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Cardiovascular Drugs
A to I

Go To Cardiovascular Drugs L to Z 

 Last Updated 04/10/00 12:26:51 PM

Adenosine (Adenocard)
Class: Antiarrhythmic
Use: Treat PSVT.
Action: Slows conduction time through the AV node, interrupting the re-entry pathways through the AV node, restoring normal sinus rhythm. Promotes K+ efflux = repolarization (hyperpolarization).
Cardiac Effect: Treat PSVT.
Administration Routes: IV
Onset Time: Effects occur rapidly
½ Life: < 10 seconds
Metabolism -- Excretion: In the blood and tissue to inosine then to AMP and hypoxanthine --
Side Effects: CP. Hypotension. Dyspnea (12%).
Anesthesia Interactions: Methylxanthines antagonize effects. Dipyrdamole (Persantine) potentiates effects. Carbamazepine (Tegretol) may increase heart block.

Amiloride (Midamor)
Class: K+ Sparing Diuretic
Use: Counteracts K+ loss induced by other diuretics. Usually used in conjunction with more potent diuretics such as thiazides or loop diuretics.
Action: Interferes with K+/Na+ exchange (active transport) in the distal tubule. Decreases Na+ reabsorption in the distal tubule
Cardiac Effect:
Administration Routes: PO
Onset Time: 2 hours
½ Life: 6-9 hours
Metabolism -- Excretion: No active metabolites. -- Excreted unchanged equally in the urine and feces
Side Effects: Hyperkalemia.
Anesthesia Interactions: ACE Inhibitor may increase chance of hyperkalemia.

Amiodarone (Cordarone)
Class: Antiarrhythmic – Class III (K+ channel blocker) (Also blocks some Na+ & Ca2+ channels and is a sympatholytic agent)
Use: Treat ventricular arrhythmias or supraventricular arrhythmias
Action: Inhibits adrenergic stimulation. Prolongs the action potential and refractory period in myocardial tissue. Decreases AV conduction and sinus node function. Doesn’t effect the resting membrane potential. ­ chance of DAD’s & EAD’s.
Cardiac Effect: Treat ventricular arrhythmias or supraventricular arrhythmias
Administration Routes: PO, IV
Onset Time: 2-3 days
½ Life: 40-55 days. Shortened in children.
Metabolism -- Excretion: In liver, major metabolite active. -- Via biliary excretion. Possible enterohepatic recirculation.
Side Effects: Pulmonary fibrosis. Interstitial pneumonitis alveolitis. CHF. Arrhythmias. Myocardial depression. Hypotension. Increases [Digitalis].
Anesthesia Interactions: Use with general anesthetics may result in hypotension, atropine-resistant bradycardia, sinus arrest or AV block. Combined use with b -blockers, digitalis or Ca2+ blockers may result in bradycardia or sinus arrest.

Amrinone (Inocor)
Class: Positive inotropic agent – Phosphodiesterase inhibitor
Use: Treatment of low cardiac output states (sepsis, CHF).
Action: Inhibits phosphodiesterase (PDE) III, the major PDE in cardiac vascular tissues. Inhibition of PDE III increases cAMP potentiating delivery of Ca2+ to myocardial contractile systems resulting in a positive inotropic effect
Cardiac Effect: Increased inotropy
Administration Routes: IV
Onset Time: IV – 2-5 minutes
½ Life: Neonates: 22.2 hrs. Infants: 6.8 hrs. Adults (normal): 3.6 hrs. Adults (with CHF): 5.8 hrs
Metabolism -- Excretion: Hepatic. -- 60-90% excreted as metabolites in urine within 24 hours
Side Effects: Supraventricular and ventricular arrhythmias, hypotension, thrombocytopenia, chest pain, hepatotoxicity
Anesthesia Interactions:

Atenolol (Tenormin)
Class: b -blocker
Use: Treatment of hypertension, alone or in combination with other agents. Management of angina pectoris, post-myocardial infarction patients
Action: Competitively blocks response to b -adrenergic stimulation. Selectively blocks b 1 receptors with little or no effect on b 2 receptors except at high doses
Cardiac Effect:
Administration Routes: PO, IV
Onset Time: PO 1 hr. IV Rapid.
½ Life: 6-7 hrs. Longest in patients with reduced renal function
Metabolism -- Excretion: None -- 40% excreted as unchanged drug in urine. 50% in feces
Side Effects: Bradycardia, hypotension, chest pain, heart failure, 2nd or 3rd degree AV block, dyspnea
Anesthesia Interactions: By decreasing the clearance of continuous infusions it may increase the effect of perioperative agents such as fentanyl, propofol, sufentanil, ketamine and etomidate. May increase the effect/toxicity of haloperidol (hypotensive effects), hydralazine.

Bretylium (Bretylol)
Class: Antiarrhythmic – Class III (K+ channel blocker)
Use: Treatment of ventricular tachycardia and fibrillation. Used in the treatment of other serious ventricular arrhythmias resistant to lidocaine
Action: Causes an initial release of Norepinephrine (NE) at the peripheral adrenergic nerve terminals. After the initial release of NE, it inhibits further release by depressing postganglionic nerve endings in response to sympathetic nerve stimulation.
Cardiac Effect:
Administration Routes: IM, IV
Onset Time: IM 2 hrs. IV 6-20 minutes
½ Life: 7-11 hrs. ESRD: 16-32 hrs.
Metabolism -- Excretion: Not metabolized -- 70-80% excreted over the first 24 hrs. Excreted unchanged in the urine.
Side Effects: Hypotension, bradycardia, hyperthermia, respiratory depression.
Anesthesia Interactions: Increases toxicity of other antiarrhythmic agents. Additive toxicity or effect by bretylium, pressor catecholamines, digitalis

Bumetanide (Bumex)
Class: Loop Diuretic
Use: Management of edema secondary to CHF or hepatic or renal disease. Can be used in furosemide-allergic patients (1 mg = 40 mg furosemide)
Action: Inhibits reabsorption of Na+ and Cl- in the ascending loop of Henle and proximal renal tubule, interfering with the Cl- binding cotransport system, thus causing increased excretion of H2O, Na+, Cl-, Mg2+, PO4 and Ca2+. It does not appear to act on the distal tubule
Cardiac Effect:
Administration Routes: PO, IM, IV
Onset Time: PO/IM 30-60 mins. IV within a few mins.
½ Life: Infants: 2.5 hrs. Children & Adults: 1-3 hrs.
Metabolism -- Excretion: Partial, occurs in the liver -- Majority of unchanged drug and metabolites excreted in urine.
Side Effects: Hypokalemia, hypochloremia, hypotension
Anesthesia Interactions: Nondepolarizing agents will have a prolonged duration. Digoxin predisposed to digoxin toxicity secondary to potential hypokalemia.

Captopril (Capoten, Capozide)
Class: Angiotensin Converting Enzyme (ACE) Inhibitor - Vasodilator
Use: Management of hypertension and treatment of CHF.
Action: Competitive inhibitor of ACE. Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. Results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion.
Cardiac Effect:
Administration Routes: PO
Onset Time: 15 mins
½ Life: Normal: 1.9 hrs. CHF: 2.06 hrs. Anuria: 20-40 hrs.
Metabolism -- Excretion: 50% Metabolized. -- 95% excreted in urine in 24 hrs.
Side Effects: Tachycardia, chest pain, Cough
Anesthesia Interactions: Increased hypotension when used with anesthetic agents

Clonidine (Catapres, Duraclon)
Class: a 2 agonist (Centrally acting)
Use: Tx. of mild to moderate HTN. Used for narcotic withdrawal and smoking cessation. Decreases the stress response to surgery, the hemodynamic response to intubation, the dose of anesthetic drugs needed to produce anesthesia. Intrathecal and epidural clonidine used to enhance postop analgesia.
Action: Stimulates a 2 receptors in the brain inhibiting NE release from SN terminals. Reduces SNS activity producing sedation and a decrease in vasomotor tone and HR. Also enhances parasympathetic tone. Epidural use produces segmental analgesia via pre and postsynaptic a 2 activation, which prevents pain signal transmission.
Cardiac Effect:
Administration Routes: PO, Transdermal, epidural
Onset Time: PO 0.5-1 hr. IV 10 mins. Epidural 20 mins.
½ Life: Normal: 6-20 hrs. Renal impairment: 18-41 hrs. Epidural CSF: 1-2 hrs.
Metabolism -- Excretion: Hepatic (50%). Metabolized to inactive metabolites -- 65% excreted in urine. 32% unchanged. 22% feces.
Side Effects: Somnolence, orthostatic hypotension, agitation, tachycardia, bradycardia, CHF
Anesthesia Interactions: b -blockers may ­ bradycardia and may ­ the rebound HTN of withdrawal

Digitoxin ()
Class: Positive inotropic agent – Cardiac Glycoside
Use: Treatment of CHF and to slow the ventricular rate in tachy arrhythmias such as atrial fibrillation, atrial flutter, and SVT. Cardiogenic shock
Action: CHF—Inhibition of the Na+/K+ ATPase pump, which acts to ­ the intracellular Na+-Ca2+ exchange to ­ intracellular Ca2+ leading to, ­ contractility. Supraventricular Arrhythmias—Direct suppression of the AV node conduction to ­ effective refractory period and ¯ conduction velocity – + inotropic effect, enhanced vagal tone, and ¯ ventricular rate to fast atrial arrhythmias.
Cardiac Effect:
Administration Routes: PO, IM, IV
Onset Time:
½ Life: 168 hrs
Metabolism -- Excretion: Liver -- In gut, by bile
Side Effects: Sinus brady, AV & SA block, atrial or nodal ectopic beats, Ventricular arrhythmias
Anesthesia Interactions: Amiodarone & Verapamil ­ [Dig]

Digoxin (Lanoxin)
Class: Positive inotropic agent – Cardiac Glycoside – Antiarrhythmic
Use: Treatment of CHF and to slow the ventricular rate in tachy arrhythmias such as atrial fibrillation, atrial flutter, and SVT. Cardiogenic shock
Action: CHF—Inhibition of the Na+/K+ ATPase pump, which acts to ­ the intracellular Na+-Ca2+ exchange to ­ intracellular Ca2+ leading to, ­ contractility. Supraventricular Arrhythmias—Direct suppression of the AV node conduction to ­ effective refractory period and ¯ conduction velocity – + inotropic effect, enhanced vagal tone, and ¯ ventricular rate to fast atrial arrhythmias.
Cardiac Effect:
Administration Routes: PO, IM, IV
Onset Time: PO 1-2 hrs. IV 5-30 mins
½ Life: Neonates: 35-170 hrs. Infants: 18-25 hrs. Children: 35 hrs. Adults: 38-48 hrs. Adults (anephric): 4-6 days.
Metabolism -- Excretion: Some metabolism in stomach or gut. Metabolites are still active. -- 50-70% excreted unchanged in urine
Side Effects: Sinus brady, AV & SA block, atrial or nodal ectopic beats, Ventricular arrhythmias
Anesthesia Interactions: Amiodarone & Verapamil ­ [Dig]

Diltiazem (Cardizem, Dilacor)
Class: Antiarrhythmic – Class IV (Ca2+ channel blocker). -- Antihypertensive agent
Use: Hypertension. Chronic stable angina or angina from coronary artery spasm. Atrial fibrillation or atrial flutter. PSVT.
Action: Inhibits Ca2+ from entering the "slow channels or select voltage-sensitive areas of VSM and myocardium during depolarization, producing a relaxation of coronary VSM and coronary vasodilation. Increases myocardial O2 delivery in patients with vasospastic angina. Compared to nifedipine it has more inhibitory effects on cardiac conduction system and less vasodilation properties.
Cardiac Effect:
Administration Routes: PO, IV
Onset Time: PO: 30-60 mins.
½ Life: 4-10 hrs. May increase with renal impairment
Metabolism -- Excretion: Extensive first-pass metabolism in liver. -- In urine and bile mostly as metabolites.
Side Effects: Bradycardia, AV block (first & second degree), pharyngitis
Anesthesia Interactions:

Dobutamine (Dobutrex)
Class: Positive inotropic agent - b -agonist
Use: Increase cardiac output in the short-term treatment of patients with cardiac decompensation caused by depressed contractility from organic heart disease, cardiac surgical procedures, or acute MI
Action: Stimulates b 1 receptors, causing increased contractility and heart rate, with little effect on b 2 or a receptors. Mimics Norepinephrine.
Cardiac Effect:
Administration Routes: IV
Onset Time: IV: 1-2 mins
½ Life: 2 mins
Metabolism -- Excretion: In tissues and the liver to inactive metabolites. -- Metabolites are excreted in urine.
Side Effects: Ectopic beats, increased HR, CP, HTN, Ventricular tachycardia (with high doses). PVC’s, dyspnea, paresthesia
Anesthesia Interactions: Increased TPR. General anesthetics and dobutamine have resulted in ventricular arrhythmias in animals.

Enalapril (Vasotec)
Class: Angiotensin Converting Enzyme (ACE) Inhibitor - Vasodilator
Use: Management of hypertension and treatment of CHF.
Action: Competitive inhibitor of ACE. Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. Results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion.
Cardiac Effect:
Administration Routes: PO, IV
Onset Time: About 1 hr.
½ Life: Infants: 6-10 hrs. Adults: 35-38 hrs.
Metabolism -- Excretion: Is a pro-drug and undergoes biotransformation in the liver to enalaprilat the active compound. -- 60-80% in urine with some fecal excretion.
Side Effects: Tachycardia, syncope, paresthesia, dyspnea, hypotension, bronchospasm
Anesthesia Interactions: Increased hypotensive effects when anesthetic agents are added.

Flecainide (Tambocor)
Class: Antiarrhythmic – Class I C (Na+ channel blocker)
Use: Prevention and suppression of documented life-threatening ventricular arrhythmias (sustained VT). Controlling symptomatic, disabling SVT in patients without structural heart disease in whom other agents fail.
Action: Slows conduction in cardiac tissue by altering transport of ions across cell membranes. Causes slight prolongation of refractory periods. Decreases the rate of rise of the action potential without affecting its duration. Increases electrical stimulation threshold of ventricle, HIS-Purkinje system. Possesses local anesthetic and moderate negative inotropic effects.
Cardiac Effect:
Administration Routes: PO
Onset Time:
½ Life: Infants: 11-12 hrs. Children: 8 hrs. Adults: 7-22 hrs. ESRD: 19-26 hrs.
Metabolism -- Excretion: In the liver. -- 80-90% excreted in urine as unchanged drug and metabolites (10-50%)
Side Effects: Dyspnea. CP, edema, tachycardia, bradycardia, heart blocks, increased PR & QRS, CHF, hypoesthesia, paresthesia
Anesthesia Interactions:

Furosemide (Lasix)
Class: Loop Diuretic
Use: Management of edema associated with CHF and hepatic or renal disease.
Action: Inhibits reabsorption of Na+ and CL- in the ascending loop of Henle and distal tubule. Increased excretion of H2O, Na+, Cl-, K+, Mg2+, Ca2+, HCO3. Decreases CSF production by interfering with Na+ transport in cerebral glial tissue.
Cardiac Effect:
Administration Routes: PO, IV, IM
Onset Time: PO: 30-60 min. IV: 5 min. IM: 30 min
½ Life: 0.5 - 1.1 hrs. Pt. With ESRD: 9 hrs
Metabolism -- Excretion: -- 50% of oral and 80% of IV dose excreted in the urine within 24 hrs. The rest by non-renal pathways.
Side Effects: Electrolyte imbalance, hypotension,
Anesthesia Interactions: Increased antihypertensive agents effects. Interferes with hypoglycemic effect of antidiabetic agents.

Hydralazine (Apresoline)
Class: Vasodilator
Use: Management of moderate to severe HTN, CHF, HTN secondary to pre-eclampsia / eclampsia. Also use in treatment of primary pulmonary HTN.
Action: Direct vasodilation of arterioles (with little effect on veins) producing decreased systemic vascular resistance. It binds to arterioles and activates guanylate cyclase producing accumulation of 6MP. It is associated with reflex tachycardia, increased cardiac output and plasma volume.
Cardiac Effect:
Administration Routes: PO, IM, IV
Onset Time: PO: 20-60 mins. IV: 5-20 mins.
½ Life: 2-8 hrs. ESRD: 7-16 hrs.
Metabolism -- Excretion: Large hepatic first pass. -- 14% excreted unchanged in urine
Side Effects: Tachycardia, hypotension
Anesthesia Interactions:

Hydrochlorothiazide (HCTZ, Ezide)
Class: Thiazide Diuretic
Use: Management of mild to moderate HTN. Treatment of edema in CHF and nephrotic syndrome
Action: Inhibits Na+ reabsorption in the distal tubules causing increased excretion of Na+ and H2O as well as K+ and H+. Allows Ca2+ reabsorption. Not as potent as loop diuretics.
Cardiac Effect:
Administration Routes: PO
Onset Time: PO: within 2 hrs
½ Life: Lasts 6-12 hrs
Metabolism -- Excretion: -- Excreted unchanged in the urine
Side Effects: Hypotension
Anesthesia Interactions:

Isosorbide Dinitrate (Isordil, Iso-Bid, Sorbitrate)
Class: Nitrate – Vasodilator
Use: Prevention and treatment of angina pectoris. For CHF. To relieve pain, dysphagia, and spasm in esophageal spasm with GE reflux
Action: Stimulation of intracellular cGMP results in VSM relaxation of both arterial and venous vasculature. Increased venous pooling decreases left ventricular pressure (preload) and art4rial dilation decreases arterial resistance (afterload). Therefore, this reduces cardiac oxygen demand. Coronary artery dilation improves collateral flow to ischemic regions. Converted in liver to its active form, mononitrate. Longer lasting than other nitrates.
Cardiac Effect:
Administration Routes: PO, Sublingual
Onset Time: SL: 2-10 mins. PO: 45-60 mins.
½ Life: 1-4 hrs. Metabolite: 4 hrs.
Metabolism -- Excretion: Extensive liver metabolism. -- In urine and feces
Side Effects: Tolerance buildup, hypotension
Anesthesia Interactions: ASA may increase serum nitrate concentration

Isradipine (DynaCirc)
Class: Ca2+ Channel blocker (Dihydropyridines) (DHP)
Use: Treatment of HTN, CHF, migraine prophylaxis
Action: Inhibits Ca2+ from entering the "slow channels" or select voltage-sensitive areas of VSM and myocardium during depolarization, producing peripheral and coronary vasodilation. Increases myocardial O2 delivery in patients with vasospastic angina. Decrease in TPR may enhance cardiac function. Closed channel blocker.
Cardiac Effect:
Administration Routes: PO
Onset Time:
½ Life: 8 hrs
Metabolism -- Excretion: 100% hepatic -- Renal excretion by metabolites.
Side Effects: Edema, tachycardia, Heart failure
Anesthesia Interactions:

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