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Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Cardiovascular Pharmacology

Treatment of primary (essential) hypertension)

A

Thiazides, ACE inhibitors, ARBs, dihydropyridine Ca2+ chanel blockers

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2
Q

Cardiovascular Pharmacology

Treatment of hypertension with heart failure

A

Diuretics, ACE inhibitors/ARBs, β blockers (compensated HF), aldosterone antagonists

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3
Q

Cardiovascular Pharmacology

Treatment of hypertension with diabetes mellitus

A

ACE inhibitors/ARBs, Ca2+ channel blockers, thiazide diuretics, β blockers

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4
Q

Cardiovascular Pharmacology

Treatment of hypertension in pregnancy

A

Hydralazine, labetalol, methyldopa, nifedipine

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5
Q

Cardiovascular Pharmacology

Calcium channel blockers

A

Examples: amlodipine, clevidipine, nicardipine, nimodipine (dihydropyridines, act on vascular smooth muscle); diltiazem, verapamil (non-hdihydropyridines, act on heart)

Mechanism: Block voltage-dependent L-type calcium channels of cardiac and smooth muscle → ↓ muscle contractility
Vascular smooth muscle: amlodipine = nifedipine > diltiazem > verapamil
Heart: verapamil > diltiazem > amlodipine = nifedipine

Clinical Use:
Dihydropyridine (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud phenomenon
Nimodipine: SAH (prevents cerebral vasospasm)
Clevidipine: Hypertensive urgency or emergency
Non-dihydropyridine: Hypertension, angina, atrial fibrillation/flutter

Adverse Effects:
Non-dihydropyridine: cardiac depression, AV block, hyperprolactinemia, constipation
Dihydropyridine: Peripheral edema, flushing, dizziness, gingival hyperplasia

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6
Q

Cardiovascular Pharmacology

Hydralazine

A

MOA: ↑ cGMP → smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction

Clinical Use: Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy. Frequently coadministered with a β-blocker to prevent reflex tachycardia.

Adverse effects: Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina. Lupus-like syndrome.

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7
Q

Cardiovascular Pharmacology

Treatment of hypertensive emergency

A

Celvidipine, fenoldopam, labetalol, nicardipine, nitroprusside

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8
Q

Cardiovascular Pharmacology

Nitroprusside

A

MOA: Short acting; ↑ cGMP via direct release of NO.

Use: Hypertensive emergency

Adverse Effects: Can cause cyanide toxicity (releases cyanide)

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9
Q

Cardiovascular Pharmacology

Fenoldopam

A

MOA: Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation → ↓ BP, ↑ natriuresis.

Use: Hypertensive emergency, postoperative antihypertensive.

Adverse Effects: Hypotension and tachycardia

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10
Q

Cardiovascular Pharmacology

Nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)

A

MOA: Vasodilate by ↑ NO in vascular smooth muscle → ↑ in cGMP & smooth muscle relaxation. Dilate veins&raquo_space; arteries. ↓ Preload.

Use: Angina, acute coronary syndrome, pulmonary edema.

Adverse Effects: Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend → tachycardia, dizziness, headache upon reexposure

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11
Q

Cardiovascular Pharmacology

Effects of nitrates on angina

A 
↓ EDV
↓ BP
No change in contractility
↑ HR (reflex response)
↓ Ejection time
↓ MVO2
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12
Q

Cardiovascular Pharmacology

Effects of β-blockers on angina

A 
No effect or ↑ EDV
↓ BP
↓ Contractility
↓ HR
↑ Ejection time
↓ MVO2
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13
Q

Cardiovascular Pharmacology

Effects of nitrates + β-blockers on angina

A 
No effect or ↓ EDV
↓ BP
Little/no effect on contractility
↓ or no effect on HR
Little or no effect on ejection time
↓↓  MVO2
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14
Q

Cardiovascular Pharmacology

Ranolazine

A

MOA: Inhibits late phase of sodium current → ↓ diastolic wall tension and O2 consumption. No effect on HR or contractility

Use: Angina refractory to other medical therapies

Adverse Effects: Constipation, dizziness, headache, nausea, QT prolongation

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15
Q

Cardiovascular Pharmacology

HMG-CoA reductase inhibitors (lovastatin, pravastatin)

A

MOA: Inhibition of HMG-CoA to mevalonate, a cholesterol precursor ; ↓ mortality in CAD patients
↓↓↓ LDL
↑ HDL
↓ TG

Adverse Effects: Hepatotoxicity (↑ LFTs), myopathy (esp. when used with fibrates or niacin)

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16
Q

Cardiovascular Pharmacology

Bile acid resins (cholestyramine, colestipol, colesevelam)

A

MOA: Prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more
↓↓ LDL
Slightly ↑ HDL
Slightly ↑ TG

Adverse Effects: GI upset, ↓ absorption of other drugs and fat-soluble vitamins

17
Q

Cardiovascular Pharmacology

Ezetimibe

A

MOA: Prevent cholesterol absorption at small intestine brush border
↓↓ LDL
No effect on HDL or TG

Adverse effects: Rare ↑ LEFTs, diarrhea

18
Q

Cardiovascular Pharmacology

Fibrates (gemfibrozil, bezafibrate, fenofibrate)

A

MOA: Upregulate LPL → ↑ clearance; activates PPAR- α to induce HDL synthesis
↓ LDL
↑ HDL
↓↓↓ TG

Adverse Effects: Myopathy, (↑ risk with statins), cholesterol gallstones

19
Q

Cardiovascular Pharmacology

Niacin (vitamin B3)

A

MOA: Inhibits lipolysis (hormone-sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis
↓↓ LDL
↑↑ HDL
↓ TG

Adverse Effects: Red flushed face, which is ↓ by NSAIDs or long-term use, hyperglycemia, hyperuricemia

20
Q

Cardiovascular Pharmacology

Digoxin

A

MOA: Direct inhibition of Na+/K+ ATPase → indirect inhibition of Na+/Ca2+ exchanger → ↑[Ca2+]i → positive inotropy. Stimulates vagus nerve → ↓ HR.

Use: HF; atrial fibrillation (↓ conduction at AV node and depression of SA node)

Adverse Effects: Cholinergic (nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block), hyperkalemia.

Toxicity Risk Factors: Renal failure, hypokalemia, drugs that displace digoxin from tissue-binding sites, and ↓ clearance.

Antidote: Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

21
Q

Cardiovascular Pharmacology

Class IA antiarrhythmics (quinidine, procainamide, disopyramide)

A

MOA: Sodium channel blocker. Slow or block conduction. ↓ slope of phase 0 depolarization → ↑ AP duration, ↑ ERP, ↑ QT interval

Use: Atrial & ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

Adverse Effects: Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de pointes due to ↑ QT interval

22
Q

Cardiovascular Pharmacology

Class IB antiarrhythmics (lidocaine, mexiletine)

A

MOA: Sodium channel blocker. Slow or block conduction. ↓ slope of phase 0 depolarization → ↓ AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

Use: Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias.

Adverse Effects: CNS stimulation/depression, cardiovascular depression

23
Q

Cardiovascular Pharmacology

Class IC antiarrhythmics (flecainide, propafenone)

A

MOA: Sodium channel blocker. Slow or block conduction. ↓ slope of phase 0 depolarization → significantly prolong ERP in AV node and accessory bypass tracts. No effect on ERP in Purkinje and ventricular tissue. Minimal effect on AP duration

Use: SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

Adverse Effects: Proarrythmic, especially post-MI

24
Q

Cardiovascular Pharmacology

Class II antiarrhythmics (metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol)

A

MOA: β-blockers. ↓ SA & AV nodal activity by ↓ cAMP, ↓ Ca2+ currents. Suppress abnormal pacemakers by ↓ slope of phase 4. AV node particularly sensitive → PR interval. Esmolol very short acting.

Use: SVT, ventricular rate control and atrial flutter.

Adverse effects: Impotence, exacerbation of COPD and asthma, CV effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Can cause unopposed α1-agonism if given alone for pheochromocytoma or cocaine toxicity. Metoprolol: dyslipidemia. Propanalol: exacerbate vasospasm in Prinzmetal angina.

Tx of overdose: saline, atropine, glucagon

25
Q

Cardiovascular Pharmacology

Class III antiarrhythmics (amiodarone, ibulitide, dofeltilide, sotalol)

A

MOA: Potassium channel blocker. ↑ AP duration, ↑ ERP, ↑ QT interval.

Use: Atrial fibrillation, atrial flutter, ventricular tachycardia (amiodarone, sotalol)

Adverse Effects:
Sotalol: torsades de pointes, excessive β blockade
Ibutilide - torsades de pointes
Amidoarone: pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, acts as hapten (corneal deposits, blue/gray skin deposits resulting in dermatitis), neurological effects, constipation, cardiovascular effects (bradycardia, heart block, HF)

26
Q

Cardiovascular Pharmacology

Class IV antiarrhythmics (verapamil, diltiazem)

A

MOA: Calcium channel blocker. ↓ conduction velocity, ↑ ERP, ↑ PR interval

Use: Prevention of nodal arrhythmias (eg. SVT), rate control in atrial fibrillation

Adverse Effects: Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression)

27
Q

Cardiovascular Pharmacology

Adenosine

A

MOA: ↑ K+ out of cells → hyperpolarzing cell and ↓ ICa. Very short acting

Use: Drug of choice in diagnosing/terminating certain forms of SVT

Adverse Effects: Flushing, hypotension, chest pain, sense of impending doom, bronchospasm

28
Q

Cardiovascular Pharmacology

Mg2+

A

Effective in torsades de pointes and digoxin toxicity

Pharmacology (17 decks)

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