoxin, beta blockers

1 (Weckenbach or Ventricular slowed • Coronary artery disease
• Rhythm: Pattern of
Mobitz I)
grouped beats
• P: normal
• PR: gradual legthening
• QRS: normal
2° AV Block type 2 • HR: Atrial normal/ Rheumatic heart disease, coronary

(mobitz II) ventricular variates artery disease, anterior myocardial
• Rhythm: Atrial regular/ infarction
Ventricular irregular
• P: normal
• PR: regular or prolonged
with non conduced beats
• QRS: >0,12sec can have
bundle branch block
3° AV Block • HR: atrial normal/ • Coronary artery disease, myocarditis,

ventricular <60 depends on amyloidosis, scleroderma
block site • Drugs: digoxin, beta blockers, calcium
• Rhythm: regular unrelated channel blockers
A-V
• P: normal
• PR: variable
• QRS: normal or wide
Ventricular • HR: vent 150-250 Myocardial infarction, coronary

tachycardia • Rhythm: regular or not artery disease, electrolyte imbalance,
• P: hidden on QTS complex cardiomyopathy, mitral valve prolapse,
• PR: not measurable Long QT syndrome, central nervous
• QRS: Distorted in system disorders
appearance, >0,12sec, ST-T
opposite direction as QRS,
R-R interval regular or not.
Ventricular • HR: not measurable Myocardial infarction, heart failure,

fibrillation • Rhythm: chaotic hyperkalemia, hypoxemia, acidosis,
• P: none drug toxicity, pulmonary embolism,
• PR: none during pacing
• QRS: none
P.292
Treatment Example
• If symptomatic: atropine or temporary

pacemaker
• If asymptomatic: observe with
transcutaneous pacemaker and haemodynamic
monitoring
• Temporary pacemaker
• Symptomatic patients: temporary pacemaker

• Drugs: atropine, epinephrine, isoprotenerol,
dopaine
• If calcium channel blocker toxicity: calcium
chloride
• Treat the cause

• If monomorphic VT and stable left ventricle
function: procainamide, amiodarone or
lidocaine.
If unstable: amiodarone or lidocaine and then
cardioversion
• If Polymorphic VT: beta blocker, amiodarone,
procainamide or sotalol and cardioversion if no
change
• CPR
• Defibrillation according guidelines
P.293
1.2.4 - Vascular disease
Figure 4 - Stanford Aortic dissection classification

P.294
1.2.5 - Acute pulmonary embolism: ESC 2019 Guidelines
Figure 5 - Geneva score

P.295 Table 8 - Pulmonary embolism severity index
Simplified
Parameter Original Version
version
Age Ager in years = number of points 1 if >80 years
Male sex 10 -
Cancer 30 1
Chronic heart failure 10 1
Chronic pulmonary disease 10 1
Pulse rate >110 20 1
Systolic BP <100 30 1
Respiratory rate >30 20 -
Temperature <36°C 20 -
Altered mental status 60 -
Arterial oxyhemoglobin
20 1
saturation <90%
Risk strata
Class I:
<65 pints.
Very low 30 days mortality risk (0-1,6%) 0 pints = 30 day
Class II: mortality risk 1.0%
66-85 pints.
Low mortality risk (1,7-3,5%)
Class III:
86-105 pints.
Moderate mortality risk (3,2-7,1%)
Class IV:
>1 points = 30 days
106-125 points
mortality risk 10,9%
High mortality risk (4.0-11,4%)
Class V:
>125 points.
Very high risk of mortality (10-24,5%)
P.296
1.2.6 - Acute respiratory distress syndrome
Figure 6 - ARDS diagnosis chart
Acute respiratory distress syndrome

(Berlin definition)
Timing
Whiting 1 week of known clinical insult, new or

worsening respiratory syndrome
Chest imaging
Bilateral opacities, not fully explained by effusions,

lobular collapse or nodules
Origin or edema
Objective assessment by echocardiography or EV
Oxygenation (with PEEP>5)
Mild: Moderate: Severe:

PaO2/FiO2 PaO2/FiO2 PaO2/FiO2
200-300 100-200 <100
P.297
Table 9 - FICM/ICS guidelines for the management of ARDS in adult

patients
Grade
Topic Conditions
recommendation
Tidal volume ≤6ml/kg ideal body weight
Tidal Volume Strongly in favour
Plateau pressure <30 cmH2O
Proning for ≥12 hours per day

Prone Positioning Strongly in favour Patients with moderate/severe ARDS
(P:F ratio ≤20kPa)
HFOV Strongly against -
Conservative Fluid
Weakly in favour -
Management
Patients with moderate or severe ARDS

Higher PEEP Weakly in favour
(PF ratio ≤27kPa)
Evidence for cisatracurium besylate

Continuous 48-hour infusion
NMBA Weakly in favour
Patients with moderate/severe ARDS
(≤20kPa)
With lung-protective mechanical

ventilation
ECMO Weakly in favour Patients with severe ARDS, lung
injury score ≥3 or pH <7.20 due to
uncompensated hypercapnoea
Inhaled Vasodilators Weakly against Evidence for inhaled nitric oxide
Corticosteroids Research recommendation -
ECCO2R Research recommendation -
Modified from: Griffiths MJD, et al. BMJ Open Respir Res. 2019. http://dx.doi.org/10.1136/bmjresp-2019-000420
P.298
1.2.7 - Sepsis
Figure 7 -qSOFA
P.299
1.2.8 - Multiple organ failure
Table 10 - SOFA
a
catecholamines administered for at least 1h (dopamine and norepinephrine μmg/kg/min).
Variables 0 1 2
PaO2/FiO2>400 PaO2/FiO2<400 PaO2/FiO2<300

Respiratory
SpO2/FiO2>302 SpO2/FiO2<302 SpO2/FiO2<221
Dopamine ≤5 or
Cardiovasculara MAP >70mmHg MAP<70mmHg
dobutamine (any)
Liver
<1,2 1,2-1,9 2-5,9
Bilirubin (mg/dl)
Renal
<12 1,2-1,9 2,0-3,4
Creatinine (mg/dl)
Coagulation
>150 <150 <100
Platelets (x103/mm3)
Neurologic
15 13-14 10-12
CGS score
P.300
3 4
PaO2/FiO2<200 PaO2/FiO2<100
SpO2/FiO2<142 SpO2/FiO2<67
Dopamine >5 Dopamine >15

Norepinephine≤0,1 Norepinephine>0,1
Phenylephrine<0,8 Phenylephrine>0,8
6-11,9 >12
3,5-4,9 >5,0
<50 <20
6-9 <6
P.301
Figure 8 - HELLP syndrome diagnosis and classification

P.302
1.2.9 - Kidney
Table 11 - RIFLE and AKIN
RIFLE
AKIN
Patients who receive RRT are

considered to have met the
criteria for stage 3 irrespective of
the stage that they are in at the
time of commencement of RRT.
303 Abbreviations
+PV = Positive Predictive Value B

BCM = Basic-standard Continuous
A Monitoring
A = Atrial Transmitral Filling Velocity Bicarb = Bicarbonate
AAA = Abdominal Aortic Aneurysm BiVAD = Biventricular Assist Devices
AbCS = Abdominal compartment syndrome BNP = Brain Natriuretic Peptide
ABG = Arterial Blood Gases BP = Blood Pressure
ABGA = Arterial Blood Gas Analyses Bpm = Beats per minute
ACA = Anterior Cerebral Artery BSA = Body Surface Area
ACC = American College of Cardiology
ACPE = Acute Cardiogenic Pulmonary C
Edema CA = Cardiac Arrest
ACS = Acute Coronary syndrome C(a-v)O2 = Arterio-venous oxygen
AHA = American Heart Association concentration difference
AHF = A cute Heart Failure CaCO2 = Arterial CO2
AI = Aortic Insufficiency CaO2 = Arterial oxygen concentration
AKI = Acute Kidney Injury CART = Cardiac Arrest Risk Triage
ALI = Acute Lung Injury CFI = Cardiac Function Index
ALVF = A cute Left Ventricular Failure CI = Cardiac Index
ALT or ALAT = Alanine Aminotransferase CICU = Cardiac Intensive Care Unit
AMP = Arterial Mean Pressure CISVC= Collapsibility Index of Superior Vena
Ao = Aorta Cava
AP = Arterial Pressure CO = Cardiac Output
APACHE = Acute Physiological And Chronic CO2= Carbon Dioxide
Health Evaluation CP = Cardiac Power
APP = Abdominal Perfusion Pressure CPI = Cardiac Power Index
AR = Aortic Regurgitation CPO = Cardiac Power Output
ARDS = A cute Respiratory Distress CPP = Cerebral Perfusion Pressure
Syndrome CPR = Cardiopulmonary Resuscitation
ARF = Acute Renal Failure cPWA = Calibrated arterial pulse wave
ASD = Atrial Septal Defect analysis
AST = Aspartate Aminotransferase Cr = Serum Creatinine
AU = Arbitrary Units CRP = C-reactive Protein
AUCH = Hyperemic Area CRT = Capillary Refill Time
AUROC = A rea Under the Receiver CS = Cardiogenic Shock
Operating Characteristic Curve Cstat = Static compliance
AV = Aortic Valve CT = Computer Tomography
CvCO2 = Mixed venous CO2
Abbreviations 304
CVP = Central Venous Pressure EDPAP = End-Diastolic Pulmonary Artery

CW= Continuous Wave Doppler Pressure
EDPVR = End-Diastolic Pressure-Volume
D Relationship
DaE = Dynamic arterial elastance EDV = End-Diastolic Volume
DAP = Diastolic Arterial Pressure EEG = Electroencephalography
DAPT = Double Antiaggregant Therapies EEO = End-Expiratory Occlusion
DBP = Diastolic blood pressure EF = Ejection fraction
DC = Dynamic Compliance Ees = End-systolic elastance
DC PM = Dual-Chamber Pacemaker with EIO = End-Expiratory Occlusion
right atrial and ventricular EKG = Electrocardiogram
stimulation and sensitivity EROA = Effective Regurgitant Orifice Area
DeO2 = Deoxygenation slope ESC = European Society of Cardiology
DIC = Disseminated Intravascular ESPVR = End-Systolic Pressure-Volume
Coagulation Relationship
DIVC = Diameter of Inferior Vena Cava ET = Ejection Time
DIIVC = Distensibility Index of Inferior Vena etCO2 = end-tidal CO2
Cava EVLW = Extravascular Lung Water
DO2 = Oxygen delivery EVLWI = Extravascular Lung Water Index
DP = Driving pressure
DSt = Exponential Downslope Time F
DSVC = : Diameter of Superior Vena Cava FAC = Fractional Area Change
DiasVel = Diastolic velocity FC = Fluid Challenge
Fio2 = Fraction Of Inspired Oxygen
E Fr = French
E = Early Transmitral Filling Velocity FT = Filling Time
E’ = Tissue Doppler (mitral) FTc = Flow Time corrected
Ea = Arterial Elastance FW = Free Wall
Eadyn = Dynamic Arterial Elastance
EC = Electrical Cardiometry G
ECCO2R = Extra-Corporeal Carbon Dioxide GCS = Glasgow Coma Score
Removal GEDV = Global End-Diastolic Volume
ECG = Electrocardiogram GEDVI = Global End-Diastolic Volume Index
ECMO = Extracorporeal Membrane GEF = Global Ejection Fraction
Oxygenation GFR = Glomerular Filtration Rate
eCPR = Extracorporeal Cardiopulmonary GIPS = Global Increased Permeability
Resuscitation Syndrome
305 Abbreviations
H J
Hb = Haemoglobin JVP = Jugular Venous Pressure
HF = Heart Failure
HFNC = High Flow Nasal Cannula L
HFOV = High Frequency Oscillation LA = Left Atrium
Ventilation LA-Ao = Left Atrial-to-Aortic
HR = Heart Rate LAD = Left Anterior Descendent
LAO = Left Anterior Oblique
I LAP = Left Atrial Pressure
IABP = Intra-Aortic Balloon Pump LCx = Left Circumflex
IAH = Intra-abdominal hypertension LDF = Laser Doppler Flowmetry
IAP = Intra-Abdominal Pressure LFT = Liver Function Test
IAS = Index Average Speed LI = Lindergaard Index
IBW = Ideal Body Weight LODS = Logistic Organ Dysfunction System
ICA = Internal Carotid Artery LUS = Lung Ultrasound
ICG = Cardiac Impedance LRM = Lung Recruitment Maneuver
ICP = Intracranial Pressure LS = Longitudinal Strain
ICU = Intensive Care Unit LV = Left Ventricle
iDO2 = Oxygen delivery index LVAD = Left Ventricular Assist Device
IJV = Internal Jugular Vein LVDd = Left ventricle diastolic diameter
IMV = Invasive Mechanical Ventilation LVEDA = Left Ventricular End-Diastolic
iNO = Inhaled Nitric Oxide Area
INTERMACS = Interagency Registry for LVEDAi = Left Ventricle End-Diastolic Area
Mechanically Assisted index
Circulatory Support LVEDP = Left Ventricular End-Diastolic
IPPV = Intermittent Positive Pressure Pressures
Ventilation LVEDv = Left Ventricle End Diastolic
ITBV = Intrathoracic Blood Volume Volume
ITBVI = Intrathoracic Blood Volume Index LVESv = Left Ventricle End Systolic Volume
ITTV = Intrathoracic Thermal Volume LVOT = Left Ventricular Outflow Tract
IV = Intravenous LVOTA = Left ventricle outflow tract area
IVC = Inferior Vena Cava LVOT MVV = L eft ventricle outflow tract
IVCd = Inferior vena Cava diameter max velocity variation
IVCDV = Inferior vena cava dyameter LVOT VTI = Left ventricle outflow tract
variation velocity integral
IVP = Intra-Vesical Pressure LVP = LV Pressure
IVRT = Isovolumic Relaxation Time LVSd = Left ventricle systolic diameter
LVV = LV Volume
Abbreviations 306
M P
MAP = Mean Arterial Pressure PA = Pulmonary Artery
MAPSE = Mitral Annular Plane Systolic PAC = Pulmonary Artery Catheter
Excursion PACO2 = Carbon Dioxide Tension
MCA = Middle Cerebral Artery PAD = Peripheral Artery Disease
MCS = Mechanical Circulatory Support PAO2 = Oxygen Tension
MEWS = Modified Early Warning Score PAO2/FiO2 = Partial pressure arterial
MFI = Microvascular Flow Index oxygen/fraction of inspired
MgSO4 = Magnesium Sulfate oxygen
MIA = Measure, Interpret, Apply PAOP = Pulmonary Artery Occlusion
MiV = Mitral Valve Pressure
MODS = Multiple Organ Dysfunction Score PAP = Pulmonary Arterial Pressure
MOF = Multiple Organ Failure PAPi = Pulmonary Artery Pulsatility index
MPAP = Mean Pulmonary Artery Pressure Paw = Mean Airway Pressure
MPMO = Mortality Probability Model PCA = Posterior Cerebral Artery
MPP = Mean perfusion pressure PCG = Phonocardiogram
MR = Mitral Regurgitation PCM = Pulse Contour Method
MRI = Magnetic Resonance Imaging pCO2 = Carbon Dioxide
MS = Mitral Stenosis PCOP = Pulmonary Artery Occlusion
MTt = Mean Transit Time Pressure
MV = Mechanical Ventilation PCP = Pulmonary Capillary Pressure
mVel = Mean Velocity PCWP = Pulmonary Capillary Wedge
MVO2 = Myocardial Oxygen Consumption Pressure
PDESi = Phosphodiesterase type 5 inhibitor
N PE = Pulmonary Embolism
N = Normal PEA = Pulseless Electrical Activity
NEWS = National Early Warning Score PEEP = Positive End-Expiratory Pressure
NI = Non-Invasive PFO = Patent Foramen Ovale
NIRS = Near Infra-Red Spectroscopy PgCO2 = Gastric intramucosal carbon
NIV = Non-Invasive Ventilation dioxide partial pressure
NMBA = Neuromuscular Blocking Agents PGI2 = Prostaglandine I2
NR = Non Reported PH = Pulmonary Hypertension
NYHA = New York Heart Association PI = Perfusion Index
PulsI = Pulsatility index
O PICC = Peripherally Inserted Central
O2ER = Oxygen extraction ratio Catheters
OCT = Oxygen Challenge Test PiCCO = Pulse Contour Cardiac Output
OPS = O
rthogonal Polarization Spectral imaging PLR = Passive Leg Raising
307 Abbreviations
pLVAD = Percutaneous LV Assist (e.g. R

Impella or TandemHeart) RA = Right Atrium
pMCS = P ercutaneous Mechanical RAP = Right Atrial Pressure
Circulatory Support RASS = Richmond Agitation and Sedation
pO2 = Partial pressure of oxygen Scale
POCUS = Point of Care Ultrasound RCA = Right Coronary Artery
PP = Pulse pressure Re02 = Reoxygenation slope
PPG = Photoplethysmography RF = Renal Function
PPI = Peripheral Perfusion Index RI = Resistance Index
PPMV = P ositive Pressure Mechanical ROSC = Return of Spontaneous Circulation
Ventilation RR = Respiratory Rate
PPV = Pulse Pressure Variation RRT = Renal Replacement Therapy
PR = Pulmonary Regurgitation RV = Right Ventricle
PRAM = P ressure Recording Analytical RVAD = Right Ventricular Assist Device
Method RVEDa = Right ventricle end diastolic area
PS = Pulmonary Stenosis RVEDV = Right ventricle end diastolic
PTE = Pulmonary Thromboembolism volume
PTV = Pulmonary Thermal Volume RVESa = Right ventricle end systolic area
PvaCO2 = Veno-arterial difference in PCO2 RVF = Right Ventricular Failure
PvCO2 = Venous partial pressure carbon RVFAC = Right Ventricle Fraction area
dioxide change
PV = Pulmonary Veins RVOT = Right Ventricular Outflow Track
PVA = Pressure-Volume Area RVSP = Right Ventricular Systolic Pressure
PVI = Plethysmographic Variability Index Rvol = Regurgitant Volume
PVPI = Pulmonary Vascular Permeability
Index S
PVR = Pulmonary Vascular Resistance SAH = Subarachnoid Haemorrhage
PVRi = Pulmonary vascular resistance SaO2 = Arterial Oxygen Saturation
index SAPS = Simplified Acute Physiologic Score
PW = Pulse Wave Doppler SBP = Systolic Blood Pressure
PWA = Pulse wave analysis SBT = Spontaneous Breathing Trial
PWTT = Pulse Wave Transit Time SCAI = Society for Cardiovascular
PWV = Pulse Wave Velocity Angiography and Interventions
Scm = Standard Continuous Monitoring
Q ScvO2 = Central Venous Oxygen Saturation
Qp/Qs = Pulmonary-systemic shunt ratio SFF = Systolic Filling Fraction
qSOFA = Quick SOFA Shi = Shock index
Abbreviations 308
SIRS = S
ystemic Inflammatory Response TTE = Transthoracic Echocardiogram/
Syndrome Echocardiography
SOFA = Sequential Organ Failure Score TTM = Targeted Temperature Management
SPAP = Systolic Pulmonary Artery Pressure TV = Tidal Volume
SpO2 = Oxygen Saturation By Pulse-
Oximetry U
SS = Septic shock UO = Urine output
SSEP = Somatosensory Evoked Potentials US = Ultrasound
St02 = Tissue Oxygen Saturation
SV = Stroke (Systolic) Volume V
SysVel = Systolic velocity VA-ECMO = Veno-Arterial Extra Corporeal
SVi = Stroke Volume index Membrane Oxygenation
SVC = Superior Vena Cava VBG = Venous Blood Gases
SvcO2 = Central Venous Oxygen Saturation Vd = Diastolic volume
SvO2 = Mixed Venous Oxygen Saturation VIVC = Inferior Vena Cava Respiratory
SVR = Systemic Vascular Resistance Variation
SVRi = Systemic vascular resistance index VO2 = Oxygen consumption
SVV = Stroke Volume Variation VOT = Vascular Occlusion Test
SW = Stroke Work VS = Vital Signs
VSD = Ventricle Septal Defect
T VSR = Ventricular Septal Rupture
T°= Temperature VT/FV = Ventricular Tachycardia/Fibrillation
TAPSE = Tricuspid Annular Plane Systolic VTI = Velocity Time Integral
Excursion VTIRVOT = Right Ventricular Outflow Tract
TdV = Tidal Volume Velocity Time Integral
TEE = Transesophageal Echocardiography VTR = Velocity of Tricuspid Valve
Temp = Body Temperature Regurgitant Flow
TI = Tricuspid Insufficiency
TIA = Transient Ischaemic Attack W
tIVT = Total Isovolumetric Time WiPO = Weaning-induced pulmonary
TOE = Transoesophageal Echocardiogram oedema
tPO2 = Tissue Oxygen Tension WSACS = The Abdominal Compartment
TPR = Total Peripheral Resistance Society, formerly known as the
TPTD = Transpulmonary thermodilution World Society of the Abdominal
TR = Tricuspid Regurgitation Compartment Syndrome
TRv = Tricuspid Regurgitation velocity WU = Wood Units
TS = Tricuspid Regurgitation
References
309 and copyright acknowledgments
PART I - 1
Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, Jaesche R, Mebazaa

A, Pinsky MR, Teboul JL, Vincent JL, Rhodes A. Consensus on Circulatory Shock and
Hemodynamic Monitoring, Task Force of the European Society of Intensive Care Medicine,
Intensive Care Med 40(12):1795-1815, 2014. (PMID: 25392034; PMCID: PMC4239778)
An excellent overview of the linkage between monitoring, pathophysiology and
strategies to monitor what is necessary to treat the patient in circulatory shock.
Pinsky MR. Functional Hemodynamic Monitoring: Current concepts in critical care. Curr
Opin Crit Care 20(3):288-293, 2014. (PMID: 24722057, PMCID: PMC4324536; NIHMS ID
NIHMS626235)
A summary paper describing the dynamic parameters available to identify tissue
hypoperfusion, volume responsiveness and arterial tone.
Teboul JV, Saugel B, Cecconi M, De Backer D, Hofer C, Monnet X, Perel A, Pinsky MR,
Reuter D, Rhodes A, Squara P, Vincent JL, Scheeren T, on behalf of the Cardiovascular
Dynamics section of the ESICM. Less invasive hemodynamic monitoring. Intensive Care
Med 42(9): 1350-1359, 2016. https://doi:10.1007/s00134-016-4375-7 (PMID: 27155605)
Expert opinion on alternatives to invasive monitoring
Chen L, Olufunmilayo O, Clermont G, Hravnak M, Pinsky MR, Dubrawski AW. Dynamic and
personalized risk forecast in step-down units: Implications for monitoring paradigms. Ann
Am Thorac Soc 14(3): 384-391, 2017. https://doi:10.1513/AnnalsATS.201611-905OC (PMID:
28033032)
One of the first studies to show that hemodynamic monitoring can identify subgroups
of patients at risk for cardiorespiratory insufficiency and that deterioration in those
that do deteriorate usually follows defined phenotypic pathways, often starting 90
minutes before overt collapse.
Hravnak M, Pellathy T, Chen L, Dubrawski A, Wertz A, Clermont G, Pinsky MR. A call

to Alarms: Current state and future directions in the battle against alarm fatigue. J
Electrocardiol 51(6S): S44-48, 2018. https://doi:10.1016/j.jelectrocard.2018.07.024 (PMID:
30077422)
A comprehensive summary of the strengths and weaknesses of hemodynamic
monitoring based clinical alarms as both useful and causing alarm fatigue.
References
and copyright acknowledgments 310
Guarracino F, Bertini P, Pinsky MR. Cardiovascular determinants of resuscitation from

septic shock. Crit Care 23(1): 118, 2019. https://doi.org/10.1186/s13054-019-2414-9 (PMID:
30987647)
An excellent clinical study systematically examining the value of advanced
hemodynamic monitoring approaches to predict and explain the hemodynamic
response of the septic patient to protocolized resuscitation based on the Surviving
Sepsis Guidelines.
PART I - 2
Saugel B, Vincent JL. Cardiac output monitoring: how to choose the optimal method for
the individual patient. Curr Opin Crit Care 2018;24:165-172
Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369:1726-34
Vincent JL, Pelosi P, Pearse R, et al. Perioperative cardiovascular monitoring of high-risk

patients: a consensus of 12. Crit Care 2015;19:224.
Vincent JL. Measure, interpret, apply — the MIA rule in critical care monitoring. Br J
Anaesth 2016;117:557-558
PART II - 1.1
Ritter S, Rudiger A, Maggiorini M. Transpulmonary thermodilution-derived cardiac

function index identifies cardiac dysfunction in acute heart failure and septic patients: an
observational study. Critical Care. 2009;13(4):R133.
Graham AS, Ozment C, Tegtmeyer K, Lai S, Braner DA. Central venous catheterization. N
Engl J Med. 2007;356(21):e21.
Kumar A, Chuan A. Ultrasound guided vascular access: efficacy and safety. Best Practice
& Research Clinical Anaesthesiology. 2009;23(3):299-311.
Moore CL, Copel JA. Point-of-Care Ultrasonography. New England Journal of Medicine.
2011;364(8):749-57.
References
Lamperti M, Bodenham AR, Pittiruti M, Blaivas M, Augoustides JG, Elbarbary M, et al.

International evidence-based recommendations on ultrasound-guided vascular access.
Intensive care medicine. 2012;38(7):1105-17.
O’grady NP, Alexander M, Burns LA, Dellinger EP, Garland J, Heard SO, et al. Guidelines for
the prevention of intravascular catheter-related infections. Clinical infectious diseases.
2011;52(9):e162-e93.
Ritter S, Rudiger A, Maggiorini M. Transpulmonary thermodilution-derived cardiac

function index identifies cardiac dysfunction in acute heart failure and septic patients: an
observational study. Critical Care. 2009;13(4):R133.
Graham AS, Ozment C, Tegtmeyer K, Lai S, Braner DA. Central venous catheterization. N
Engl J Med. 2007;356(21):e21.
Moore CL, Copel JA. Point-of-Care Ultrasonography. New England Journal of Medicine.
2011;364(8):749-57.
PART II - 1.2
Reuter DA, Huang C, Edrich T, Shernan SK, Eltzschig HK. Cardiac output monitoring
using indicator-dilution techniques: basics, limits, and perspectives. Anesth Analg.
2010;110(3):799-811. doi:10.1213/ANE.0b013e3181cc885a
Jozwiak M, Monnet X, Teboul JL. Pressure Waveform Analysis. Anesth Analg.

2018;126(6):1930-1933. doi:10.1213/ANE.0000000000002527
Jozwiak M, Monnet X, Teboul JL. Less or more hemodynamic monitoring in critically ill
patients. Curr Opin Crit Care. 2018;24(4):309-315. doi:10.1097/MCC.0000000000000516
Monnet X, Teboul JL. Transpulmonary thermodilution: advantages and limits. Crit Care.
2017;21(1):147. Published 2017 Jun 19. doi:10.1186/s13054-017-1739-5
References
PART II - 2.1
Section III. Monitoring and investigations in the intensive care unit. In ESC Textbook of
Intensive and Acute Cardiovascular Care. M. Tubaro, P. Wranckx, S. Price and C. Vrints.
Oxford press. In coming third edition
PART II - 2.2.1
Sangkum L, Liu GL, Yu L, Yan H, Kaye AD, Liu H. Minimally invasive or noninvasive cardiac
output measurement: an update. J Anesth. 2016;30(3):461-80
Harjola VP, Parissis J, Brunner-La Rocca HP, Celutkiene J, Chioncel O, Collins SP, et al.
Comprehensive in-hospital monitoring in acute heart failure: applications for clinical
practice and future directions for research. A statement from the Acute Heart Failure
Committee of the Heart Failure Association (HFA) of the European Society of Cardiology
(ESC). Eur J Heart Fail. 2018;20(7):1081-99
Caillard A, Gayat E, Tantot A, Dubreuil G, M’Bakulu E, Madadaki C, et al. Comparison of

cardiac output measured by oesophageal Doppler ultrasonography or pulse pressure
contour wave analysis. Br J Anaesth. 2015;114(6):893-900.
PART II - 2.2.2
Saugel B, Cecconi M, Wagner JY, Reuter DA. Noninvasive continuous cardiac output
monitoring in perioperative and intensive care medicine. Br J Anaesth. 2015;114:562-575.
Sodolski T, Kutarski A. Impedance cardiography: A valuable method of evaluating

haemodynamic parameters. Cardiol J. 2007;14:115-126.
Phillips. ICG. 2019 - http://incenter.medical.philips.com/doclib/enc/fet

ch/2000/4504/577242/577243/577247/582646/583147/PM_-_ICG_Brochure.
pdf%3fnodeid%3d585359%26vernum%3d-2
References
G Cotter, A Schachner, L Sasson, H Dekel and Y Moshkovitz. Impedance cardiography

revisited (comparison to Thoracic Impedance). Physiological Measurement. 2006;27:817-
827.
Wagner JY, Grond J, Fortin J, et a. Continuous noninvasive cardiac output determination

using the CNAP system: evaluation of a cardiac output algorithm for the analysis of
volume clamp method-derived pulse contour. J Clin Monit Comput. 2016 Aug;30(4):487-
93.
Wagner JY, Sarwari H, Schön G: Radial artery applanation tonometry for continuous
noninvasive cardiac output measurement: a comparison with intermittent pulmonary
artery thermodilution in patients after cardiothoracic surgery. Crit Care Med 2015; 43:
1423-1428.
Mercado P, Maizel J, Beyls C, Titeca-Beauport D, Joris M, Kontar L, Riviere A, Bonef

O, Soupison T, Tribouilloy C, de Cagny B, Slama M. Transthoracic echocardiography: an
accurate and precise method for estimating cardiac ouput in the critically ill patient. Crit
Care. 2017 Jun 9;21(1):136.
Sageman WS, Amundson DE. Thoracic electrical bioimpedance measurement of cardiac

output in postaortocoronary bypass patients. Crit Care Med. 1993 Aug;21(8):1139-42.
PART II - 2.2.3
De Backer D, Ospina-Tascon G, Salgado D, et al. Monitoring the microcirculation in the

critically ill patient: Current methods and future approaches. Intensive Care Med 2010;
36:1813-1825
Ince C, Boerma EC, Cecconi M, De Backer D, Shapiro NL, Duranteau J, et al. Second
consensus on the assessment of sublingual microcirculation in critically ill patients:
results from a task force of the European Society of Intensive Care Medicine. Intensive
Care Med 2018; 44(3):281-299
Mesquida J, Espinal C, Gruartmoner G. Skeletal muscle oxygen saturation (StO2)

measured by near-infrared spectroscopy in the critically ill patients. Biomed Res Int 2013;
2013:502194
References
Ince C. Hemodynamic coherence and the rationale for monitoring the microcirculation.
Crit Care 2015, 19:S8
PART II - 2.3.1
Echocardiography and lung ultrasonography for the assessment and management of

acute heart failure. Price S, Platz E, Cullen L et al., Nature Reviews Cardiology 2017;
14:427-440 Haemodynamic monitoring using echo in the critically ill, de Backer et al
How I do it: lung ultrasound. Gargani L, Volpicelli G. Cardiovasc Ultrasound 2014 Jul 4;
12:25
PART II - 2.3.2
Harjola VP et al. Contemporary management of acute right ventricular failure: a

statement from the Heart Failure Association and the Working Group on Pulmonary
Circulation and Right Ventricular Function of the European Society of Cardiology. Eur J
Heart Fail. 2016 Mar;18(3):226-41. doi: 10.1002/ejhf.478.
Konstam MA et al. American Heart Association Council on Clinical Cardiology;

Council on Cardiovascular Disease in the Young; and Council on Cardiovascular
Surgery and Anesthesia. Evaluation and Management of Right-Sided Heart Failure:
A Scientific Statement From the American Heart Association. Circulation. 2018 May
15;137(20):e578-e622. doi: 10.1161/CIR.0000000000000560.
Rudski LG et al. Guidelines for the echocardiographic assessment of the right heart
in adults: a report from the American Society of Echocardiography endorsed by the
European Association of Echocardiography, a registered branch of the European Society
of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr
2010;23:685–713. doi: 10.1016/j.echo.2010.05.010.
References
PART II - 2.3.3
Pivetta E, Goffi A, Nazerian P, Castagno D, Tozzetti C, Tizzani P, Tizzani M, Porrino G,

Ferreri E, Busso V, Morello F, Paglieri C, Masoero M, Cassine E, Bovaro F, Grifoni S, Maule
MM, Lupia E, Study Group on Lung Ultrasound from the M and Careggi H. Lung ultrasound
integrated with clinical assessment for the diagnosis of acute decompensated heart
failure in the emergency department: a randomized controlled trial. Eur J Heart Fail.
2019;21:754-766.
Rivas-Lasarte M, Alvarez-Garcia J, Fernandez-Martinez J, Maestro A, Lopez-Lopez L,

Sole-Gonzalez E, Pirla MJ, Mesado N, Mirabet S, Fluvia P, Brossa V, Sionis A, Roig E and
Cinca J. Lung ultrasound-guided treatment in ambulatory patients with heart failure: a
randomized controlled clinical trial (LUS-HF study). Eur J Heart Fail. 2019.[Epub ahead of
print]
Platz E, Lewis EF, Uno H, Peck J, Pivetta E, Merz AA, Hempel D, Wilson C, Frasure SE,
Jhund PS, Cheng S and Solomon SD. Detection and prognostic value of pulmonary
congestion by lung ultrasound in ambulatory heart failure patients. Eur Heart J.
2016;37:1244-51.
Platz E, Campbell RT, Claggett B, Lewis EF, Groarke JD, Docherty KF, Lee MMY, Merz
AA, Silverman M, Swamy V, Lindner M, Rivero J, Solomon SD and McMurray JJV. Lung
Ultrasound in Acute Heart Failure: Prevalence of Pulmonary Congestion and Short- and
Long-Term Outcomes. JACC Heart Fail. 2019;7:849-858.
PART II - 2.3.4
Parulekar P, Neil-Gallacher E, Harrison A. Intensive care unit physician-delivered point of

care renal tract ultrasound in acute kidney injury is feasible. Journal of the Intensive Care
Society. 2018;19(4):313-318. doi:10.1177/1751143718762685
Qian Z, Yang M, Li L, et al. Ultrasound assessment of diaphragmatic dysfunction as a

predictor of weaning outcome from mechanical ventilation: a systematic review and meta-
analysis. BMJ Open 2018;8:e021189. doi: 10.1136/bmjopen-2017-021189.
References
Gao, T., Cheng, MH., Xi, FC. et al. Predictive value of transabdominal intestinal sonography
in critically ill patients: a prospective observational study. Crit Care 23, 378 (2019).
https://doi.org/10.1186/s13054-019-2645-9.
Volpicelli G, Elbarbary M, Blaivas M, Lichtenstein DA, Mathis G, Kirkpatrick AW, Melniker

L, Gargani L, Noble VE, Via G, Dean A, Tsung JW, Soldati G, Copetti R, Bouhemad B,
Reissig A, Agricola E, Rouby JJ, Arbelot C, Liteplo A, Sargsyan A, Silva F, Hoppmann R,
Breitkreutz R, Seibel A, Neri L, Storti E, Petrovic T; International Liaison Committee on
Lung Ultrasound (ILC-LUS) for International Consensus Conference on Lung Ultrasound
(ICC-LUS). International evidence-based recommendations for point-of-care lung
ultrasound. Intensive Care Med. 2012 Apr;38(4):577-91. doi: 10.1007/s00134-012-2513-4.
Epub 2012 Mar 6. PMID: 22392031.
Robba C, Poole D, Citerio G, Taccone FS, Rasulo FA; Consensus on brain ultrasonography
in critical care group. Brain Ultrasonography Consensus on Skill Recommendations and
Competence Levels Within the Critical Care Setting. Neurocrit Care. 2020 Apr;32(2):502-
511. doi: 10.1007/s12028-019-00766-9. PMID: 31264072.
PART II - 3
Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and

hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine.
Intensive Care Med. 2014;40:1795-815.
Boyd JH, Forbes J, Nakada TA, et al. Fluid resuscitation in septic shock: a positive fluid
balance and elevated central venous pressure are associated with increased mortality.
Critical Care Med. 2011;39:259-65.
Rosenberg AL, Dechert RE, Park PK, et al. Review of a large clinical series: association
of cumulative fluid balance on outcome in acute lung injury: a retrospective review of the
ARDSnet tidal volume study cohort. J Intensive Care Med. 2009;24:35-46.
Kelm DJ, Perrin JT, Cartin-Ceba R, et al. Fluid overload in patients with severe sepsis and
septic shock treated with early goal-directed therapy is associated with increased acute
need for fluid-related medical interventions and hospital death. Shock. 2015;43:68-73.
References
Payen D, de Pont AC, Sakr Y, et al. A positive fluid balance is associated with a worse
outcome in patients with acute renal failure. Crit Care. 2008;12:R74.
Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of
the evidence. Chest. 2002;121:2000-8.
Cecconi M, Hofer C, Teboul JL, et al. Fluid challenges in intensive care: the FENICE study:
A global inception cohort study. Intensive Care Med. 2015;41:1529-37.
Marik PE, Cavallazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived
variables and fluid responsiveness in mechanically ventilated patients: A systematic
review of the literature. Crit Care Med. 2009;37:2642-7.
Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International

Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;
43:304-77.
Varpula M, Tallgren M, Saukkonen K, et al. Hemodynamic variables related to outcome in

septic shock. Intensive Care Med. 2005;31:1066-71.
Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of
the evidence. Chest. 2002;121:2000-8.
Vieillard-Baron A, Evrard B, Repessé X, et al. Limited value of end-expiratory inferior

vena cava diameter to predict fluid responsiveness impact of intra-abdominal pressure.
Cecconi M, Parsons AK, Rhodes A. What is a fluid challenge? Curr Opin Crit Care.
2011;17:290-5.
Konrad FM, Mik EG, Bodmer SI, et al. Acute normovolemic hemodilution in the pig is
associated with renal tissue edema, impaired renal microvascular oxygenation, and
functional loss. Anesthesiology. 2013;119:256-69.
Muller L, Toumi M, Bousquet PJ, et al. An increase in aortic blood flow after an infusion
of 100 ml colloid over 1 minute can predict fluid responsiveness: the mini-fluid challenge
study. Anesthesiology. 2011;115:541-7.
References
Messina A, Dell’Anna A, Baggiani M, et al. Functional hemodynamic tests: A systematic

review and a metanalysis on the reliability of the end-expiratory occlusion test and of the
mini-fluid challenge in predicting fluid responsiveness. Crit Care. 2019;23:264.
Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in
the critically ill. Crit Care Med. 2006;34:1402-7.
Monnet X, Marik P, Teboul JL. Passive leg raising for predicting fluid responsiveness: a
systematic review and meta-analysis. Intensive Care Med. 2016;42:1935-47.
Monnet X, Teboul JL. Passive leg raising: five rules, not a drop of fluid! Crit Care. 2015;19:
18.
Jabot J, Teboul JL, Richard C, et al. Passive leg raising for predicting fluid responsiveness:
importance of the postural change. Intensive Care Med. 2009;35:85-90.
Beurton A, Teboul JL, Girotto V, et al. Intra-Abdominal Hypertension Is Responsible for

False Negatives to the Passive Leg Raising Test. Crit Care Med. 2019;47:e639-47.
Chacko CJ, Wise MP, Frost PJ. Passive leg raising and compression stockings: a note of
caution. Crit Care. 2015;19:237.
Michard F, Teboul JL. Using heart-lung interactions to assess fluid responsiveness during
mechanical ventilation. Crit Care. 2000;4:282-9.
Jozwiak M, Monnet X, Teboul JL. Prediction of fluid responsiveness in ventilated patients.

Ann Transl Med. 2018;6:352.
Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial

pulse pressure and fluid responsiveness in septic patients with acute circulatory failure.
Am J Respir Crit Care Med. 2000;162:134-8.
Monnet X, Dres M, Ferre A, et al. Prediction of fluid responsiveness by a continuous non-

invasive assessment of arterial pressure in critically ill patients: comparison with four
other dynamic indices. Br J Anaesth. 2012;109:330-8.
References
Monnet X, Rienzo M, Osman D, et al. Esophageal Doppler monitoring predicts fluid

responsiveness in critically ill ventilated patients. Intensive Care Med. 2005;31:1195-201.
Sandroni C, Cavallaro F, Marano C, et al. Accuracy of plethysmographic indices as

predictors of fluid responsiveness in mechanically ventilated adults: a systematic review
and meta-analysis. Intensive Care Med. 2012;38:1429-37.
Yang X, Du B. Does pulse pressure variation predict fluid responsiveness in critically ill
patients? A systematic review and meta-analysis. Crit Care. 2014;18:650.
Michard F, Chemla D, Teboul JL. Applicability of pulse pressure variation: how many
shades of grey? Crit Care. 2015;19:144.
Myatra SN, Prabu NR, Divatia JV, et al. The Changes in Pulse Pressure Variation or Stroke
Volume Variation After a «Tidal Volume Challenge» Reliably Predict Fluid Responsiveness
During Low Tidal Volume Ventilation. Crit Care Med. 2017;45:415-21.
Messina A, Montagnini C, Cammarota G, et al. Tidal volume challenge to predict fluid

responsiveness in the operating room: An observational study. Eur J Anaesthesiol.
2019;36:583-91.
Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter
are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care
Med. 2004;30:1740-6.
Charron C, Caille V, Jardin F, et al. Echocardiographic measurement of fluid

responsiveness. Curr Opin Crit Care. 2006;12:249-54.
Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge

of volume status in ventilated septic patients. Intensive Care Med. 2004;30:1734-9.
Das SK, Choupoo NS, Pradhan D, et al. Diagnostic accuracy of inferior vena caval
respiratory variation in detecting fluid unresponsiveness: A systematic review and meta-
analysis. Eur J Anaesthesiol. 2018;35:831-9.
References
Vignon P, Repesse X, Begot E, et al. Comparison of Echocardiographic Indices Used

to Predict Fluid Responsiveness in Ventilated Patients. Am J Respir Crit Care Med.
2017;195:1022-32.
Muller L, Bobbia X, Toumi M, et al. Respiratory variations of inferior vena cava diameter to
predict fluid responsiveness in spontaneously breathing patients with acute circulatory
failure: need for a cautious use. Crit Care. 2016;16:R188.
Via G, Tavazzi G, Price S. Ten situations where inferior vena cava ultrasound may fail to
accurately predict fluid responsiveness: a physiologically based point of view. Intensive
Care Med. 2016;42:1164-7.
Monnet X, Osman D, Ridel C, et al. Predicting volume responsiveness by using the end-
expiratory occlusion in mechanically ventilated intensive care unit patients. Crit Care Med.
2009;37:951-6.
Gavelli F, Teboul JL, Monnet X. The end-expiratory occlusion test: please, let me hold your
breath! Crit Care. 2019;23:274.
Gavelli F, Shi R, Teboul JL, Azzolina D, Monnet X. The end-expiratory occlusion test for
detecting preload responsiveness: a systematic review and meta-analysis. Ann Intensive
Care. 2020;10:65.
Jozwiak M, Mercado P, Teboul J-L, et al. What is the lowest change in cardiac output that
transthoracic echocardiography can detect? Crit Care. 2019;23:116.
Jozwiak M, Depret F, Teboul JL, et al. Predicting Fluid Responsiveness in Critically

Ill Patients by Using Combined End-Expiratory and End-Inspiratory Occlusions With
Echocardiography. Crit Care Med. 2017;45:e1131-8.
Depret F, Jozwiak M, Teboul JL, et al. Esophageal Doppler Can Predict Fluid
Responsiveness Through End-Expiratory and End-Inspiratory Occlusion Tests. Crit Care
Med. 2019;47:e96-102.
Ali A, Aygun E, Abdullah T, et al. A challenge with 5 cmH2O of positive end-expiratory

pressure predicts fluid responsiveness in neurosurgery patients with protective
ventilation: an observational study. Minerva anestesiologica. 2019. [Epub ahead of print].
References
Wilkman E, Kuitunen A, Pettila V, et al. Fluid responsiveness predicted by elevation of

PEEP in patients with septic shock. Acta Anaesthesiologica Scandinavica. 2014;58:27-35.
Biais M, Lanchon R, Sesay M, et al. Changes in Stroke Volume Induced by Lung

Recruitment Maneuver Predict Fluid Responsiveness in Mechanically Ventilated Patients
in the Operating Room. Anesthesiology. 2017;126:260-7.
Messina A, Colombo D, Barra FL, et al. Sigh maneuver to enhance assessment of fluid
responsiveness during pressure support ventilation. Crit Care. 2019;23:31.
Monnet X, Marik PE, Teboul JL. Prediction of fluid responsiveness: an update. Ann
Intensive Care. 2016;6:111.
Sanghvi VR, Khaja F, Mark AL, et al. Effects of blood volume expansion on left ventricular
hemodynamics in man. Circulation. 1972;46:780-7.
Jozwiak M, Hamzaoui O, Monnet X, et al. Fluid resuscitation during early sepsis: a need for
individualization. Minerva Anestesiol. 2018;84:987-92.
Jozwiak M, Silva S, Persichini R, et al. Extravascular lung water is an independent

prognostic factor in patients with acute respiratory distress syndrome. Crit Care Med.
2013;41:472-80.
Upadya A, Tilluckdharry L, Muralidharan V, et al. Fluid balance and weaning outcomes.

Malbrain M, Van Regenmortel N, Saugel B, et al., Principles of fluid management and

stewardship in septic shock: it is time to consider the four D’s and the four phases of fluid
therapy. Ann Intensive Care. 2018;8:66.
Schortgen F. Hypotension during intermittent hemodialysis: new insights into an old

problem. Intensive Care Med. 2003;29:1645-9.
Monnet X, Cipriani F, Camous L, et al.The passive leg raising test to guide fluid removal in
critically ill patients. Ann Intensive Care. 2016;6:46.
References
Liu J, Shen F, Teboul JL, et al., Cardiac dysfunction induced by weaning from mechanical
ventilation: incidence, risk factors, and effects of fluid removal. Crit Care. 2016;20:369.
Teboul JL. Weaning-induced cardiac dysfunction: where are we today? Intensive Care Med.
2014;40:1069-79.
Dres M, Teboul JL, Anguel N, et al. Passive leg raising performed before a spontaneous
breathing trial predicts weaning-induced cardiac dysfunction. Intensive Care Med.
2015;41:487-94.
PART III - 1
Vincent JL et al. Circulatory shock. New England Journal of Medicine. 2013: 1726-1734.
Mullens W et al. The use of diuretics in heart failure with congestion - a position statement
from the Heart Failure Association of the European Society of Cardiology. European
Journal of Heart Failure. 2019: 137-155.
Cecconi M et al. Consensus on circulatory shock and hemodynamic monitoring. Task force
of the European Society of Intensive Care Medicine. Intensive Care Medicine. 2014: 1795-
1815.
Ponikowski P et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and
chronic heart failure. European Journal of Heart Failure. 2016: 891-975.
PART III - 2.1
Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med 2005;
353:2788-2796
Masip J, Peacock WF, Price S, et al. Indications and practical approach to non-invasive
ventilation in acute heart failure. Eur Heart Journal 2018 39:17-25
References
Harjola VP, Parissis J, Brunner-La Rocca HP, et al. Comprehensive in-hospital monitoring
in acute heart failure: applications for clinical practice and future directions for research.
A statement from the Acute Heart Failure Committee of the Heart Failure Association
(HFA) of the European Society of Cardiology (ESC). Eur J Heart Fail 2018; 20:1081-1099
PART III - 2.2
Zeymer U, Bueno H, Granger CB, Hochman J, Huber K, Lettino M, Price S, Schiele F,

Tubaro M, Vranckx P, Zahger D and Thiele H. ACCA - Position paper for the diagnosis and
treatment of patients with acute myocardial infarction complicated by cardiogenic shock.
Eur Heart J Acute Cardiovasc Care. 2020;9:183-197.
Thiele H, Ohman EM, de Waha-Thiele S, Zeymer U and Desch S. Management of

cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J.
2019;40:2671-2683.
Van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic A, Menon
V, Ohman EM, Sweitzer NK, Thiele H, Washam JB and Cohen MG. Contemporary
management of cardiogenic shock - A scientific statement. Circulation.
2017;136:e232-e268.
Thiele H, Jobs A, Ouweneel DM, Henriques JPS, Seyfarth M, Desch S, Eitel I, Pöss J,
Fuernau G and de Waha S. Percutaneous short-term active mechanical support devices
in cardiogenic shock: a systematic review and collaborative meta-analysis of randomized
trials Eur Heart J. 2017;38:3523-3531.
PART III - 3
Lahm T, Douglas I, Archer S, et al. Assessment of right ventricular function in the research
setting: knowledge gaps and pathway forward. Am J respire Crit Care Med 2018, 198:
e15-e43
References
Harjola VP, Mebazaa A, Celutkiene J, et al. Contemporary management of acute right

ventricular failure: a statement from the heart failure association and the working group
on pulmonary circulation and right ventricular function of the European Society of
Cardiology. European Journal of Heart Failure 2016; 18: 226-41
Vieillard-Baron A, Naeije R, Haddad F, et al. Diagnostic workup, etiologies, and

management of acute right ventricle failure. A state-of-the-art paper. Intensive Care Med
2018; 44: 774-790
Mullens W, Abrahams Z, Francis G, et al. Importance of venous congestion for worsening

of renal function in advanced decompensated heart failure. J Am Coll Cardiol 2009; 53:
589-596
PART III - 4
Harjola VP, Parissis J, Brunner-La Rocca HP, et al. Comprehensive in-hospital monitoring
in acute heart failure: applications for clinical practice and future directions for research.
A statement from the Acute Heart Failure Committee of the Heart Failure Association
(HFA) of the European Society of Cardiology (ESC). Eur J Heart Fail. 2018;20(7):1081-1099.
Price S, Platz E, Cullen L, et al. Expert consensus document: Echocardiography and lung
ultrasonography for the assessment and management of acute heart failure. Nat Rev
Cardiol. 2017;14(7):427-440.
Chioncel, O., Parissis, J., Mebazaa, A.,et all . Epidemiology, Pathophysiology and
Contemporary Management of Cardiogenic Shock - A position statement from the Heart
Failure Association (HFA) of the European Society of Cardiology (ESC). Eur J Heart Fail
(2020),doi:10.1002/ejhf.1922
Watanabe N Acute mitral regurgitation Heart 2019;105:671-677.
Jones BM, Kapadia SR, Smedira NG, et al. Ventricular septal rupture complicating acute
myocardial infarction: a contemporary review. Eur Heart J. 2014;35(31):2060-2068.
References
PART III - 5
Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac
tamponade. Am J Cardiol. 1990 Dec 15;66(20):1487-91. PubMed PMID: 2251997.
Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003 Aug 14;349(7):684-90.
Review. PubMed PMID: 12917306.
Little WC, Freeman GL. Pericardial disease. Circulation. 2006 Mar28;113(12):1622-32.

Review. Erratum in: Circulation. 2007 Apr 17;115(15):e406. Dosage error in article text.
PubMed PMID: 16567581.
Saito Y, Donohue A, Attai S, Vahdat A, Brar R, Handapangoda I, Chandraratna PA. The

syndrome of cardiac tamponade with «small» pericardial effusion. Echocardiography.
2008 Mar;25(3):321-7. doi: 10.1111/j.1540-8175.2007.00567.x. Review. PubMed PMID:
18307446.
Hoit BD. Anatomy and Physiology of the Pericardium. Cardiol Clin. 2017 Nov;35(4):481-
490. doi: 10.1016/j.ccl.2017.07.002. Review. PubMed PMID: 29025540.
Appleton C, Gillam L, Koulogiannis K. Cardiac Tamponade. Cardiol Clin. 2017

Nov;35(4):525-537. doi: 10.1016/j.ccl.2017.07.006. Review. PubMed PMID: 29025544.
Gluer R, Murdoch D, Haqqani HM, Scalia GM, Walters DL. Pericardiocentesis – How to do
it. Heart Lung Circ. 2015 Jun;24(6):621-5. doi: 10.1016/j.hlc.2014.11.009. Epub 2014 Dec 12.
Review. PubMed PMID: 25637941.
Geske JB, Anavekar NS, Nishimura RA, Oh JK, Gersh BJ. Differentiation of Constriction
and Restriction: Complex Cardiovascular Hemodynamics. J Am Coll Cardiol. 2016 Nov
29;68(21):2329-2347.
PART III - 6
Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-34.

References
Cecconi M, De Backer D, Antonelli M, Beale RJ, Bakker J, Hofer C, et al. Consensus on

Circulatory Shock and Hemodynamic Monitoring. Task Force of the European Society of
Intensive Care Medicine. Intensive Care Med. 2014;40(12):1795-815.
Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving Sepsis
Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016.
Intensive Care Med. 2017;43(3):304-77.
PART III - 7
Shokoohi H, Boniface KS, Pourmand A, et al. Bedside Ultrasound Reduces Diagnostic

Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit
Care Med 2015; 43:2562.
Bentzer P, Griesdale DE, Boyd J, MacLean K, Sirounis D, Ayas NT. Will This
Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? JAMA.
2016 Sep 27;316(12):1298-309.
PART III - 8
Kirkpatrick AW1, Roberts DJ, Malbrain ML, et al. Intra-abdominal hypertension and the
abdominal compartment syndrome: updated consensus definitions and clinical practice
guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive
Care Med. 2013 Jul;39(7):1190-206
Malbrain ML, Marik PE, Witters I, et al. Fluid overload, de-resuscitation, and outcomes in
critically ill or injured patients: a systematic review with suggestions for clinical practice.
Anaesthesiol Intensive Ther. 2014 Nov-Dec;46(5):361-80
Amestoy É. Secondary intra-abdominal hypertension in shock after resuscitation. Thesis.

Universitat Autònoma de Barcelona. ISBN: 9788449072369. [Internet]. 2017. Available
from: http://hdl.handle.net/10803/405522
References
Lozada MJ, Goyal V, Levin D, Malbrain M, et al. Management of peripartum intra-abdominal

hypertension and abdominal compartment syndrome. First published: 09 May 2019.
https://doi.org/10.1111/aogs.13638
Regli A, Pelosi P, Malbrain. Ventilation in patients with intra-abdominal hypertension: what

every critical care physician needs to know. Ann Intensive Care. 2019 Apr 25;9(1):52
Depauw PRAM, Groen RJM, Van Loon J, Peul WC, Malbrain MLNG, De Waele JJ. The
significance of intra-abdominal pressure in neurosurgery and neurological diseases: a
narrative review and a conceptual proposal. Acta Neurochir (Wien). 2019 May;161(5):855-
864
Malbrain ML, Peeters Y, Wise R. The neglected role of abdominal compliance in organ-
organ interactions. Crit Care. 2016 Mar 16;20:67
Malbrain ML, Roberts DJ, Sugrue M, et al. The polycompartment syndrome: a concise
state-of-the-art review. Anaesthesiol Intensive Ther. 2014 Nov-Dec;46(5):433-50
Malbrain ML. Different techniques to measure intra-abdominal pressure (IAP): time for a
critical re-appraisal. Intensive Care Med. 2004 Mar;30(3):357-71
PART III - 9
Sharkey SW. Respiration, in “A Guide to Interpretation of Hemodynamic Data in the

Coronary Care Unit”/ by Sharkey SW. Lippincott Williams and Wilkins. 1st Ed. 1997
Alviar CL, Miller PE, McAreavey D, Katz JN, Lee B, Moriyama B, et al. Positive Pressure
Ventilation in the Cardiac Intensive Care Unit. J Am Coll Cardiol. 2018 Sep;72(13):1532–53.
PART III - 10
Noll G, Wenzel RR, Binggeli C, Corti C, Luscher TF. Role of sympathetic nervous system in
hypertension and effects of cardiovascular drugs. European heart journal. 1998;19 Suppl
F:F32-8.
References
Thiele H, Jobs A, Ouweneel DM, Henriques JPS, Seyfarth M, Desch S, et al. Percutaneous
short-term active mechanical support devices in cardiogenic shock: a systematic
review and collaborative meta-analysis of randomized trials. European heart journal.
2017;38(47):3523-31.
Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of Mechanical Circulatory Support.

Journal of the American College of Cardiology. 2015;66(23):2663-74.
Burkhoff D, Mirsky I, Suga H. Assessment of systolic and diastolic ventricular properties

via pressure-volume analysis: a guide for clinical, translational, and basic researchers.
American journal of physiology Heart and circulatory physiology. 2005;289(2):H501-12.
Katz AM. Influence of altered inotropy and lusitropy on ventricular pressure-volume loops.
Journal of the American College of Cardiology. 1988;11(2):438-45.
Doshi D, Burkhoff D. Cardiovascular Simulation of Heart Failure Pathophysiology and

Therapeutics. Journal of cardiac failure. 2016;22(4):303-11.
Woodard JC, Farrar DJ, Chow E, Santamore WP, Burkhoff D, Hill JD. Computer model of
ventricular interaction during left ventricular circulatory support. ASAIO transactions.
1989;35(3):439-41.
Rihal CS, Naidu SS, Givertz MM, Szeto WY, Burke JA, Kapur NK, et al. 2015 SCAI/ACC/
HFSA/STS Clinical Expert Consensus Statement on the Use of Percutaneous Mechanical
Circulatory Support Devices in Cardiovascular Care: Endorsed by the American
Heart Assocation, the Cardiological Society of India, and Sociedad Latino Americana
de Cardiologia Intervencion; Affirmation of Value by the Canadian Association of
Interventional Cardiology-Association Canadienne de Cardiologie d’intervention. Journal
of the American College of Cardiology. 2015;65(19):e7-e26.
Burkhoff D, Naidu SS. The science behind percutaneous hemodynamic support: a review
and comparison of support strategies. Catheterization and cardiovascular interventions :
official journal of the Society for Cardiac Angiography & Interventions. 2012;80(5):816-29.
Naidu SS. Novel percutaneous cardiac assist devices: the science of and indications for
hemodynamic support. Circulation. 2011;123(5):533-43.
References
Weil BR, Konecny F, Suzuki G, Iyer V, Canty JM, Jr. Comparative Hemodynamic Effects of
Contemporary Percutaneous Mechanical Circulatory Support Devices in a Porcine Model
of Acute Myocardial Infarction. JACC Cardiovascular interventions. 2016;9(22):2292-303.
Prasad A, Ghodsizad A, Brehm C, Kozak M, Korner M, El Banayosy A, et al. Refractory

Pulmonary Edema and Upper Body Hypoxemia During Veno-Arterial Extracorporeal
Membrane Oxygenation-A Case for Atrial Septostomy. Artificial organs. 2018;42(6):664-9.
Russo JJ, Aleksova N, Pitcher I, Couture E, Parlow S, Faraz M, et al. Left Ventricular
Unloading During Extracorporeal Membrane Oxygenation in Patients With Cardiogenic
Shock. Journal of the American College of Cardiology. 2019;73(6):654-62.
Kim WH, Hong TH, Byun JH, Kim JW, Kim SH, Moon SH, et al. Flow Rate Through Pigtail
Catheter Used for Left Heart Decompression in an Artificial Model of Extracorporeal
Membrane Oxygenation Circuit. ASAIO journal (American Society for Artificial Internal
Organs : 1992). 2017;63(3):346-50.
Mets B, Frumento RJ, Bennett-Guerrero E, Naka Y. Validation of continuous thermodilution

cardiac output in patients implanted with a left ventricular assist device. Journal of
cardiothoracic and vascular anesthesia. 2002;16(6):727-30.
Wiesenack C, Prasser C, Liebold A, Schmid FX. Assessment of left ventricular cardiac

output by arterial thermodilution technique via a left atrial catheter in a patient on a right
ventricular assist device. Perfusion. 2004;19(1):73-5.
Thiele RH, Bartels K, Gan TJ. Cardiac output monitoring: a contemporary assessment and
review. Critical care medicine. 2015;43(1):177-85.
Crowley J, Cronin B, Essandoh M, D’Alessandro D, Shelton K, Dalia AA. Transesophageal

Echocardiography for Impella Placement and Management. Journal of cardiothoracic and
vascular anesthesia. 2019;33(10):2663-8.
Fiedler AG, Dalia A, Axtell AL, Ortoleva J, Thomas SM, Roy N, et al. Impella Placement
Guided by Echocardiography Can Be Used as a Strategy to Unload the Left Ventricle
During Peripheral Venoarterial Extracorporeal Membrane Oxygenation. Journal of
References
Pappalardo F, Pieri M, Arnaez Corada B, Ajello S, Melisurgo G, De Bonis M, et al. Timing

and Strategy for Weaning From Venoarterial ECMO are Complex Issues. Journal of
Donker DW, Meuwese CL, Braithwaite SA, Broome M, van der Heijden JJ, Hermens JA, et
al. Echocardiography in extracorporeal life support: A key player in procedural guidance,
tailoring and monitoring. Perfusion. 2018;33(1_suppl):31-41.
Cardiac ultrasound and extracorporeal life support: the two go together. Journal of the
American Society of Echocardiography : official publication of the American Society of
Echocardiography. 2015;28(4):A18-9.
Platts DG, Sedgwick JF, Burstow DJ, Mullany DV, Fraser JF. The role of echocardiography
in the management of patients supported by extracorporeal membrane oxygenation.
Journal of the American Society of Echocardiography : official publication of the American
Society of Echocardiography. 2012;25(2):131-41.
Aissaoui N, Luyt CE, Leprince P, Trouillet JL, Leger P, Pavie A, et al. Predictors of
successful extracorporeal membrane oxygenation (ECMO) weaning after assistance for
refractory cardiogenic shock. Intensive care medicine. 2011;37(11):1738-45.
PART III - 11
Hassager C, Nagao K, Hildick-Smith D., Out-of-hospital cardiac arrest: in-hospital

intervention strategies., Lancet 2018; 391: 989-998
THE FUTURE
Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, et al. Consensus on

circulatory shock and hemodynamic monitoring. Task force of the European Society of
Intensive Care Medicine. Intensive care medicine 2014; 40: 1795-815
Messina A, Greco M, Cecconi M. What should I use next if clinical evaluation and
echocardiographic haemodynamic assessment is not enough? Current opinion in critical
care 2019; 25: 259-65
References
Singer M. Critical illness and flat batteries. Critical care 2017; 21: 309
Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving Sepsis
Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016.
Intensive Care Med 2017; 43: 304-77
Komorowski M, Celi LA, Badawi O, Gordon AC, Faisal AA. The Artificial Intelligence
Clinician learns optimal treatment strategies for sepsis in intensive care. Nat Med 2018;
24: 1716-20
Sanchez-Pinto LN, Luo Y, Churpek MM. Big Data and Data Science in Critical Care. Chest
2018; 154: 1239-48
Rajkomar A, Dean J, Kohane I. Machine Learning in Medicine. N Engl J Med 2019; 380:
1347-58
APPENDIX
Pinsky M, Teboul J, Vincent J (Eds). Hemodynamic monitoring (2019) Lessons from the
ICU. doi:10.1007/978-3-319-69269-2
Chacon-Lozsan F, Lebedeva E, Peinado-Acevedo J. Novel formula to measure

mean pulmonary artery pressure (2016) Cardiometry (9); 74-76. DOI:10.12710/
cardiometry.2016.9.7476
Cao, H., Eshelman, L., Nielsen, L., Gross, B., Saeed, M., & Frassica, J. Hemodynamic
Instability Prediction Through Continuous Multiparameter Monitoring in ICU (2010)
Journal of Healthcare Engineering, 1(4), 509–534. doi:10.1260/2040-2295.1.4.509
Varon, J., & Fromm,, R. E. (2014). Acute and Critical Care Formulas and Laboratory Values.
doi:10.1007/978-1-4614-7510-1
M Tubaro, P Vranckx, S Price, C Vrints. The ESC textbook of intensive and

acute cardiovascular care 2nd ed (2015). Oxford University press. DOI: 10.1093/
med/9780199687039.001.0001.
References
Lancellotti P, Zamorano J, Habib G, Badano L (Eds). The EACVI Textbook

of Echocardiography 2nd Ed (2016). Oxford University press. DOI: 10.1093/
med/9780198726012.001.0001
Liu, Y. C., Liu, J. H., Fang, Z. A., Shan, G. L., Xu, J., Qi, Z. W., … Yu, X. Z. (2012). Modified
shock index and mortality rate of emergency patients. World journal of emergency
medicine, 3(2), 114–117. doi:10.5847/wjem.j.1920-8642.2012.02.006
Peura JL, et al. Circulation. 2012;126:2648-2667. DOI: 10.1161/CIR.0b013e3182769a54
Baran DA, et al. This document was endorsed by the American College of Cardiology
(ACC), the American Heart Association (AHA), the Society of Critical Care Medicine
(SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheter Cardiovasc
Interv. 2019;94:29–37.
Argiriou M, et al. Right heart failure post left ventricular assist device implantation. J
Thorac Dis. 2014 Mar;6 Suppl 1:S52-9. doi: 10.3978/j.issn.2072-1439.2013.10.26.
Stainback RF, et al. J Am Soc Echocardiogr 2015;28:853-909.

http://dx.doi.org/10.1016/j.echo.2015.05.008
Silvia Moreira Ayub-Ferreira. Arq Bras Cardiol. 2018; 111(1):4-12. DOI: 10.5935/
abc.20180126
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Prof. Josep Masip

Prof. Josep Masip, MD, PhD, FESC

GENERAL APPROACH  P.2

PART I - OVERVIEW OF HAEMODYNAMIC MONITORING

2 - INDICATIONS FOR HAEMODYNAMIC MONITORING  P.15

PART II - TECHNIQUES FOR HAEMODYNAMIC MONITORING

2 - NON-INVASIVE HAEMODYNAMIC MONITORING P.41

3 - PRELOAD RESPONSIVENESS  P.125

PART III - SPECIFIC CLINICAL SCENARIOS

2 - ACUTE LEFT VENTRICULAR FAILURE  P.154

3 - RIGHT VENTRICULAR FAILURE  P.173

4 - ACUTE MITRAL REGURGITATION AND

5 - CARDIAC TAMPONADE AND CONSTRICTION  P.197

6 - SEPTIC SHOCK  P.204

7 - HYPOVOLEMIC SHOCK  P.218

8 - INTRA-ABDOMINAL HYPERTENSION  P.225

9 - HAEMODYNAMICS DURING MECHANICAL VENTILATION  P.235

10 - HAEMODYNAMICS DURING MECHANICAL CIRCULATORY SUPPORT  P.250

11 - CARDIAC ARREST AND POST-CARDIAC ARREST P.260

REFERENCES AND COPYRIGHT ACKNOWLEDGMENTS P.309

2 - INDICATIONS FOR HAEMODYNAMIC MONITORING  P.15

1 - CRUCIAL PARAMETERS AND

Prof. Michael R. Pinsky, MD, FCCP, MCCM

Prof. Marilyn Hravnak, RN, PhD, FAAN, MCCM

Haemodynamic monitoring comprises a broad array of monitoring devices and analyses.

Table 1 - List of various haemodynamic monitoring devices and

Monitor Invasive Intermittent

1.1 - Goals of haemodynamic monitoring

1.2 - Haemodynamic monitoring landscape

1.3 - Fused parameters and monitoring systems

As an aid to clinical decision making, haemodynamic monitoring is often used as a simple

Table 2 - Summary of dynamic parameters and methods for functional hae-

Method Variable Threshold Limitations

Table 3 - Fused parameter critical illness scoring systems

System Timing Outcome Source Intent

General illness scoring systems

In-hospital Worst values: bedside Group severity of

In-hospital Worst values: bedside Group severity of

In-hospital Bedside assessment Probability of

Organ dysfunction scores

In-hospital Bedside assessment Severity of organ

First Organ Bedside assessment Severity of organ

qSOFA As needed None Bedside assessment Identify risk of sepsis

Early warning scores

Sous-titre ligne 1 P.14

Variables Variable selection

34 Machine learning regression

20 Machine learning regression

16 Machine learning regression

Haemodynamic monitoring is a very large

4 Machine learning regression

Multiple Logistic regression

26 Machine learning regression

Prof. Jean-Louis Vincent, MD, PhD, FCCM, FCCP

2.1 - Indications for haemodynamic monitoring

2.1.1 - Preemptive monitoring

2.1.2 - Diagnostic monitoring

2.1.3 - Monitoring to guide management

2.2 - Different aspects of haemodynamic monitoring

GENERAL APPROACH P.2

2 - INDICATIONS FOR HAEMODYNAMIC MONITORING P.15

2 - NON-INVASIVE HAEMODYNAMIC MONITORING P.41

3 - PRELOAD RESPONSIVENESS P.125

2 - ACUTE LEFT VENTRICULAR FAILURE P.154

3 - RIGHT VENTRICULAR FAILURE P.173

4 - ACUTE MITRAL REGURGITATION AND

5 - CARDIAC TAMPONADE AND CONSTRICTION P.197

6 - SEPTIC SHOCK P.204

7 - HYPOVOLEMIC SHOCK P.218

8 - INTRA-ABDOMINAL HYPERTENSION P.225

9 - HAEMODYNAMICS DURING MECHANICAL VENTILATION P.235

10 - HAEMODYNAMICS DURING MECHANICAL CIRCULATORY SUPPORT P.250

11 - CARDIAC ARREST AND POST-CARDIAC ARREST P.260

REFERENCES AND COPYRIGHT ACKNOWLEDGMENTS P.309

2 - INDICATIONS FOR HAEMODYNAMIC MONITORING P.15

2 - NON-INVASIVE HAEMODYNAMIC MONITORING P.41

3 - PRELOAD RESPONSIVENESS P.125