Angina pectoris is a clinical syndrome characterized by episodes of chest pain. It occurs when there is a deficit in myocardial oxygen supply (myocardial ischemia) in relation to myocardial oxygen demand. It is most often caused by atherosclerotic plaque in the coronary arteries but may also be caused by coronary vasospasm. The development and progression of atherosclerotic plaque is called coronary artery disease (CAD). Atherosclerotic plaque narrows the lumen, decreases elasticity, and impairs dilation of coronary arteries. The result is impaired blood flow to the myocardium, especially with exercise or other factors that increase the cardiac workload and need for oxygen. The continuum of CAD progresses from angina to myocardial infarction. There are three main types of angina: classic angina, variant angina, and unstable angina. The Canadian Cardiovascular Society classifies clients with angina according to the amount of physical activity they can tolerate before anginal pain occurs. These categories can assist in clinical assessment and evaluation of therapy.

Classic anginal pain is usually described as substernal chest pain of a constricting, squeezing, or suffocating nature. It may radiate to the jaw, neck, or shoulder, down the left or both arms, or to the back. The discomfort is sometimes mistaken for arthritis, or for indigestion, as the pain may be associated with nausea, vomiting, dizziness, diaphoresis, shortness of breath, or fear of impending doom. The discomfort is usually brief, typically lasting 5 minutes or less until the balance

of oxygen supply and demand is restored.

For clients at any stage of CAD development, irrespective of symptoms of myocardial ischemia, optimal management involves lifestyle changes and medications, if necessary, to control or reverse risk factors for disease progression. Risk factors are frequently additive in nature and are classified as nonmodifiable and modifiable. Nonmodifiable risk factors include age, race, gender, and family history. The risk factors that can be altered include smoking, hypertension, hyperlipidemia, obesity, sedentary lifestyle, stress, and the use of drugs that increase cardiac workload (eg, adrenergics, corticosteroids).

Thus, efforts are needed to assist clients in reducing blood pressure, weight, and serum cholesterol levels, when indicated, and developing an exercise program. For clients with diabetes mellitus, glucose and blood pressure control can reduce the microvascular changes associated with the condition. In addition, clients should avoid circumstances known to precipitate acute attacks, and those who smoke should stop. Smoking is harmful to clients because:

Nicotine increases catecholamines which, in turn, increase heart rate and blood pressure.

Carboxyhemoglobin, formed from the inhalation of carbon monoxide in smoke, decreases delivery of blood and oxygen to the heart, decreases myocardial contractility, and increases the risks of life-threatening cardiac dysrhythmias

(eg, ventricular fibrillation) during ischemic episodes.

Both nicotine and carbon monoxide increase platelet adhesiveness and aggregation, thereby promoting thrombosis.

Smoking increases the risks for myocardial infarction, sudden cardiac death, cerebrovascular disease (eg, stroke), peripheral vascular disease (eg, arterial insufficiency), and hypertension. It also reduces high-density lipoprotein, the good cholesterol.

Additional nonpharmacologic management strategies include surgical revascularization (eg, coronary artery bypass graft) and interventional procedures that reduce blockages (eg, percutaneous transluminal coronary angioplasty [PTCA], intracoronary stents, laser therapy, and rotoblators). However, most clients still require antianginal and other cardiovascular medications to manage their disease.

Drugs used for myocardial ischemia are the organic nitrates, the beta-adrenergic blocking agents, and the calcium channel blocking agents. These drugs relieve anginal pain by reducing myocardial oxygen demand or increasing blood supply to the myocardium. Nitrates and beta blockers are described in the following sections and dosage ranges are listed in Drugs at a Glance: Nitrates and Beta Blockers. Calcium channel blockers are described in a following section; indications for use and dosage ranges are listed in Drugs at a Glance: Calcium Channel Blockers.

Organic nitrates (and nitrates) are simple nitric and nitrous acid esters of alcohols. These compounds cause a rapid reduction in myocardial oxygen demand followed by rapid relief of symptoms. They are effective in stable and anstable angina, as well as Prinzmetals or variant angina pectoris.

Nitrates, b-blockers, and calcium channel-blockers are equally effective for relief of anginal symptoms. However, for prompt relief of an ongoing attack of angina precipitated by exercise or emotional stress, sublingual (or spray form) nitroglycerin (NITROSTAT) is the drug of choice.

At therapeutic doses, nitroglycerin has two major effects. First, it causes dilation of the large veins, resulting in pooling blood in the veins. This diminishes preload (venous return to the heart), and reduces the work of the heart. Second, nitroglycerin dilates the coronary vasculature, providing increased blood supply to the heart muscle. Nitroglycerin causes a decrease in myocardial oxygen consumption because of decreased cardiac work.

Adverse effects. The most common adverse effect of nitroglycerin, as well as the other nitrates, is headache. 30 to 60 % of patients receiving intermittent nitrate therapy with long-acting agents develop headaches. High doses of organic nitrates can also cause postural hypotension, facial flushing, and tachycardia.

Tolerance to the actions of nitrates develops rapidly. It can be overcome by provision of a daily nitrate-free interval to restore sensitivity to the drug. This interval is typically 6 to 8, 10-12 hours, usually at night because there is decreased demand on the heart at that time. Nitroglycerin patches are worn for 12 hours and removed for 12 hours. However, Prinzmetals or variant angina worsens early in the morning, perhaps due to circardian catecholamine surges. These patients nitrate-free interval should be late afternoon.

Indication and usage:

1. Control of blood pressure in perioperative hypertension: hypertension associated with surgical procedures, especially cardiovascular procedures, such as hypertension seen during intratracheal intubation, anesthesia, skin incision, sternotomy, cardiac bypass.

2. Congestive heart failure associated with acute myocardial infarction.

3. Treatment of angina pectoris.

4. Production of controlled hypotension during surgical procedures.

Isosorbide dinitrate is an orally active nitrate. The drug is not readily metabolized by the liver or smooth muscle and has lower potency than nitroglycerin in relaxing vascular smooth muscle. Isosorbide dinitrate (Isordil, Sorbitrate) is used to reduce the frequency and severity of acute anginal episodes. When given sublingually or in chewable tablets, it acts in about 2 minutes, and its effects last 2 to 3 hours. When higher doses are given orally, more drug escapes metabolism in the liver and produces systemic effects in approximately 30 minutes. Therapeutic effects last about 4 hours after oral administration. The effective oral dose is usually determined by increasing the dose until headache occurs, indicating the maximum tolerable dose. Sustained-release capsules also are available. Isosorbide mononitrate (Ismo, Imdur) is the metabolite and active component of isosorbide dinitrate. It is well absorbed after oral administration and almost 100% bioavailable. Unlike other oral nitrates, this drug is not subject to first-pass hepatic metabolism. Onset of action occurs within 1 hour, peak effects occur between 1 and 4 hours, and the elimination half-life is approximately 5 hours. It is used only for prophylaxis of angina; it does not act rapidly enough to relieve acute attacks.

In angina pectoris, beta-adrenergic blocking agents are used in long-term management to decrease the frequency and severity of anginal attacks, decrease the need for sublingual nitroglycerin, and increase exercise tolerance. When a beta blocker is being discontinued after prolonged use, it should be tapered in dosage and gradually discontinued or rebound angina can occur.

These drugs should not be given to clients with known or suspected coronary artery spasms because they may intensify the frequency and severity of vasospasm. This probably results from unopposed stimulation of alpha-adrenergic receptors, which causes vasoconstriction, when beta-adrenergic receptors are blocked by the drugs. Clients who continue to smoke may have reduced efficacy with the use of beta blockers. Clients with asthma should be observed for bronchospasm from blockage of beta2 receptors in the lung. Beta blockers should be used with caution in clients with diabetes mellitus because they can conceal signs of hypoglycemia except for sweating).

The b-adrenergic blockers agents supress the activation of the heart by blocking b1 receptors. They also reduce the work of the heart by decreasing cardiac output and causing a slight decrease in blood pressure. Propranolol is the prototype of this class of compounds, but other b-blockers, such as metoprolol and atenolol are equally effective. Propranolol decreases the oxygen requirement of heart muscle and therefore is effective in reducing the chest pain on exertion that is common in angina. Propranolol is therefore useful in the chronic management of stable angina (not for acute treatment). Tolerance to moderate exercise is increased and this is noticeable by improvement in the electrocardiogram. Agents with intrinsic sympathomymetic activity (for example, pindolol and acebutolol) are less effective and should be avoided. The b-blockers reduce the frequency and severity oh angina attacks. These agents are particularly useful in the treatment of patients with myocardial infarction. The b-blockers can be used with nitrates to increase exercise duration and tolerance. They are, however, contraindicated in patients with diabetes, peripheral vascular disease, or chronic pulmonary disease.

Calcium channel blockers act on contractile and conductive tissues of the heart and on vascular smooth muscle. For these cells to function normally, the concentration of intracellular calcium must be increased. This is usually accomplished by movement of extracellular calcium ions into the cell (through calcium channels in the cell membrane) and release of bound calcium from the sarcoplasmic reticulum in the cell. Thus, calcium plays an important role in maintaining vasomotor tone, myocardial contractility, and conduction. Calcium channel blocking agents prevent the movement of extracellular calcium into the cell. As a result, coronary and peripheral arteries are dilated, myocardial contractility is decreased, and the conduction system is depressed in relation to impulse formation (automaticity) and conduction velocity.

In angina pectoris, the drugs improve the blood supply to the myocardium by dilating coronary arteries and decrease the workload of the heart by dilating peripheral arteries. In variant angina, calcium channe l blockers reduce coronary artery vasospasm. In atrial fibrillation or flutter and other supraventricular tachydysrhythmias, diltiazem and verapamil slow the rate of ventricular response. In hypertension, the drugs lower blood pressure primarily by dilating peripheral arteries.

Calcium channel blockers are well absorbed after oral administration but undergo extensive first-pass metabolism in the liver. Most of the drugs are more than 90% protein bound and reach peak plasma levels within 1 to 2 hours (6 hours or longer for sustained-release forms). Most also have short elimination half-lives (<5 hours), so doses must be given three or four times daily unless sustained-release formulations are used. Amlodipine (30 to 50 hours), bepridil (24 hours), and felodipine (11 to 16 hours) have long elimination half-lives and therefore can be given once daily. The drugs are metabolized in the liver, and dosage should be reduced in clients with severe liver disease. Dosage reductions are not required with renal disease. The calcium channel blockers approved for use in the United States vary in their chemical structures and effects on body tissues. Seven of these are chemically dihydropyridines, of which nifedipine is the prototype. Bepridil, diltiazem, and verapamil differ chemically from the dihydropyridines and each other. Nifedipine and related drugs act mainly on vascular smooth muscle to produce vasodilation, whereas verapamil and diltiazem have greater effects on the cardiac conduction system.

The drugs also vary in clinical indications for use; most are used for angina or hypertension, and only diltiazem and verapamil are used to manage supraventricular tachydysrhythmias. In clients with CAD, the drugs are effective as monotherapy but are commonly prescribed in combination with beta blockers. In addition, nimodipine is approved for use only in subarachnoid hemorrhage, in which it decreases spasm in cerebral blood vessels and limits the extent of brain damage. In animal studies, nimodipine exerted greater effects on cerebral arteries than on other arteries, probably because it is highly lipid soluble and penetrates the bloodbrain barrier. Contraindications include second- or third-degree heart block, cardiogenic shock, and severe bradycardia, heart failure, or hypotension. The drugs should be used cautiously with milder bradycardia, heart failure, or hypotension and with renal or hepatic impairment.

In addition to antianginal drugs, several other drugs may be used to control risk factors and prevent progression of myocardial ischemia to myocardial infarction and sudden cardiac death. These may include:

Aspirin. This drug has become the standard of care because of its antiplatelet (ie, antithrombotic) effects. Recommended doses vary from 81 mg daily to 325 mg daily or every other day; apparently all doses are beneficial in reducing the possibility of myocardial reinfarction, stroke, and death. Clopidogrel, 75 mg/day,

is an acceptable alternative for individuals with aspirin allergy.

Antilipemics. These drugs may be needed by clients who are unable to lower serum cholesterol levels sufficiently with a low-fat diet. Lovastatin or a related statin is often used. The goal is usually to reduce the serum cholesterol level below 200 mg/dL and lowdensity lipoprotein cholesterol to below 130 mg/dL.

Antihypertensives. These drugs may be needed for clients with hypertension. Because beta blockers and calcium channel blockers are used to manage hypertension as well as angina, one of these drugs may be effective for both disorders.

The goals of drug therapy are to relieve acute anginal pain; reduce the number and severity of acute anginal attacks; improve exercise tolerance and quality of life; delay progression of CAD; prevent myocardial infarction; and prevent sudden cardiac death.

For relief of acute angina and prophylaxis before events that cause acute angina, nitroglycerin (sublingual tablets or translingual spray) is usually the primary drug of choice. Sublingual or chewable tablets of isosorbide dinitrate also may be used. For long-term prevention or management of recurrent angina, oral or topical nitrates, beta-adrenergic blocking agents, or calcium channel blocking agents are used.

Combination drug therapy with a nitrate and one of the other drugs is common and effective. Clients taking one or more long-acting antianginal drugs should carry a short-acting drug as well, to be used for acute attacks.

Dosage of all antianginal drugs should be individualized to achieve optimal benefit and minimal adverse effects. This is usually accomplished by starting with relatively small doses and increasing them at appropriate intervals as necessary. Doses may vary widely among individuals.

Clients who take long-acting dosage forms of nitrates on a regular schedule develop tolerance to the vasodilating (antianginal) effects of the drug. The clients more likely to develop tolerance are those on high-dose, uninterrupted therapy. Although tolerance decreases the adverse effects of hypotension, dizziness, and headache, therapeutic effects also may be decreased. As a result, episodes of chest pain may occur more often or be more severe than expected. In addition, shortacting nitrates may be less effective in relieving acute pain. Opinions seem divided about the best way to prevent or manage nitrate tolerance. Some authorities recommend using short-acting nitrates when needed and avoiding the long-acting forms. Others recommend using the long-acting forms for 12 to 16 hours daily during active periods and omitting them during inactive periods or sleep.

Thus, a dose of an oral nitrate or topical ointment would be given every 6 hours for three doses daily, allowing a rest period of 6 hours without a dose. Transdermal discs should be removed at bedtime. If anginal symptoms occur during sleeping hours, short-acting nitrates may be beneficial in relieving the symptoms. All nitrates should be administered at the lowest effective dosage.

The safety and effectiveness of antianginal drugs have not been established for children. Nitroglycerin has been given IV for heart failure and intraoperative control of blood pressure, with the initial dose adjusted for weight and later doses titrated to response.

Antianginal drugs are often used because cardiovascular disease and myocardial ischemia are common problems in older adults. Adverse drug effects, such as hypotension and syncope, are likely to occur, and they may be more severe than in younger adults. Blood pressure and ability to ambulate safely should be closely monitored, especially when drug therapy is started or dosages are increased. Ambulatory clients also should be monitored for their ability to take the drugs correctly.

With calcium channel blockers, older adults may have higher plasma concentrations of verapamil, diltiazem, nifedipine, and amlodipine. This is attributed to decreased hepatic metabolism of the drugs, probably because of decreased hepatic blood flow. In addition, older adults may experience more hypotension with verapamil, nifedipine, and felodipine than younger clients. Blood pressure should be monitored with these drugs.

Little information is available about the use of antianginal drugs in clients with impaired renal function. A few studies indicate that advanced renal failure may alter the pharmacokinetics of calcium channel blockers. Although the pharmacokinetics of diltiazem and verapamil are quite similar in clients with normal and impaired renal function, caution is still advised. With verapamil, about 70% of a dose is excreted as metabolites in urine.

Dosage reductions are considered unnecessary with verapamil and diltiazem but may be needed with nifedipine and several other dihydropyridine derivatives. With nifedipine, protein binding is decreased and the elimination half-life is prolonged with renal impairment. In a few clients, reversible elevations in blood urea nitrogen and serum creatinine have occurred. With nicardipine, plasma concentrations are higher in clients with renal impairment, and dosage should be reduced. Bepridil should be used with caution because its metabolites are excreted mainly in urine.

Nitrates, beta blockers, and calcium channel blockers are metabolized in the liver, and all should be used with caution in clients with significant impairment of hepatic function from reduced blood flow or disease processes.

With oral nitrates, it is difficult to predict effects. On the one hand, first-pass metabolism is reduced, which increases bioavailability (amount of active drug) of a given dose. On the other hand, the nitrate reductase enzymes that normally deactivate the drug may increase if large doses are given. In this case, more enzymes are available and the drug is metabolized more rapidly, possibly reducing therapeutic effects of a given dose. Relatively large doses of oral nitrates are sometimes given to counteract the drug tolerance (reduced hemodynamic effects) associated with chronic use. In addition, metabolism of nitroglycerin and isosorbide dinitrate normally produces active metabolites. Thus, if metabolism is reduced by liver impairment, drug effects may be decreased and shorter in duration.

With calcium channel blockers, impairment of liver function has profound effects on the pharmacokinetics and pharmacodynamics of most of these drugs. Thus, the drugs should be used with caution, dosages should be substantially reduced, and clients should be closely monitored for drug effects (including periodic measurements of liver enzymes). These recommendations stem from the following effects:

An impaired liver produces fewer drug-binding plasma proteins such as albumin. This means that a greater proportion of a given dose is unbound and therefore active.

In clients with cirrhosis, bioavailability of oral drugs is greatly increased and metabolism (of both oral and parenteral drugs) is greatly decreased. Both of these effects increase plasma levels of drug from a given dose (essentially an overdose). The effects result from shunting of blood around the liver so that drug molecules circulating in the bloodstream do not come in contact with drug-metabolizing enzymes and therefore are not metabolized. For example, the bioavailability of verapamil, nifedipine, felodipine, and nisoldipine is approximately double and their clearance is approximately one third that of clients without cirrhosis.

Although hepatotoxicity is uncommon, clinical symptoms of hepatitis, cholestasis, or jaundice and elevated liver enzymes (eg, alkaline phosphatase, creatine kinase [CK], lactate dehydrogenase [LDH], aspartate aminotransferase [AST], alanine aminotransferase [ALT]) have occurred, mainly with diltiazem, nifedipine, and verapamil. These changes resolve if the causative drug is stopped.

Antianginal drugs have multiple cardiovascular effects and may be used alone or in combination with other cardiovascular drugs in clients with critical illness. They are probably used most often to manage severe angina, severe hypertension, or serious cardiac dysrhythmias. For example, IV nitroglycerin may be used for angina and hypertension; an IV beta blocker or calcium channel blocker may be used to improve cardiovascular function with angina, hypertens ion, or supraventricular tachydysrhythmias. With any of these drugs, dosage must be carefully titrated and clients must be closely monitored for hypotension and other drug effects.

In addition, absorption of oral drugs or topical forms of nitroglycerin may be impaired in clients with extensive edema, heart failure, hypotension, or other conditions that impair blood flow to the gastrointestinal tract or skin.

CARDIAC DYSRHYTHMIAS can originate in any part of the conduction system or from atrial or ventricular muscle. They result from disturbances in electrical impulse formation (automaticity), conduction (conductivity), or both. The characteristic of automaticity allows myocardial cells other than the SA node to depolarize and initiate the electrical impulse that culminates in atrial and ventricular contraction. This may occur when the SA node fails to initiate an impulse or does so too slowly. When the electrical impulse arises anywhere other than the SA node, it is an abnormal or ectopic focus. If the ectopic focus depolarizes at a rate faster than the SA node, the ectopic focus becomes the dominant pacemaker. Ectopic pacemakers may arise in the atria, AV node, Purkinje fibers, or ventricular muscle. They may be activated by hypoxia, ischemia, or hypokalemia. Ectopic foci indicate myocardial irritability (increased responsiveness to stimuli) and potentially serious impairment of cardiac function.

Dysrhythmias may be mild or severe, acute or chronic, episodic or relatively continuous. They are clinically significant if they interfere with cardiac function (ie, the hearts abil-ity to pump sufficient blood to body tissues). The normal heartcan maintain an adequate cardiac output with ventricular rates ranging from 40 to 180 beats per minute. The diseased heart, however, may not be able to maintain an adequate cardiac output with heart rates below 60 or above 120. Dysrhythmias are usually categorized by rate, location, or patterns of conduction.

Antidysrhythmic agents are diverse drugs used for prevention and management of cardiac dysrhythmias. Dysrhythmias, also called arrhythmias, are abnormalities in heart rate or rhythm. They become significant when they interfere with cardiac function and ability to perfuse body tissues. To aid in understanding of dysrhythmias and antidysrhythmic drug therapy, the physiology of cardiac conduction and contractility is reviewed.

Most of antiarrhythmic agents suppress automaticity (1) by decreasing the slope of diastolic depolarization and/or by raising the threshold of discharge to a less negative voltage. Such drugs cause the frequency of discharge to decrease, an effect that is more pronounced in cells with ectopic pacemaker activity than in normal cells.

Indications for Use

Antidysrhythmic drug therapy commonly is indicated in the following conditions:

1. To convert atrial fibrillation (AF) or flutter to normalsinus rhythm (NSR)

2. To maintain NSR after conversion from AF or flutter

3. When the ventricular rate is so fast or irregular that cardiac output is impaired. Decreased cardiac output leads to symptoms of decreased systemic, cerebral, and coronary circulation.

4. When dangerous dysrhythmias occur and may be fatal if not quickly terminated. For example, ventricular tachycardia may cause cardiac arrest.

Effects of drugs on conduction abnormalities: Antiarrhythmic agents prevent reentry by slowing conduction and/or increasing the refractory period to convent a unidirectional block into a bidirectional block.

As noted above, the antiarrhythmic drugs can modify impulse generation and conduction. More than a dozen such drugs that are patentially usefull in treating arrhythmias are currently available. However, only a limited number of these agents are clinically beneficial in the treatment of selected arrhythmias. For example, the acute termination of ventricular tachycardia by lidocaine or supraventricular tachycardia by adenosine or verapamil are examples in which antiarrhythmic therapy results in decreased morbidity. In contrast, many of the antiarrhythmic agents are now known to have lethal proarrhythmic actions, that is, to cause arrhythmias.

The antiarrhythmic drugs can be classified according to their predominant effects on the action potential. Although this classification is convenient, it is not entirely clear-cut, because many of the drugs have actions relating to more than one class or they have active metabolites with a different class of action.

Classification of antiarrhythmic drugs



Mechanism of Action

Drug name


Na+Channel blocker

Disopyramide, procainamide, quinidine


Na+Channel blocker

Lidocaine, mexiletine, tocainide


Na+Channel blocker

Flecainide, propafenone


b Adrenoreceptor blocker

Esmolol, metoprolol, pindolol, propranolol


K+Channel blocker

Amiodarone, bretylium, sotalol


Ca++ Channel blocker

Diltiazem, verapamil

Other antiarrhythmic drugs

Adenosine, digoxin


Class I drugs have been subdivided into three groups according to their effect on the duration of the action potential. Class IA agents slow the rate of rise of the action potential, thus slowing conduction, and prolong the action potential and increase the ventricular effective refractory period. They have an intermediate speed of association with activated/inactivated sodium channels, and an intermediate rate of dissociation from resting channels. Class IB drugs have little effect on the rate of depolarization, but rather they decrease the duration of the action potential by shortening repolarization. They rapidly interact with sodium channels. Class IC agents markedly depress the rate of rise of the membrane action potential, and therfore they cause marked conduction slowing but have little effect on the duration of the membrane action potential or the ventricular effective refractory period. They bind slowly to sodium channels.

The Class II agents include the b-adrenergic antagonists. These drugs diminish Phase 4 depolarisation, thus depressing automaticity, prolonging AV conduction, and decreasing heart rate and contractility.

These agents exert antidysrhythmic effects by blocking sympathetic nervous system stimulation of beta receptors in the heart and decreasing risks of ventricular fibrillation. Blockage of receptors in the SA node and ectopic pacemakers decreases automaticity, and blockage of receptors in the AV node increases the refractory period. The drugs are effective for management of supraventricular dysrhythmias and those resulting from excessive sympathetic activity. Thus, they are most often used to slow the ventricular rate of contraction in supraventricular tachydysrhythmias (eg, AF, atrial flutter, paroxysmal supraventricular tachycardia [PSVT]).

As a class, beta blockers are being used more extensively because of their effectiveness and their ability to reduce mortality in a variety of clinical settings, including postmyocardial infarction and heart failure. Reduced mortality may result from the drugs ability to prevent ventricular fibrillation.Only four of the beta blockers marketed in the United States are approved by the Food and Drug Administration (FDA) for management of dysrhythmias.

Class II agents are useful in treating tachyarrhythmias caused by increased sympathetic activity. They are also used for atrial flutter and fibrillation, and for AV nodal reentrant tachycardia.

Class III agents block potassium channels and thus diminish the outward potassium current during repolarization of cardiac cells. They prolong the effective refractory period. All Class III drugs have the potential to induce arrhythmias.

Although the drugs share a common mechanism of action, they are very different drugs. As with beta blockers, clinical use of class III agents is increasing because they are associated with less ventricular fibrillation and decreased mortality compared with class I drugs.

The Class IV drugs are calcium channel blockers. They decrease the inward current carried by calcium and slowed conduction in tissues dependent on calcium currents, such as the AV node.

Other antiarrhythmic drugs:

Digoxin (tab. 0.125, 0.25, 0.5 mg, amp. 1, 2 ml 0.025 %) shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in Purkinje fibers. Digoxin is used to control the ventricular response rate in atrial fibrillation and flutter. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation. [This arrhythmia is usually treated with lidocaine or phenytoin].

Adenosine is a naturally occurring nucleoside, but at high doses the drug decreases conduction velocity, prolongs the refractory period, and decreases automaticity in the AV node. Intravenous adenosine is the drug of choice for abolishing acute supraventricular tachycardia. It has low toxicity, but causes flushing, chest pain and hypotension. Adenosine has an extremely short duration of action (about 15 seconds).

 Magnesium sulfate is given IV in the management of several dysrhythmias, including prevention of recurrent episodes of torsades de pointes and management of digitalis-induced dysrhythmias. Its antidysrhythmic effects may derive from imbalances of magnesium, potassium, and calcium. Hypomagnesemia increases myocardial irritability and is a risk factor for both atrial and ventricular dysrhythmias. Thus, serum magnesium levels should be monitored in clients at risk

and replacement therapy instituted when indicated. However, in some instances, the drug seems to have antidysrhythmic effects even when serum magnesium levels are normal.

Therapeutic indications for some commonly encountered arrhythmias

Type of arrhythmia

Class I

Class II

Class III

Class IV



Atrial flutter






Commonly used drugs






Alternative drugs






Atrial fibrillation






Commonly used drugs





Anticoagulant therapy

Alternative drugs







AV nodal reentry






Commonly used drugs






Alternative drugs






Acute supraventricular tachycardia






Commonly used drugs






Alternative drugs







Acute ventricular tachycardia






Commonly used drugs






Alternative drugs



Sotalol, amiodarone



Ventricular fibrillation (not responding to electrical defibrillation)






Commonly used drugs






Alternative drugs



Bretylium, amiodarone