Exam 1- Cardiac Drugs PDF

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Nurs 223 theory course exam 1- Cardiac drugs to study...

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DRUG

INDICATION

Digoxin (Lanoxin)

Heart failure. Atrial fibrillation and atrial flutter (slows ventricular rate). Paroxysmal atrial tachycardia

DRUG CLASS CARDIAC Antiarrhythmics, Inotrope

ACTION Increases the force of myocardial contraction. Prolongs refractory period of the AV node. Decreases conduction through the SA and AV nodes.

NOTE/SE Fatigue, bradycardia, nausea, vomiting

Therapeutic Effects: Increased cardiac output (positive inotropic effect) and slowing of the heart rate (negative chronotropic effect). 0. 52ng/mli st he c or r ec tdi goxi nl e vel

Lidocaine (Xylocaine)

Amiodarone (Cordarone)

Ventricular arrhythmias

Life-threatening ventricular arrhythmias unresponsive to less toxic agents.

Antiarrhythmics Sodium channel blockers

Antiarrhythmics Potassium channel blockers

Suppresses automaticity and spontaneous depolarization of the ventricles during diastole by altering the flux of sodium ions across cell membranes with little or no effect on heart rate. Therapeutic Effects: Control of ventricular arrhythmias. Prolongs action potential and refractory period. Inhibits adrenergic stimulation. Slows the sinus rate, increases PR and QT intervals, and decreases peripheral vascular resistance (vasodilation). Therapeutic Effects:

Confusion, drowsiness, cardiac arrest, arrhythmias, bradycardia, hypotension

CHF, WORSENING OF ARRHYTHMIAS, bradycardia, hypotension.

Atropine

Metoprolol (Toprol)

Verapamil (Calan)

Treatment of sinus bradycardia and heart block.

Antiarrhythmics anticholinergic

Hypertension. Angina pectoris. Prevention of MI and decreased mortality in patients with recent MI. Management of stable, symptomatic (class II or III) heart failure due to ischemic, hypertensive or cardiomyopathc origin (may be used with ACE inhibitors, diuretics and/or digoxin; Toprol XL only).

Antiarrhythmics Beta blocker Antihypertensive

Management of hypertension, angina pectoris, and/or vasospastic (Prinzmetal’s) angina. Management of supraventricular arrhythmias and rapid ventricular rates in atrial flutter or fibrillation.

Antiarrhythmics Calcium channel blocker

Suppression of arrhythmias. Therapeutic Effects: Increased heart rate. Blocks stimulation of beta1(myocardial)adrenergic receptors. Does not usually affect beta2(pulmonary, vascular, uterine)adrenergic receptor sites. Therapeutic Effects: Decreased BP and heart rate. Decreased frequency of attacks of angina pectoris. Decreased rate of cardiovascular mortality and hospitalization in patients with heart failure. Inhibits the transport of calcium into myocardial and vascular smooth muscle cells, resulting in inhibition of excitationcontraction coupling and subsequent contraction. Decreases SA and AV conduction and prolongs AV node refractory period in conduction tissue. Therapeutic Effects: Systemic vasodilation resulting in decreased BP. Coronary vasodilation resulting in decreased frequency and

Tachycardia, palpitations, arrhythmias. Bradycardia, HF, Pulmonary edema, hypotension, peripheral vasoconstriction

ARRHYTHMIAS, HF, bradycardia, chest pain, hypotension, palpitations, peripheral edema, syncope, tachycardia.

Aspirin (ASA, ECASA)

Inflammatory disorders. Mild-mod pain Prophylaxis of transient ischemic attacks and MI.

Platelet Aggregation Inhibitors

severity of attacks of angina. Reduction of ventricular rate during atrial fibrillation or flutter. Produce analgesia and inflammation/fever inhibits production of prostaglandins. platelet aggregation.

Dyspepsia, epigastric distress, nausea, abdominal pain, hepatoxicity, vomiting

Therapeutic Effects: Analgesia. Reduction of inflammation. Reduction of fever. Decreased incidence of transient ischemic attacks and MI. Clopidogrel (Plavix)

Warfarin (Coumadin, Jantoven)

Reduction of atherosclerotic events (MI, stroke, vascular death) in patients at risk for such events including recent MI, acute coronary syndrome (unstable angina/non– Q-wave MI), stroke, or peripheral vascular disease.

Platelet Aggregation Inhibitors

Prophylaxis and treatment of: Venous thrombosis, Pulmonary embolism, Atrial fibrillation with embolization. Management of myocardial infarction: Decreases risk of death, Decreases risk of subsequent MI, Decreases risk of future thromboembolic events. Prevention of thrombus formation and embolization after prosthetic valve placement.

Anticoagulants

Inhibits platelet aggregation by irreversibly inhibiting the binding of ATP to platelet receptors. Therapeutic Effects: Decreased occurrence of atherosclerotic events in patients at risk. Interferes with hepatic synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X). Therapeutic Effects: Prevention of thromboembolic events.

Chest pain, hypertension, edema

Bleeding, cramps, nausea, fever

Heparin

Lovastatin (Mevacor)

Cholestyramine (Questran)

Prophylaxis and treatment of various thromboembolic disorders including: Venous thromboembolism, Pulmonary emboli, Atrial fibrillation with embolization, Acute and chronic consumptive coagulopathies, Peripheral arterial thromboembolism. Used in very low doses (10– 100 units) to maintain patency of IV catheters (heparin flush).

Anticoagulants

Primary prevention of coronary heart disease (myocardial infarction, unstable angina, and coronary revascularization) in asymptomatic patients with increased total and low-density lipoprotein (LDL) cholesterol and decreased high-density lipoprotein (HDL) cholesterol. Slows the progression of coronary atherosclerosis in patients with coronary artery disease.

Anti-hyperlipidemics Statin

Management of primary hypercholesterolemia. Pruritus associated with elevated levels of bile acids.

Anti-hyperlipidemics Bile Acid Sequestrant

Potentiates the inhibitory effect of antithrombin on factor Xa and thrombin. In low doses, prevents the conversion of prothrombin to thrombin by its effects on factor Xa. Higher doses neutralize thrombin, preventing the conversion of fibrinogen to fibrin. Therapeutic Effects: Prevention of thrombus formation. Prevention of extension of existing thrombi (full dose). Therapeutic Effects: Lowering of total and LDL cholesterol and triglycerides. Slightly increases HDL cholesterol. Slows the progression of coronary atherosclerosis with resultant decrease in coronary heart disease-related events. Lowers LDL by 20-40%  Lowers triglycerides by 10-20%  Increases HDL by 5-15%  Take in evening Bind bile acids in the GI tract, forming an insoluble complex. Result is increased clearance of cholesterol. Therapeutic Effects:



Bleeding, anemia

Abdominal cramps, constipation, diarrhea, flatus, heartburn. Interferes with grapefruit Adverse effects: Headache, Fatigue, Rhabdomyolosisdamage to muscles, hurts ache, Hepatotoxicity (rare) – check liver enzymes Q8 wks)

Abdominal discomfort, constipation, nausea. Adverse effects: Constipation, flatulence, abd

Decreased plasma cholesterol and low-density lipoproteins (LDLs). Decreased pruritus. Lowers LDL 30% Increases HDL minimally  May increase triglycerides  Removes bile acid from body Decreases the cholesterol in blood stream Large doses decrease lipoprotein and triglyceride synthesis by inhibiting the release of free fatty acids from adipose tissue and decreasing hepatic lipoprotein synthesis. Cause peripheral vasodilation in large doses.

pain, Decreased absorption of fatsoluble vitamins (ADEK)

 

Niacin (Niaspan)

Treatment and prevention of niacin deficiency (pellagra). Adjunctive therapy in certain hyperlipidemias (niacin only).

Anti-hyperlipidemics Vitamin B3

HEPATOTOXICITY, GI upset, flushing of the face and neck, pruritus. Adverse effects: Severe cutaneous flushing- premed w/ ASA or NSAID, take w/ or after meals. Vasodilate?

Therapeutic Effects: Decreased blood lipids (niacin only). Supplementation in deficiency states.    



Gemfibrozil (Lopid)

Management of type IIb hyperlipidemia (decreased HDL, increased LDL, increased triglycerides) in patients

Anti-hyperlipidemics

Lowers LDL 20% Increases HDL 20% Lowers triglycerides 40% Decreases production of VLDL Decreases lipoprotein synthesis

Inhibits peripheral lipolysis. Decreases triglyceride production by the liver. Decreases production of the

Abdominal pain, diarrhea, epigastric pain. Adverse effects: Nausea, abdominal

who do not yet have clinical coronary artery disease and have failed therapy with diet, exercise, weight loss, or other agents (niacin, bile acid sequestrants).

triglyceride carrier protein.Increases HDL. Therapeutic Effects: Decreased plasma triglycerides and increased HDL. 

 

Ezetimibe (Zetia)

Prazosin (Minipress)

Lisinopril (Prinivil)

Alone or with other agents (HMG-CoA reductase inhibitors) in the management of dyslipidemias including primary hypercholesterolemia, homozygous familial hypercholesterolemia and homozygous sitosterolemia. Mild to moderate hypertension.

Alone or with other agents in the management of hypertension. Management of heart failure. Reduction of risk

Lowers triglycerides 2050% Increases HDL 10-25% Minimally lowers LDL

pain, cholelithiasis, weight gain, Hepatotoxicity (check liver enzymes routinely). Combines w/ lovastatin= increase effective of lowering cholesterol

Anti-hyperlipidemics

Inhibits absorption of cholesterol in the small intestine. Therapeutic Effects: Lowering of cholesterol, a known risk factor for atherosclerosis.

cholecystitis, nausea,  liver enzymes

Alpha-1 adrenergic blockers

Dilates both arteries and veins by blocking postsynaptic alpha1adrenergic receptors. Decreases contractions in smooth muscle of prostatic capsule.

Dizziness, headache, weakness, first dose orthostatic hypotension, palpitations

ACE inhibitors

Therapeutic Effects: Lowering of BP. Decreased cardiac preload and afterload. Decreased symptoms of prostatic hyperplasia (urinary urgency, urinary hesitancy, nocturia). Angiotensinconverting enzyme (ACE) inhibitors block the conversion of angiotensin I to the

Dizziness, fatigue, first dose hypotension, cough

of death or development of heart failure after myocardial infarction.

Losartan (Cozaar)Cozzy the Cozaar

Clonidine (Catapres)

vasoconstrictor angiotensin II. ACE inhibitors also prevent the degradation of bradykinin and other vasodilatory prostaglandins. ACE inhibitors alsoqplasma renin levels andpaldosterone levels. Net result is systemic vasodilation.

Alone or with other agents in the management of hypertension. Treatment of diabetic nephropathy in patients with type 2 diabetes. Prevention of stroke in patients with hypertension and left ventricular hypertrophy.

Angiotensin II receptor blocker (ARB)

Mild to moderate

Centrally acting alpha

Therapeutic Effects: Lowering of BP in hypertensive patients. Increased survival and decreased Symptoms in patients with heart failure. Increased survival after myocardial infarction. Blocks the vasoconstrictor and aldosteronesecreting effects of angiotensin II at various receptor sites, including vascular smooth muscle and the adrenal glands. Therapeutic Effects: Lowering of BP in hypertensive patients. Decreased progression of diabetic nephropathy. Decreased incidence of stroke in patients with hypertension and left ventricular hypertrophy (effect may be less in black patients). Stimulates alpha-

Diarrhea, hyperkalemia,

Drowsiness, dry

hypertension.

Nitroglycerin

Furosemide (Lasix)

Management of angina pectoris. Adjunct treatment of acute MI. Production of controlled hypotension during surgical procedures. Treatment of HF associated with acute MI.

Edema due to heart failure, hepatic impairment or renal disease. Hypertension.

agonist Antihypertensives

Nitrates

Antihypertensives Diuretics

adrenergic receptors in the CNS, which results in decreased sympathetic outflow inhibiting cardioacceleration and vasoconstriction centers. Prevents pain signal transmission to the CNS by stimulating alpha-adrenergic receptors in the spinal cord. Therapeutic Effects: Decreased BP. Decreased pain. Improvement in ADHD symptoms. Increases coronary blood flow by dilating coronary arteries and improving collateral flow to ischemic regions. Produces vasodilation (venous greater than arterial). Decreases left ventricular enddiastolic pressure and left ventricular end-diastolic volume (preload). Reduces myocardial oxygen consumption. Therapeutic Effects: Relief or prevention of anginal attacks. Increased cardiac output. Reduction of BP. Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water, sodium, chloride, magnesium,

mouth, withdrawal phenomenon

Dizziness, headache, hypotension, tachycardia

Dehydration, hypocalcemia, hypochloremia, hypokalemia, hypomagnesemia, hyponatremia, hypovolemia, metabolic alkalosis.

potassium, and calcium. Effectiveness persists in impaired renal function.

Propranolol (Inderal)

Metoprolol (Toprol) – SEE ABOVE

Hydralazine (Apresoline)

Management of hypertension, angina, arrhythmias, hypertrophic cardiomyopathy, thyrotoxicosis, essential tremors, pheochromocytoma. Also used in the prevention and management of MI, and the prevention of vascular headaches.

Antihypertensives Beta blocker

Moderate to severe hypertension (with a diuretic).

Antihypertensives Direct vasodilator

Therapeutic Effects: Diuresis and subsequent mobilization of excess fluid (edema, pleural effusions). Decreased BP. Blocks stimulation of beta1(myocardial) and beta2 (pulmonary, vascular, and uterine)adrenergic receptor sites. Therapeutic Effects: Decreased heart rate and BP. Suppression of arrhythmias. Prevention of MI. Direct-acting peripheral arteriolar vasodilator. Therapeutic Effects: Lowering of BP in hypertensive patients and decreased afterload in patients with HF.

Diltiazem (Cardizem)

Management of: Hypertension. Angina pectoris and vasospastic (Prinzmetal’s) angina. Supraventricular tachyarrhythmias and rapid ventricular rates in atrial flutter or fibrillation.

Antihypertensives Calcium channel blocker nondihydropyridine

Inhibits transport of calcium into myocardial and vascular smooth muscle cells, resulting in inhibition of excitationcontraction coupling and subsequent contraction. Therapeutic Effects:

Fatigue, weakness, erectile dysfunction

Tachycardia, dizziness, drowsiness, sodium retention, drug induced-lupus syndrome

Abnormal dreams, peripheral edema, anxiety, confusion, dizziness Hypotension, bradycardia, dizziness, facial flushing, headache

Nifedipine (Procardia)

Aliskiren (Tekturna)

Management of: Hypertension (extended-release only), Angina pectoris, Vasospastic (Prinzmetal’s) angina.

Treatment of hypertension (alone or with other agents).

Antihypertensives Calcium channel blocker nondihydropyridine

Antihypertensives Direct renin inhibitor

Systemic vasodilation resulting in decreased BP. Coronary vasodilation resulting in decreased frequency and severity of attacks of angina. Reduction of ventricular rate in atrial fibrillation or flutter. Inhibits calcium transport into myocardial and vascular smooth muscle cells, resulting in inhibition of excitationcontraction coupling and subsequent contraction.

Therapeutic Effects: Systemic vasodilation, resulting in decreased BP. Coronary vasodilation, resulting in decreased frequency and severity of attacks of angina. Inhibition of renin results in decreased formation of angiotensin II, a powerful vasoconstrictor. Therapeutic Effects: Decreased BP.

Headache, peripheral edema, flushing of face. Hypotension, bradycardia, dizziness, facial flushing, headache

Cough, hypotension, abdominal pain, angioedema...