PROPHECY GENERAL ICU RN A V2 EXAM 2026 |
Questions & Answers | Verified Answers | 85
Questions w/ Detailed Rationales |
Comprehensive Practice | Pass Guaranteed - A+
Graded
SECTION 1: CARDIOVASCULAR (Questions 1-15)
Q1: A patient with cardiogenic shock has the following hemodynamic parameters: MAP
58 mmHg, CI 1.8 L/min/m², CVP 18 mmHg, PAOP 24 mmHg, SVR 1800 dynes·sec/cm⁵.
The patient is on norepinephrine 0.5 mcg/kg/min and dobutamine 10 mcg/kg/min.
Which adjustment is most appropriate?
● A. Increase norepinephrine to achieve MAP >65 mmHg
● B. Add vasopressin 0.03 units/min to reduce catecholamine doses [CORRECT]
● C. Increase dobutamine to improve cardiac output
● D. Initiate phenylephrine to augment afterload
Correct Answer: B
Rationale: This patient presents cardiogenic shock with biventricular failure (elevated
CVP and PAOP indicating right and left ventricular congestion, low CI, elevated SVR
from compensatory vasoconstriction).
Why B is correct: The patient is on high-dose norepinephrine (0.5 mcg/kg/min exceeds
typical maximum 0.3-0.5 mcg/kg/min) with inadequate response. Vasopressin
deficiency occurs in septic shock but also in prolonged cardiogenic shock. Adding
vasopressin 0.03 units/min allows reduction of norepinephrine dose, reducing
,catecholamine toxicity (arrhythmias, myocardial oxygen demand, renal
vasoconstriction). The 2021 SCCM guidelines support vasopressin as second-line to
reduce norepinephrine exposure.
Why A is incorrect: Increasing norepinephrine further increases myocardial oxygen
demand without addressing the fundamental problem of pump failure. High-dose
catecholamines increase mortality in cardiogenic shock.
Why C is incorrect: Dobutamine is already at 10 mcg/kg/min (high dose). Further
increase risks significant tachycardia, arrhythmias, and hypotension from beta-2
mediated vasodilation. The problem is not inadequate inotropy but rather mechanical
pump failure requiring mechanical circulatory support consideration.
Why D is incorrect: Phenylephrine is a pure alpha-agonist that increases afterload
without inotropic support. In cardiogenic shock with elevated SVR already, increasing
afterload further reduces cardiac output (afterload mismatch) and worsens pump
failure.
Next Steps: Consider mechanical circulatory support (Impella, IABP, or VA-ECMO) if not
already evaluated. Hemodynamics suggest isolated medical therapy will be insufficient.
Q2: A patient with ST-elevation MI develops a new holosystolic murmur at the left lower
sternal border, acute pulmonary edema, and hypotension 5 days post-infarction.
Hemodynamics show prominent V waves on PAOP tracing. Which complication has
occurred?
● A. Acute mitral regurgitation from papillary muscle rupture [CORRECT]
● B. Ventricular septal defect (VSD)
● C. Free wall rupture with tamponade
● D. Right ventricular infarction
Correct Answer: A
,Rationale: The presentation is classic for acute severe mitral regurgitation (MR) from
papillary muscle rupture, a mechanical complication of inferior MI (posteromedial
papillary muscle, single blood supply from posterior descending artery).
Why A is correct:
● Timing: 2-7 days post-MI (inflammatory weakening, necrosis)
● Murmur: Holosystolic at left lower sternal border (radiates to axilla, may be soft
due to equalization of pressures)
● Hemodynamics: Prominent V waves on PAOP (reflective of systolic regurgitant
flow into non-compliant left atrium)
● Presentation: Acute pulmonary edema (sudden volume overload of left
atrium/pulmonary circuit), hypotension (reduced forward cardiac output)
Why B is incorrect: VSD produces harsh holosystolic murmur at left lower sternal border
with thrill, but prominent V waves are less characteristic. Step-up in oxygen saturation
from RA to PA would be present. Murmur is typically louder and more harsh.
Why C is incorrect: Free wall rupture presents with sudden hemodynamic collapse,
electromechanical dissociation, tamponade (pulsus paradoxus, elevated CVP with
equalization to PAOP), not a murmur and pulmonary edema. Usually fatal without
immediate pericardiocentesis/surgery.
Why D is incorrect: RV infarction presents with hypotension, clear lungs, elevated CVP
with normal/low PAOP (right failure without left failure), Kussmaul sign, not a new
murmur or pulmonary edema.
Management: Emergency surgical consultation, IABP for afterload reduction,
vasodilators if BP permits, inotropes, avoid mechanical ventilation if possible (reduces
venous return worsens RV function), surgical repair or replacement.
, Q3: [Select All That Apply] A patient with septic shock has the following parameters
after 30 mL/kg fluid resuscitation: MAP 54 mmHg, CVP 14 mmHg, ScvO₂ 58%, lactate
6.2 mmol/L. Which interventions are appropriate? (Select all that apply)
● A. Administer additional crystalloid 500-1000 mL bolus
● B. Initiate norepinephrine to achieve MAP ≥65 mmHg [CORRECT]
● C. Consider dobutamine if ScvO₂ remains <70% after MAP restored [CORRECT]
● D. Check capillary refill time to assess peripheral perfusion [CORRECT]
● E. Administer hydrocortisone 50 mg IV q6h immediately
Correct Answer: B, C, D
Rationale:
A is incorrect: CVP 14 mmHg suggests adequate preload (or excessive preload).
Additional fluid without evidence of fluid responsiveness (passive leg raise, stroke
volume variation, echo assessment) risks fluid overload, particularly given elevated CVP.
The patient likely needs vasopressors, not more fluid.
B is correct: MAP <65 mmHg after adequate fluid resuscitation indicates
vasopressor-dependent shock. Norepinephrine is first-line to restore perfusion pressure
to critical organs.
C is correct: ScvO₂ 58% indicates inadequate oxygen delivery (normal 70-75%). After
MAP restoration, if ScvO₂ remains low, dobutamine (2-5 mcg/kg/min) increases cardiac
output and oxygen delivery. This addresses the "D" in early goal-directed therapy
principles.
D is correct: Capillary refill time (CRT) is a simple, validated assessment of peripheral
perfusion. Prolonged CRT (>3 seconds) despite "normal" MAP indicates persistent
microcirculatory dysfunction and may guide therapy beyond macrohemodynamic
targets.
Questions & Answers | Verified Answers | 85
Questions w/ Detailed Rationales |
Comprehensive Practice | Pass Guaranteed - A+
Graded
SECTION 1: CARDIOVASCULAR (Questions 1-15)
Q1: A patient with cardiogenic shock has the following hemodynamic parameters: MAP
58 mmHg, CI 1.8 L/min/m², CVP 18 mmHg, PAOP 24 mmHg, SVR 1800 dynes·sec/cm⁵.
The patient is on norepinephrine 0.5 mcg/kg/min and dobutamine 10 mcg/kg/min.
Which adjustment is most appropriate?
● A. Increase norepinephrine to achieve MAP >65 mmHg
● B. Add vasopressin 0.03 units/min to reduce catecholamine doses [CORRECT]
● C. Increase dobutamine to improve cardiac output
● D. Initiate phenylephrine to augment afterload
Correct Answer: B
Rationale: This patient presents cardiogenic shock with biventricular failure (elevated
CVP and PAOP indicating right and left ventricular congestion, low CI, elevated SVR
from compensatory vasoconstriction).
Why B is correct: The patient is on high-dose norepinephrine (0.5 mcg/kg/min exceeds
typical maximum 0.3-0.5 mcg/kg/min) with inadequate response. Vasopressin
deficiency occurs in septic shock but also in prolonged cardiogenic shock. Adding
vasopressin 0.03 units/min allows reduction of norepinephrine dose, reducing
,catecholamine toxicity (arrhythmias, myocardial oxygen demand, renal
vasoconstriction). The 2021 SCCM guidelines support vasopressin as second-line to
reduce norepinephrine exposure.
Why A is incorrect: Increasing norepinephrine further increases myocardial oxygen
demand without addressing the fundamental problem of pump failure. High-dose
catecholamines increase mortality in cardiogenic shock.
Why C is incorrect: Dobutamine is already at 10 mcg/kg/min (high dose). Further
increase risks significant tachycardia, arrhythmias, and hypotension from beta-2
mediated vasodilation. The problem is not inadequate inotropy but rather mechanical
pump failure requiring mechanical circulatory support consideration.
Why D is incorrect: Phenylephrine is a pure alpha-agonist that increases afterload
without inotropic support. In cardiogenic shock with elevated SVR already, increasing
afterload further reduces cardiac output (afterload mismatch) and worsens pump
failure.
Next Steps: Consider mechanical circulatory support (Impella, IABP, or VA-ECMO) if not
already evaluated. Hemodynamics suggest isolated medical therapy will be insufficient.
Q2: A patient with ST-elevation MI develops a new holosystolic murmur at the left lower
sternal border, acute pulmonary edema, and hypotension 5 days post-infarction.
Hemodynamics show prominent V waves on PAOP tracing. Which complication has
occurred?
● A. Acute mitral regurgitation from papillary muscle rupture [CORRECT]
● B. Ventricular septal defect (VSD)
● C. Free wall rupture with tamponade
● D. Right ventricular infarction
Correct Answer: A
,Rationale: The presentation is classic for acute severe mitral regurgitation (MR) from
papillary muscle rupture, a mechanical complication of inferior MI (posteromedial
papillary muscle, single blood supply from posterior descending artery).
Why A is correct:
● Timing: 2-7 days post-MI (inflammatory weakening, necrosis)
● Murmur: Holosystolic at left lower sternal border (radiates to axilla, may be soft
due to equalization of pressures)
● Hemodynamics: Prominent V waves on PAOP (reflective of systolic regurgitant
flow into non-compliant left atrium)
● Presentation: Acute pulmonary edema (sudden volume overload of left
atrium/pulmonary circuit), hypotension (reduced forward cardiac output)
Why B is incorrect: VSD produces harsh holosystolic murmur at left lower sternal border
with thrill, but prominent V waves are less characteristic. Step-up in oxygen saturation
from RA to PA would be present. Murmur is typically louder and more harsh.
Why C is incorrect: Free wall rupture presents with sudden hemodynamic collapse,
electromechanical dissociation, tamponade (pulsus paradoxus, elevated CVP with
equalization to PAOP), not a murmur and pulmonary edema. Usually fatal without
immediate pericardiocentesis/surgery.
Why D is incorrect: RV infarction presents with hypotension, clear lungs, elevated CVP
with normal/low PAOP (right failure without left failure), Kussmaul sign, not a new
murmur or pulmonary edema.
Management: Emergency surgical consultation, IABP for afterload reduction,
vasodilators if BP permits, inotropes, avoid mechanical ventilation if possible (reduces
venous return worsens RV function), surgical repair or replacement.
, Q3: [Select All That Apply] A patient with septic shock has the following parameters
after 30 mL/kg fluid resuscitation: MAP 54 mmHg, CVP 14 mmHg, ScvO₂ 58%, lactate
6.2 mmol/L. Which interventions are appropriate? (Select all that apply)
● A. Administer additional crystalloid 500-1000 mL bolus
● B. Initiate norepinephrine to achieve MAP ≥65 mmHg [CORRECT]
● C. Consider dobutamine if ScvO₂ remains <70% after MAP restored [CORRECT]
● D. Check capillary refill time to assess peripheral perfusion [CORRECT]
● E. Administer hydrocortisone 50 mg IV q6h immediately
Correct Answer: B, C, D
Rationale:
A is incorrect: CVP 14 mmHg suggests adequate preload (or excessive preload).
Additional fluid without evidence of fluid responsiveness (passive leg raise, stroke
volume variation, echo assessment) risks fluid overload, particularly given elevated CVP.
The patient likely needs vasopressors, not more fluid.
B is correct: MAP <65 mmHg after adequate fluid resuscitation indicates
vasopressor-dependent shock. Norepinephrine is first-line to restore perfusion pressure
to critical organs.
C is correct: ScvO₂ 58% indicates inadequate oxygen delivery (normal 70-75%). After
MAP restoration, if ScvO₂ remains low, dobutamine (2-5 mcg/kg/min) increases cardiac
output and oxygen delivery. This addresses the "D" in early goal-directed therapy
principles.
D is correct: Capillary refill time (CRT) is a simple, validated assessment of peripheral
perfusion. Prolonged CRT (>3 seconds) despite "normal" MAP indicates persistent
microcirculatory dysfunction and may guide therapy beyond macrohemodynamic
targets.
