NR 547 CEA
NR 547 CEA Exam 2026 - Comprehensive
Practice Questions & Answers
Page 1: Cardiovascular System
Q1: A patient with chronic heart failure is started on a new medication that reduces mortality by
decreasing preload and afterload. Which class of drugs achieves this effect and what is the
primary mechanism of action?
A1: ACE inhibitors (e.g., lisinopril) inhibit conversion of angiotensin I to angiotensin II, leading
to vasodilation and decreased sodium/water retention.
Q2: A 60-year-old patient presents with chest pain radiating to the left arm. Troponins are
elevated. What is the likely diagnosis and first-line management?
A2: Acute myocardial infarction; first-line management includes MONA (Morphine, Oxygen,
Nitroglycerin, Aspirin) and reperfusion therapy.
Q3: Explain the Frank-Starling law in heart failure.
A3: The stroke volume increases with increased end-diastolic volume up to an optimal point;
beyond that, excessive preload leads to decreased cardiac output.
Q4: Differentiate systolic vs diastolic heart failure.
A4: Systolic HF: reduced ejection fraction (EF <40%). Diastolic HF: preserved EF (≥50%) with
impaired ventricular filling.
Q5: A patient on digoxin develops nausea, vomiting, and arrhythmia. What is the most likely
cause?
A5: Digoxin toxicity, often due to renal impairment or drug interactions.
Page 2: Respiratory System
Q6: Interpret this ABG: pH 7.29 | PaCO2 55 | HCO3 25.
A6: Acute respiratory acidosis; no metabolic compensation.
NR 547 CEA
, NR 547 CEA
Q7: A patient with COPD has increased PaCO2 and chronic hypoxemia. What is the expected
compensation?
A7: Renal compensation: increased HCO3- retention to buffer chronic respiratory acidosis.
Q8: What are hallmark findings in ARDS on imaging?
A8: Bilateral pulmonary infiltrates without cardiogenic cause; diffuse alveolar damage.
Q9: Explain the mechanism of hypoxemia in ARDS.
A9: Impaired gas exchange due to alveolar-capillary membrane injury and intrapulmonary
shunting.
Q10: What is the recommended tidal volume strategy in ARDS?
A10: Low tidal volume ventilation (6 mL/kg ideal body weight) to reduce ventilator-induced
lung injury.
Page 3: Renal System
Q11: A patient with long-standing diabetes presents with microalbuminuria. Which part of the
nephron is initially damaged?
A11: Glomerular basement membrane; thickening due to glycation increases permeability.
Q12: List indications for urgent dialysis.
A12: Hyperkalemia, severe acidosis, fluid overload unresponsive to diuretics, uremic symptoms.
Q13: Differentiate prerenal, intrinsic, and postrenal AKI.
A13: Prerenal: decreased perfusion. Intrinsic: tubular/glomerular damage. Postrenal: obstruction
of urinary tract.
Q14: What electrolyte imbalance is most dangerous in AKI?
A14: Hyperkalemia, due to risk of cardiac arrhythmias.
Q15: Explain the rationale for using loop diuretics in acute decompensated heart failure.
A15: Inhibit Na+/K+/2Cl- symporter in the loop of Henle, promoting diuresis to reduce preload.
NR 547 CEA
NR 547 CEA Exam 2026 - Comprehensive
Practice Questions & Answers
Page 1: Cardiovascular System
Q1: A patient with chronic heart failure is started on a new medication that reduces mortality by
decreasing preload and afterload. Which class of drugs achieves this effect and what is the
primary mechanism of action?
A1: ACE inhibitors (e.g., lisinopril) inhibit conversion of angiotensin I to angiotensin II, leading
to vasodilation and decreased sodium/water retention.
Q2: A 60-year-old patient presents with chest pain radiating to the left arm. Troponins are
elevated. What is the likely diagnosis and first-line management?
A2: Acute myocardial infarction; first-line management includes MONA (Morphine, Oxygen,
Nitroglycerin, Aspirin) and reperfusion therapy.
Q3: Explain the Frank-Starling law in heart failure.
A3: The stroke volume increases with increased end-diastolic volume up to an optimal point;
beyond that, excessive preload leads to decreased cardiac output.
Q4: Differentiate systolic vs diastolic heart failure.
A4: Systolic HF: reduced ejection fraction (EF <40%). Diastolic HF: preserved EF (≥50%) with
impaired ventricular filling.
Q5: A patient on digoxin develops nausea, vomiting, and arrhythmia. What is the most likely
cause?
A5: Digoxin toxicity, often due to renal impairment or drug interactions.
Page 2: Respiratory System
Q6: Interpret this ABG: pH 7.29 | PaCO2 55 | HCO3 25.
A6: Acute respiratory acidosis; no metabolic compensation.
NR 547 CEA
, NR 547 CEA
Q7: A patient with COPD has increased PaCO2 and chronic hypoxemia. What is the expected
compensation?
A7: Renal compensation: increased HCO3- retention to buffer chronic respiratory acidosis.
Q8: What are hallmark findings in ARDS on imaging?
A8: Bilateral pulmonary infiltrates without cardiogenic cause; diffuse alveolar damage.
Q9: Explain the mechanism of hypoxemia in ARDS.
A9: Impaired gas exchange due to alveolar-capillary membrane injury and intrapulmonary
shunting.
Q10: What is the recommended tidal volume strategy in ARDS?
A10: Low tidal volume ventilation (6 mL/kg ideal body weight) to reduce ventilator-induced
lung injury.
Page 3: Renal System
Q11: A patient with long-standing diabetes presents with microalbuminuria. Which part of the
nephron is initially damaged?
A11: Glomerular basement membrane; thickening due to glycation increases permeability.
Q12: List indications for urgent dialysis.
A12: Hyperkalemia, severe acidosis, fluid overload unresponsive to diuretics, uremic symptoms.
Q13: Differentiate prerenal, intrinsic, and postrenal AKI.
A13: Prerenal: decreased perfusion. Intrinsic: tubular/glomerular damage. Postrenal: obstruction
of urinary tract.
Q14: What electrolyte imbalance is most dangerous in AKI?
A14: Hyperkalemia, due to risk of cardiac arrhythmias.
Q15: Explain the rationale for using loop diuretics in acute decompensated heart failure.
A15: Inhibit Na+/K+/2Cl- symporter in the loop of Henle, promoting diuresis to reduce preload.
NR 547 CEA
