Exam IV: Cardiovascular Drugs Flashcards Preview

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Flashcards in Exam IV: Cardiovascular Drugs Deck (12):

RAAS Drugs

1. Aliskiren: inhibit renin to Ang I
2. Captopril: inhibit Ang I to Ang II (ACE inhibitor)
3. Losartan: inhibit Ang II to aldosterone (ARB)

Adverse effects of all: hyperkalemia, angioedema, hypotension
Captopril: causes cough
Losartan: acute renal failure


Captopril 5 Advantages

1. Anti fibrosis
2. Vasodilation
3. Increase prostaglandins
4. Increase Ang 1-7
5. Increase bradykinin levels – can cause the cough and angioedema



use for acute angina
1. NTG (Nitroglycerin): organic and selective for dilating veins and coronary arteries, which causes a decrease in preload and afterload
Averse effects: headache, overt syncope, and hypotension (decrease O2 to heart)

2. SNP: inorganic and non-specific, so dilates veins and arteries
Adverse effects: cyanide build up if liver not functioning properly


Ca2+ Channel Blockers

1. Dihydropyridine: Nifedipine
2. Non-dihydropyridine: Verapamil and Diltiazem

Effects of both: dilate arterioles, increase coronary blood flow, no effect on venous beds
Non-dihydropyridine effects: selective for heart, so do not use for heart failure patients

Adverse Effects of both: edema


Beta Blockers

Propanolol: beta 1 and beta 2; bad for asthma
Metropolol: beta 1 only

Adverse effects of both: impotence, bradycardia, and vivid dreams


Alpha Receptors

Prazosin: alpha 1 antagonist that dilates arteries and veins; decreases preload, intact negative feedback, and decrease sympathetic flow; side effect is 1st dose postural hypotension

Clonidine: alpha 2 agonist that decreases sympathetic flow and side effect is dry mouth


Loop Diuretics

affects the thick ascending limb of loop of Henle by blocking the Na/K/2Cl cotransporter
monotherapy for CHF

Furosemide: secreted by organic acid
Effects: decrease in Na/H2O, Cl, Mg, and K
alkalosis, gout, ear issues, and allergy causing necrosis of cells that may lead to death


K-sparing Diuretics

affect the collecting ducts

Spironolactone: MR antagonist (aldosterone) thereby blocking the Na/K pump; antagonist of androgens
Amiloride: ENaC blocker secreted by organic base

Effects: increases K and Cl while causing acidosis


Thiazide Diuretics

affects distal convoluted tubule by inhibiting the Na/Cl cotransporter

HCT: decreases Na/H2O, K, and causes alkalosis
secreted by organic acid
1st line diuretic for hypertension


Treatment for Angina Pectoris

Effort Induced: nitrates, calcium channel blockers, and beta blockers

Variant: nitrates and calcium channel blockers


Treatment for Heart Failure

Preload Reduction: loop diuretics (monotherapy), K sparing (combination), venodilators (nitrates)

Afterload Reduction: ACEI/ARB, beta antagonists

Not used:
Alpha receptor antagonists: because neurotransmitters would bind to beta instead and increase renin angiotensin system = bad
Ca channel blockers: it blocks Ca2+ channels reducing Ca2+ in cells and decreases contractility = bad


Compensation for Heart Failure

1. Increase preload to increase SV to decrease HR while maintaining CO because CO = SV * HR

2. In heart failure no longer have enough blood pumped out aka increase in afterload, so increase vasoconstriction to increase BP to drive the blood flow through the tissues to decrease afterload

3. Increase contractility to make the contraction longer lasting thereby decreasing afterload, or the amount of blood left in the heart after contraction

4. HR isn’t as important because when reduced SV, sympathetic is increased more and more until maximized so that means HR is maximized and won’t go any higher