PathoPhysiology Chapter 20

Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.

CHAPTER 20SHOCK


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


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





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



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


TYPES OF SHOCK


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


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


CARDIOGENIC SHOCK


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



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





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





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



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



Anaphylactic Shock • Clinical symptoms include:

• Urticaria• Bronchoconstriction• Stridor• Wheezing• Itching

• Treatment includes maintenance of airway patency, use of epinephrine, antihistamines, vasopressors, and fluids



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



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



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





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



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


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



(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



(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



(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


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


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



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



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)



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

Education

PathoPhysiology Chapter 20