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Flashcards in Pharm: Cardiovascular Deck (21):

Class IA anti-arrhythmics (quinidine, procainamide, dispyramide)

Mechanism: bind and block activated Na channels > prolong phase 0 depolarization; minor interaction with K channels also prolongs phase 3 repolarization > increases AP duration
Use: atrial and ventricular arrhythmias, WPW
SE: prolonged QT, cardiac arrhythmia, cinchonism (quinidine), drug-induced Lupus (procainamide), psychosis


Class IB anti-arrhythmics (lidocaine, tocainide, mexiletine)

Mechanism: bind activated and inactivated Na channels > inhibit activation of Na channels > shorten AP duration and decrease excitability of cardiac myocyte
Use: acute ventricular arrhythmias (post-MI), digitalis-induced arrhythmia
SE: arrhythmia, hypotension, tremor, fatigue, neurotoxicity (lidocaine)


Class 1C anti-arrhythmics (flecainide, encainide, propafenone)

Mechanism: block Na channels > prolong phase 0 depolarization and decrease rate of cardiac contraction; no effect on AP duration
Use: SVTs
SE: life-threatening arrhythmia; avoid in pts with structurally abnormal hearts


Class III anti-arrhythmics (amiodarone, ibutilide, dofetilide, sotalol)

Mechanism: block K channels > prolong phase 3 repolarization, increase AP duration; amiodarone has class I, II, III, and IV effects; sotalol is also a beta blocker
Use: atrial and ventricular arrhythmias
SE: prolonged QT (except amiodarone), arrhythmia; pulmonary fibrosis, hepatotoxicity, thyroid dysfunction, photosensitivity (amiodarone)


Class IV anti-arrhythmics (non-dihydropyridine Ca channel blockers: verapamil, diltiazem)

Mechanism: block Ca channels on cardiac and smooth muscle > prolong phase 4 spontaneous depolarization in SA and AV nodal cells, delay myocyte repolarization
Use: SVT (also HTN and angina)
SE: constipation, flushing, edema, heart block



Mechanism: increases K efflux in SA and AV nodes > hyperpolarization of both nodes
Use: SVT, cardiac stress testing
SE: flushing, dyspnea, heart block, chest pain



Mechanism: increases extracellular K concentration > raise AP threshold
Use: suppress ectopic pacemakers, digoxin toxicity
SE: hyperkalemia, arrhythmia, shock, paralysis



Mechanism: inhibits Na/K ATPase > increases intracellular Na > decreases efflux of Ca via Na/Ca exchanger > increased contractility
Use: heart failure
SE: blurry yellow vision, ECG changes, cholinergic effects (nausea, vomiting, diarrhea)


Nitroglycerin, isosorbide mononitrate

Mechanism: converted to NO > increases cGMP synthesis > dephosphorylation of myosin light chain > smooth muscle relaxation > reduced preload
Use: angina, pulmonary edema, heart failure
SE: headache, orthostatic hypotension, reflex tachycardia



Mechanism: converted to NO > increases cGMP synthesis > dephosphorylation of myosin light chain > smooth muscle relaxation > reduced preload; IV only
Use: hypertensive crisis
SE: cyanide toxicity (treat w/thiosulfate)


ACE inhibitors (captopril, enalapril, lisinopril)

Mechanism: inhibit ACE > blocks vasoconstriction mediated by ATII and water/Na retention via aldosterone; increases levels of bradykinin
Use: HTN, CHF, diabetic nephropathy
SE: cough, angioedema, teratogenic, elevated Cr (decrease GFR), hyperkalemia, hypotension


Angiotensin Receptor Blockers (losartan)

Mechanism: block the ATII receptor and therefore the effects of ATII and aldosterone
Use: HTN, CHF, diabetic nephropathy
SE: hyperkalemia, decrease GFR, teratogenic, rash



Mechanism: increases cGMP > relaxation of arteriolar smooth muscle > decreases afterload
Use: HTN (esp. in pregnancy), CHF
SE: reflex tachycardia, fluid retention, drug-induced lupus


Ca channel blockers (dihydropyridine: amlodipine, nifedipine)

Mechanism: block Ca channels > vasodilation
Use: HTN, angina (Prinzmetal), Raynaud
SE: hypotension, edema, cardiac depression



Mechanism: increases osmolarity in the proximal tubule and descending loop of Henle > draws water into lumen for excretion
Use: to decrease ICP or intraocular pressure; also in drug overdose
SE: pulmonary edema, dehydration, headache


Carbonic anhydrase inhibitors (acetazolamide)

Mechanism: inhibits carbonic anhydrase in the PCT > blocks HCO3- reabsorption and promotes Na excretion
Use: glaucoma, toxin ingestion (to alkalize urine), metabolic alkalosis, altitude sickness, pseudotumor cerebri
SE: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy


Loop diuretics (furosemide)

Mechanism: inhibits Na/K/2 Cl cotransporter in the thick ascending loop of Henle
Use: CHF, renal failure, HTN, hypercalcemia, edema
SE: ototoxicity, hypokalemia, dehydration, (sulfa) allergy, (interstitial) nephritis, gout (OH DANG)


Thiazides (hydrochlorothiazide)

Mechanism: inhibits Na/Cl cotransporter in early DCT; also decreases Ca excretion
Use: HTN, CHF, nephrogenic diabetes insipidus, hypercalciuria, osteoperosis
SE: hypokalemia and natremia, hyperGlycemia, Lipidemia, Uricemia, and Calcemia (hyperGLUC), sulfa allergy


Ethacrynic acid

Mechanism: same as furosemide but not a sulfonamide
Use: diuresis in patients allergic to sulfas
SE: hyperuricemia, effects similar to furosemide


Aldosterone receptor blockers (spironolactone)

Mechanism: blocks action of aldosterone in the late DCT and collecting duct; K sparing; has anti-androgen effect
Use: primary hyperaldosteronism, edema, HTN; female hirsutism in PCOS
SE: hyperkalemia (arrhythmia), metabolic acidosis, gynecomastia


Amiloride, triamterene

Mechanism: blocks Na channels in the collecting duct; K sparing
Use: edema, HTN
SE: hyperkalemia (arrhythmia), metabolic acidosis