Shock

Objective
• Define the etiology , pathophysiology ,
diagnosis of shock
• Identify the three main categories of
shock with their pathophysiology and
clinical manifestations.
• identify goal of therapy .
• Discuss the pharmacotheraputic
approaches in treatment of shock.
 Introduction
• Shock is a medical emergency requiring
prompt recognition and treatment because it
can quickly lead to serious pathophysiologic
consequence including death.
• It Is heterogeneous group of syndromes that
cause an acute, generalized form of circulatory
failure associated with inadequate oxygen
utilization by the cells.
• It is characterized as a systolic blood pressure of
<90 mmhg or acute reduction of at least 40
mmhg from baseline.
• MAP < 70 mmhg ,tachycardia and organ
perfusion abnormality.
 Etiology
• Circulatory shock develops when the CVS is
unable to deliver un adequate oxygen supply
to meet tissue oxygen demands, resulting in
cellular dysfunction.
• Dysoxia leads to a shift in cellular metabolism
to anaerobic pathways and results in elivated
blood lactate concentrations.
• Physiologically, tissue metabolic requirements
are met both adequate
- mean atrial pressure
- adequate oxygen delivery (DO2)
 Etiology
• The mean atrial pressure is the driving pressure for
peripheral blood flow and end organ perfusion.
• Tissue blood flow cant be directly measured:-
• therefore , map is used a surrogate estimate
because component of bp are cardiac output
and (SVR) – systemic vascular resistance and co is
the determinant of do2 i.e. bp is integrally related
to Do2.
• Low bp is commonly present in patients with
shock. But it is not required to define shock
because compensatory mechanisms such as
vasoconstriction may preserve blood pressure
while tissue perfusion is inadequate.
 Etiology
• Shock can be classified into four
 - hypovolemic
 - cardiogenic
 both are encountered in 16 % of all cases
 - obstructive
 about 2% of cases
 - distributive / vasodilatory
 Most common , in about 4% of all cases.
• Patient may have component of more than
one shock syndrome or presentation. They
may transit from one shock to another.
 Pathophysiology
• Each shock syndrome has a different etiology and
resultant pathophysiology. However, since all shock
syndromes lead to inadequate tissue perfusion and
cellular dysoxia, they have the same effect on cellular
metabolism.
• Shock results in failure of the circulatory system to deliver
sufficient oxygen (O2) to body tissues.
• As the syndrome evolves, compensatory mechanisms
will be activated and overwhelmed.
• This compensatory mechanisms encompass:
 Increase in sympathetic outflow,
 Activation of the renin-angiotensin system, and
 Activation of humoral factors that stimulate peripheral
vasoconstriction.
 Pathophysiology
• COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
 SNS - Neurohormonal response
Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (SVR-Afterload)
Increased Preload
 Pathophysiology
 SNS - Hormonal: Renin-angiotensin
system
Decrease renal perfusion
Releases renin angiotensin I
angiotensin II potent vasoconstriction
releases aldosterone adrenal cortex
sodium & water retention
 Pathophysiology
 SNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus
stimulated
 ADH released by Posterior pituitary
gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water
 Pathophysiology
 SNS - Hormonal: Adrenal Cortex
Anterior pituitary releases
• adrenocorticotropic hormone (ACTH)
Stimulates adrenal Cx to release
• glucocorticoids
Blood sugar increases to meet
increased
• metabolic needs
 Pathophysiology
• Failure of Compensatory Response
 Decreased blood flow to the tissues
causes cellular hypoxia
 Anaerobic metabolism begins
Cell swelling, mitochondrial disruption,
and eventual cell death
If Low Perfusion States persists:
IRREVERSIBLE - DEATH
Pathophysiology
 Diagnosis
• The diagnosis of shock is based on the finding of
impaired tissue perfusion on examination.3 These
findings may include the following:
• Systolic blood pressure (SBP) less than 90 mm Hg,
or a greater than 40 mm Hg decrease from
baseline in a hypertensive patient, or a mean
arterial pressure (MAP) less than 65 mm Hg
• Tachycardia (heart rate [HR] >90 beats/minute)
• Tachypnea (respiratory rate [RR] >20
breaths/minute)
• Cutaneous vasoconstriction: cold, clammy,
mottled skin
 Diagnosis
• (although not typical of distributive shock)
• Mental confusion (agitation, stupor, or coma)
• Oliguria: urine output less than 20 mL/hour
• Elevated blood lactate level leading to
metabolic acidosis
• Decreased venous oxygen saturation (mixed
[Svo2], central [Scvo2]) (reflects increased V˙
o2 or impaired oxygen supply)
• Not all these described findings are
encountered in every patient with shock, and
considerable variability exists in both the
rapidity and sequence of onset.
 Stages of shock
 Initial stage - tissues are under perfused, decreased CO,
• increased anaerobic metabolism, building of lactic acid
 Compensatory stage - it is Reversible. SNS activated by
low CO, attempting to compensate for the decrease
tissue perfusion.
 Progressive stage - Failing compensatory mechanisms:
• profound vasoconstriction from the SNS ISCHEMIA
• Lactic acid production is high - metabolic acidosis
 Irreversible or refractory stage - Cellular necrosis and
Multiple Organ Dysfunction Syndrome may occur.
• DEATH
 Types of shock
 Three types of shock are recognized:
1.Hypovolemic
• It is a consequence of preload due to
intravascular volume loss.
2.Cardiogenic
• It is a consequence of cardiac pump failure.
3.Distributive
• It is a consequence of severely decreased
SVR & is characterized by an overt loss of
vascular tone, causing acute tissue hypo
perfusion.
 Hypovolemic shock
• Hypovolemic shock is extracellular
volume depletion that may result from
blood loss (plasma and red blood
cells) due to trauma, surgery, or
internal hemorrhage or from plasma
loss due to fluid sequestered within the
body or lost from the body.
 Etiology
 Major Hypovolemic Shock Etiologies
I. Hemorrhagic
• Trauma
• GI bleeding
• Abdominal aortic aneurysm
II. Non hemorrhagic (dehydration)
• Vomiting
• Diarrhea
• Third spacing
• Burns
• Fistulae
 Pathophysiology
• Decreased intravascular volume
Decreased venous return (Preload, RAP)
Decreased
ventricular filling (Preload, PAWP)
Decreased stroke volume (HR, Preload,
& Afterload) Decreased CO
(Compensatory mechanisms)
Inadequate tissue perfusion
 Clinical presentation
Patients will be in acute distress, although
symptoms and signs will vary depending on the
severity of the hypovolemic and
• whether the etiology is hemorrhagic versus no
hemorrhagic.
• Hypotension (SBP <90 mmHg) [or >40 mmHg
decrease from baseline in a hypertensive patient]
• Tachycardia (HR >90 bpm)
• Tachypnea (RR >20 bpm)
• Oliguria (urine output <20 mL/hour)
• Depressed cardiac index (CI < 2.2 L/min/m2)
• Change in mental status
• Metabolic acidosis
 Clinical presentation
• Symptoms
• Thirst
• Weakness
• Light-headedness
• Scanty urine output and dark-yellow-
colored urine.
 Cardiogenic shock
• Cardiogenic shock is inadequate
cardiac output from an intracardiac
cause leading to tissue hypo perfusion. In
about 80% of cases cardiogenic shock is
caused by acute myocardial infarction
leading to left ventricular dysfunction.
• It is the most severe form of heart failure
and it is distinguished from chronic heart
failure by the presence of
- hypotension ,hypo perfusion and the
need for different therapeutic interventions.
 Etiology
Mechanical - complications of MI:
– Papillary Muscle Rupture
– Ventricular aneurysm
– Ventricular septal rupture
Other causes:
– Cardiomyopathies
– tamponade
– tension pneumothorax
– arrhythmias
– valve disease
 Pathophysiology
 Impaired pumping ability of LV leads to…
• Decreased stroke volume Decreased
CO
Decreased BP Compensatory
mechanism which may lead to Decreased
tissue perfusion.
• Inadequate systolic emptying Increase in
Left ventricular filling pressures (preload)
Increase in Left atrial pressures Increase in
Pulmonary capillary pressure Pulmonary
interstitial & intraalveolar edema.
 Clinical presentation
 Mean arterial pressure below 70 mmHg
 Abnormal heart sounds
• Murmurs
• Pathologic S3 (ventricular gallop)
• Pathologic S4 (atrial gallop)
 Pericardial tamponade
– muffled heart tones, elevated neck veins
 Tension pneumothorax
• JVD, tracheal deviation, decreased or
absent unilateral breath sounds, and
chest hyper resonance on affected side
 Clinical presentation
• Syndrome of inadequate tissue perfusion
associated with normal circulating BV,
and low cardiac output
 Symptoms: dyspnea, poor exercise
tolerance,
• confusion, sweating, PND
 Signs: tachycardia, cold skin, high JVP,
added
• heart sounds, engorged liver, peripheral
edema.
 Distributive shock
• Inadequate perfusion of tissues
through maldistribution of blood flow.
• Intravascular volume is maldistributed
because of alterations in blood vessels.
• Cardiac pump & blood volume are
normal but blood is not reaching the
tissues.
 Etiology
• Septic Shock (Most Common) - Syndrome of profound
hypotension due to release of endotoxins / TNF /
vasoactive peptides following bacterial destruction
Usually associated with normal blood volume, high / low
CO, and low SVR

• Anaphylactic Shock - A type of distributive shock that

results from widespread systemic allergic reaction to an
antigen This hypersensitive reaction is LIFE THREATENING

• Neurogenic Shock - A type of distributive shock that

results from the loss or suppression of sympathetic tone
Causes massive vasodilatation in the venous vasculature,
decreased venous return to heart, decreased cardiac
output.
 Pathophysiology
• Septic Shock - Initiated by gram-
negative (most common) or gram
positive bacteria, fungi, or viruses
• Cell walls of organisms contain
Endotoxins
• Endotoxins release inflammatory
mediators
• Causes Vasodilation & increase capillary
permeability
• leads to Shock due to alteration in
peripheral circulation & massive dilation
 Pathophysiology
• Anaphylactic shock – Antigen exposure
of the
body stimulates production IgE
antibodies
specific to antigen.
• Antigens like drugs, bites, contrast, blood,
foods, vaccines
• re - Exposure to antigen
• IgE binds to mast cells and basophils
 Anaphylactic response
 Pathophysiology
• Neurogenic shock - Disruption of
sympathetic nervous system
• Loss of sympathetic tone
• Venous and arterial vasodilation
• Decreased venous return
• Decreased stroke volume
• Decreased cardiac output
• Decreased cellular oxygen supply
• Impaired tissue perfusion
• Impaired cellular metabolism
 Clinical manifestation
Early hyper Cutaneous - Hypothermia

Neurogenic
septic

Anaphylactic
dynamic manifestation - Hypotension
response - urticaria , - Bradycardia
- tachypnea angioedema
,pruritis - Flaccid paralysis
- decreased SVR below level of the
- massive Respiratory spinal lesion
vasodilation comproimise
- Warm dry skin
Late hypo - wheezing
- Decrease in
dynamic - respiratory cardiac output
response distress
vasoconstriction Circulatory
- significant collapse
tachycardia - Tachycardia
- increased SVR - Vasodilation
 Goal of Therapy
 Initial goals: To support O2 delivery through by
assuring:
• Effective intravascular plasma volume,
• Optimal O2-carrying capacity, and
• Adequate BP (maintaining MAP above 65 mm
Hg)
 Ultimate goals: To prevent further disease
progression with subsequent organ damage
there by reducing morbidity.
• If possible, to reverse organ dysfunction that
has already occurred.
 General Management
Approaches
• Initiate supplemental O2 at the earliest signs of
shock, beginning with 4 to 6 L/min via nasal
cannula or 6 to 10 L/min by face mask.
(Maintaining airway/ventilation)
• Adequate fluid resuscitation to maintain
circulating blood volume is essential in managing
all forms of shock.
• If fluid administration does not achieve desired
end points, pharmacologic support is necessary
with inotropic and vasoactive drugs.
• NB: Supportive care measures for: pain, anxiety,
delirium….
 Pharmacotherapy
1. fluid resuscitation
• The use of fluids is the cornerstone of managing
all forms of shock including hypovolemic shock.
• Three major therapeutic options are available to
clinicians for restoring circulating blood volume:
• Crystalloids (low Molecular wt electrolyte-based
solutions),
• Colloids (large molecular weight solutions), and
• Blood products
• Choice of fluid is based on O2- carrying capacity,
cause of shock, accompanying disease states,
degree of fluid loss, and required speed of fluid
delivery
Isotonic crystalloids are the first line liquid of choice for forms of circulatory
insufficiency that are associated with hemodynamic instability.
 Pharmacotherapy
• Crystalloids are generally advocated as the initial
choice of resuscitation fluid in hypovolemic shock
because of:
• Rapid and easy administration, good availability,
good compatibility with most drugs, low cost, and
equivalent outcomes compared with colloids.
• If volume resuscitation is suboptimal following
several litters of crystalloid, colloids should be
considered.
• Blood products are used only in instances
involving hemorrhage (or severe pre-existing
anemia): Ex:- in case of sustained blood losses
from hemorrhage > 1,500 mL.
 Pharmacotherapy
2. Inotropic agents and vasopressors –
• are generally not indicated in the initial treatment
of hypovolemic shock (assuming that fluid
therapy is adequate).
• These medications are needed in patients who
continue to have signs and symptoms of
inadequate tissue perfusion despite correction of
cause and optimal fluid.
• They are fast acting and are given as continuous
infusions and titrated rapidly to predetermined
effects.
• A rapid-acting inotropic agent (e.g., dopamine,
dobutamine, epinephrine) also can be used to
increase myocardial contractility and CO.
 Pharmacotherapy
 Norepinephrine
• It is a combined α- and β-agonist, but it
primarily produces vasoconstriction, thereby
increasing SVR.
• It produces either no change or a slight
decrease in CO.
• It is considered the first-line option for initial
vasopressor therapy of septic shock.
• It is less likely to cause tachydysrhythmias and
a decrease in splanchnic oxygen utilization.
• It is initiated at 0.05 to 0.1 mcg/kg/min and
rapidly titrated to pre-set goals of MAP.
 Pharmacotherapy
 Phenylephrine
• It is a pure α1-agonist and is thought to increase BP
through vasoconstriction.
• It may also increase contractility and CO.
• Useful alternative
• in pts who cannot tolerate the tachycardia with use of
dopamine or NE
• in pts with known underlying myocardial dysfunction
• in pts refractory to dopamine or NE (b/c of β-receptor
desensitization)
• It is initiated at a dosage of 0.5 mcg/kg/min and may be
titrated every 5 to 15 min to desired effects.
 Pharmacotherapy
 Dopamine
• It has inotropic, chronotropic, and vasoactive properties,
all of which are dose dependent. (High
dose….Vasoconstriction)
• Doses of 5 to 10 mcg/kg/min increase CI by improving
contractility and heart rate, primarily from its β1 effects.
• It increases MAP and SVR as a result of both increased
CO and, at higher doses (>10 mcg/kg/min), its α1
agonist effects.
• Clinical utility of dopamine is limited b/c large dosages
are frequently necessary to maintain CO and MAP & its
ADRs.
• NB: Infusion rate should be limited to less than 10 to 15
mcg/kg/min in patients with cardiac failure.
 Pharmacotherapy
 Dobutamine
• It is a potent positive inotropic agent with predominant
direct β1-agonist effects and weak β2- and α1-
adrenergic effects.
• It is an inotrope with vasodilatory properties
(“Inodilator”).
• It is used to increase the CI, typically by 25% to 50%.
• Produces a larger increase in CO and is less
arrhythmogenic than D.
• Unlike D, it lowers PCWP and SVR with increasing doses.
• Preferred in pts with depressed CO, increase PCWP &
SVR with mild hypotension.
• Starting dosages ranges from 2.5 to 5 mcg/kg/min.
 Pharmacotherapy
 Epinephrine
• Similar to D, it has dose-dependent hemodynamic
effects.
• At lower infusion ranges (0.01– 0.1 mcg/kg/min), it
stimulates β1, causing in increased HR and contractility.
• As the dose increases, more α1- stimulation occurs,
resulting in vasoconstriction and corresponding increases
in SVR.
• It should be reserved for patients with a markedly
depressed CO in conjunction with severe hypotension.
• Because it is associated with tachydysrhythmias and
lactate elevation, it is considered as last resort.
 Pharmacotherapy
 Vasopressin
• It produces rapid & sustained improvement in
hemodynamic parameters at dosages not
exceeding 0.04 units/min.
• It should be used only if response to one or two
adrenergic agents is inadequate or as a method
for reducing the dosage of these therapies.
• Doses above 0.04 units/min are associated with
negative changes in CO and mesenteric mucosal
perfusion.
• In order to minimize adverse events and maximize
beneficial effects, it should be used as add-on
therapy
 Pharmacotherapy
 Corticosteroids
• It can be initiated in cases of septic shock
when:-
• Adrenal insufficiency is suspected (e.g.,
patients receiving long-term corticosteroid
therapy for other indications prior to the onset
of shock),
• Vasopressor dosages are escalating, or
• Weaning of vasopressor therapy proves futile
• A daily dose equivalent to 200 to 300 mg
hydrocortisone should be continued for 7
days.
• After we treat the patient with the
previously listed medications ,the next
treatment will focus on treating the
cause of each type of shock by:-
Using percutaneous coronary
intervention (PCI)
Broad spectrum antibiotics
Anti histamine
Anti arrhythmia and so on..
 Evaluation of therapeutic
outcomes
 Successful treatment of shock is measured by the
restoration of BP to baseline values and reversal of
associated organ dysfunction.
 Vital signs, UO, mental status, Lab & PE has to be
monitored.
 Therapy goals include:
• Arterial SBP > 90 mm Hg (MAP > 60 mm Hg) within 1 hour
• PAOP to a goal pressure of 14 to 18 mm Hg & CVP to 8
to 15 mm Hg)
• Organ dysfunction reversal evident by increased UO to >
0.5 mL/kg/h (1.0 mL/kg/h in pediatrics), return of mental
status to baseline, and normalization of skin color and
temperature over the first 24 hours.
• Normalization of laboratory measurements is expected
within hours to days following fluid resuscitation.
Thank You
 Group 3
NAME
1. ABAY GEBRIE 0005/12

SUBMISSION DATE – 22 – 04 – 2015

SUBMITTED TO – MR TEKLEHAYMANOT
DESSIE , ETHIOPIA