Which of the following best defines shock?
A. A state of persistent hypotension
B. A reduction in circulating blood volume
C. Inadequate tissue perfusion leading to cellular hypoxia
D. Failure of the heart to pump blood
C. Inadequate tissue perfusion leading to cellular hypoxia
Rationale: Shock is fundamentally defined by inadequate tissue perfusion and oxygen delivery, not hypotension alone.
Which variable most directly determines oxygen delivery (DO₂) to tissues?
A. Systemic vascular resistance
B. Cardiac output and arterial oxygen content
C. Mean arterial pressure alone
D. Hemoglobin level alone
B. Cardiac output and arterial oxygen content
Rationale: DO₂ depends on cardiac output × arterial oxygen content, making both circulation and oxygen-carrying capacity essential.
Which metabolic change occurs earliest at the cellular level in shock?
A. Apoptosis
B. Anaerobic metabolism
C. Coagulation activation
D. Cytokine exhaustion
B. Anaerobic metabolism
Rationale: Reduced oxygen delivery causes an early shift to anaerobic metabolism, leading to lactate production.
The primary cause of lactic acidosis in shock is:
A. Renal failure
B. Hepatic dysfunction
C. Anaerobic glycolysis
D. Respiratory alkalosis
C. Anaerobic glycolysis
Which compensatory response is mediated by the sympathetic nervous system during early shock?
A. Bradycardia
B. Vasodilation
C. Tachycardia and vasoconstriction
D. Decreased catecholamine release
C. Tachycardia and vasoconstriction
Rationale: Sympathetic activation increases heart rate and peripheral vasoconstriction to maintain perfusion.
Which hormone system is activated to conserve sodium and water during shock?
Renin–angiotensin–aldosterone system
RAAS activation promotes vasoconstriction and fluid retention.
Which mechanism explains persistent tissue hypoxia despite normal blood pressure?
A. Reduced hemoglobin concentration
B. Microcirculatory dysfunction
C. Increased preload
D. Bradycardia
B. Microcirculatory dysfunction
Rationale: Shock involves microvascular failure, preventing effective oxygen extraction even when macrocirculation appears adequate.
Which ion pump failure is central to cellular injury in shock?
A. Ca²⁺ ATPase
B. Na⁺/K⁺ ATPase
C. H⁺ pump
D. Cl⁻ channel
B. Na⁺/K⁺ ATPase
Rationale: ATP depletion causes Na⁺/K⁺ pump failure, leading to cellular swelling and death.
Which inflammatory mediator is most responsible for vasodilation in septic shock?
A. Histamine
B. Nitric oxide
C. Thromboxane A₂
D. Endothelin
B. Nitric oxide
Rationale: Excess nitric oxide causes profound vasodilation and low SVR.
Which organ is most sensitive to hypoperfusion in early shock?
A. Liver
B. Brain
C. Skin
D. Kidneys
D. Kidneys
Rationale: The kidneys have high metabolic demand and limited tolerance to ischemia, making oliguria an early sign.
Which stage of shock is characterized by failure to respond to therapy?
A. Compensated
B. Decompensated
C. Progressive
D. Irreversible
D. Irreversible
Rationale: In irreversible shock, widespread cellular death prevents recovery.
Which feature best distinguishes distributive shock from other types?
A. Decreased preload
B. Increased SVR
C. Pathologic vasodilation
D. Myocardial failure
C. Pathologic vasodilation
Rationale: Distributive shock is marked by loss of vascular tone.
Which coagulation abnormality may occur in severe shock?
A. Hyperfibrinogenemia
B. Polycythemia
C. Disseminated intravascular coagulation
D. Thrombocytosis
C. Disseminated intravascular coagulation
Rationale: Inflammatory activation of coagulation may lead to DIC.
Which statement about shock is MOST accurate?
A. Hypotension is required for diagnosis
B. Shock is purely a cardiovascular disorder
C. Shock is a systemic disease involving inflammation
D. Shock always presents with cold skin
C. Shock is a systemic disease involving inflammation
Rationale: Shock is a systemic, immuno-inflammatory process, not merely circulatory failure.
Which factor primarily determines preload?
A. Arterial resistance
B. Venous return
C. Heart rate
D. Afterload
B. Venous return
Rationale: Preload reflects ventricular filling, which depends on venous return.
A trauma patient with massive hemorrhage develops tachycardia and cold clammy skin. Which shock type is present?
A. Septic
B. Cardiogenic
C. Hypovolemic
D. Neurogenic
C. Hypovolemic
Rationale: Blood loss causes reduced preload and CO → hypovolemic shock.
Warm, flushed skin with bounding pulses is MOST consistent with:
A. Hypovolemic shock
B. Early septic shock
C. Cardiogenic shock
D. Obstructive shock
B. Early septic shock
Rationale: Early septic shock presents with vasodilation and high CO.
A patient with acute myocardial infarction develops pulmonary edema and hypotension. Which mechanism explains the shock?
A. Vasodilation
B. Reduced preload
C. Pump failure
D. Cytokine storm
C. Pump failure
Rationale: Myocardial dysfunction leads to cardiogenic shock.
A hypotensive patient with bradycardia after a cervical spine injury is in which type of shock?
A. Septic
B. Cardiogenic
C. Neurogenic
D. Hypovolemic
Answer: C
Rationale: Loss of sympathetic tone causes hypotension with bradycardia.
Elevated jugular venous pressure with hypotension and muffled heart sounds suggests:
A. Massive pulmonary embolism
B. Cardiac tamponade
C. Hypovolemia
D. Septic shock
B. Cardiac tamponade
Rationale: Beck’s triad indicates obstructive shock due to tamponade.
Why may blood pressure be normal in early septic shock?
A. Increased SVR
B. Increased preload
C. Increased cardiac output
D. Reduced oxygen consumption
C. Increased cardiac output
Rationale: Early sepsis is a high-output, low-SVR state.
Which finding best indicates inadequate tissue perfusion despite normal blood pressure?
A. Normal urine output
B. Elevated serum lactate
C. Bounding pulses
D. Wide pulse pressure
B. Elevated serum lactate
Rationale: Elevated lactate reflects cellular hypoxia.
Which shock type is primarily associated with decreased SVR?
A. Hypovolemic
B. Cardiogenic
C. Septic
D. Obstructive
C. Septic
Rationale: Septic shock causes vasoplegia.
Which mechanism contributes MOST to ARDS in shock?
A. Alveolar hemorrhage
B. Endothelial injury and capillary leak
C. Bronchospasm
D. Atelectasis
B. Endothelial injury and capillary leak
Rationale: Inflammatory injury increases alveolar–capillary permeability.