Cardiac Pharmacology Drugs

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Essential hypertension therapy

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Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs) , calcium channel blockers.

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HTN + CHF therapy

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Diuretics, ACE inhibitors/ARBs, beta-blockers (in compensated CHF), K+ sparing diuretics

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contra-indicated in cardiogenic shock:

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beta-blockers

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HTN + Diabetes mellitus

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ACE inhibitors/ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers

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Calcium channel blocker names

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Nifedipine, verapamil , diltiazem, amlodipine.

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MOA of Nifedipine, verapamil , diltiazem, amlodipine.

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Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

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Most effective Ca channel blockers for heart

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verapamil > diltiazem > amlodipine = nifedipine

(verapamil = ventricle)

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Most effective Ca channel blockers for Vascular smooth muscle

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amlodipine = nifedipine > diltiazem > verapamil .

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adv. effects of Ca channel blockers

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Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation

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adv effects of which drugs: Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation

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Ca channel blockers

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Hydralazine clinical use

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Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa.Frequently co-administered with a beta-blocker to prevent reflex tachycardia .

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Hydralazine MOA

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inc. cGMP -> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction .

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Hydralazine adverse effects

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

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adverse effects of what drug: Compensatory tachycardia (contraindicated in angina/CAD ) , fluid retention, nausea , headache,angina. Lupus-like syndrome

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Hydralazine

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use which drug?: Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently coadministered with a beta-blocker to prevent reflex tachycardia

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Hydralazine

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use which drugs in this clinical situation?: Hypertension, angina, arrhythmias, Prinzmetal 's angina, Raynaud's

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Ca channel blockers: nifedipine, verapamil, diltiazem, amlodipine

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Treatment for malignant Hypertension:

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nitroprusside, fenoldopam

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fenoldopam MOA:

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Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation. dec. BP and inc. natriuresis (Na excretion).

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Nitroprusside MOA:

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Short acting; t cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)

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which drug's MOA: Short acting; inc. cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)

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nitroprusside

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which drug's MOA: Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation. dec. BP and inc. natriuresis (Na excretion).

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fenoldopam

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MOA Nitroglycerin, isosorbide dinitrate:

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Vasodilate by releasing nitric oxide in smooth muscle, causing inc in cGMP and smooth musclerelaxation . Dilate veins >> arteries. dec. preload.

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which drug's MOA: Vasodilate by releasing nitric oxide in smooth muscle, causing inc in cGMP and smooth musclerelaxation . Dilate veins >> arteries. dec. preload.

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Nitroglycerin, isosorbide dinitrate

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Nitroglycerin, isosorbide dinitrate, CLINICAL USE:

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Angina, pulmonary oedema

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Nitroglycerin, isosorbide dinitrate adverse effect

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Reflex tachycardia, hypotension, flushing, headache,

" Monday disease" in industrial exposure:development of tolerance for the vasodilating action during the workweek and loss of toleranceover the weekend results in tachycardia, dizziness, and headache upon re-exposure .

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which drug's adverse effect?: Reflex tachycardia, hypotension, flushing, headache

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Nitroglycerin, isosorbide dinitrate

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HMG -CoA reductase inhibitors

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Lovastatin, pravastatin,simvastatin, atorvastatin,rosuvastatin

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adv. effects of: lovastatin, pravastatin,simvastatin, atorvastatin,rosuvastatin

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Hepatotoxicity (inc. LFTs), rhabdomyolysis

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which drugs have this adv. effect?: Hepatotoxicity(inc. LFTs),rhabdomyolysis

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lovastatin, pravastatin,simvastatin, atorvastatin, rosuvastatin

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desirable effects lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

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+++ dec LDL, + inc HDL, + dec triglycerides

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MOA: lovastatin, pravastatin,simvastatin, atorvastatin, rosuvastatin

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Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

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Which drug's MOA: Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

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Lovastatin, pravastatin,simvastatin, atorvastatin, rosuvastatin

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MOA: Niacin (vitamin b3)

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Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

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Which drug's MOA: Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

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Niacin (vit. B3)

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Adv. effects of Niacin (vit B3)

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Red, flushed face, which is dec. by aspirin or long-term use. Hyperglycemia (acanthosis nigricans) Hyperuricemia (exacerbates gout)

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Adv effects of which drug: Red, flushed face,which is dec. by aspirinor long-term use. Hyperglycemia (therefore acanthosis nigricans) Hyperuricemia (exacerbates gout)

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Niacin aka vit b3

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desirable effects of Niacin:

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++ dec. LDL, ++ inc HDL, + dec triglycerides

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Bile acid resins (cholestyramine, colestipol, colesevelam) MOA:

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Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

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Which drug's MOA: Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

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Bile acid resins (cholestyramine, colestipol, colesevelam)

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Bile acid resin names:

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cholestyramine, colestipol, colesevelam

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cholestyramine, colestipol, colesevelam adv. effects:

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Patients hate it - tastesbad and causes GI discomfort, dec. absorption of fat-soluble vitamins, Cholesterol gallstones

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adv effects of which drug: Patients hate it - tastes bad and causes GI discomfort, dec. absorption of fat-soluble vitamins, Cholesterol gallstones

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cholestyramine, colestipol, colesevelam

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5x Lipid lowering agents:

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HMG - CoA reductase inhibitors, Niacin (vitamin B3), Bile acid resins, Cholesterol absorption blockers, Fibrates

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desirable effects: cholestyramine, colestipol, colesevelam

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++ dec. LDL, + inc HDL, + inc triglycerides

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name of the cholesterol absorption blocker:

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ezetimibe

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ezetimibe class

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cholesterol absorption blocker

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ezetimibe desirable effect:

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++ dec. LDL. (no effect on HDL/triglycerides)

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LDL lowering drug that has no effect on HDL of triglyceride levels:

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ezetimibe; cholestrol absorption blocker

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ezetimibe MOA

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Prevent cholesterol reabsorption at small intestine brush border

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MOA of what drug: Prevent cholesterol reabsorption at small intestine brush border

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ezetimibe

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name of fibrates:

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gemfibrozil, clofibrate, bezafibrate, fenofibrate

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gemfibrozil, clofibrate, bezafibrate, fenofibrate: class and MOA

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Fibrates, Upregulate LPL -> TG clearance

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MOA of what drug: Upregulate LPL -> TG clearance

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fibrates: gemfibrozil, clofibrate, bezafibrate, fenofibrate

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ezetimibe adverse effects:

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(Rare): inc. LFTs, diarrhea

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what drug's adverse effects: Rare inc. LFTs, diarrhea

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ezetimibe: cholestrol reabsorption blockers

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Fibrates adverse effects:

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Myositis, hepatotoxicity (inc. LFTs), cholesterol gallstones

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what drug's adverse effects: Myositis, hepatotoxicity (inc. LFTs), cholesterol gallstones

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fibrates: gemfibrozil,clofibrate, bezafibrate,fenofibrate

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effect of nitrates (Nitroglycerin, isosorbide dinitrate) on contractility and HR

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increased: as a reflex response to decreased preload

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Treatment of Angina:

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nitrates/beta-blockers/Ca channel blockers

(Nifedipine acts like nitrates, verapamil acts like beta-blockers)

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Cardiac Glycosides name:

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Digoxin

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Digoxin's pharmacokinetics

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75% bioavailable. 20-40% is protein bound. half life: 40 hours

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Digoxin Clinical use:

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CHF (inc. contractility); atrial fibrillation (dec. conduction at AV node and depression of SA node).

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Digoxin's class:

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cardiac glycoside

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Clinical use of what drug?:

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CHF (inc. contractility) ; atrial fibrillation (dec. conduction at AV node and depression of SA node).

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Digoxin's MOA

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Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. inc. i.cellular [Ca2+] -> positive inotropy. Also stimulates vagus nerve -> dec. HR

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MOA of what drug: Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. inc. i.cellular [Ca2+] -> positive inotropy. Also stimulates vagus nerve -> dec. HR

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digoxin

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adverse effects of digoxin:

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Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG - inc PR, dec. QT, ST scooping (Salvador Dali), T-wave inversion, arrhythmia , AV block. Can lead to hyperkalemia (das bad).

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factors that predispose to digoxin toxicity:

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Factors predisposing to toxicity- renal failure (dec. excretion ), hypokalemia (permissive for digoxin binding at K+ binding site on Na+/K+ ATPase), quinidine (dec. digoxin clearance; displaces digoxin from tissue-binding sites)

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antidote to digoxin toxicity:

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Slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab (fragment antigen binding) fragments, Mg2+.

mech: (Magnesium suppresses digoxin-induced ventricular arrhythmias while phenytoin and lidocaine suppresses digoxin-induced ventricular automaticity and delay after-depolarizations)

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Class one antiarrythmics MOA

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- Na+channel blockers.

- Local anesthetics.

- Slow or block (dec.) conduction (especially in depolarized cells).

- dec. slope of phase 0 depolarization and inc. threshold for firing in abnormal pacemaker cells.

- Are state dependent(therefore selectively depress tissue that is frequently depolarized [e.g., tachycardia])

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factors increasing toxicity of class one antiarrythmics:

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hyperkalaemia

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names of class 1A antiarrythmics:

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Quinidine, Procainamide, Disopyramide

- "The Queen Proclaims Diso's pyramid ."

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quinidine toxicity:

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cinchonism- headache,tinnitus; thrombocytopenia; torsades de pointes due to inc QT interval

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procainamide toxicity:

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reversible SLE-like syndrome; thrombocytopenia; torsades de pointes due to inc QT interval

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disopyramide toxicity:

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heart failure; thrombocytopenia; torsades de pointes due to inc QT interval

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adv. effects of which drug: cinchonism- headache,tinnitus; thrombocytopenia; torsades de pointes due to inc QT interval

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quinidine

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adv. effects of which drug: reversible SLE-like syndrome; thrombocytopenia; torsades de pointes due to inc QT interval

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procainamide

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adv. effects of which drug: heart failure; thrombocytopenia; torsades de pointes due to inc QT interval

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disopyramide

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quinidine, procainamide, disopyramide desirable effects:

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class 1a anti-arrythmic: inc. AP duration, inc. effective refractory period (ERP), inc. QT interval. Affect both atrial and ventricular arrhythmias, especially re-entrantand ectopic supraventricular and ventricular tachycardia.

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desirable effects of which drug: inc. AP duration, inc. effective refractory period (ERP), inc. QT interval. Affect both atrial andventricular arrhythmias, especially re-entrant and ectopic supraventricular and ventricular tachycardia.

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quinidine, procainamide, disopyramide (class 1a antiarrythmics)

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class 1B anti-arrythmics names and primary use:

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lidocaine, mexiletine, tocainide. (+phenytoin)

- "1'd Buy LIDO's MEXIcan Tacos"

Use: post MI. "1B is Best post MI"

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lidocaine, mexiletine, tocainide. Desirable effects:

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dec. AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

therefore useful in acute ventricular arrhythmias (especially post-MI) and in digitalis-induced arrhythmias

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desirable effects of which drugs: dec. AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

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class 1b anti-a.ics: lidocaine, mexiletine, tocainide

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lidocaine, mexiletine, tocainide: adverse effects

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local anesthetic. CS stimulation/depression, cardiovascular depression

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adv. FX of which drugs: local anesthetic. CS stimulation/depression, cardiovascular depression.

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lidocaine tocainide, mexiletine

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class 1c antiarrymics names:

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Flecainide, propafenone

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Flecainide, propafenone: desirable effects:

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class 1c a-a: No effect on AP duration. Useful in ventricular tachycardias that progress to VF and inintractable SVT. Usually used only as last resort in refractory tachyarrhythmias

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contraindication of Flecainide, propafenone:

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post-MI, Structural heart disease

"1C is Contraindicated in structural heart diseaseand post-MI."

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adverse effect of Flecainide, propafenone

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Proarrhythmic, especially post-MI (contraindicated) . Significantly prolongs refractory period in AV node

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desirable effects of which drug: Useful in ventricular tachycardias that progress to VF and inintractable SVT. Usually used only as last resort in refractory tachyarrhythmias

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Flecainide, propafenone; class 1c antiarrythmics

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class 2 antiarrythmics: names and what they block:

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beta blockers: Metoprolol, propranolol, esmolol, atenolol, timolol.

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metaprolol selectivity:

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B1 selective blocker

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propanolol selectivity:

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B non-sel blocker

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esmolol selectivity:

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B1 selective. particularly short acting

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atenolol selectivity

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B1-selective blocker

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timolol selectivity

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B-non selective blocker

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class 2 antiarrythmics' MOA:

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B blockers: Decreases SA and AV nodal activity by dec. cAMP, dec. Ca2 + currents. Suppress abnormal pacemakers by dec. slope of phase 4.

AV node particularly sensitive: inc. PR interval

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B1 selective class 2 a-a drugs:

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atenolol, esmolol, metoprolol

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B non-sel class 2 a-a drugs:

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propanolol, timolol

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Metoprolol, propranolol, esmolol, atenolol , timolol adverse effects:

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class 2 a-as: B blockers: Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNSeffects (sedation, sleep alterations).

+ May mask the signs of hypoglycemia.

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metoprolol specific adverse effect:

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dyslipidemia. Treat overdose with glucagon

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propanolol specific adverse effect:

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exacerbate vasospasm in Prinzmetal's angina

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which drug has this adverse effect?: exacerbate vasospasm in Prinzmetal's angina

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propanolol

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which drug has this adverse effect?: dyslipidemia

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metoprolol: treat overdose with glucagon

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class 3 anti-arrythmics: names and what they block:

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Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS). K channel blockers.

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Amiodarone, Ibutilide, Dofetilide, Sotalol. class and MOA:

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class 3 a-as: K channel blockers: inc AP duration, inc ERP. Used when other anti-arrhythmics fail. inc QT interval.

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sotalol class and toxicity:

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class 3 a-a: torsades de pointes, excessive beta block

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ibutilide class and toxicity:

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class 3 a-a: torsades de pointes

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amiodarone class and toxicity:

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mostly class 3 a-a but has class 1, 2, 3, and 4, effects.

pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF).

Front 110

tests that are necessary to monitor for a patient on amiodarone:

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PFT, LFT, TFT. can cause hyper/hypothyroidism, hepatotoxicity, pulm. fibrosis amongst other adv. effects

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class four a-as: names and MOA:

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verapamil and diltiazem (Ca2+ blockers with cardiac selectivity)

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diltiazem MOA as an a-a:

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Ca2+ channel blocker: dec. conduction velocity, inc. ERP, inc. PR interval. Used in prevention of nodal arrhythmias (e.g., SVT)

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class four a-a names and toxicity:

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verapamil, and diltiazem: Constipation, flushing, oedema, CV effects (CHF, AV block, sinus node depression).

Front 114

adverse effects of which drugs: Constipation, flushing, oedema, CV effects (CHF, AV block, sinus node depression).

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class 4 a-as: verapamil and diltiazem

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a-a Used in prevention of nodal arrhythmias (e.g., SVT

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class 4: verapamil and diltiazem

Adenosine

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Adenosine MOA:

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inc. K+ out of cells -> hyperpolarizing the cell + dec. i.cellular Ca2+.

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Adenosine desirable effects and half life:

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Drug of choice in diagnosing/abolishingsupraventricular tachycardia. Very short acting (15 sec)

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Adenosine toxicity and antidote:

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Toxicity includes flushing, hypotension,chest pain. Effects blocked by theophylline and caffeine

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Mg2+ desirable effects

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Effective in torsades de pointes and digoxin toxicity.

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therapy for torsades de pointes and dig. toxicity:

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Mg2+