Understanding Shock: Types, Causes, and Effects

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Questions and Answers

In the context of septic shock, which of the following best illustrates the progression from initial infection to multiple organ failure?

  • Microbial presence causes an increase in blood volume, leading to pulmonary edema and subsequent respiratory failure.
  • Microbial infection leads directly to cardiac tamponade, inhibiting heart function and causing immediate organ failure.
  • Microorganisms trigger an inflammatory response, causing vasodilation and endothelial injury, progressing to disseminated intravascular coagulation (DIC), metabolic dysfunction, and ultimately, multiple organ failure. (correct)
  • Infection results in vasoconstriction, reducing blood flow to vital organs and causing immediate tissue necrosis.

A patient presents with hypotension, tachycardia, and cool, clammy skin following a severe burn injury. Which of the following mechanisms contributes most significantly to the development of hypovolemic shock in this patient?

  • Vasoconstriction to shunt blood to vital organs.
  • Loss of intravascular fluid due to increased capillary permeability and evaporation from the burn wound. (correct)
  • Increased venous return due to peripheral vasodilation.
  • Increased myocardial contractility due to catecholamine release.

Which statement best captures the rationale for classifying pulmonary embolism (PE) as a potential cause of cardiogenic shock?

  • PE causes direct compression of the heart, restricting its ability to fill and eject blood effectively.
  • PE directly damages the myocardium, impairing its contractile function and reducing cardiac output.
  • PE obstructs the pulmonary arteries, increasing right ventricular afterload, leading to right ventricular failure and reduced left ventricular preload, ultimately causing systemic hypoperfusion. (correct)
  • PE induces systemic vasodilation, leading to reduced systemic vascular resistance and subsequent hypotension.

A patient in septic shock exhibits elevated cardiac output but persistent hypotension. Which of the following best explains this seemingly paradoxical finding?

<p>The elevated cardiac output is a compensatory mechanism to counteract the severely reduced systemic vascular resistance, but it is insufficient to maintain adequate blood pressure and tissue perfusion. (C)</p> Signup and view all the answers

In late-stage septic shock, disseminated intravascular coagulation (DIC) significantly contributes to which of the following pathophysiological processes?

<p>Microvascular thrombosis, leading to tissue ischemia and organ dysfunction. (A)</p> Signup and view all the answers

Which of the following best describes the role of endothelial activation and injury in the pathogenesis of septic shock?

<p>Endothelial activation increases vascular permeability, promotes vasodilation, and induces a pro-coagulant state, contributing to hypotension, edema, and microvascular thrombosis. (C)</p> Signup and view all the answers

A patient with adrenal insufficiency develops endocrine shock. Which of the following hormonal deficiencies primarily contributes to the patient's hypotension and poor stress response?

<p>Lack of cortisol, impairing vascular tone and stress response. (D)</p> Signup and view all the answers

How does anaphylactic shock differ mechanistically from septic shock in terms of initial triggers and primary mediators?

<p>Anaphylactic shock is triggered by allergens and mediated by IgE antibodies, causing mast cell degranulation, whereas septic shock is triggered by microbial infections and mediated by cytokines, leading to systemic inflammation. (B)</p> Signup and view all the answers

In the progressive stage of shock, what is the most significant consequence of the shift from aerobic to anaerobic metabolism at the cellular level?

<p>Accumulation of lactic acid, leading to metabolic acidosis and impaired cellular function. (D)</p> Signup and view all the answers

A patient with cirrhosis develops non-hemorrhagic hypovolemic shock. Which of the following mechanisms contributes most directly to this condition?

<p>Leakage of protein-rich fluid into the peritoneal cavity (ascites), leading to third-space fluid loss and reduced intravascular volume. (C)</p> Signup and view all the answers

Flashcards

Shock

Circulatory failure that impairs tissue perfusion and leads to cellular hypoxia.

Cardiogenic Shock

Low cardiac output due to heart conditions like myocardial infarction or embolism.

Hypovolemic Shock

Low blood volume typically due to fluid loss such as hemorrhage or burns.

Septic Shock

Systemic inflammatory response caused by overwhelming infection or similar inflammatory issues.

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Distributive Shock

Widespread vasodilation and blood pooling due to systemic inflammation or allergic reaction.

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Anaphylactic Shock

A severe, IgE-mediated hypersensitivity reaction causing cardiovascular collapse.

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Neurogenic Shock

Trauma disrupting autonomic pathways, leading to hypotension and bradycardia.

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Initial Stage of Shock

Compensatory mechanisms activated to maintain tissue perfusion.

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Non-Progressive Shock

Tissue hypoperfusion, potentially reversible with intervention.

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Progressive Stage of Shock

Irreversible cellular injury and death due to prolonged hypoperfusion.

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Study Notes

  • Shock is circulatory failure impairing tissue perfusion and leading to cellular hypoxia
  • Untreated shock can lead to multiple organ failure and death

Types of Shock

  • Cardiogenic shock is pump failure
    • Low cardiac output means tissues and organs receive insufficient oxygen and nutrients
    • Etiology includes myocardial infarction, ventricular rupture, arrhythmias, cardiac tamponade, pulmonary embolism
    • The body compensates by increasing the heart rate (tachycardia) and vascular resistance, but these mechanisms eventually fail
  • Hypovolemic shock is low blood volume
    • A loss of blood or fluid reduces preload
    • This leads to low stroke volume and decreased cardiac output
    • Compensatory mechanisms (vasoconstriction, tachycardia) attempt to maintain blood pressure
    • Etiology can be hemorrhagic (blood loss) or non-hemorrhagic (fluid loss)
  • Septic shock is infection-induced vasodilation and inflammation
    • Infection triggers a systemic inflammatory response (SIRS)
    • Vasodilation and endothelial dysfunction lead to leaky blood vessels, causing fluid loss into tissues
    • Widespread coagulation activation (DIC) results in microthrombi formation
    • Tissue hypoxia leads to multiple organ failure if untreated
    • Etiology can be overwhelming microbial infection, severe trauma or burns, or pancreatitis

Classifications of Shock

  • Distributive shock involves severe vasodilation and blood pooling, where blood vessels lose their tone
  • Septic shock is caused by infection-induced SIRS
    • High cardiac output with low vascular resistance leads to hypoperfusion
  • Anaphylactic shock is caused by severe IgE-mediated hypersensitivity reaction
    • Massive histamine release causes vasodilation, airway constriction, and fluid leakage, leading to cardiovascular collapse and respiratory distress
  • Neurogenic shock is caused by spinal cord injury or brain trauma, disrupting autonomic regulation
    • Loss of sympathetic tone leads to unopposed parasympathetic activity, causing severe hypotension and bradycardia
  • Endocrine shock is caused by endocrine failure
    • Adrenal insufficiency (lack of cortisol) leads to poor stress response
    • Myxedema coma (severe hypothyroidism) leads to low metabolism and vasodilation
  • Hypovolemic shock involves loss of circulating volume
    • Hemorrhagic hypovolemic shock is caused by blood loss
    • Reduced vascular volume leads to inadequate cardiac output
    • Non-hemorrhagic hypovolemic shock is caused by GI losses, renal losses, skin losses, or third-space losses
  • Cardiogenic shock involves intracardiac causes
    • Acute myocardial infarction causes cardiac muscle damage
    • Myocarditis causes inflammation of the heart muscle
    • Arrhythmias causes abnormal rhythms, reducing output
    • Valvular heart disease creates mechanical obstruction of blood flow
  • Obstructive shock involves extra cardiac causes
    • Pulmonary embolism causes a clot that blocks pulmonary circulation, increasing right heart strain
    • Tension pneumothorax causes a collapsed lung that compresses heart and vessels
    • Cardiac tamponade is fluid accumulation restricting heart movement

Pathogenesis of Septic Shock

  • Microorganisms trigger inflammatory cells, causing a cytokine storm
  • Endothelial activation and injury increase vascular permeability which causes fluid leaks out of vessels
  • Damaged endothelial tissue activates the coagulation cascade, resulting in DIC
  • Uncontrolled clotting leads to microvascular thrombosis, causing tissue ischemia and organ dysfunction
  • Cytokines and reactive oxygen species released by leukocytes damage the mitochondria.
    • Impaired oxidative phosphorylation leads to cells not being able to generate enough ATP, reflecting metabolic abnormalities
    • Mitochondrial dysfunction leads to cellular energy failure due to a shift toward anaerobic metabolism which produces lactic acid and causes metabolic acidosis
    • failure to generate ATP also causes sodium-potassium pump dysfunction, leading to cellular swelling and apoptosis
  • These combined effects lead to multiple organ dysfunction syndrome (MODS) that is the failure of lungs, kidneys, heart, and brain
  • Irreversible stage leads to death due to cardiogenic shock and end-organ failure

Stages of Shock

  • Initial stage: oxygen delivery slightly decreases, but compensatory mechanisms prevent major symptoms
    • Cells still rely on aerobic metabolism, but oxygen extraction increases to compensate
    • ATP production remains sufficient for function
    • Clinical signs are often subtle or absent, as vital organs still receive adequate perfusion
  • Non-progressive stage (compensated shock): the body detects low blood pressure or reduced perfusion and activates additional compensatory mechanisms
    • Activation of baroreceptors increases the heart rate and vasoconstriction
    • Baroreceptors stimulate the sympathetic nervous system, causing increased heart rate (tachycardia), which aims to raise blood pressure and increases myocardial contractility
    • RAAS activation: kidneys retain sodium and water to increase blood pressure
    • Low renal perfusion pressure stimulates the renin-angiotensin-aldosterone system (RAAS)
    • Hypothalamus detects hypovolemia, causing ADH (vasopressin) release from the posterior pituitary, which leads to an increase in water reabsorption in the kidneys and vasoconstriction
  • Progressive stage (decompensated shock): hypoxia worsens, leading to anaerobic metabolism and lactic acidosis, while vasodilation causes worsening hypotension
  • Irreversible stage: cellular death leads to multiple organ failure and death

Morphology of Shock (Tissue Changes Due to Hypoxia)

  • Microvascular thrombosis (clots in small vessels)
  • Fibrin thrombi in kidneys, leading to acute kidney injury
  • Adrenocortical lipid depletion, leading to adrenal gland dysfunction
  • Diffuse alveolar damage, leading to pulmonary dysfunction and acute respiratory distress syndrome (ARDS)

Clinical Features of Shock

  • Hypotension (low blood pressure): blood flow cannot sustain organ function
  • Weak, rapid pulse: compensation for low cardiac output
  • Cold, clammy, cyanotic skin: vasoconstriction to preserve vital organs
  • Cardiac, cerebral, and pulmonary dysfunction: altered mental status, shortness of breath
  • Worsening renal function: reduced urine output (oliguria)

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