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CVT Pharmacology & Cardiac Medications Flashcards

6 cards from real CVT practice questions. Tap to flip, then mark Knew It or Still Learning โ€” missed cards come back until you master them.

Read the first 6 CVT Pharmacology & Cardiac Medications flashcards as text
  1. ACE inhibitors are beneficial in heart failure patients primarily because they:

    Answer: Block the renin-angiotensin-aldosterone system to reduce preload and afterload

    ACE inhibitors block angiotensin II production and aldosterone release, causing vasodilation and sodium excretion that reduce both preload and afterload, improving cardiac function.

  2. Which antithrombotic agent works by irreversibly inhibiting platelet ADP receptors (P2Y12)?

    Answer: Clopidogrel

    Clopidogrel (Plavix) is a thienopyridine that irreversibly blocks the P2Y12 ADP receptor on platelets, preventing platelet aggregation for the platelet's lifetime.

  3. What is the primary mechanism of action of calcium channel blockers in treating cardiac arrhythmias?

    Answer: Block L-type calcium channels to slow SA and AV node activity

    Non-dihydropyridine CCBs (verapamil, diltiazem) block L-type calcium channels in the SA and AV nodes, slowing automaticity and conduction to control rate.

  4. Thrombolytics (e.g., tPA) are used in acute STEMI to:

    Answer: Dissolve existing thrombus by activating plasminogen

    Thrombolytics convert plasminogen to plasmin, which degrades fibrin clots, restoring coronary blood flow when primary PCI is not available within the recommended time window.

  5. Which electrolyte imbalance most commonly potentiates digoxin toxicity?

    Answer: Hypokalemia

    Hypokalemia increases digoxin binding to Na-K-ATPase and enhances its toxic effects, leading to increased risk of life-threatening arrhythmias.

  6. Epinephrine is administered during cardiac arrest primarily to:

    Answer: Increase coronary and cerebral perfusion pressure via alpha-1 vasoconstriction

    Epinephrine's alpha-1 adrenergic effects cause peripheral vasoconstriction, increasing aortic diastolic pressure and thus coronary and cerebral perfusion pressure during CPR.