Cardiac Vascular Nursing Exam Cardiac Vascular Nursing Exam Pharmacology & Medications 1 — Questions and Answers
Question 1: Which mechanism of action explains why beta-blockers reduce mortality in heart failure with reduced ejection fraction?
- Blocking catecholamine overstimulation reduces cardiac remodeling, improves ejection fraction, and prevents arrhythmic death (Correct answer)
- Beta-blockers primarily reduce preload by blocking aldosterone receptors
- Beta-blockers increase cardiac output acutely by improving contractility
- Beta-blockers prevent heart failure by directly inhibiting RAAS activation
Correct answer: Blocking catecholamine overstimulation reduces cardiac remodeling, improves ejection fraction, and prevents arrhythmic death
Chronic sympathetic overstimulation in HFrEF causes maladaptive remodeling; beta-blockers block this, reversing remodeling, improving EF, and reducing sudden cardiac death.
Question 2: A nurse is administering IV heparin for STEMI management. Which laboratory value must be monitored to guide dosing?
- Activated partial thromboplastin time (aPTT) (Correct answer)
- International normalized ratio (INR)
- Anti-Xa level only (not aPTT for unfractionated heparin)
- Platelet count exclusively
Correct answer: Activated partial thromboplastin time (aPTT)
Unfractionated heparin's anticoagulant effect is monitored with aPTT, targeting 60–100 seconds (1.5–2.5× control) to maintain therapeutic anticoagulation during ACS management.
Question 3: Which class of medication is contraindicated in patients with bilateral renal artery stenosis and must be avoided when initiating heart failure treatment?
- ACE inhibitors and ARBs (Correct answer)
- Beta-blockers
- Loop diuretics
- Aldosterone antagonists
Correct answer: ACE inhibitors and ARBs
ACE inhibitors and ARBs block efferent arteriolar constriction that maintains GFR in renal artery stenosis; in bilateral disease this can precipitate acute kidney injury.
Question 4: A patient on amiodarone for atrial fibrillation also takes warfarin. The nurse anticipates which drug interaction?
- Amiodarone inhibits warfarin metabolism, increasing INR and bleeding risk (Correct answer)
- Amiodarone increases warfarin metabolism, decreasing anticoagulant effect
- Amiodarone displaces warfarin from protein binding, reducing its effectiveness
- No significant interaction exists between amiodarone and warfarin
Correct answer: Amiodarone inhibits warfarin metabolism, increasing INR and bleeding risk
Amiodarone inhibits CYP2C9, the primary enzyme metabolizing warfarin's S-enantiomer, causing warfarin accumulation and significantly elevated INR requiring dose reduction.
Question 5: Which pharmacological property of digoxin makes narrow therapeutic index monitoring essential?
- Digoxin has a narrow margin between therapeutic and toxic plasma concentrations, with toxicity enhanced by hypokalemia (Correct answer)
- Digoxin is rapidly metabolized requiring frequent large doses to maintain levels
- Digoxin toxicity is prevented solely by renal dose adjustment without serum level monitoring
- Digoxin's therapeutic index is wide; monitoring is done for cost efficiency only
Correct answer: Digoxin has a narrow margin between therapeutic and toxic plasma concentrations, with toxicity enhanced by hypokalemia
Therapeutic digoxin levels (0.5–2 ng/mL) are close to toxic levels, and hypokalemia sensitizes the Na/K-ATPase pump to digoxin, dramatically increasing toxicity risk.
Question 6: Nitroglycerin relieves angina primarily through which mechanism?
- Venous dilation reduces cardiac preload, decreasing myocardial oxygen demand (Correct answer)
- Direct coronary artery vasodilation increasing oxygen supply only
- Arterial vasodilation reducing afterload as the primary antianginal mechanism
- Negative chronotropic effect slowing heart rate to reduce oxygen consumption
Correct answer: Venous dilation reduces cardiac preload, decreasing myocardial oxygen demand
Nitroglycerin releases nitric oxide causing smooth muscle relaxation predominantly in venous capacitance vessels, reducing preload and ventricular filling pressure, lowering myocardial oxygen demand.
Which mechanism of action explains why beta-blockers reduce mortality in heart failure with reduced ejection fraction?