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CHAPTER 20SHOCK
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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
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PATHOGENESIS OF SHOCK (CONT.)
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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.)
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.)
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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