Shock

Causes and
Management
• a state of cellular and tissue hypoxia

• This most commonly occurs when there is

circulatory failure manifested as hypotension
(ie, reduced tissue perfusion);

• however, it is crucial to recognize that a patient

in shock can present normotensive, or
hypotensive.

• Shock is initially reversible, but must be

recognized and treated immediately to prevent
progression to irreversible organ dysfunction
 Distributive

• Distributive shock is characterized by severe peripheral

vasodilatation (vasodilatory shock).

• Sepsis is the most common cause of distributive shock.

 Systemic inflammatory response syndrome (SIRS)

• a clinical syndrome that is characterized by an inflammatory response, usually

induced by a major body insult that can be infectious or noninfectious

• The majority of patients presenting to the ED or admitted to the hospital who have
SIRS are not in shock and will not develop shock during their admission; the
presence of SIRS, however, should increase a clinician’s vigilance for progression of
disease severity.
Examples of noninfectious conditions that can be
complicated by SIRS include the following:

●Pancreatitis
●Burns .
●Significant blunt trauma and crush injury .
●Amniotic fluid embolism .
●Air embolism .
●Fat embolism .
 Neurogenic shock

• severe traumatic brain injury

• spinal cord injury.
• Interruption of autonomic pathways, causing decreased vascular resistance and
altered vagal tone, is thought to be responsible for distributive shock in patients with
spinal cord injury.
 Anaphylactic shock

• Most commonly encountered in patients with

• severe immunoglobulin-E (Ig-E) mediated,
– allergic reactions to insect stings
– food
– drugs
• Direct release of mediators from mast cells and basophils produced by
various triggers (eg, contrast media).
 Endocrine shock
Addisonian crisis (adrenal failure due to mineralocorticoid deficiency)
• In states of mineralocorticoid deficiency, vasodilatation can occur due to altered
vascular tone and aldosterone-deficiency-mediated hypovolemia.

myxedema
• with myxedema; concurrent myocardial depression or pericardial effusions likely
contribute to hypotension and shock in this population.

thyrotoxicosis

can develop high-output cardiac failure and do not develop shock per se.

• However, with progression, these patients can develop left ventricular systolic
dysfunction and/or tachyarrhythmia, leading to hypotension.
 Cardiogenic shock
intracardiac causes of cardiac pump failure that result in reduced cardiac output (CO).
Cardiomyopathy

• Myocardial infarction involving greater than 40 percent of the left ventricular

myocardium.
• Myocardial infarction of any size if accompanied by severe extensive ischemia due to
multivessel coronary artery disease
• Severe right ventricular infarction
• Acute exacerbation of heart failure in patients with severe underlying dilated
cardiomyopathy
• Stunned myocardium following cardiac arrest
• Myocardial depression due to advanced septic or neurogenic shock, and myocarditis.
 Arrhythmia

• Both atrial and ventricular tachy-arrhythmias brady-arrhythmias may

induce hypotension, often contributing to states of shock.

• However, when CO is severely compromised by significant rhythm

disturbances (eg, sustained ventricular tachycardia, complete heart
block), patients can present with cardiogenic shock.
 Mechanical causes of cardiogenic shock

• Acute mitral incompetence

rupture of a papillary muscle or chordae tendineae
• Acute aortic incompetence
dissection of the ascending aorta

Critical aortic stenosis or mitral stenosis rarely present with cardiogenic shock, but often
contribute to hypotension and shock from other causes (eg, sepsis, hypovolemia).

• Rupture of the intraventricular septum

• Ruptured ventricular free wall aneurysm.
 Hypovolemic shock
• reduced intravascular volume (ie, reduced preload), which, in turn, reduces CO.

• Hypovolemic shock can be divided into two categories:

Hemorrhagic —
• Reduced intravascular volume from blood loss can result in shock
• Causes :
– blunt or penetrating trauma (includes multiple fractures without vessel injury) is
the most common,
– upper gastrointestinal bleeding. (eg, variceal hemorrhage, peptic ulcer)
– lower gastrointestinal bleeding. (eg, diverticular, arteriovenous malformation)
• Less common causes include
– intraoperative and postoperative bleeding.
– ruptured abdominal aortic aneurysm,
– hemorrhagic pancreatitis,
– tumors or abscess erosion into major vessels,
– postpartum hemorrhage,
– uterine or vaginal hemorrhage from other causes (eg, infection, tumors,
lacerations), spontaneous peritoneal hemorrhage from bleeding diathesis,
 Non-hemorrhagic

• ●Gastrointestinal losses (eg, diarrhea, vomiting, external drainage)

• ●Skin losses (eg, heat stroke, burns, severe dermatologic conditions
including Stevens-Johnson syndrome)
• ●Renal losses (eg, excessive drug-induced or osmotic diuresis, salt-
wasting nephropathies)
• ●Third space losses into the extravascular space or body cavities (eg,
postoperative and trauma, intestinal obstruction, crush injury,
pancreatitis, cirrhosis)
 Obstructive shock
• is mostly due to extracardiac causes of cardiac pump failure and often associated with poor right ventricular
output.

Pulmonary vascular

• Right ventricular failure from hemodynamically significant pulmonary embolism (PE) or severe pulmonary
hypertension (PH).

• In these cases, the right ventricle fails because it is unable to generate enough pressure to overcome the high
pulmonary vascular resistance associated with PE or PH.

• Acute right heart syndrome can, given ventricular interdependence, mimic left ventricular dysfunction
resulting in cardiogenic shock.

Mechanical causes:

• primary physiologic disturbance is reduced venous return to the right atrium or inadequate right ventricle
filling.
Mechanical causes of obstructive shock include the following:
●Tension pneumothorax
●Pericardial tamponade
 Combined
•
pancreatitis
 Distributive shock (due to the effects of
inflammatory and anti-inflammatory cascades on
vascular permeability and peripheral vasodilation);

 Hypovolemic component (due to decreased oral

intake, insensible losses, vomiting, diarrhea)
 Cardiogenic component (due to inflammation-
related myocardial depression).
●Patients with underlying cardiomyopathy

may present with hypovolemic shock (from over-diuresis)

and cardiogenic shock (from inadequate compensatory tachycardia
and/or stroke volume).

●Patients with severe traumatic injury

may have hemorrhagic shock from blood loss
as well as distributive shock from SIRS
less commonly, fat embolism.
 Stages of shock —

• The early stages of shock (pre-shock, shock) are more amenable to therapy and are more likely to be
reversible, compared with end-stage shock, which is associated with irreversible end-organ damage and death.

• ●Pre-shock
• . It is characterized by compensatory responses to diminished tissue perfusion
• compensatory tachycardia
• peripheral vasoconstriction
• Thus, tachycardia or mild to moderate hyperlactatemia, may be the only clinical signs of early shock

• ●Shock –
• During shock, the compensatory mechanisms become overwhelmed,
• signs and symptoms of organ dysfunction appear including symptomatic tachycardia, restlessness, diaphoresis,
metabolic acidosis, hypotension, oliguria, and cool, clammy skin.

• ●End-organ dysfunction – Progressive shock leads to irreversible organ damage

• multiorgan failure (MOF), and death.
• anuria and acute renal failure develop,
• acidemia further depresses CO,
• hypotension becomes severe and recalcitrant to therapy,
• hyperlactatemia often worsens
• restlessness evolves into coma.
• Death is common in this phase of shock.
 Initial approach

• Assess airway, breathing, circulation —

• The first priorities are to stabilize the airway and breathing with
oxygen and/or mechanical ventilation, when necessary

• Patients with respiratory distress and/or marked hemodynamic

instability are typically intubated.

• The exception is those with suspected tension pneumothorax,

where the prompt drainage of air from the pleural space may
quickly reverse shock and avoid intubation (mechanical ventilation
can worsen tension and precipitate cardiac arrest).
• Peripheral venous access (14 to 18 gauge catheters)
• immediately intravenous fluids to restore adequate tissue
perfusion.

• Intravenous fluids, should not be delayed for a detailed clinical

assessment, nor should clinicians be conservative in terms of fluid
resuscitation to patients with heart failure or kidney injury as a
rule.
 Central venous access

• whom peripheral access cannot be obtained,

• who need infusions of large volumes of fluids and/or blood
products or multiple intravenous infusions,
• who are expected to need prolonged infusions of vasopressors.
• Frequent blood draws for laboratory studies
• For hemodynamic monitoring (eg, central venous pressure).
• the administration of resuscitative fluids and medications,
including vasoactive medications, should not be delayed because
central venous access is not available.
• ●Clinicians should obtain

• A brief history and examination,

• bedside telemetry monitoring
• electrocardiography [ECG], to assess whether an immediate or
early lifesaving therapy is required.

• ●Patients with milder forms of shock/hypotension or critically ill

patients who have been stabilized should undergo a thorough
diagnostic evaluation while resuscitation continues.

• However, the evaluation remains time-sensitive.

Common conditions needing lifesaving
interventions
 Anaphylactic shock

• Hypotension
• Inspiratory stridor
• Oral and facial edema,
• History of recent exposure to common allergens eg, bee stings
• intramuscular epinephrine.
• The typical adult dose is 0.3 mg of 1:1000 epinephrine injected into the mid-
outer thigh and repeated every 5 to 15 minutes as needed .

• Other pharmacologic agents frequently administered following epinephrine

include antihistamines (eg, diphenhydramine 25 to 50 mg

• nebulized albuterol (2.5 mg in 3 mL of normal saline)

• methylprednisolone (1 to 2 mg/kg intravenously).

 Tension
pneumothorax
• Tachypnea,
• Unilateral pleuritic chest pain
• Diminished breath sounds,
• Distended neck veins,
• Tracheal deviation away from the affected side,
• Risk factors for tension pneumothorax (eg, trauma, recent procedure,
mechanical ventilation, underlying cystic lung disease).

• Patients strongly suspected to have a tension pneumothorax do not

require a chest radiograph

• Emergent tube thoracostomy

• Ultrasound guidance is preferable for both diagnosis and tube

placement.

• Radiographic confirmation of re-expansion should be performed after

drainage
 Pericardial tamponade

• Dyspnea,
• Tachycardia
• Hypotension,
• Elevated jugular venous pressure,
• Distant heart sounds.
• Pulsus paradoxus.
• Known risk factors (eg, trauma, bleeding diathesis, known pericardial
effusion, recent thoracic or pericardial procedure).

• Bedside echocardiography is preferred before pericardiocentesis.

• Ultrasonography also guides needle or catheter placement and

examines the response to drainage of fluid from the pericardial sac.
Hemodynamically significant hemorrhage

• ●Traumatic

• history of blunt or penetrating trauma benefit from rapid

multiorgan bedside ultrasonography to identify blood in the
abdomen.

• A positive study indicates the need for surgical exploration to

identify and control the source of hemorrhage .

• A negative study does not rule out intraabdominal hemorrhage,

and continued assessment should be pursued as clinically
indicated.
• ●Nontraumatic –

• Patients suspected of having a ruptured aorta

• hypotension, abdominal, chest or back pain, known history of aneurysm or
dissection
• contrast-enhanced computed tomography (CT).
• Transesophageal echocardiography (thoracic aorta)
• Abdominal ultrasound (abdominal aorta), to identify perioaortic hematoma or
aneurysmal disease.

• For patients with the manifestations of upper or lower gastrointestinal

hemorrhage (eg, hematemesis)

• endoscopic intervention, embolization, or surgery may be indicated

•
• This population typically requires large volumes of blood products,
and vasopressors are avoided.

• Adequate peripheral access (two 14 to 18 gauge IVs)

• A type and crossmatch, a complete blood count, and coagulation

studies should be obtained in all patients with suspected
hemorrhage.
 Life-threatening arrhythmias

• Patients with rhythm disturbances resulting in shock can be cardioverted

(tachyarrhythmias)
• receive atropine or undergo temporary pacemaker placement
(bradyarrhythmias) as part of the advanced cardiac life support protocol.

• Arrhythmias can be the primary cause or contribute to shock.

• secondary to the metabolic disturbances associated with shock (eg, hypokalemia,

acidosis)

• secondary to the underlying cause of shock (eg, sepsis ,pulmonary embolism,

myocardial infarction).

• Thus, their presence should prompt additional investigations (eg, serum

chemistries, arterial blood gas analysis, toxicology screen, bedside cardiac
ultrasound, and cultures in those with suspected infection).
 Septic shock

• fever.
• hypotension
• suspected septic source

• benefit from the early administration of intravenous antibiotics

• If the source is unknown and Pseudomonas is unlikely,

• we favor combining vancomycin with a third- or fourth-generation

cephalosporin (eg, ceftriaxone or cefotaxime, cefepime)

• or a beta-lactam/beta-lactamase inhibitor (eg,

piperacillin-tazobactam, or a carbapenem (eg, imipenem or
meropenem).
• If Pseudomonas is likely,
• vancomycin should be combined with two
antipseudomonal agents (eg, fluoroquinolone,
aminoglycoside, piperacillin-tazobactam, cefepime,
ceftazidime).

• A leukocytosis and, in particular, a bandemia, as well

as laboratory and imaging findings suggestive of a
source, all support the presence of sepsis as a cause
of shock.

• Blood and other appropriate body fluid cultures

should be obtained, preferably prior to the
administration of antibiotics,
• in addition to imaging when necessary to facilitate
timely source control.
 Cardiogenic shock from
myocardial infarction

• Patients who present with hypotension

associated with anterior crushing chest pain,
respiratory distress, and the ECG changes
consistent with ST elevation myocardial infarction
(STEMI) benefit from early intervention.
• Elevated troponin and pulmonary edema on
chest radiography are supportive of the
diagnosis.
• Interventions include the administration of
pharmacologic agents (eg, antiplatelet agents,
heparin), coronary revascularization procedures
(eg, balloon angioplasty), and/or an intraaortic
balloon pump.
Cardiogenic shock from acute aortic or mitral valve
insufficiency

• chest pain
• hypotension,
• new low-pitched early diastolic murmur consistent with aortic insufficiency

• should undergo POC ultrasonography or echocardiography prior to surgical

intervention.

• CT chest for aortic dissection, blood cultures and transesophageal

echocardiography for aortic root abscess.

• Patients with acute respiratory distress and new systolic murmur following an
acute (MI) should preferably undergo urgent echo to look for MR or VSR, which
also typically needs urgent surgical intervention.
Patients with descending thoracic
aortic dissection

• Hypertension
• Tearing chest or back pain.
• Associated with acute aortic insufficiency, pericardial
tamponade, or MI.
• Transesophageal echocardiography, or contrast-enhanced CT to
evaluate the ascending aorta and aortic valve
• Ascending aortic dissection is a cardiac surgical emergency and
immediate consultation with a cardiac surgeon should be
obtained.
 Hemodynamically significant
pulmonary embolism

• hypotension,
• acute dyspnea,
• hypoxemia
• may benefit from the administration of systemic thrombolytic therapy
• Normal chest radiography
• elevated D-dimer,
• troponin.
• Computed tomographic pulmonary angiography is the preferred diagnostic
modality in this population.
• Echocardiography (eg, right ventricle enlargement, thrombus) to justify the
administration of a thrombolytic agent.
Patients suspected of having an
adrenal crisis

• hypotension,
• volume depletion
• history of glucocorticoid deficiency or withdrawal
• should receive fluid resuscitation and dexamethasone 4 mg
intravenously.

Insect or animal bites —

Some insect and animal bites require antivenom to reverse shock
 Initial diagnostic evaluation

• Clinical bedside evaluation

• An initial efficient and targeted history
• Physical examination including electrocardiography should be
directed towards uncovering the type, severity, and cause of
shock.

• ●General assessment –

• The evaluation should include a thorough history

• Assessment of lips , tongue, neck veins, lungs, heart, and
abdomen, as well as skin and joints.
• Hypotension, oliguria, mental status changes, and cool, clammy skin are
sentinel clinical findings that should raise the suspicion of shock

• prompt immediate treatment with intravenous fluids and further evaluation with
laboratory studies and relevant imaging.

• ●Electrocardiogram –
• Arrhythmia
• ST segment changes consistent with ischemia, infarction, or pericarditis.
• A low-voltage ECG may be suggestive of a pericardial effusion.
• The classic signs of pulmonary embolism (S1, Q3, T3) or right ventricular strain
may also be evident.

• ●Assessment for the etiology –

A comprehensive assessment for the underlying etiology of shock should be
performed after stabilization.
 Laboratory tests to identify the cause of
shock and/or early organ failure

●Serum lactate
●A complete metabolic panel, including renal and liver function tests
●Cardiac enzymes and natriuretic peptides
●Complete blood count and differential
●Coagulation studies and D-dimer level
●Blood gas analysis
 Serum lactate level

• poor tissue perfusion

• increased production from anaerobic metabolism and/or decreased clearance by
the liver, kidneys, and skeletal muscle
• elevated lactate is a sensitive tool for the diagnosis of shock.
• it is not specific and can also be found in conditions including metformin toxicity,
diabetic ketoacidosis,

• Lactate has been best studied in patients with sepsis where elevated levels >2
mmol/L.

• in particular those >4 mmol/L are associated with increased mortality

independent of organ dysfunction or hypotension.

• In addition, lactate levels can be serially measured to follow the response to

therapies.
• ●Renal and liver function tests –

• Elevated blood urea nitrogen (BUN), creatinine, and transaminases

are usually due to shock-induced end-organ damage (eg, acute
kidney injury, shock liver)

• May also explain the etiology of shock (eg, renal abscess, acute
hepatitis, chronic cirrhosis).

• ●Cardiac enzymes and natriuretic peptides –

• Elevated troponin-I or -T levels,
• brain natriuretic peptide,
• N-terminal pro-brain natriuretic peptide may indicate cardiogenic
shock from ischemia but can also be due to demand ischemia or to
pulmonary embolism (PE).
 Complete blood count and differential

• ●A high hematocrit may suggest hemoconcentration from hypovolemia.

• Anemia in the setting of bleeding supports hemorrhagic shock.

• Concurrent thrombocytopenia may suggest an etiology for hemorrhage.

• An elevated eosinophil count may suggest an allergy to support anaphylaxis.

• Although a leukocytosis may suggest septic shock, it is not specific for the
diagnosis and may simply indicate a stress response.

• A low white blood cell count and especially a bandemia are more for sepsis in
the setting of undifferentiated shock.
 Coagulation studies and D-
dimer level
• Elevations in PT & INR as well as APTT may suggest a cause for
underlying hemorrhagic shock

• Elevated in patients with sepsis, systemic inflammatory response

syndrome due to nonspecific activation of the coagulation cascade, and
liver disease.

• Evidence of DIC (elevated fibrin split products and D-dimer level with
low fibrinogen level) can also be found in patients with severe shock.

• Elevated D-dimer levels are not specific for the diagnosis of PE but,
when normal, can significantly reduce the probability of PE.

• A normal D-dimer level also significantly reduces the likelihood of

aortic dissection
 Arterial blood gas analysis
(ABG)
pulse oximetry may be unreliable due to poor tissue perfusion.

• Hypoxemia can be due to

• obstructive shock from pulmonary embolism,
• cardiogenic shock from myocardial infarction,
• septic shock from pneumonia,
• acute respiratory distress syndrome (ARDS) resulting from shock.

• Compensatory hypocapnia can be seen in those with a metabolic acidosis.

• Hypercapnia may occur in patients with encephalopathy, brain injury, or
increased dead space ventilation in patients with severe ARDS.

• Metabolic acidosis may be due to hyperlactatemia, acute kidney injury, or toxin

ingestion.
• A toxicology screen may be useful in those suspected of having
shock from drug intoxication

• An amylase and lipase should be obtained in those with suspected

pancreatitis.

• Urinalysis and gram stain of material from sites of possible

infection (eg, blood, sputum, urine, wounds)

• A cortisol level or corticotrophin stimulation test may be helpful

in those suspected to have an adrenal crisis

• Thyroid function tests may identify those with suspected

myxedema coma.
 Imaging

• ●Chest radiography –
• Demonstrate a pneumonia, pneumothorax, pulmonary edema, or
widened mediastinum
• Complications of shock (eg, ARDS).
• Clear in hypovolemic shock or obstructive shock from PE.

• Free air under the diaphragm to suggest viscus perforation,

emergent surgical consultation and additional testing, (CT) of the
abdomen and pelvis if the patient is stable, or immediate
laparotomy if the patient is unstable.
• Point-of-care (POC) ultrasonography –
• focused cardiac ultrasound (FOCUS)
• focused assessment with sonography for trauma [FAST]
 First, limited views of the heart should be
performed to examine the following:
• •Pericardium –
• pericardial effusion ,chamber collapse may support tamponade as a cause
of shock .

•Left ventricle –
• A large left ventricle with reduced contractility may suggest primary pump failure
• Small cardiac chambers and a hyperdynamic LV may indicate distributive shock
from sepsis or hypovolemia
•
• •Right ventricle –
• Reduced right ventricle (RV) contractility may suggest RV myocardial infarction;
increased size of the RV (eg, >1:1 RV/LV ratio) may suggest a large pulmonary
embolism (PE)
• . A floating thrombus in the right atrium/ventricle or clot in transit also support
PE.

• •Inferior vena cava –

• A collapsing inferior vena cava (IVC) at the end of expiration suggests
hypovolemia from hemorrhagic or nonhemorrhagic causes.
• A dilated IVC may support cardiac tamponade or PE.
 Second, brief imaging of the chest and abdomen
should be performed to examine the following:

• •Lung and pleural space –

• Pulmonary edema as evidenced by the presence of B lines may
support primary pump failure or volume overload subsequent to
fluid resuscitation

• A pleural effusion may support empyema or hemothorax and

guide thoracentesis

• •Peritoneal cavity –
• Evidence of significant peritoneal fluid accumulation may suggest
a source of blood loss in trauma
• or a potential source of infection (ie, spontaneous bacterial
peritonitis in the patient with cirrhosis
 Third, brief imaging of the major arteries and veins
should be performed to examine the following:

• •Aorta –
• Transesophageal echocardiography
• ultrasonography may detect a thoracic or abdominal aneurysm or
an intimal flap consistent with dissection of the aorta.

• •Proximal lower extremity veins –

• Lack of compressibility of thigh veins may be indicative of deep
venous thrombosis, thereby raising the suspicion for PE.
 CT of
• the head (traumatic brain injury, stroke),
• Spine (spinal injury),
• Chest (pneumonia, pneumothorax, ruptured aneurysm,
dissection),
• Abdomen and pelvis (intestinal obstruction, perforation, abscess),
and pulmonary artery (pulmonary embolism)
 Pulmonary arterial catheterization (PAC)

• has never been shown to improve patient-centered outcomes, such that the
routine insertion of Swan-Ganz catheters has fallen out of favor

• However, when the diagnosis or the type of shock remains undetermined or

mixed, hemodynamic measurements obtained by PAC can be helpful

• Additional patients that may benefit from PAC are those with unknown volume
status despite adequate fluid resuscitation, those with severe cardiogenic shock
• can also be used to guide fluid resuscitation, titrate vasopressors

• The major hemodynamic indices measured on PAC are cardiac output (ie,
cardiac index), systemic vascular resistance, pulmonary artery occlusion
pressure (ie, pulmonary capillary wedge pressure), right atrial pressure, and
mixed venous oxyhemoglobin saturation (SvO2).

•
 Hemodynamic support

• intravenous fluids (IVFs),

• followed by vasopressors, should IVFs fail to restore adequate tissue perfusion;

• the exception is hypovolemic shock where more fluids is preferred.

• in general, we suggest maintaining the mean arterial pressure between 65 to 70 mmHg

• We prefer to administer IVFs in well-defined boluses (eg, 500 to 1000 mL) over discrete
time intervals (eg, over 15 to 30 minutes) that can be repeated until blood pressure and
tissue perfusion are acceptable, pulmonary edema or fluid fails to augment perfusion.

• The total volume infused is determined by the etiology of shock.

• As an example,

• patients with obstructive shock from pulmonary embolism usually require small
volumes of IVF (500 to 1000 mL),
• while those with RV infarction or sepsis often need 2 to 5 L,
• with hemorrhagic shock frequently require volumes >3 to 5 L (often inclusive of
blood products).

• The administration of diuretic therapy should be avoided in hypotensive patients

with pulmonary edema until the need for hemodynamic support has been
weaned.

• most patients are treated with crystalloids (eg, Ringer’s lactate or normal saline),

• those with hemorrhagic shock should be preferentially treated with blood

products.
• Vasopressors :

• Importantly, the use of vasopressors in patients with hemorrhagic

or hypovolemic shock may be harmful,

• vasopressors should only be used as an additional form of

hemodynamic support when resuscitation has failed to restore
adequate tissue perfusion

• Norepinephrine (Levophed; initial dosing 8 to 12 mcg/minute

intravenously)
• ●Inotropic agents – Dobutamine (initial dose 0.5 to 1 mcg/kg/minute
but frequently 2.5 mcg/kg/minute when cardiac decompensation is
severe) is the most commonly used inotropic agent in patients who
have cardiogenic shock.

• Dobutamine is often administered together with norepinephrine to

offset the fall in peripheral vascular resistance that occurs when low
doses of dobutamine are used.

• Vasopressor support should be titrated according to the response (ie,

indices of tissue perfusion including blood pressure, urine output,
mental status, and skin color) and limiting side effects (eg, tachycardia).
 Distributive shock

• ●General clinical manifestations –

• hypotension

• without the clinical and hemodynamic signs of reduced preload (eg, normal skin turgor, moist mucous membranes,
normal inferior vena cava [IVC] on imaging)

• or fluid overload (eg, no peripheral edema or distended neck veins, normal central venous pressure [CVP] [8 to 12
mmHg].

• A preserved or hyperdynamic left ventricle is typically observed on echocardiography.

• ●Etiologic manifestations –

• The clinical features that distinguish one cause of distributive shock from the other depend upon the etiology.

• As an example, patients may present with hypotension in association with

• Clinical manifestations of pneumonia (septic shock),
• Brain or spinal trauma (neurogenic shock),
• Anaphylaxis (anaphylactic shock), a history of toxin exposure (toxic shock),
• Steroid withdrawal (adrenal crisis)
• Hypothyroidism (myxedema coma).
 Cardiogenic shock

• ●General clinical manifestations –

• Hypotension

• in association with the clinical and radiologic manifestations of pulmonary edema

• (eg, diffuse lung crackles, distended neck veins),

• elevated CVP (>12 mmHg)
• large dilated ventricle(s) and poor left ventricle function, or valvular or septal abnormalities on echocardiography.

• ●Etiologic manifestations –

• Patients with cardiogenic shock from myocardial infarction (MI) may have crushing substernal chest pain, acute dyspnea with
elevated cardiac isoenzymes, and electrocardiographic (ECG) findings of MI.

• Cardiogenic shock from arrhythmias may be sudden in onset with palpitations or syncope and may be evident on telemetry or
ECG.

• A ruptured valve or septal defect may present with the manifestations of acute pulmonary edema and a new murmur in the
setting of a recent MI.

• Patients with myocarditis may present with pleuritic chest pain and a pericardial rub.
 Hypovolemic shock

• ●General clinical manifestations –

• reduced skin turgor,
• dry mucous membranes,
• a collapsible IVC on imaging,
• low CVP (<8 mmHg)

• ●Etiologic manifestations –

• a history of heat exposure,

• vomiting,
• diarrhea,
• hematemesis
 Obstructive shock
• ●General clinical manifestations –

• hypotension

• distended neck veins but usually without the clinical signs of fluid overload or reduced preload.

• The exceptions are patients with subacute cardiac tamponade who often have evidence of fluid overload on
examination.

• On bedside ultrasonography or echocardiography,

• an effusion with a small right and left ventricle and a dilated IVC may be seen in patients with pericardial tamponade
• ; a dilated right ventricle and small left ventricle may be seen in patients with PE

• ●Etiologic manifestations –

• Depending upon the cause of obstructive shock, patients may present with pleuritic chest pain and acute dyspnea
(from pulmonary embolism [PE]),

• chest pain, tracheal deviation, unilateral reduced breath sounds, and elevated plateau pressures on mechanical
ventilation (tension pneumothorax

• quiet heart sounds, pulsus paradoxus, and distended neck veins (cardiac tamponade).
 Combined

• Hypovolemia may induce or coexist with cardiogenic shock

(eg, low ejection fraction with dry mucous membranes and a
collapsible IVC).
• In such cases, following the response to empiric therapies targeted
at the suspected causes of shock may allow the clinician to
determine which form of shock is predominant.

• The combination of bradycardia, renal failure, AV nodal blockade,

shock, and hyperkalemia