PathoPhysiology Chapter 20

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CHAPTER 20
SHOCK

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PATHOGENESIS OF SHOCK
• Shock represents a diverse group of life-threatening
conditions
• Common factor among all types of shock is
hypoperfusion and impaired cellular oxygen
utilization
• Inadequate cellular oxygenation may result from:
• Decreased cardiac output
• Maldistribution of blood flow
• Reduced blood oxygen content

3. Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.
PATHOGENESIS OF SHOCK (CONT.)

4. Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.
PATHOGENESIS OF SHOCK (CONT.)
Impaired Tissue Oxygenation
• Results in cellular hypoxia, which causes:
• Anaerobic metabolism
• Free radical production
• Macrophage induction
• Failure of microcirculation to autoregulate blood
flow leads to activation of coagulation

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PATHOGENESIS OF SHOCK (CONT.)

6. Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.
PATHOGENESIS OF SHOCK (CONT.)
Compensatory Mechanisms and Stages
of Shock
• Compensatory stage: homeostatic mechanisms are
sufficient to maintain adequate tissue perfusion
despite a reduction in CO
• SNS activation attempts to maintain blood pressure
even though CO has fallen

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PATHOGENESIS OF SHOCK (CONT.)
Compensatory Mechanisms and Stages
of Shock
• Progressive stage of shock is marked by
hypotension and marked tissue hypoxia
• Lactate production increases with anaerobic metabolism
• Lack of ATP leads to cellular swelling, dysfunction, and
death
• Cellular and organ dysfunction result from oxygen-free
radicals, release of inflammatory cytokines, and activation
of the clotting cascade

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TYPES OF SHOCK

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TYPES OF SHOCK
Cardiogenic Shock
• Usually result of severe ventricular dysfunction
associated with MI
• Diagnostic features:
• Decreased CO
• Elevated left ventricular end-diastolic pressure
• S3 heart sounds
• Pulmonary edema

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TYPES OF SHOCK (CONT.)
Cardiogenic Shock
• Low CO = reduced oxygen delivery to tissues =
higher oxygen extraction = low SvO2
• Therapy aimed at improving CO and myocardial
oxygen delivery, decreasing workload
• Inotropic, preload reducing, and afterload
reducing agents
• Intraaortic balloon counterpulsation, ventricular
assist devices, heart transplantation

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CARDIOGENIC SHOCK

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TYPES OF SHOCK
Obstructive Shock
• Results from mechanical obstructions that prevent
effective cardiac filling and stroke volume
• Common causes include pulmonary embolism,
cardiac tamponade, and tension pneumothorax
• Rapid management of underlying obstruction is
required to prevent cardiovascular collapse

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TYPES OF SHOCK (CONT.)
Hypovolemic Shock
• Results from inadequate circulation blood volume
precipitated by hemorrhage, burns, dehydration, or
leakage of fluid into interstitial spaces
• Low CO and intracardiac pressures lead to SNS
activation = elevated HR, vasoconstriction,
increased contractility

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TYPES OF SHOCK (CONT.)

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TYPES OF SHOCK (CONT.)
Hypovolemic Shock
• Severity of symptoms correlates with amount of
blood loss
• Therapy is aimed at fluid replacement and control
of the source of volume loss
• Colloids, crystalloids, and blood products used for
fluid replacement

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TYPES OF SHOCK (CONT.)

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TYPES OF SHOCK (CONT.)
Distributive Shock
• Characterized by excessive vasodilation and
peripheral pooling of blood
• CO inadequate due to reduced preload
• Types include:
• Anaphylactic shock
• Neurogenic shock
• Septic shock

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TYPES OF SHOCK (CONT.)
Anaphylactic Shock
• Result of excessive mast cell degranulation
mediated by IgE antibodies in response to antigen
• Mast cells release vasodilatory mediators resulting in
severe hypotension

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TYPES OF SHOCK (CONT.)
Anaphylactic Shock
• Clinical symptoms include:
• Urticaria
• Bronchoconstriction
• Stridor
• Wheezing
• Itching
• Treatment includes maintenance of airway
patency, use of epinephrine, antihistamines,
vasopressors, and fluids

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TYPES OF SHOCK (CONT.)
Neurogenic Shock
• Results from loss of sympathetic activation of
arteriolar smooth muscle
• Causes include medullary depression (brain injury,
drug overdose) or lesions of sympathetic nerve
fibers (spinal cord injury)
• Treatment includes vasopressors, fluids

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TYPES OF SHOCK (CONT.)
Septic Shock
• Results from severe systemic inflammatory response
to infection
• Common causes include gram-negative and gram-
positive bacteria, fungal infections
• Gram-negative shock: endotoxins in bacterial cell
walls stimulation massive immune system activation

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TYPES OF SHOCK (CONT.)
Septic Shock
• Characterized by release of immune mediators
resulting in widespread inflammation
• Clotting cascade, complement system, and kinin
system are activated
• Widespread inflammation leads to profound
peripheral vasodilation with hypotension,
maldistribution of blood flow with cellular hypoxia,
and increased capillary permeability with edema
formation

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TYPES OF SHOCK (CONT.)

24. Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.
TYPES OF SHOCK (CONT.)
Septic Shock
• Initially characterized by high CO due to
sympathetic activation of the heart
• Even though CO is high, cellular hypoxia is present
• Reduced cellular oxygen utilization is manifested as
high SvO2

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TYPES OF SHOCK (CONT.)
Septic Shock
• Therapy aimed at improving the distribution of
blood flow and managing infection with antibiotics
• Administration of fluids and drugs to improve
cardiac and vascular performance to improve
distribution of blood flow

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ASSESSMENT AND
HEMODYNAMIC MONITORING
• Helpful for assessing CO, volume status and
oxygen delivery and consumption
• Right atrial pressure, pulmonary artery
pressure, and left atrial pressure monitored
• Used to guide management of cardiac
preload, afterload, and contractility to
optimize CO and minimize workload

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ASSESSMENT AND
HEMODYNAMIC MONITORING
(CONT.)
Cardiac Output
• Preload—amount of blood in the ventricle at the
end of diastole
• Afterload—aortic impedance that the left ventricle
must overcome to eject blood during systole
• Contractility—inherent state of activation of
cardiac muscle fibers

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ASSESSMENT AND
HEMODYNAMIC MONITORING
(CONT.)
Arterial Oxygen Content
• Oxygen delivery (DO2)
• Oxygen consumption (VO2)
• Normally 25% of oxygen in arterial blood is
extracted from tissues, so mixed venous oxygen
saturation is 75%
• Low CO results in greater oxygen extraction and
lower SVO2
• Maldistribution of flow results in less oxygen
extraction and higher SVO2

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ASSESSMENT AND
HEMODYNAMIC MONITORING
(CONT.)
Hemodynamic Monitoring
• Pulmonary artery catheter inserted via jugular or
subclavian vein allows measurement of
intracardiac pressures, CO, and SVO2
• Right atrial pressure used to manage blood volume
(right preload)
• Pulmonary pressure used to detect pulmonary
complications
• Pulmonary artery diastolic pressure reflects left
preload
• Pulmonary capillary occlusion pressure is a direct
measure of left atrial pressure

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COMPLICATIONS OF SHOCK
• Shock states result in reduced or inadequate
cellular oxygen consumption and may affect all
organs and systems of the body
• Complications are inflammatory in nature
• Inflammation triggered by hypoxic injury to cells,
by antigen or endotoxin
• Excessive immune response leads to leaking
capillaries, damage from proteolytic enzymes,
and systemic activation of the clotting,
complement, and kinin systems

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COMPLICATIONS OF SHOCK (CONT.)
Acute Respiratory Distress Syndrome
(ARDS)
• Most commonly associated with septic shock
• Development of refractory hypoxemia, decreased
pulmonary compliance, and radiographic
evidence of pulmonary edema
• Neutrophils release proteolytic enzymes, produce
oxygen-free radicals, and secrete inflammatory
chemicals that make pulmonary capillaries leaky

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COMPLICATIONS OF SHOCK (CONT.)
Disseminated Intravascular Coagulopathy
(DIC)
• Immune activation of the clotting cascade
• Microcirculation obstructions lead to ischemic tissue
damage
• Widespread clot formation consumes platelets and
clotting factors
• Platelet count and fibrinogen levels are low, fibrin
degradation products (D-dimer) are elevated

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COMPLICATIONS OF SHOCK (CONT.)
Acute Renal Failure (ARF)
• Kidneys undergo long periods of hypoperfusion
• Vasoconstriction causes decreased glomerular
blood flow—reduced hydrostatic pressure and
filtration rates
• Acute tubular necrosis (ATN) associated with
decreased urinary excretion of waste products
(creatinine and urea)

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COMPLICATIONS OF SHOCK (CONT.)
Multiple Organ Dysfunction Syndrome
(MODS)
• Most common causes: sepsis and septic shock
• Initiated by immune mechanisms that are
overactive and destructive
• Cytokines affect endothelium, recruit neutrophils,
and activate inflammation in vascular beds leading
to tissue destruction and organ dysfunction