NRMS 5190 — Pathophysiology Exam 4 SUNY Downstate Medical
Center Questions with Answers| Pass Guaranteed| Updated
1. A 68-year-old man presents after an acute MI with BP 78/50, HR 128, cool
clammy skin, and pulmonary crackles. Cardiac index is 1.6 L/min/m2 and PCWP
is 24 mmHg. Which type of shock best explains this presentation?
A. Hypovolemic shock
B. Cardiogenic shock
C. Distributive (septic) shock
D. Neurogenic shock
Answer: B
Rationale: Cardiogenic shock results from primary pump failure, producing low
cardiac index with high filling pressures (elevated PCWP) as blood backs up behind
the failing left ventricle, causing pulmonary edema. Compensatory sympathetic
activation causes tachycardia and vasoconstriction (cool, clammy skin).
Hypovolemic and septic/neurogenic shock present with low or normal filling
pressures, not elevated PCWP.
2. In early (compensated) shock, which neurohormonal response is primarily
responsible for maintaining blood pressure despite falling cardiac output?
A. Decreased renin-angiotensin-aldosterone activity
B. Baroreceptor-mediated sympathetic activation increasing heart rate and
systemic vascular resistance
C. Release of atrial natriuretic peptide causing vasodilation
D. Parasympathetic dominance slowing heart rate
Answer: B
Rationale: Falling blood pressure unloads arterial baroreceptors (carotid sinus,
aortic arch), reducing inhibitory signaling to the medulla and triggering a
sympathetic surge. This raises heart rate, contractility, and systemic vascular
resistance (via alpha-1 vasoconstriction) to preserve perfusion pressure to the
brain and heart. RAAS is activated, not suppressed, and ANP would worsen
hypotension.
,3. A patient in septic shock has warm extremities, bounding pulses, BP 82/40,
and a markedly widened pulse pressure despite tachycardia. What underlying
pathophysiologic mechanism explains this hemodynamic pattern?
A. Profound peripheral vasodilation from nitric-oxide-mediated loss of vascular
tone
B. Pure hypovolemia from third-spacing
C. Primary myocardial pump failure
D. Mechanical obstruction of venous return
Answer: A
Rationale: Early septic (distributive) shock is characterized by massive nitric oxide-
and cytokine-mediated vasodilation, causing warm skin, bounding pulses, and low
systemic vascular resistance with a wide pulse pressure, even though cardiac
output may initially be normal or increased. This differs from
cardiogenic/hypovolemic shock, which present with cool, vasoconstricted
extremities.
4. Which laboratory/hemodynamic finding best indicates progression from
compensated to decompensated (irreversible) shock?
A. Lactate 1.0 mmol/L with normal mentation
B. Rising serum lactate with persistent metabolic acidosis and multi-organ
dysfunction
C. Mild tachycardia with normal urine output
D. Transient orthostatic hypotension that resolves with fluids
Answer: B
Rationale: Decompensated shock is marked by a shift from aerobic to anaerobic
metabolism, producing rising lactate and worsening metabolic (lactic) acidosis,
along with evidence of end-organ hypoperfusion (oliguria, altered mentation,
rising creatinine/LFTs). Mild, reversible findings reflect compensated shock where
perfusion is still adequate to vital organs.
5. A trauma patient has lost approximately 35% of circulating blood volume.
Which class of hemorrhagic shock and expected clinical picture is most
consistent?
A. Class I: HR normal, BP normal
B. Class II: HR >100, BP normal, narrowed pulse pressure
, C. Class III: HR >120, BP decreased, confusion, decreased urine output
D. Class IV: HR <60, BP markedly elevated
Answer: C
Rationale: Class III hemorrhagic shock (30-40% blood volume loss) produces
marked tachycardia (>120), hypotension, decreased urine output, and altered
mental status as compensatory mechanisms begin to fail. Class IV (>40% loss) is
more severe with profound hypotension and tachycardia >140, not bradycardia.
6. Which combination of findings would best differentiate obstructive shock
(e.g., cardiac tamponade) from hypovolemic shock?
A. Jugular venous distention and muffled heart sounds with hypotension
B. Flat neck veins and dry mucous membranes
C. Bounding peripheral pulses and warm skin
D. Elevated hemoglobin and hematocrit
Answer: A
Rationale: Obstructive shock from tamponade impairs diastolic filling, producing
Beck's triad (hypotension, jugular venous distention, muffled heart sounds)
because venous return backs up against the compressed heart. Hypovolemic shock
instead shows flat neck veins from reduced intravascular volume, the opposite
venous pressure pattern.
7. A patient with a T4 spinal cord injury develops hypotension and bradycardia.
What is the primary pathophysiologic mechanism?
A. Excess catecholamine release causing vasoconstriction
B. Loss of sympathetic outflow below the lesion leading to unopposed
parasympathetic tone and vasodilation
C. Primary cardiac ischemia
D. Acute blood loss from the spinal injury
Answer: B
Rationale: Neurogenic shock results from disruption of descending sympathetic
pathways below a high spinal cord lesion, leaving parasympathetic (vagal) tone
unopposed. This causes bradycardia (rather than the tachycardia seen in other
shock states) and widespread vasodilation with hypotension due to loss of
vasomotor tone.
, 8. Which compensatory renal mechanism helps maintain intravascular volume
during early hypovolemic shock?
A. Increased glomerular filtration rate and diuresis
B. Renin release triggering angiotensin II vasoconstriction and aldosterone-
mediated sodium/water retention
C. Suppression of antidiuretic hormone
D. Increased natriuretic peptide release promoting sodium excretion
Answer: B
Rationale: Decreased renal perfusion pressure activates the renin-angiotensin-
aldosterone system. Angiotensin II causes systemic and efferent arteriolar
vasoconstriction to preserve GFR and raise BP, while aldosterone increases sodium
and water reabsorption; ADH release is also increased (not suppressed) to
conserve free water.
9. A patient in shock is receiving aggressive fluid resuscitation. Which finding
suggests fluid responsiveness has been exceeded and volume overload is
developing?
A. Improved urine output and warming extremities
B. New crackles, rising CVP/PCWP, and worsening oxygenation
C. Decreasing heart rate toward baseline
D. Rising blood pressure with stable respiratory status
Answer: B
Rationale: Once the heart operates on the flat portion of the Frank-Starling curve,
additional preload no longer improves stroke volume and instead raises filling
pressures, producing pulmonary congestion (crackles), rising CVP/PCWP, and
hypoxemia — signaling that fluid resuscitation should be reassessed rather than
continued.
10. Which statement about anaphylactic shock pathophysiology is most
accurate?
A. It is mediated by IgG-driven complement activation only
B. Mast cell/basophil degranulation releases histamine and mediators causing
vasodilation, increased capillary permeability, and bronchoconstriction
C. It primarily involves loss of sympathetic tone from spinal injury
D. It is characterized by primary pump failure with elevated filling pressures
Center Questions with Answers| Pass Guaranteed| Updated
1. A 68-year-old man presents after an acute MI with BP 78/50, HR 128, cool
clammy skin, and pulmonary crackles. Cardiac index is 1.6 L/min/m2 and PCWP
is 24 mmHg. Which type of shock best explains this presentation?
A. Hypovolemic shock
B. Cardiogenic shock
C. Distributive (septic) shock
D. Neurogenic shock
Answer: B
Rationale: Cardiogenic shock results from primary pump failure, producing low
cardiac index with high filling pressures (elevated PCWP) as blood backs up behind
the failing left ventricle, causing pulmonary edema. Compensatory sympathetic
activation causes tachycardia and vasoconstriction (cool, clammy skin).
Hypovolemic and septic/neurogenic shock present with low or normal filling
pressures, not elevated PCWP.
2. In early (compensated) shock, which neurohormonal response is primarily
responsible for maintaining blood pressure despite falling cardiac output?
A. Decreased renin-angiotensin-aldosterone activity
B. Baroreceptor-mediated sympathetic activation increasing heart rate and
systemic vascular resistance
C. Release of atrial natriuretic peptide causing vasodilation
D. Parasympathetic dominance slowing heart rate
Answer: B
Rationale: Falling blood pressure unloads arterial baroreceptors (carotid sinus,
aortic arch), reducing inhibitory signaling to the medulla and triggering a
sympathetic surge. This raises heart rate, contractility, and systemic vascular
resistance (via alpha-1 vasoconstriction) to preserve perfusion pressure to the
brain and heart. RAAS is activated, not suppressed, and ANP would worsen
hypotension.
,3. A patient in septic shock has warm extremities, bounding pulses, BP 82/40,
and a markedly widened pulse pressure despite tachycardia. What underlying
pathophysiologic mechanism explains this hemodynamic pattern?
A. Profound peripheral vasodilation from nitric-oxide-mediated loss of vascular
tone
B. Pure hypovolemia from third-spacing
C. Primary myocardial pump failure
D. Mechanical obstruction of venous return
Answer: A
Rationale: Early septic (distributive) shock is characterized by massive nitric oxide-
and cytokine-mediated vasodilation, causing warm skin, bounding pulses, and low
systemic vascular resistance with a wide pulse pressure, even though cardiac
output may initially be normal or increased. This differs from
cardiogenic/hypovolemic shock, which present with cool, vasoconstricted
extremities.
4. Which laboratory/hemodynamic finding best indicates progression from
compensated to decompensated (irreversible) shock?
A. Lactate 1.0 mmol/L with normal mentation
B. Rising serum lactate with persistent metabolic acidosis and multi-organ
dysfunction
C. Mild tachycardia with normal urine output
D. Transient orthostatic hypotension that resolves with fluids
Answer: B
Rationale: Decompensated shock is marked by a shift from aerobic to anaerobic
metabolism, producing rising lactate and worsening metabolic (lactic) acidosis,
along with evidence of end-organ hypoperfusion (oliguria, altered mentation,
rising creatinine/LFTs). Mild, reversible findings reflect compensated shock where
perfusion is still adequate to vital organs.
5. A trauma patient has lost approximately 35% of circulating blood volume.
Which class of hemorrhagic shock and expected clinical picture is most
consistent?
A. Class I: HR normal, BP normal
B. Class II: HR >100, BP normal, narrowed pulse pressure
, C. Class III: HR >120, BP decreased, confusion, decreased urine output
D. Class IV: HR <60, BP markedly elevated
Answer: C
Rationale: Class III hemorrhagic shock (30-40% blood volume loss) produces
marked tachycardia (>120), hypotension, decreased urine output, and altered
mental status as compensatory mechanisms begin to fail. Class IV (>40% loss) is
more severe with profound hypotension and tachycardia >140, not bradycardia.
6. Which combination of findings would best differentiate obstructive shock
(e.g., cardiac tamponade) from hypovolemic shock?
A. Jugular venous distention and muffled heart sounds with hypotension
B. Flat neck veins and dry mucous membranes
C. Bounding peripheral pulses and warm skin
D. Elevated hemoglobin and hematocrit
Answer: A
Rationale: Obstructive shock from tamponade impairs diastolic filling, producing
Beck's triad (hypotension, jugular venous distention, muffled heart sounds)
because venous return backs up against the compressed heart. Hypovolemic shock
instead shows flat neck veins from reduced intravascular volume, the opposite
venous pressure pattern.
7. A patient with a T4 spinal cord injury develops hypotension and bradycardia.
What is the primary pathophysiologic mechanism?
A. Excess catecholamine release causing vasoconstriction
B. Loss of sympathetic outflow below the lesion leading to unopposed
parasympathetic tone and vasodilation
C. Primary cardiac ischemia
D. Acute blood loss from the spinal injury
Answer: B
Rationale: Neurogenic shock results from disruption of descending sympathetic
pathways below a high spinal cord lesion, leaving parasympathetic (vagal) tone
unopposed. This causes bradycardia (rather than the tachycardia seen in other
shock states) and widespread vasodilation with hypotension due to loss of
vasomotor tone.
, 8. Which compensatory renal mechanism helps maintain intravascular volume
during early hypovolemic shock?
A. Increased glomerular filtration rate and diuresis
B. Renin release triggering angiotensin II vasoconstriction and aldosterone-
mediated sodium/water retention
C. Suppression of antidiuretic hormone
D. Increased natriuretic peptide release promoting sodium excretion
Answer: B
Rationale: Decreased renal perfusion pressure activates the renin-angiotensin-
aldosterone system. Angiotensin II causes systemic and efferent arteriolar
vasoconstriction to preserve GFR and raise BP, while aldosterone increases sodium
and water reabsorption; ADH release is also increased (not suppressed) to
conserve free water.
9. A patient in shock is receiving aggressive fluid resuscitation. Which finding
suggests fluid responsiveness has been exceeded and volume overload is
developing?
A. Improved urine output and warming extremities
B. New crackles, rising CVP/PCWP, and worsening oxygenation
C. Decreasing heart rate toward baseline
D. Rising blood pressure with stable respiratory status
Answer: B
Rationale: Once the heart operates on the flat portion of the Frank-Starling curve,
additional preload no longer improves stroke volume and instead raises filling
pressures, producing pulmonary congestion (crackles), rising CVP/PCWP, and
hypoxemia — signaling that fluid resuscitation should be reassessed rather than
continued.
10. Which statement about anaphylactic shock pathophysiology is most
accurate?
A. It is mediated by IgG-driven complement activation only
B. Mast cell/basophil degranulation releases histamine and mediators causing
vasodilation, increased capillary permeability, and bronchoconstriction
C. It primarily involves loss of sympathetic tone from spinal injury
D. It is characterized by primary pump failure with elevated filling pressures
