Antianginal Drugs

Critical Thinking ScenarioMrs. Sinatro, a 56-year-old housewife, experiences chest pressure after exercise. She is the mother of sixand works 30 hours a week word-processing documents for a law firm. When she is told that her chest dis-comfort is probably secondary to coronary artery disease, she cannot believe it. She states, “I’m just tooyoung to have heart problems!” Mrs. Sinatro is referred to her primary care health care provider and givensublingual nitroglycerin tablets to use PRN for chest pain.

Reflect on:� What assessment questions will you ask to determine Mrs. Sinatro’s risk factors for heart disease?� Evaluate Mrs. Sinatro’s reaction to her new diagnosis and the client teaching implications.� What lifestyle modifications would help minimize the progression of coronary artery disease?

774

chapter 53

1. Describe the types, causes, and effects ofangina pectoris.

2. Describe general characteristics and types ofantianginal drugs.

3. Discuss nitrate antianginals in terms of indica-tions for use, routes of administration, adverseeffects, nursing process implications, and drugtolerance.

4. Differentiate between short-acting and long-acting dosage forms of nitrate antianginal drugs.

5. Discuss calcium channel blockers in terms oftheir effects on body tissues, clinical indicationsfor use, common adverse effects, and nursingprocess implications.

6. Teach clients ways to prevent, minimize, ormanage acute anginal attacks.

Antianginal Drugs

ObjectivesAFTER STUDYING THIS CHAPTER, THE STUDENT WILL BE ABLE TO:

OVERVIEW

Angina pectoris is a clinical syndrome characterized byepisodes of chest pain. It occurs when there is a deficit inmyocardial oxygen supply (myocardial ischemia) in relationto myocardial oxygen demand. It is most often caused byatherosclerotic plaque in the coronary arteries but may alsobe caused by coronary vasospasm. The development and pro-gression of atherosclerotic plaque is called coronary arterydisease (CAD). Atherosclerotic plaque narrows the lumen,decreases elasticity, and impairs dilation of coronary arteries.The result is impaired blood flow to the myocardium, espe-cially with exercise or other factors that increase the cardiacworkload and need for oxygen.

The continuum of CAD progresses from angina to myocar-dial infarction. There are three main types of angina: classicangina, variant angina, and unstable angina (Box 53–1). TheCanadian Cardiovascular Society classifies clients with angina

according to the amount of physical activity they can toleratebefore anginal pain occurs (Box 53–2). These categories canassist in clinical assessment and evaluation of therapy.

Classic anginal pain is usually described as substernalchest pain of a constricting, squeezing, or suffocating nature.It may radiate to the jaw, neck, or shoulder, down the left orboth arms, or to the back. The discomfort is sometimes mis-taken for arthritis, or for indigestion, as the pain may be asso-ciated with nausea, vomiting, dizziness, diaphoresis, shortnessof breath, or fear of impending doom. The discomfort is usu-ally brief, typically lasting 5 minutes or less until the balanceof oxygen supply and demand is restored.

Current research indicates that gender differences exist inthe type and quality of cardiac symptoms, with women re-porting epigastric or back discomfort. Additionally, olderadults may have atypical symptoms of CAD and may experi-ence “silent” ischemia that may delay them from seeking pro-fessional help. Individuals with diabetes mellitus may present

CHAPTER 53 ANTIANGINAL DRUGS 775

without classic angina, although they may experience relatedsymptoms. The American Heart Association has releasedguidelines for the management of angina.

Numerous overlapping factors contribute to the develop-ment and progression of CAD. To aid understanding of drugtherapy for angina, these factors are described in the followingsections.

Coronary Atherosclerosis

Atherosclerosis (see Chap. 58) begins with accumulation oflipid-filled macrophages (ie, foam cells) on the inner lining of

coronary arteries. Foam cells, which promote growth of ather-osclerotic plaque, develop in response to elevated blood cho-lesterol levels. Initially, white blood cells (monocytes) becomeattached to the endothelium and move through the endotheliallayer into subendothelial spaces, where they ingest lipid andbecome foam cells. These early lesions progress to fibrousplaques containing foam cells covered by smooth muscle cellsand connective tissue. Advanced lesions also contain hemor-rhages, ulcerations, and scar tissue. Factors contributing to plaque development and growth include endothelial in-jury, lipid infiltration (ie, cholesterol), recruitment of in-flammatory cells (mainly monocytes and T lymphocytes),and smooth muscle cell proliferation. Endothelial injury may

causes platelets to aggregate at the site of injury, form a throm-bus, and release chemical mediators that cause vasoconstriction(eg, thromboxane, serotonin, platelet-derived growth factor). Thedisrupted plaque, thrombus, and vasoconstriction combine to obstruct blood flow further in the affected coronary artery. Whenthe plaque injury is mild, blockage of the coronary artery may beintermittent and cause silent myocardial ischemia or episodes ofanginal pain at rest. Thrombus formation and vasoconstrictionmay progress until the coronary artery is completely occluded,producing myocardial infarction. Endothelial injury, with subse-quent thrombus formation and vasoconstriction, may also resultfrom therapeutic procedures (eg, angioplasty, atherectomy).

The Agency for Healthcare Research and Quality, in its clinicalpractice guidelines for the management of angina, defines unstableangina as meeting one or more of the following criteria:

• Anginal pain at rest that usually lasts longer than 20 minutes• Recent onset (<2 months) of exertional angina of at least

Canadian Cardiovascular Society Classification (CCSC)class III severity

• Recent (<2 months) increase in severity as indicated by pro-gression to at least CCSC class III.

However, myocardial ischemia may also be painless or silentin a substantial number of clients. Overall, the diagnosis is usu-ally based on chest pain history, electrocardiographic evidence ofischemia, and other signs of impaired cardiac function (eg, heartfailure).

Because unstable angina often occurs hours or days beforeacute myocardial infarction, early recognition and effective man-agement are extremely important in preventing progression to in-farction, heart failure, or sudden cardiac death.

ClassicClassic angina (also called stable, typical, or exertional angina)occurs when atherosclerotic plaque obstructs coronary arteries andthe heart requires more oxygenated blood than the blocked arter-ies can deliver. Chest pain is usually precipitated by situations thatincrease the workload of the heart, such as physical exertion, ex-posure to cold, and emotional upset. Recurrent episodes of classicangina usually have the same pattern of onset, duration, and in-tensity of symptoms. Pain is usually relieved by rest, a fast-actingpreparation of nitroglycerin, or both.

VariantVariant angina (also called atypical, Prinzmetal’s, or vasospasticangina) is caused by spasms of the coronary artery that decreaseblood flow to the myocardium. The spasms occur most often incoronary arteries that are already partly blocked by atheroscleroticplaque. Variant angina usually occurs during rest or with minimalexercise and often occurs at night. It often occurs at the same timeeach day. Pain is usually relieved by nitroglycerin. Long-termmanagement includes avoidance of conditions that precipitate va-sospasm, when possible (eg, exposure to cold, smoking, and emo-tional stress), as well as antianginal drugs.

UnstableUnstable angina (also called rest, preinfarction, and crescendoangina) is a type of myocardial ischemia that falls between classicangina and myocardial infarction. It usually occurs in clients withadvanced coronary atherosclerosis and produces increased fre-quency, intensity, and duration of symptoms. It often leads tomyocardial infarction.

Unstable angina usually develops when a minor injury rupturesatherosclerotic plaque. The resulting injury to the endothelium

BOX 53–1 TYPES OF ANGINA PECTORIS

stairs at a normal pace and in normal conditions can elicitangina.

Class III: Marked limitations of ordinary physical activity.Angina occurs on walking one or two blocks on the level andclimbing one flight of stairs in normal conditions and at a nor-mal pace.

Class IV: Inability to carry on any physical activity withoutdiscomfort—anginal symptoms may be present at rest.

Class I: Ordinary physical activity (eg, walking, climbingstairs) does not cause angina. Angina occurs with strenuous,rapid, or prolonged exertion at work or recreation.

Class II: Slight limitation of ordinary activity. Angina oc-curs on walking or climbing stairs rapidly, walking uphill,walking or stair climbing after meals, or in cold, in wind,or under emotional stress. Walking more than two blockson the level and climbing more than one flight of ordinary

BOX 53–2 CANADIAN CARDIOVASCULAR SOCIETY CLASSIFICATION OF PATIENTS WITH ANGINA PECTORIS

776 SECTION 9 DRUGS AFFECTING THE CARDIOVASCULAR SYSTEM

be the initiating factor in plaque formation because it allowsmonocytes, platelets, cholesterol, and other blood com-ponents to come in contact with and stimulate abnormalgrowth of smooth muscle cells and connective tissue in thearterial wall.

Atherosclerosis commonly develops in the coronary ar-teries. As the plaque lesions develop over time, they becomelarger and extend farther into the lumen of the artery. The le-sions may develop for decades before they produce symp-toms of reduced blood flow. Eventually, such events asplaque rupture, mural hemorrhage, formation of a thrombusthat partly or completely occludes an artery, and vasocon-striction precipitate myocardial ischemia. Thus, serious im-pairment of blood flow may occur with a large atheroscleroticplaque or a relatively small plaque with superimposed va-sospasm and thrombosis. If stenosis blocks approximately80% of the artery, blood flow cannot increase in response toincreased need; if stenosis blocks 90% or more of the artery,blood flow is impaired when the client is at rest.

When coronary atherosclerosis develops slowly, collateralcirculation develops to increase blood supply to the heart.Collateral circulation develops from anastomotic channelsthat connect the coronary arteries and allow perfusion of anarea by more than one artery. When one artery becomesblocked, the anastomotic channels become larger and allowblood from an unblocked artery to perfuse the area typicallysupplied by the occluded artery. Endothelium-derived relax-ing factors such as nitric oxide (NO) can dilate collateral ves-sels and facilitate regional myocardial blood flow. Althoughcollateral circulation may prevent myocardial ischemia in theclient at rest, it has limited ability to increase myocardial per-fusion with increased cardiac workload.

Myocardial ischemia impairs blood flow to the myo-cardium, especially with exercise, mental stress, exposure tocold, or other factors that increase the cardiac workload. Mostindividuals with myocardial ischemia have advanced coro-nary atherosclerosis. Hypertension is also a major risk factorfor myocardial ischemia.

Myocardial Ischemia

Myocardial ischemia occurs when the coronary arteries areunable to provide sufficient blood and oxygen for normal car-diac functions. Also known as ischemic heart disease, CAD,and coronary heart disease, myocardial ischemia may presentas an acute coronary syndrome with three main consequences.One consequence is unstable angina, with the occurrence ofpain (symptomatic myocardial ischemia). A second is myo-cardial infarction (MI) that is silent or asymptomatic and diag-nosed by biochemical markers only. A third is MI, with orwithout ST-segment elevation, which occurs when the ischemiais persistent or severe.

Resultant Cardiovascular Impairments

1. With normal cardiac function, coronary blood flow canincrease to meet needs for an increased oxygen supply

with exercise or other conditions that increase cardiacworkload. When coronary arteries are partly blocked byatherosclerotic plaque, vasospasm, or thrombi, bloodflow may not be able to increase sufficiently.

2. The endothelium of normal coronary arteries synthe-sizes numerous substances (see Chap. 50) that protectagainst vasoconstriction and vasospasm, bleeding andclotting, inflammation, and excessive cell growth. Im-paired endothelium (eg, by rupture of atheroscleroticplaque or the shear force of hypertension) leads tovasoconstriction, vasospasm, clot formation, formationof atherosclerotic plaque, and growth of smooth mus-cle cells in blood vessel walls.

One important substance produced by the endothe-lium of coronary arteries is NO (also called endothelium-derived relaxing factor). NO, which is synthesized fromthe amino acid arginine, is released by shear stress on theendothelium, sympathetic stimulation of exercise, andinteractions with acetylcholine, histamine, prostacyclin,serotonin, thrombin, and other chemical mediators. NOrelaxes vascular smooth muscle and inhibits adhesionand aggregation of platelets. When the endothelium isdamaged, these vasodilating and antithrombotic effectsare lost. At the same time, production of strong vaso-constrictors (eg, angiotensin II, endothelin-1, thrombox-ane A2) is increased. In addition, inflammatory cellsenter the injured area and growth factors stimulategrowth of smooth muscle cells. All of these factors par-ticipate in blocking coronary arteries.

3. Sympathetic nervous system stimulation normally pro-duces dilation of coronary arteries, tachycardia, and in-creased myocardial contractility to handle an increasedneed for oxygenated blood. Atherosclerosis of coronaryarteries, especially if severe, may cause vasoconstrictionas well as decrease blood flow by obstruction.

Nonpharmacologic Management of Angina

For clients at any stage of CAD development, irrespective ofsymptoms of myocardial ischemia, optimal management in-volves lifestyle changes and medications, if necessary, to con-trol or reverse risk factors for disease progression. Risk factorsare frequently additive in nature and are classified as non-modifiable and modifiable. Nonmodifiable risk factors includeage, race, gender, and family history. The risk factors that canbe altered include smoking, hypertension, hyperlipidemia,obesity, sedentary lifestyle, stress, and the use of drugs that in-crease cardiac workload (eg, adrenergics, corticosteroids).Thus, efforts are needed to assist clients in reducing bloodpressure, weight, and serum cholesterol levels, when indi-cated, and developing an exercise program. For clients withdiabetes mellitus, glucose and blood pressure control can re-duce the microvascular changes associated with the condition.

In addition, clients should avoid circumstances known toprecipitate acute attacks, and those who smoke should stop.Smoking is harmful to clients because:


• Nicotine increases catecholamines which, in turn, in-crease heart rate and blood pressure.

• Carboxyhemoglobin, formed from the inhalation of car-bon monoxide in smoke, decreases delivery of blood andoxygen to the heart, decreases myocardial contractility,and increases the risks of life-threatening cardiac dys-rhythmias (eg, ventricular fibrillation) during ischemicepisodes.

• Both nicotine and carbon monoxide increase plateletadhesiveness and aggregation, thereby promoting throm-bosis.

• 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 lipopro-tein, the “good” cholesterol.

Additional nonpharmacologic management strategies in-clude surgical revascularization (eg, coronary artery bypassgraft) 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 cardiovascularmedications to manage their disease.

ANTIANGINAL DRUGS

Drugs used for myocardial ischemia are the organic nitrates,the beta-adrenergic blocking agents, and the calcium channelblocking agents. These drugs relieve anginal pain by reduc-ing myocardial oxygen demand or increasing blood supply tothe myocardium. Nitrates and beta blockers are described inthe following sections and dosage ranges are listed in Drugsat a Glance: Nitrates and Beta Blockers. Calcium channelblockers are described in a following section; indications foruse and dosage ranges are listed in Drugs at a Glance: Cal-cium Channel Blockers.

Organic Nitrates

Organic nitrates relax smooth muscle in blood vessel walls.This action produces vasodilation, which relieves anginal pain

Drugs at a Glance: Nitrate and Beta-Blocker Antianginal Drugs

Generic/Trade Name Indications for Use Routes and Dosage Ranges

Nitrates

Nitroglycerin (Nitro-Bid, others)

Isosorbide dinitrate(Isordil, Sorbitrate)

Isosorbide mononitrate(Ismo, Imdur)

Beta Blockers

Propranolol (Inderal)

Atenolol (Tenormin)

Metoprolol (Lopressor)

Nadolol (Corgard)

Relieve acute anginaPrevent exercise-induced anginaLong-term prophylaxis to decrease the

frequency and severity of acute anginalepisodes

Treatment and prevention of angina

Treatment and prevention of angina

Long-term management of angina, to re-duce frequency and severity of anginalepisodes

Same as propranolol

Same as propranolol

Same as propranolol

PO Immediate-release tablets, 2.5–9 mg 2 or 3 times per day

PO Sustained-release tablets or capsules, 2.5 mg 3 or 4 times per day

SL 0.15–0.6 mg PRN for chest painTranslingual spray, one or two metered doses (0.4 mg/dose)

sprayed onto oral mucosa at onset of anginal pain, to amaximum of 3 doses in 15 min

Transmucosal tablet, 1 mg q3–5h while awake, placedbetween upper lip and gum or cheek and gum

Topical ointment, 1⁄2–2 inches q4–8h; do not rub inTopical transdermal disc, applied once dailyIV 5–10 mcg/min initially, increased in 10- to 20-mcg/min

increments up to 100 mcg/min or more if necessary torelieve pain

SL 2.5–10 mg PRN or q2–4hPO Regular tablets, 10–60 mg q4–6hPO Chewable tablets, 5–10 mg q2–3hPO Sustained-release capsules, 40 mg q6–12hPO 20 mg twice daily, with first dose on arising and the

second dose 7 h laterPO Extended-release tablets (Imdur), 30–60 mg once

daily in the morning, increased after several days to120 mg once daily if necessary

PO 10–80 mg 2 to 4 times per day IV 0.5–3 mg q4h until desired response is obtained

PO 50 mg once daily, initially, increased to 100 mg/dafter 1 wk if necessary

PO 50 mg twice daily initially, increased up to 400 mgdaily if necessary

PO 40–240 mg/d in a single dose


by several mechanisms. First, dilation of veins reduces venouspressure and venous return to the heart. This decreases bloodvolume and pressure within the heart (preload), which in turndecreases cardiac workload and oxygen demand. Second, ni-trates dilate coronary arteries at higher doses and can increaseblood flow to ischemic areas of the myocardium. Third, ni-trates dilate arterioles, which lowers peripheral vascular resis-tance (afterload). This results in lower systolic blood pressureand, consequently, reduced cardiac workload. The prototypeand most widely used nitrate is nitroglycerin.

Nitrates are converted to NO in vascular smooth muscle.NO activates guanylate cyclase, an enzyme that catalyzes for-mation of cyclic guanine monophosphate, which decreasescalcium levels in vascular smooth muscle cells. Because in-tracellular calcium is required for contraction of vascularsmooth muscle, the result of decreased calcium is vasodila-tion. The NO derived from nitrate medications can be con-sidered a replacement or substitute for the NO that a damagedendothelium can no longer produce.

Clinical indications for nitroglycerin and other nitrates aremanagement and prevention of acute chest pain caused by

myocardial ischemia. For acute angina and prophylaxis beforea situation deemed likely to precipitate acute angina, fast-act-ing preparations (sublingual or chewable tablets, transmucosalspray or tablet) are used. For management of recurrent angina,long-acting preparations (oral and sustained-release tablets ortransdermal ointment and discs) are used. However, they maynot be effective long-term because tolerance develops to theirhemodynamic effects. Intravenous (IV) nitroglycerin is used tomanage angina that is unresponsive to organic nitrates viaother routes or beta-adrenergic blocking agents. It also may beused to control blood pressure in perioperative or emergencysituations and to reduce preload and afterload in severe heartfailure.

Contraindications include hypersensitivity reactions, severeanemia, hypotension, and hypovolemia. The drugs shouldbe used cautiously in the presence of head injury or cerebralhemorrhage because they may increase intracranial pressure.Additionally, males taking nitroglycerin or any other nitrateshould not take sildenafil (Viagra) for erectile dysfunction.Both drugs decrease blood pressure and the combined effectcan produce profound, life-threatening hypotension.

Drugs at a Glance: Calcium Channel Blockers

Generic/Trade Name Indications Routes and Dosage Ranges

Amlodipine (Norvasc)

Bepridil (Vascor)

Diltiazem (Cardizem)

Felodipine (Plendil)Isradipine (DynaCirc)Nicardipine (Cardene)

Nifedipine (Adalat, Procardia)

Nimodipine (Nimotop)

Nisoldipine (Sular)

Verapamil(Calan, Isoptin)

PSVT, paroxysmal supraventricular tachycardia.

AnginaHypertensionAngina

AnginaHypertensionAtrial fibrillation and flutterPSVT

HypertensionHypertensionAnginaHypertension

AnginaHypertension

Subarachnoid hemorrhage

Hypertension

AnginaAtrial fibrillation or flutterPSVTHypertension

PO 5–10 mg once daily

PO 200 mg/d initially, increased to 300 mg daily after 10 d if neces-sary; maximum dose, 400 mg daily

Angina or hypertension, immediate-release, PO 60–90 mg 4 timesdaily before meals and at bedtime

Hypertension, sustained-release only, PO 120–180 mg twice dailyDysrhythmias (Cardizem IV only) IV injection 0.25 mg/kg (average dose

20 mg) over 2 min with a second dose of 0.35 mg/kg (average dose25 mg) in 15 min if necessary, followed by IV infusion of 5–15 mg/hup to 24 h

PO 5–10 mg once dailyPO 2.5–5 mg twice dailyAngina, immediate-release only, PO 20–40 mg 3 times dailyHypertension, immediate-release, same as for angina, above; sustained-

release, PO 30–60 mg twice dailyAngina, immediate-release, PO 10–30 mg 3 times daily; sustained-

release, PO 30–60 mg once dailyHypertension, sustained-release only, 30–60 mg once dailyPO 60 mg q4h for 21 consecutive d. If patient unable to swallow,

aspirate contents of capsule into a syringe with an 18-gauge needle, administer by nasogastric tube, and follow with 30 mL normal saline.

PO, initially 20 mg once daily, increased by 10 mg/wk or longer intervalsto a maximum of 60 mg daily. Average maintenance dose, 20–40 mgdaily. Adults with liver impairment or >65 y, PO, initially 10 mg oncedaily

Angina, PO 80–120 mg 3 times dailyDysrhythmias, PO 80–120 mg 3 to 4 times daily; IV injection, 5–10 mg

over 2 min or longer, with continuous monitoring of electrocardiogramand blood pressure

Hypertension, PO 80 mg 3 times daily or 240 mg (sustained release)once daily


Individual Nitrates

Nitroglycerin (Nitro-Bid, others), the prototype drug, is usedto relieve acute angina pectoris, prevent exercise-inducedangina, and decrease the frequency and severity of acuteanginal episodes. Oral dosage forms are rapidly metabolizedin the liver, and relatively small proportions of doses reachthe systemic circulation. In addition, oral doses act slowlyand do not help relieve acute chest pain.

For these reasons, several alternative dosage forms havebeen developed, including transmucosal tablets and spraysadministered sublingually or buccally, transdermal ointmentsand adhesive discs applied to the skin, and an IV preparation.When given sublingually, nitroglycerin is absorbed directlyinto the systemic circulation. It acts within 1 to 3 minutes andlasts 30 to 60 minutes. When applied topically to the skin, ni-troglycerin is also absorbed directly into the systemic circu-lation. However, absorption occurs at a slower rate, andtopical nitroglycerin has a longer duration of action thanother forms. It is available in an ointment, which is effectivefor 4 to 8 hours, and a transdermal disc, which is effective forabout 12 hours. An IV form of nitroglycerin is used to relieveacute anginal pain that does not respond to other agents. Regardless of the route, nitroglycerin has a half-life of 1 to 5 minutes, supporting the beneficial use of transdermal patchesand sustained-release tablets.

Isosorbide dinitrate (Isordil, Sorbitrate) is used to re-duce the frequency and severity of acute anginal episodes.When given sublingually or in chewable tablets, it acts inabout 2 minutes, and its effects last 2 to 3 hours. Whenhigher doses are given orally, more drug escapes metabo-lism in the liver and produces systemic effects in approxi-mately 30 minutes. Therapeutic effects last about 4 hoursafter oral administration. The effective oral dose is usuallydetermined by increasing the dose until headache occurs,indicating the maximum tolerable dose. Sustained-releasecapsules also are available.

Isosorbide mononitrate (Ismo, Imdur) is the metaboliteand active component of isosorbide dinitrate. It is well ab-sorbed after oral administration and almost 100% bioavail-able. Unlike other oral nitrates, this drug is not subject tofirst-pass hepatic metabolism. Onset of action occurs within1 hour, peak effects occur between 1 and 4 hours, and theelimination half-life is approximately 5 hours. It is usedonly for prophylaxis of angina; it does not act rapidlyenough to relieve acute attacks.

Beta-Adrenergic Blocking Agents

Beta-adrenergic blocking agents are often prescribed in avariety of clinical conditions. Their actions, uses, and adverseeffects are discussed in Chapter 19. In this chapter, the drugsare discussed only in relation to their use in angina pectoris.

Sympathetic stimulation of beta1 receptors in the heart in-creases heart rate and force of myocardial contraction, bothof which increase myocardial oxygen demand and may pre-cipitate acute anginal attacks. Beta-blocking drugs prevent orinhibit sympathetic stimulation. Thus, the drugs reduce heartrate and myocardial contractility, particularly when sympa-thetic output is increased during exercise. A slower heart ratemay improve coronary blood flow to the ischemic area. Betablockers also reduce blood pressure, which in turn decreasesmyocardial workload and oxygen demand. In angina pectoris,beta-adrenergic blocking agents are used in long-term man-agement to decrease the frequency and severity of anginalattacks, decrease the need for sublingual nitroglycerin, andincrease exercise tolerance. When a beta blocker is being dis-continued after prolonged use, it should be tapered in dosageand gradually discontinued or rebound angina can occur.

These drugs should not be given to clients with known orsuspected coronary artery spasms because they may intensifythe frequency and severity of vasospasm. This probably re-sults from unopposed stimulation of alpha-adrenergic recep-tors, which causes vasoconstriction, when beta-adrenergicreceptors are blocked by the drugs. Clients who continue tosmoke may have reduced efficacy with the use of beta block-ers. Clients with asthma should be observed for broncho-spasm from blockage of beta2 receptors in the lung. Betablockers should be used with caution in clients with diabetesmellitus because they can conceal signs of hypoglycemia(except for sweating).

Propranolol, the prototype beta blocker, is used to re-duce the frequency and severity of acute attacks of angina.It is usually added to the antianginal drug regimen when ni-trates do not prevent anginal episodes. It is especially usefulin preventing exercise-induced tachycardia, which can pre-cipitate anginal attacks. Studies indicate that beta blockersare more effective than nitrates or calcium channel blockersin decreasing the likelihood of silent ischemia and improv-ing the mortality rate after transmural MI.

Propranolol is well absorbed after oral administration. It isthen metabolized extensively in the liver; a relatively small

Nursing Notes: Apply Your Knowledge

Mrs. Sinatro, a patient with newly diagnosed coronary artery dis-ease (CAD), has been started on a nitroglycerin patch that she isto apply in the morning and remove before going to bed at night.Sublingual nitroglycerin, PRN, is ordered for episodes of chestpain. Discuss appropriate teaching for Mrs. Sinatro.

Mr. Ely has Nitropaste (nitroglycerin ointment), 1 inch, orderedevery 6 hours to decrease blood pressure and control angina. Thenurse carefully measures out 1 inch of ointment on the measuringpaper and spreads the ointment with her finger. Before she is ableto administer the medication, she feels dizzy and unwell. Shehands the medication to another nurse and asks her to give it.Identify the error and how it could be prevented.

How Can You Avoid This Medication Error?


proportion of an oral dose (approximately 30%) reaches thesystemic circulation. For this reason, oral doses of propranololare much higher than IV doses. Onset of action is 30 minutesafter oral administration and 1 to 2 minutes after IV injection.Because of variations in the degree of hepatic metabolism,clients vary widely in the dosages required to maintain a ther-apeutic response.

Atenolol, metoprolol, and nadolol have the same actions,uses, and adverse effects as propranolol, but they have longhalf-lives and can be given once daily. They are excreted bythe kidneys, and dosage must be reduced in clients with renalimpairment.

Calcium Channel Blocking Agents

Calcium channel blockers act on contractile and conductive tis-sues of the heart and on vascular smooth muscle. For these cellsto function normally, the concentration of intracellular calciummust be increased. This is usually accomplished by movementof extracellular calcium ions into the cell (through calciumchannels in the cell membrane) and release of bound cal-cium from the sarcoplasmic reticulum in the cell. Thus, calciumplays an important role in maintaining vasomotor tone, myo-cardial contractility, and conduction. Calcium channel block-ing agents prevent the movement of extracellular calcium intothe cell. As a result, coronary and peripheral arteries are dilated,myocardial contractility is decreased, and the conductionsystem is depressed in relation to impulse formation (auto-maticity) and conduction velocity (Fig. 53–1).

In angina pectoris, the drugs improve the blood supply tothe myocardium by dilating coronary arteries and decrease theworkload of the heart by dilating peripheral arteries. In vari-ant angina, calcium channel blockers reduce coronary arteryvasospasm. In atrial fibrillation or flutter and other supraven-tricular tachydysrhythmias, diltiazem and verapamil slow therate of ventricular response. In hypertension, the drugs lowerblood pressure primarily by dilating peripheral arteries.

Calcium channel blockers are well absorbed after oral ad-ministration but undergo extensive first-pass metabolism in theliver. Most of the drugs are more than 90% protein bound andreach peak plasma levels within 1 to 2 hours (6 hours or longerfor sustained-release forms). Most also have short eliminationhalf-lives (<5 hours), so doses must be given three or fourtimes daily unless sustained-release formulations are used.Amlodipine (30 to 50 hours), bepridil (24 hours), and felodi-pine (11 to 16 hours) have long elimination half-lives and there-fore can be given once daily. The drugs are metabolized in theliver, and dosage should be reduced in clients with severe liverdisease. Dosage reductions are not required with renal disease.

The calcium channel blockers approved for use in theUnited States vary in their chemical structures and effects onbody tissues. Seven of these are chemically dihydropyridines,of which nifedipine is the prototype. Bepridil, diltiazem, andverapamil differ chemically from the dihydropyridines andeach other. Nifedipine and related drugs act mainly on vascu-lar smooth muscle to produce vasodilation, whereas verapamil

and diltiazem have greater effects on the cardiac conductionsystem.

The drugs also vary in clinical indications for use; most areused for angina or hypertension, and only diltiazem and verap-amil are used to manage supraventricular tachydysrhythmias.In clients with CAD, the drugs are effective as monotherapybut are commonly prescribed in combination with beta block-ers. In addition, nimodipine is approved for use only in sub-arachnoid hemorrhage, in which it decreases spasm in cerebralblood vessels and limits the extent of brain damage. In animalstudies, nimodipine exerted greater effects on cerebral arteriesthan on other arteries, probably because it is highly lipid solu-ble and penetrates the blood–brain barrier.

Contraindications include second- or third-degree heartblock, cardiogenic shock, and severe bradycardia, heart fail-ure, or hypotension. The drugs should be used cautiouslywith milder bradycardia, heart failure, or hypotension andwith renal or hepatic impairment.

Muscle relaxation

Musclecell******************************

Calcium-blocking drugs

Musclecell

Muscle contraction

Musclecell

Figure 53–1 Calcium channel blockers: mechanism of action. (A) Dur-ing muscle relaxation, potassium ions are inside the muscle cell andcalcium and sodium ions are outside the muscle cell. (B) For musclecontraction to occur, potassium ions leave the cell and sodium and cal-cium ions enter the cell through open channels in the cell membrane.(C) When calcium channels are blocked by drug molecules, musclecontraction is decreased because calcium ions cannot move throughthe cell membrane into the muscle cell. (Calcium ions = �; sodium ions = ■ ; potassium ions = ∗ ; calcium channel blocking drugs = �.)

A

B

C


Adjunctive Antianginal Drugs

In addition to antianginal drugs, several other drugs may beused to control risk factors and prevent progression of myo-cardial ischemia to myocardial infarction and sudden cardiacdeath. These may include:

• Aspirin. This drug has become the standard of care be-cause of its antiplatelet (ie, antithrombotic) effects. Rec-ommended doses vary from 81 mg daily to 325 mg dailyor every other day; apparently all doses are beneficial inreducing the possibility of myocardial reinfarction,stroke, and death. Clopidogrel (see Chap. 57), 75 mg/day,is an acceptable alternative for individuals with aspirinallergy.

• Antilipemics. These drugs (see Chap. 58) may be neededby clients who are unable to lower serum cholesterol lev-els sufficiently with a low-fat diet. Lovastatin or a related“statin” is often used. The goal is usually to reduce theserum cholesterol level below 200 mg/dL and low-density lipoprotein cholesterol to below 130 mg/dL.

• Antihypertensives. These drugs (see Chap. 55) may beneeded for clients with hypertension. Because betablockers and calcium channel blockers are used to man-age hypertension as well as angina, one of these drugsmay be effective for both disorders.

Nursing Process

AssessmentAssess the client’s condition in relation to angina pectoris.Specific assessment data vary with each client but usuallyshould include the following:

• During the initial nursing history interview, try to answerthe following questions:• How long has the client been taking antianginal drugs?

For what purpose are they being taken (prophylaxis,treatment of acute attacks, or both)?

• What is the frequency and duration of acute anginalattacks? Has either increased recently? (An increasecould indicate worsening coronary atherosclerosisand increased risk of myocardial infarction.)

• Do symptoms other than chest pain occur during acuteattacks (eg, sweating, nausea)?

• Are there particular activities or circumstances that pro-voke acute attacks? Do attacks ever occur when theclient is at rest? Where does the client fit in the CanadianCardiovascular Society classification system?

• What measures relieve symptoms of acute angina?• If the client takes nitroglycerin, ask how often it is re-

quired, how many tablets are needed for relief of pain,how often the supply is replaced, and where the clientstores or carries the drug.

• Assess blood pressure and pulse, electrocardiogram (ECG)reports, serum cholesterol, and cardiac enzyme reports.

Elevated cholesterol is a significant risk factor for coronaryatherosclerosis and angina and the risk is directly related tothe degree of elevation. Cardiac enzyme levels, such as tro-ponin, creatine kinase (CK), lactate dehydrogenase (LDH),and aspartate aminotransferase (AST), should all be nor-mal in clients with angina.

• During an acute attack, assess the following:• Location and quality of the pain. Chest pain is non-

specific. It may be a symptom of numerous disorders,such as pulmonary embolism, esophageal spasm orinflammation (heartburn), costochondritis, or anxiety.Chest pain of cardiac origin is caused by myocardialischemia and may indicate angina pectoris or myo-cardial infarction.

• Precipitating factors. For example, what was the clientdoing, thinking, or feeling just before the onset of chestpain?

• Has the client had invasive procedures to diagnose or treat his or her coronary artery disease (CAD) (eg, cardiac catheterization, angioplasty, revascular-ization surgery)?

Nursing Diagnoses• Decreased Cardiac Output related to altered stroke volume

or drug therapy• Acute pain in chest related to inadequate perfusion of the

myocardium• Activity Intolerance related to chest pain• Noncompliance related to drug therapy and lifestyle

changes• Deficient Knowledge related to management of disease

process and drug therapy• Ineffective Individual Coping related to chronic disease

process• Sexual Dysfunction related to fear of precipitating chest

pain

Planning/GoalsThe client will:

• Receive or take antianginal drugs accurately• Experience relief of acute chest pain• Have fewer episodes of acute chest pain• Have increased activity tolerance• Identify and manage situations that precipitate anginal

attacks• Be closely monitored for therapeutic and adverse effects,

especially when drug therapy is started• Avoid preventable adverse effects• Verbalize essential information about the disease process,

needed dietary and lifestyle changes to improve healthstatus, and drug therapy

• Recognize signs and symptoms that necessitate profes-sional intervention

• Keep appointments for follow-up care and monitoring


InterventionsUse the following measures to prevent acute anginal attacks:

• Assist in preventing, recognizing, and managing contrib-utory disorders, such as atherosclerosis, hypertension,hyperthyroidism, hypoxia, and anemia. For example,hypertension is a common risk factor for CAD and mor-bidity and mortality increase progressively with the de-gree of either systolic or diastolic elevation. Managementof hypertension reduces morbidity and mortality rates.However, most studies indicate that the reductions stemmore from fewer strokes, less renal failure, and less heartfailure, than from less CAD.

• Help the client recognize and avoid precipitating factors(eg, heavy meals, strenuous exercise) when possible. Ifanxiety is a factor, relaxation techniques or psychologi-cal counseling may be helpful.

• Help the client to develop a more healthful lifestyle interms of diet and weight control, adequate rest and sleep,regular exercise, and not smoking. Ideally, these self-helpinterventions are practiced before illness occurs and theycan help prevent or delay illness. However, most indi-viduals are unmotivated until illness develops, and per-haps after it develops as well. These interventions arebeneficial at any stage of CAD. For example, for a clientwho already has angina, a supervised exercise programhelps to develop collateral circulation. Smoking has nu-merous ill effects on the client with angina and decreaseseffectiveness of antianginal drugs.During an acute anginal attack in a client known to have

angina or CAD:

• Assume that any chest pain may be of cardiac origin.• Have the client lie down or sit down to reduce cardiac

workload and provide rest.• Check vital signs and compare them with baseline values.• Record the characteristics of chest pain and the presence

of other signs and symptoms.• Have the client take a fast-acting nitroglycerin prepara-

tion (previously prescribed), up to three sublingual tabletsor three oral sprays, each 5 minutes apart, as necessary.

• If chest pain is not relieved with rest and nitroglycerin,assume that a myocardial infarction has occurred untilproven otherwise. In a health care setting, keep the clientat rest and notify the client’s physician immediately.Outside of a health care setting, call 911 for immediateassistance.

• Leave sublingual nitroglycerin at the bedside of hospi-talized clients (per hospital policy). The tablets or sprayshould be within reach so they can be used immediately.Record the number of tablets used daily, and ensure anadequate supply is available.

Evaluation• Observe and interview for relief of acute chest pain.• Observe and interview regarding the number of episodes

of acute chest pain.

• Identify CAD lifestyle factors that are being successfullymodified or require modification (eg, diet, weight, activity,and smoking cessation).

• Interview regarding success and compliance with drugtherapy.

PRINCIPLES OF THERAPY

Goals of Therapy

The goals of drug therapy are to relieve acute anginal pain;reduce the number and severity of acute anginal attacks; im-prove exercise tolerance and quality of life; delay progressionof CAD; prevent myocardial infarction; and prevent suddencardiac death.

Choice of Drug and Dosage Form

For relief of acute angina and prophylaxis before events thatcause acute angina, nitroglycerin (sublingual tablets ortranslingual spray) is usually the primary drug of choice.Sublingual or chewable tablets of isosorbide dinitrate alsomay be used. For long-term prevention or management ofrecurrent angina, oral or topical nitrates, beta-adrenergic block-ing agents, or calcium channel blocking agents are used.Combination drug therapy with a nitrate and one of the otherdrugs is common and effective. Clients taking one or morelong-acting antianginal drugs should carry a short-actingdrug as well, to be used for acute attacks.

Titration of Dosage

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

Tolerance to Long-Acting Nitrates

Clients who take long-acting dosage forms of nitrates on aregular schedule develop tolerance to the vasodilating (anti-anginal) effects of the drug. The clients more likely to developtolerance are those on high-dose, uninterrupted therapy.Although tolerance decreases the adverse effects of hypoten-sion, dizziness, and headache, therapeutic effects also may bedecreased. As a result, episodes of chest pain may occur moreoften or be more severe than expected. In addition, short-acting nitrates may be less effective in relieving acute pain.

Opinions seem divided about the best way to prevent ormanage nitrate tolerance. Some authorities recommendusing short-acting nitrates when needed and avoiding the


Several calcium channel blockers are available in bothimmediate-acting and long-acting (sustained-release)forms. The brand names often differ very little (eg, Procar-dia is a brand name of immediate-release nifedipine;Procardia XL is a long-acting formulation). It is extremelyimportant that the correct formulation is used consistently.

Self- or Caregiver Administration

Take or give as instructed; specific instructions differ withthe type of antianginal drug being taken.Take or give antianginal drugs on a regular schedule, atevenly spaced intervals. This increases drug effectivenessin preventing acute attacks of angina.With nitroglycerin and other nitrate preparations:

Use according to instructions for the particular dosageform. The dosage forms were developed for specificroutes of administration and are not interchangeable.For sublingual nitroglycerin tablets, place them underthe tongue until they dissolve. Take at the first sign ofan anginal attack, before severe pain develops. Ifchest pain is not relieved in 5 minutes, dissolve asecond tablet under the tongue. If pain is not relievedwithin another 5 minutes, dissolve a third tablet. Ifpain continues or becomes more severe, notify yourhealth care provider immediately or report to the near-est hospital emergency room. Sit down when you takethe medications. This may help to relieve your painand prevent dizziness from the drug.For the translingual solution of nitroglycerin, sprayonto or under the tongue; do not inhale the spray.For transmucosal tablets of nitroglycerin, place themunder the upper lip or between the cheek and gumand allow them to dissolve slowly over 3 to 5 hours.Do not chew or swallow the tablets.Take oral nitrates on an empty stomach with a glassof water. Oral isosorbide dinitrate is available in reg-ular and chewable tablets; be sure each type istaken appropriately. Do not crush or chew sustained-release nitroglycerin tablets.For sublingual isosorbide dinitrate tablets, placethem under the tongue until they dissolve.If an oral nitrate and topical nitroglycerin are beingused concurrently, stagger the times of administra-tion. This minimizes dizziness from low blood pressureand headache, which are common adverse effects ofnitrate drugs.For nitroglycerin ointment, use the special paper tomeasure the dose. Place the ointment on a nonhairypart of the upper body and apply with the applicatorpaper. Cover the area with plastic wrap or tape. Rotateapplication sites (because the ointment can irritate theskin) and wipe off the previous dose before applying anew dose. Wash hands after applying the ointment.

The measured paper must be used for accuratedosage. The paper is used to apply the ointment

General Considerations

Angina is chest pain that occurs because your heart is notgetting enough blood and oxygen. The most commoncauses are hypertension and atherosclerosis of the coro-nary arteries. The chest pain usually lasts less than 5 minutes and episodes can be managed for years with-out causing permanent heart damage. However, if thepain is severe or prolonged, a heart attack and heart dam-age may develop. You need to seek information aboutyour heart condition to prevent or decrease episodes ofangina and prevent a heart attack.Several types of drugs are used in angina, and you mayneed a combination of drugs for the best effects. Mostclients take one or more long-acting drugs to preventanginal attacks and a fast, short-acting drug (usually ni-troglycerin tablets that you dissolve under your tongue, ora nitroglycerin solution that you spray into your mouth) torelieve acute attacks. You should seek emergency careimmediately if rest and three sublingual tablets or oralsprays 5 minutes apart do not relieve your chest pain.The long-acting medications are not effective in relievingsudden anginal pain.As with any medications for serious or potentially seriousconditions, it is extremely important to take antianginalmedications as prescribed. Do not increase dosage ordiscontinue the drugs without specific instructions fromyour health care provider.With sublingual nitroglycerin tablets, keep them in theoriginal container, carry them so that they are alwayswithin reach but not where they are exposed to body heat,and replace them approximately every 6 months becausethey become ineffective.It may be helpful to record the number and severity ofanginal episodes, the number of nitroglycerin tablets re-quired to relieve the attack, and the total number oftablets taken daily. Such a record can help your healthcare provider know when to change your medications oryour dosages.Headache and dizziness may occur with nitrate antianginaldrugs, especially sublingual nitroglycerin. These effectsare usually temporary and dissipate with continued ther-apy. If dizziness occurs, avoid strenuous activity and standup slowly for approximately an hour after taking the drugs.If headache is severe, you may take aspirin or aceta-minophen with the nitrate drug. Do not reduce drug dosageor take the drug less often to avoid headache. Loss ofeffectiveness may occur.Keep family members or support individuals informedabout the location and use of antianginal medications incase help is needed.Avoid over-the-counter decongestants, cold remedies,and diet pills, which stimulate the heart and constrictblood vessels and thus may cause angina.With nitrate antianginal drugs, avoid alcohol. Both thedrugs and alcohol dilate blood vessels and an excessivereduction in blood pressure (with dizziness and fainting)may occur with the combination.

CLIENT TEACHING GUIDELINESAntianginal Drugs

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long-acting forms. Others recommend using the long-actingforms for 12 to 16 hours daily during active periods andomitting them during inactive periods or sleep. Thus, a doseof an oral nitrate or topical ointment would be given every6 hours for three doses daily, allowing a rest period of 6 hourswithout a dose. Transdermal discs should be removed atbedtime. If anginal symptoms occur during sleeping hours,short-acting nitrates may be beneficial in relieving thesymptoms. All nitrates should be administered at the lowesteffective dosage.

Use in Children

The safety and effectiveness of antianginal drugs have notbeen established for children. Nitroglycerin has been givenIV for heart failure and intraoperative control of blood pres-sure, with the initial dose adjusted for weight and later dosestitrated to response.

Use in Older Adults

Antianginal drugs are often used because cardiovasculardisease and myocardial ischemia are common problems inolder adults. Adverse drug effects, such as hypotension andsyncope, are likely to occur, and they may be more severethan in younger adults. Blood pressure and ability to ambu-late safely should be closely monitored, especially whendrug therapy is started or dosages are increased. Ambula-tory clients also should be monitored for their ability to takethe drugs correctly.

With calcium channel blockers, older adults may havehigher plasma concentrations of verapamil, diltiazem, nifedi-pine, and amlodipine. This is attributed to decreased hepaticmetabolism of the drugs, probably because of decreased hepaticblood flow. In addition, older adults may experience morehypotension with verapamil, nifedipine, and felodipine thanyounger clients. Blood pressure should be monitored withthese drugs.

Use in Renal Impairment

Little information is available about the use of antianginaldrugs in clients with impaired renal function. A few studiesindicate that advanced renal failure may alter the pharmaco-kinetics of calcium channel blockers. Although the pharma-cokinetics of diltiazem and verapamil are quite similar inclients with normal and impaired renal function, caution isstill advised. With verapamil, about 70% of a dose is excretedas metabolites in urine.

Dosage reductions are considered unnecessary with verap-amil and diltiazem but may be needed with nifedipine andseveral other dihydropyridine derivatives. With nifedipine,protein binding is decreased and the elimination half-life isprolonged with renal impairment. In a few clients, reversibleelevations in blood urea nitrogen and serum creatinine haveoccurred. With nicardipine, plasma concentrations are higherin clients with renal impairment, and dosage should be re-duced. Bepridil should be used with caution because itsmetabolites are excreted mainly in urine.

Use in Hepatic Impairment

Nitrates, beta blockers (see Chap. 19), and calcium channelblockers are metabolized in the liver, and all should be usedwith caution in clients with significant impairment of hepaticfunction from reduced blood flow or disease processes.

With oral nitrates, it is difficult to predict effects. On theone hand, first-pass metabolism is reduced, which increasesbioavailability (amount of active drug) of a given dose. Onthe other hand, the nitrate reductase enzymes that normallydeactivate the drug may increase if large doses are given. Inthis case, more enzymes are available and the drug is metab-olized more rapidly, possibly reducing therapeutic effects ofa given dose. Relatively large doses of oral nitrates are some-times given to counteract the drug tolerance (reduced hemo-dynamic effects) associated with chronic use. In addition,metabolism of nitroglycerin and isosorbide dinitrate nor-mally produces active metabolites. Thus, if metabolism is re-

effective and consistent drug absorption. The drugis not as well absorbed from distal portions of theextremities because of decreased blood flow. Rota-tion of sites decreases skin irritation. Also, usedpatches must be disposed of properly because thereis enough residual nitroglycerin to be harmful, espe-cially to children and pets.

With sustained-release forms of calcium channel blockers,which are usually taken once daily, do not take moreoften than prescribed and do not crush or chew.

because the drug is readily absorbed through the skin.Skin contact should be avoided except on the desig-nated area of the body. Plastic wrap or tape aids ab-sorption and prevents removal of the drug. It alsoprevents soiling of clothes and linens.For nitroglycerin patches, apply at the same timeeach day to clean, dry, hairless areas on the upperbody or arms. Rotate sites. Avoid applying below theknee or elbow or in areas of skin irritation or scar tissue. Correct application is necessary to promote

CLIENT TEACHING GUIDELINESAntianginal Drugs (Continued )

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duced by liver impairment, drug effects may be decreasedand shorter in duration.

With calcium channel blockers, impairment of liverfunction has profound effects on the pharmacokinetics andpharmacodynamics of most of these drugs. Thus, the drugsshould be used with caution, dosages should be substan-tially reduced, and clients should be closely monitored fordrug effects (including periodic measurements of liver en-zymes). These recommendations stem from the followingeffects:

• An impaired liver produces fewer drug-binding plasmaproteins such as albumin. This means that a greater pro-portion of a given dose is unbound and therefore active.

• In clients with cirrhosis, bioavailability of oral drugs isgreatly increased and metabolism (of both oral and par-enteral drugs) is greatly decreased. Both of these effectsincrease plasma levels of drug from a given dose (es-sentially an overdose). The effects result from shuntingof blood around the liver so that drug molecules circu-lating in the bloodstream do not come in contact withdrug-metabolizing enzymes and therefore are not me-tabolized. For example, the bioavailability of verapamil,nifedipine, felodipine, and nisoldipine is approximatelydouble and their clearance is approximately one thirdthat of clients without cirrhosis.

• Although hepatotoxicity is uncommon, clinical symp-toms of hepatitis, cholestasis, or jaundice and elevatedliver enzymes (eg, alkaline phosphatase, creatine kinase[CK], lactate dehydrogenase [LDH], aspartate amino-transferase [AST], alanine aminotransferase [ALT])have occurred, mainly with diltiazem, nifedipine, andverapamil. These changes resolve if the causative drugis stopped.

Use in Critical Illness

Antianginal drugs have multiple cardiovascular effects andmay be used alone or in combination with other cardio-vascular drugs in clients with critical illness. They are probablyused most often to manage severe angina, severe hypertension,or serious cardiac dysrhythmias. For example, IV nitroglycerinmay be used for angina and hypertension; an IV beta blockeror calcium channel blocker may be used to improve cardio-vascular function with angina, hypertension, or supraventricu-lar tachydysrhythmias. With any of these drugs, dosage mustbe carefully titrated and clients must be closely monitored forhypotension and other drug effects.

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

Home Care

The role of the home care nurse may vary, depending largelyon the severity of the client’s illness. Initially, the nurse shouldassess the frequency and severity of anginal attacks and howthe attacks are managed. In addition, the nurse can assess thehome setting for lifestyle and environmental factors that mayprecipitate myocardial ischemia. When causative factors areidentified, plans can be developed to avoid or minimize them.Other aspects of home care may include monitoring theclient’s response to antianginal medications; teaching clientsand caregivers how to use, store, and replace medications toensure a constant supply; and discussing circumstances forwhich the client should seek emergency care.

Antianginal Drugs

NURSING ACTIONS RATIONALE/EXPLANATION

1. Administer accurately

a. Check blood pressure and heart rate before each dose of anantianginal drug. Withhold the drug if systolic blood pressureis below 90 mm Hg. If the dose is omitted, record and report tothe health care provider.

b. Give antianginal drugs on a regular schedule, at evenlyspaced intervals.

c. If oral nitrates and topical nitroglycerin are being used con-currently, stagger times of administration.

d. For sublingual nitroglycerin and isosorbide dinitrate, in-struct the client to place the tablets under the tongue until theydissolve.

e. For oral isosorbide dinitrate, regular and chewable tabletsare available. Be sure each type of tablet is taken appropriately.

f. For sublingual nitroglycerin, check the expiration date onthe container.

Hypotension is an adverse effect of antianginal drugs. Bradycar-dia is an adverse effect of propranolol and nadolol. Dosage ad-justments may be necessary if these effects occur.

To increase effectiveness in preventing acute attacks of angina

To minimize risks of additive hypotension and headache

Sublingual tablets of nitroglycerin are volatile. Once the bottle hasbeen opened, they become ineffective after approximately 6 moand should be replaced.

NURSINGACTIONS

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g. To apply nitroglycerin ointment, use the special paper tomeasure the dose. Place the ointment on a nonhairy part of thebody, and apply with the applicator paper. Cover the area withplastic wrap or tape. Rotate application sites and wipe off pre-vious ointment before applying a new dose.

h. For nitroglycerin patches, apply at the same time each dayto clean, dry, hairless areas on the upper body or arms. Rotatesites. Avoid applying below the knee or elbow or in areas ofskin irritation or scar tissue.

i. For intravenous (IV) nitroglycerin, dilute the drug and giveby continuous infusion, with frequent monitoring of bloodpressure and heart rate. Use only with the special administra-tion set supplied by the manufacturer to avoid drug adsorptiononto tubing.

j. With IV verapamil, inject slowly, over 2–3 min.

2. Observe for therapeutic effects

a. Relief of chest pain with acute attacks

b. Reduced incidence and severity of acute attacks with pro-phylactic antianginal drugs

c. Increased exercise tolerance

3. Observe for adverse effects

a. With nitrates, observe for hypotension, dizziness, light-headedness, tachycardia, palpitations, and headache.

b. With beta-adrenergic blocking agents, observe for hypoten-sion, bradycardia, bronchospasm, and heart failure.

c. With calcium channel blockers, observe for hypotension,dizziness, lightheadedness, weakness, peripheral edema, head-ache, heart failure, pulmonary edema, nausea, and constipation.Bradycardia may occur with verapamil and diltiazem; tachy-cardia may occur with nifedipine and nicardipine.

4. Observe for drug interactions

a. Drugs that increase effects of antianginal drugs:

(1) Antidysrhythmics, antihypertensive drugs, diuretics,phenothiazine antipsychotic agents

The measured paper must be used for accurate dosage. The paperis used to apply the ointment because the drug is readily absorbedthrough the skin. Skin contact should be avoided except on thedesignated area of the body. Plastic wrap or tape aids absorptionand prevents removal of the drug. It also prevents soiling ofclothes and linens. Application sites should be rotated because theointment can irritate the skin.

To promote effective and consistent drug absorption. The drug isnot as well absorbed from distal portions of the extremities be-cause of decreased blood flow. Rotation of sites decreases skin irritation.

The drug should not be given by direct IV injection. The drug ispotent and may cause hypotension. Dosage (flow rate) is adjustedaccording to response (pain relief or drop in systolic blood pres-sure of 20 mm Hg).

To decrease hypotension and other adverse effects

Sublingual nitroglycerin usually relieves pain within 5 min. If painis not relieved, two additional tablets may be given, 5 min apart.If pain is not relieved after three tablets, report to the health careprovider or seek emergency care.

Adverse effects are extensions of pharmacologic action. Vasodi-lation causes hypotension, which in turn causes dizziness fromcerebral hypoxia and tachycardia from compensatory sympatheticnervous system stimulation. Hypotension can decrease blood flowto coronary arteries and precipitate angina pectoris or myocardialinfarction. Hypotension is most likely to occur within an hour afterdrug administration. Vasodilation also causes headache, the mostcommon adverse effect of nitrates.

Beta blockers lower blood pressure by decreasing myocardial con-tractility and cardiac output. Excessive bradycardia may con-tribute to hypotension and cardiac dysrhythmias. Bronchospasmis more likely to occur in clients with asthma or other chronic res-piratory problems.

Adverse effects result primarily from reduced smooth musclecontractility. These effects, except constipation, are much morelikely to occur with nifedipine and other dihydropyridines.Nifedipine may cause profound hypotension, which activates thecompensatory mechanisms of the sympathetic nervous systemand the renin–angiotensin–aldosterone system. Peripheral edemamay require the administration of a diuretic. Constipation ismore likely to occur with verapamil. Diltiazem reportedly causesfew adverse effects.

Additive hypotension

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Review and Application Exercises

1. What is angina pectoris?

2. What is the role of endothelial dysfunction in the devel-opment of coronary artery atherosclerosis and myocardialischemia?

3. How do nitrates relieve angina?4. Develop a teaching plan for a client who is beginning

nitrate therapy.5. How do beta blockers relieve angina?6. Why should beta blockers be tapered and discontinued

slowly in clients with angina?7. How do calcium channel blockers relieve angina?8. Develop a teaching plan for a client taking a calcium chan-

nel blocker.

SELECTED REFERENCESBrater, D. C. (2000). Clinical pharmacology of cardiovascular drugs. In H. D.

Humes (Ed.), Kelley’s Textbook of internal medicine, 4th ed., pp. 651–672.Philadelphia: Lippincott Williams & Wilkins.

Braunwald, E., Antman, E. M., Beasley, J. W., et al. (2000). ACC/AHAguidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: Executive summary andrecommendations. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Com-mittee on the Management of Patients with Unstable Angina). Circula-tion, 102, 1193–1209.

Drug facts and comparisons. (Updated monthly). St. Louis: Facts andComparisons.

Jones, S. (2001). Oral or intravenous beta blockers in acute myocardialinfarction. Emergency Medicine Journal, 18(4), 270–271.

Porth, C. M. (2002). Pathophysiology: Concepts of altered health states,6th ed., pp. 487–530. Philadelphia: Lippincott Williams & Wilkins.

Rockett, J. L. (1999). Endothelial dysfunction and the promise of ACE in-hibitors. American Journal of Nursing, 99(10), 44–49.

Smith, S. C. & Goldberg, A. C. (2001). Ischemic heart disease. In S. N. Ahya,K. Flood, & S. Paranjothi (Eds.), The Washington manual of medical thera-peutics, 30th ed., pp. 96–130. Philadelphia: Lippincott Williams & Wilkins.

Talbert, R. L. (2002). Ischemic heart disease. In J. T. DiPiro, R. L. Talbert,G. C. Yee, G. R. Matzke, B. G. Wells, & L. M. Posey (Eds.), Pharma-cotherapy: A pathophysiologic approach, 5th ed., pp. 219–250. NewYork: McGraw-Hill.


(2) Cimetidine

(3) Digoxin

b. Drugs that decrease effects of antianginal drugs:

(1) Adrenergic drugs (eg, epinephrine, isoproterenol)

(2) Anticholinergic drugs

(3) Calcium salts

(4) Carbamazepine, phenytoin, rifampin

May increase beta-blocking effects of propranolol by slowing itshepatic clearance and elimination. Increases effects of all calciumchannel blockers by inhibiting hepatic metabolism and increasingserum drug levels.

Additive bradycardia when given with beta-blocking agents

Adrenergic drugs, which stimulate beta receptors, can reversebradycardia induced by beta blockers.

Drugs with anticholinergic effects can increase heart rate, offsettingslower heart rates produced by beta blockers.

May decrease therapeutic effectiveness of calcium channel blockers

May decrease effects of calcium channel blockers by inducinghepatic enzymes and thereby increasing their rate of metabolism

Nursing Notes: Apply Your Knowledge

Answer: Assess Mrs. Sinatro’s knowledge about CAD and herreadiness to learn about her new medications and other methodsto manage this problem. Give Mrs. Sinatro written handoutsabout CAD and written information about her antianginal med-ications. Demonstrate how to apply the patch, stressing to rotatesites and not use hairy or scarred areas because they may decreasedrug absorption. The patch is removed at night because the oxy-gen demand of the heart is usually less at rest, and continuous ap-plication can increase the development of drug tolerance. Discussside effects, including headache and hypotension, that can causedizziness and falls.

Teaching must include how to manage an episode of chestpain. First stress the importance of never ignoring chest pain.Some clients may deny they are experiencing chest pain and delaytreatment. Tell her to rest if chest pain occurs. If pain does not sub-side, instruct her to place a nitroglycerin tablet under the tongue todissolve and avoid swallowing the tablet. This can be repeatedevery 5 minutes up to three nitroglycerin tablets. If the pain has notsubsided with rest and nitroglycerin, the client or family shouldcall 911. The client should not drive or be driven by family to thehospital or clinic because she may be having a heart attack (myo-cardial infarction). The nurse should also stress the importance ofkeeping nitroglycerin with her at all times and making sure the pre-scription is refilled before it reaches the expiration date. The tabletsshould be kept in the original amber bottle to protect them fromsunlight and stored away from moisture and excessive heat.

Answer: Actually, there are two errors in this situation. A nurse canonly safely administer medication that she has prepared. In thissituation, after the medication has been spread on the paper, thedosage will be unclear. Also, a nurse or a family member shouldnever touch Nitropaste without wearing gloves. Hands should bewashed after administration. This potent vasodilator is absorbedthrough the skin, causing systemic effects such as dizziness andheadache.

How Can You Avoid This Medication Error?

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Antianginal Drugs