Practice nursing care for Clients

Practice nursing care for Clients

with Cardiac Problems II

 

Valvular heart disease (VHD) encompasses a number of common cardiovascular conditions that account for 10% to 20% of all cardiac surgical procedures in the United States. A better understanding of the natural history coupled with the major advances in diagnostic imaging, interventional cardiology, and surgical approaches have resulted in accurate diagnosis and appropriate selection of patients for therapeutic interventions. A thorough understanding of the various valvular disorders is important to aid in the management of patients with VHD. Appropriate work-up for patients with VHD includes a thorough history for evaluation of causes and symptoms, accurate assessment of the severity of the valvular abnormality by examination, appropriate diagnostic testing, and accurate quantification of the severity of valve dysfunction and therapeutic interventions, if necessary. It is also important to understand the role of the therapeutic interventions vs the natural history of the disease in the assessment of outcomes. Prophylaxis for infective endocarditis is no longer recommended unless the patient has a history of endocarditis or a prosthetic valve.

The heart pumps blood in one direction. To ensure that blood enters and leaves the heart in the correct direction, with no backflow, the heart has a set of leaflets, or valves — flaps that continually open and close. Heart valve disease results when a valve loses its ability to regulate blood flow properly.

Heart Valves: An Overview

The heart has four one-way valves:

On the right side of the heart:

The tricuspid valve (1) allows blood to pass from the right atrium (a) to the right ventricle (b); it prevents blood from flowing back into the right atrium as the heart pumps.

The pulmonary valve (2) allows blood to pass into the pulmonary arteries (c); it prevents blood from flowing back into the right ventricle.

On the left side of the heart: The mitral valve (3) allows oxygenated blood to flow from the lungs, into the left ventricle (d); it prevents blood from flowing back into the left atrium (e). The aortic valve (4) allows blood to pass from the left ventricle to the aorta (f), which transports blood to the rest of the body; it also prevents backflow of blood into the left ventricle.

Heart valve disease occurs when a valve doesn’t work properly, by not opening or closing completely, which result in blood not moving through the heart’s chambers as it should. To compensate, the heart muscle has to work harder to ensure that the appropriate amount of blood is circulated throughout the body. Heart valve disease can affect any of the heart’s four valves.

 

 

Common Valve Disorders

The vast majority of valve repair and replacement procedures performed every year in the U.S. involve the mitral and aortic valves. These valves are located on left side of the heart — the side tasked with pumping oxygen-rich blood to the rest of the body. The left side therefore works much harder than the right side.

Generally speaking, valve disorders fall into these categories:

·                     Stenosis, or narrowing of the valve: Because the valve cannot open as widely as it should, it restricts blood flow. Narrowing is typically caused when valve leaflets thicken, stiffen or fuse together. It can be the result of scarring related to rheumatic fever, which is associated with strep throat or scarlet fever; rheumatic fever is less common in the U.S., but is prevalent in developing nations. Stenosis also may be present at birth (congenital). Older adults may develop degenerative calcification (calcium buildup) of the aortic valves.

·                     Prolapse: Tissue buildup that thickens and enlarges valve flaps and strings that anchor the leaflets to the heart muscle. In effect, the valves cannot close tightly. They flop or bulge instead. Mitral valve prolapse is the most common heart valve disease. It occurs when mitral valve’s two leaflets flop backward into the left atrium.

·                     Regurgitation: When blood leaks backward. This is typically caused by prolapse.

It is possible for a patient to have both valvular stenosis and prolapse, in one or more valves, at the same time.

Causes of Heart Valve Disease

A patient can be born with heart valve disease or acquire it later in life.

·                     Heart valve disease that develops before birth is considered congenital. Congenital heart valve disease usually involves pulmonary or aortic valves that don’t form properly. These valves may not have enough tissue flaps, may be the wrong size or shape, or may lack an opening through which blood can flow properly.

·                     Acquired heart valve develops over time, throughout one’s life, due to wear and tear. Acquired heart valve disease usually affects the aortic or mitral valve.

Symptoms of Heart Valve Disease

Many people have heart valve defects or disease but do not experience symptoms. The condition can remain the same throughout one’s life, without causing problems. However, for many people, heart valve disease can gradually worsen, until symptoms develop.

Symptoms of valve disease include chest pain or tightness; feeling faint; shortness of breath; fatigue; heart palpitations (fluttering heartbeat); irregular heartbeat (arrhythmia); and heart murmur.

As aortic and mitral valve stenosis develop, the muscles of the left ventricle must pump harder to compensate for inadequate blood flow. Muscle tissue becomes stiffer, resulting in chest pain. Blood may back up in the lungs as well, causing shortness of breath and fatigue.

VALVULAR HEART DISEASE

Approximately 5 million Americans have some form of valvular heart disease. Valvular heart disease occurs when the heart valves cannot open fully (valvular stenosis) or close completely (valvular insufficiency or regurgitation). Acquired valvular dysfunctions most often involve the left side of the heart, especially the mitral valve. Acquired valvular dysfunc­tions, in decreasing order of occurrence, are mitral stenosis, mitral regurgitation, mitral valve prolapse, aortic stenosis, and aortic regurgitation.

 

 

The tricuspid valve is affected infrequently—primarily following endocarditis in IV drug abusers. The pulmonic valve is rarely involved. Stenosis and regurgitation often occur si­multaneously in a defect called a mixed lesion.

Mitral Stenosis

Mitral  stenosis  usually results  from rheumatic carditis, which can cause valve thickening by fibrosis and calcification. Rheumatic fever is the most common cause of mitral stenosis. Nonrheumatic causes include atrial myxoma (tumor), calcium accumulation, and thrombus formation.

In this condition, the valve leaflets fuse and become stiff, and the chordae tendineae contract and shorten. The valvular orifice narrows, preventing normal blood flow from the left atrium to the left ventricle. As a result of these changes, left atrial pressure rises, the left atrium dilates, pulmonary artery pressures increase, and the right ventricle hypertrophies.

Pulmonary congestion and right-sided heart failure ini­tially occur. Later, when the left ventricle receives insufficient blood volume, preload is decreased and cardiac output falls.

Clients with mild mitral stenosis are usually asympto­matic. As the valvular orifice narrows and pressure in the lungs increases, the client experiences dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea (sudden dyspnea at night), and dry cough. Hemoptysis and pulmonary edema ap­pear as pulmonary hypertension and congestion progress. Right-sided heart failure can cause hepatomegaly, neck vein distention, and pitting edema late in the disorder.

On palpation, the pulse may be normal, tachycardiac, or irregularly irregular (as in atrial fibrillation). Because the development of atrial fibrillation indicates that the client may decompensate, the physician should be notified immediately of the development of an irregularly irregular rhythm. On auscultation, the nurse notes a rumbling, apical diastolic murmur.

 

 Mitral stenosis

 

Mitral Regurgitation (Insufficiency)

 

The fibrotic and calcific changes occurring in mitral regurgi­tation prevent the mitral valve from closing completely during systole. Incomplete closure of the valve allows the backflow of blood into the left atrium when the left ventricle contracts. During diastole, regurgitant output again flows from the left atrium to the left ventricle along with the normal blood flow. This increases the volume that must be ejected during the next systole. To compensate for the increased volume and pressure, the left atrium and ventricle dilate and hypertrophy.

Mitral insufficiency usually progresses slowly; clients may remain symptom free for decades. Symptoms begin to occur when the left ventricle fails in response to increased blood volumes. The client most often reports fatigue and chronic weakness as a result of reduced cardiac output. Dyspnea on exertion and orthopnea develop later. A significant number of clients complain of anxiety, atypical chest pains, and palpita­tions. Nursing assessment may reveal normal blood pressure, atrial fibrillation (an irregularly irregular rhythm occurring in 75% of clients), or changes in respirations characteristic of left ventricular failure.

When right-sided heart failure develops, the neck veins be­come distended, the liver enlarges (hepatomegaly), and pitting edema is noted. On auscultation, the nurse hears a high-pitched systolic murmur at the apex, with radiation to the left axilla. Severe regurgitation often exhibits a third heart sound.

Rheumatic heart disease is the predominant cause of mitral insufficiency. When mitral insufficiency results from rheu­matic heart disease, it usually coexists with some degree of mitral stenosis. Nonrheumatic causes include papillary mus­cle dysfunction or rupture resulting from ischemic heart disease, infective endocarditis, and a congenital anomaly. Mitral regurgitation resulting from rheumatic heart disease is more common in women than in men. Mitral regurgitation of a nonrheumatic etiology occurs more often in men.

Mitral Valve Prolapse

Mitral valve prolapse occurs because the valvular leaflets enlarge and prolapse into the left atrium during systole. This abnormality is usually benign but may progress to pro­nounced mitral regurgitation.

Most clients with mitral valve prolapse are asymptomatic. However, they may report chest pain, palpitations, or exercise intolerance. Chest pain is usually atypical, with clients describing a sharp pain localized to the left side of the chest. Dizziness, syncope, and palpitations may be associated with atrial or ventricular dysrhythmias.

The nurse usually finds a normal heart rate and blood pres­sure on physical examination. A midsystolic click and a late systolic murmur may be audible at the apex.

The etiology of mitral valve prolapse is variable and has been associated with conditions such as Marfan’s syndrome and other congenital cardiac defects. However, most of the time no other cardiac abnormality is found. A familial occurrence is well established.

Mitral valve prolapse affects 5% to 10% of people. Al­though it is present in all age-groups, it is most common in women between 20 and 54 years of age.

Aortic Stenosis

In aortic stenosis, the aortic valve orifice narrows and obstructs left ventricular outflow during systole. This increased resistance to ejection or afterload results in ventricular hypertrophy. As stenosis progresses, cardiac output becomes fixed and unable to increase to meet the demands of the body dur­ing exertion, and symptoms develop. Eventually the left ven­tricle fails, volume backs up in the left atrium, and the pulmonary system becomes congested. Right-sided heart failure can occur late in the disease.

The classic symptoms of aortic stenosis result from the fixed cardiac output: dyspnea, angina, and syncope occurring on ex­ertion. When cardiac output falls in the late stages of the disease, the client experiences marked fatigue, debilitation, and periph­eral cyanosis. A narrow pulse pressure is noted when the blood pressure is examined. A diamond-shaped, systolic crescendo-decrescendo murmur is usually noted on auscultation.

Congenital valvular disease or malformation is the pre­dominant etiologic factor in aortic stenosis. Bicuspid or unicuspid aortic valves are the primary reason for aortic stenosis in clients younger than 30 years and account for about 50% of the disease in clients 30 to 70 years of age. Rheumatic aortic stenosis is always concomitant with rheumatic disease of the mitral valve and develops in clients between 30 and 70 years of age. Atherosclerosis and degenerative calcification of the aortic valve are the predominant factors in people older than age 70. Aortic stenosis has become the most common valvu­lar disorder in countries with aging populations. Of clients with aortic stenosis, 80% are men.

 

 

 Aortic valve stenosis

 

Aortic Regurgitation (Insufficiency)

 

In clients with aortic regurgitation, the aortic valve leaflets do not close properly during diastole, and the annulus (the valve ring that attaches to the leaflets) may be dilated, loose, or deformed. This allows regurgitation of blood from the aorta back into the left ventricle during diastole. The left ventricle, in compensation, dilates to accommodate the greater blood volume and eventually hypertrophies.

Clients with aortic regurgitation remain asymptomatic for many years because of the compensatory mechanisms of the left ventricle. As the disease progresses and left ventricular failure occurs, the principal concerns are exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Palpitations may be noted with severe disease, especially while lying on the left side. Many clients with aortic regurgitation experience nocturnal angina with diaphoresis.

On palpation, the nurse notes a “bounding” arterial pulse. The pulse pressure is usually widened, with an elevated sys­tolic pressure and diminished diastolic pressure. The classic auscultatory finding is a high-pitched, blowing, decrescendo diastolic murmur.

Aortic insufficiency usually results from nonrheumatic conditions such as infective endocarditis, congenital anatomic aortic valvular abnormalities, hypertension, and Marfan’s syndrome (a rare, generalized, systemic disease of connective tissue). Approximately 75% of clients with aortic regurgitation are men.

 

COLLABORATIVE MANAGEMENT

Assessment

 

A client with valvular disease may suddenly become ill or may slowly develop symptoms over many years. Information is collected about the client’s family health history, including valvular or other forms of heart disease to which he or she may be genetically predisposed. The nurse questions about at­tacks of rheumatic fever, the specific dates when these oc­curred, and the use of antibiotic prophylaxis against the re­currence of rheumatic fever. The client should also be questioned about a history of IV drug abuse. The client’s fa­tigue level and tolerated activity level, the presence of angina or dyspnea, and the occurrence of palpitations, if present, are also discussed.

As part of the physical assessment, the nurse obtains the client’s vital signs, inspects for signs of edema, palpates and auscultates the heart and lungs, and palpates the peripheral pulses.

In clients with mitral stenosis, the chest x-ray study shows left atrial enlargement, prominent pulmonary arteries, and an enlarged right ventricle. In those with mitral regurgitation, the chest x-ray study reveals an increased cardiac shadow, indi­cating left ventricular and left atrial enlargement.

 

 Mitral stenosis Image

 

In the later stages of aortic stenosis, the chest x-ray study may show left ventricular enlargement and pulmonary conges­tion. Left atrial and left ventricular dilation appear on the chest x-ray film of clients with aortic insufficiency. If heart failure is present, pulmonary venous congestion is also evident.

 

 Aortic stenosis Image

 

For clients with valvular heart disease, echocardiography is the diagnostic procedure of choice because it is an excellent noninvasive tool for defining cardiac structure, movement of the valve leaflets, and size and function of the cardiac chambers.

Exercise tolerance testing (ETT) is sometimes per­formed to evaluate symptomatic response, assess functional capacity, and enhance auscultatory findings. In clients with either mitral or aortic stenosis, cardiac catheterization is often indicated to assess the severity of the stenosis and its other ef­fects on the heart.

The health care provider also orders an electrocardiogram (ECG) to assess abnormalities such as left ventricular hyper­trophy, as seen with mitral regurgitation and aortic regurgita­tion, or right ventricular hypertrophy, as seen in severe mitral stenosis. Atrial fibrillation is a common finding in both mitral stenosis and mitral regurgitation and may develop in aortic stenosis because of left atrial dilation.

 

Interventions

Management of valvular heart disease depends on which valve is affected and the degree of valve impairment. Some clients can be managed with yearly monitoring and medica­tions, whereas other clients require invasive procedures or heart surgery.

NONSURGICAL MANAGEMENT.

Nonsurgical manage­ment focuses on drug therapy and rest. During the course of valvular disease, clients may develop left ventricular failure with pulmonary or systemic congestion. Diuretics, digoxin, and oxygen are often administered to improve the symptoms of heart failure. Nitrates are administered cautiously to clients with aortic stenosis because of the po­tential for syncope associated with a reduction in left ventric­ular volume (preload). Vasodilators such as nifedipine (Adalat, Procardia) may be used to reduce the regurgitant flow for clients with aortic or mitral stenosis.

Prophylactic antibiotic therapy is required for all clients with valve disease before any invasive procedure. Procedures for which clients require antibiotic coverage include bronchoscopy, endoscopy, sigmoidoscopy, colonoscopy, geni­tourinary instrumentation, surgery, and dental procedures of any type.

A major concern in valvular heart disease is maintaining cardiac output should atrial fibrillation develop. With mitral valvular disease, left ventricular filling is especially dependent on atrial contraction. When atrial fibrillation develops, there is no longer a single, coordinated atrial contraction. Cardiac out­put can decrease by 25% to 30%, and heart failure may occur. Ineffective atrial contraction may also lead to the stasis of blood and thrombi in the left atrium. The nurse monitors the client for the development of an irregularly irregular rhythm and notifies the primary care provider should it develop.

The primary care provider usually institutes therapy to re­store normal sinus rhythm or, if that is unsuccessful, to slow ventricular rate. The physician might elect to convert a client from atrial fibrillation to sinus rhythm using IV diltiazem (Cardizem). The client should be on a unit where nurses are able to monitor cardiac rhythm and blood pressure closely. Synchronized countershock (cardioversion) may be attempted if atrial fibrillation is rapid and the client is unresponsive to medical treatment.

Whether the client is converted to sinus rhythm or remains in an atrial fibrillation, digoxin is often prescribed to slow ventricular rate and increase the force of contraction. If atrial   fibrillation does not resolve, quinidine gluconate (Quinaglute, Quinate) or procainamide hydrochloride (Pronestyl hydrochloride, Procanbid) may be added to the regimen. A beta-blocking agent, such as propranolol hydrochloride (Inderal, Apo-Propranolol), or a calcium channel blocker, such as verapamil hydrochloride (Calan), may also be considered to slow the ventricular response.

For valvular heart disease and chronic atrial fibrillation, an­ticoagulation with sodium warfarin (Coumadin, Warfilone) is usually a part of the medical treatment plan to prevent thrombus formation. Thrombi may form in the atria or on de­fective valve segments, resulting in systemic emboli. As a result, one or more strokes may occur. Therefore the nurse as­sesses the client’s baseline neurologic status and regularly reassesses for neurologic changes.

Rest is often an important part of treatment. Activity may be limited because cardiac output cannot meet increased metabolic demands, and angina or heart failure can result.

 

SURGICAL MANAGEMENT.

Surgical repair or replace­ment of heart valves has a major effect on the prognosis of valvular heart disease. Correct timing is crucial. Repair or re­placement of the valve is usually performed after symptoms of left ventricular failure have developed but before irre­versible dysfunction occurs. Surgical therapy is the only de­finitive treatment of aortic stenosis and is recommended when angina, syncope, or dyspnea on exertion develop.

REPARATIVE PROCEDURES. Reparative procedures are gaining in popularity because of continuing problems with thrombi, endocarditis, and left ventricular dysfunction after valvular replacement. Reparative procedures do not result in a normal valve, but they usually “turn back the clock.” This results in a more functional valve and an improvement in car­diac output. Turbulent blood flow through the valve may per­sist, and degeneration of the repaired valve is possible.

Balloon Valvuloplasty. Balloon valvuloplasty, an inva­sive nonsurgical procedure, is possible for stenotic mitral and aortic valves. Careful selection of clients is necessary. Valvu­loplasty may be the initial treatment of choice for people with noncalcified, mobile, mitral valves. Clients selected for aortic valvuloplasty are usually older and are at high risk for surgi­cal complications or have refused operative treatment. The benefits of aortic valvuloplasty for aortic stenosis tend to be short lived, rarely lasting longer than 6 months.

When performing mitral valvuloplasty, the physician passes a balloon catheter from the femoral vein, through the atrial septum, and to the mitral valve. The balloon is inflated to enlarge the mitral orifice. For aortic valvuloplasty, the physician inserts the catheter through the femoral artery and advances it to the aortic valve, where it is inflated to enlarge the orifice. Valvuloplasty usually offers immediate relief of symptoms because the balloon has dilated the orifice and im­proved leaflet mobility. The results are comparable with those of surgical commissurotomy for appropriately selected clients.

After the procedure, the nurse observes the client closely for bleeding from the catheter insertion site and institutes pre­cautions for arterial puncture if appropriate. Bleeding is likely after valvuloplasty because of the large size of the catheter. The nurse also observes for signs of a regurgitant valve by closely monitoring heart sounds, cardiac output, and heart rhythm. Because vegetations (thrombi) may have been dis­lodged from the valve, the nurse observes for any indication of systemic emboli.

Direct, or Open, Commissurotomy.

Direct commissurotomy is accomplished with cardiopulmonary bypass during open heart surgery. The surgeon visualizes the valve, re­moves thrombi from the atria, incises the fused commissures (leaflets), and debrides calcium from the leaflets, widening the orifice.

Mitral Valve Reconstruction.

Mitral valve reconstruction is the reparative procedure of choice for most clients with acquired mitral insufficiency. To make the annulus (the valve ring that attaches to and supports the leaflets) smaller, the physician may suture the leaflets to an annuloplasty ring or take tucks in the client’s annulus. Leaflet repair is often performed at the same time. Elongated leaflets may be shortened, and shortened leaflets may be repaired by lengthening the chordae that bind them in place. Perforated leaflets may be patched with synthetic grafts.

Annuloplasty and leaflet repair result in an annulus of the appropriate size and in leaflets that can close completely. Thus regurgitation is eliminated or markedly reduced.

REPLACEMENT PROCEDURES.

The development of prosthetic (synthetic) and biologic (tissue) valves has improved the surgical therapy and prognosis of valvular heart disease. Prosthetic valves come in a wide variety (Figure 35-2). Al­though prosthetic valves are very durable, all clients must re­ceive oral anticoagulation for the rest of their lives because of the possibility of clot formation.

Biologic valves may be xenograft (from other species), such as a porcine valve (from a pig) (Figure 35-3) or a bovine valve (from a cow). Because tissue valves are associated with little risk of clot formation, long-term anticoagulation is not indicated. However, xenografts are not as durable as pros­thetic valves and usually must be replaced every 7 to 10 years. The durability of a xenograft is related to the age of the re­cipient. Calcium in the blood, which is present in larger quan­tities in younger clients, breaks down the valves. The older the client, the longer the xenograft will last. Valves donated from human cadavers and pulmonary autographs (relocation of the client’s own pulmonary valve to the aortic position) are also being used for valve replacement, especially in younger clients.

Figure 3 5 – 3 • Examples of biologic (tissue) heart valves.

A, Freestyle, a stentless pig valve with no frame.

B, Hancock II, a stented pig valve.

C, Carpentier-Edwards pericardial bioprosthesis.

(A and B  courtesy Medtronic, Inc., Minneapolis, MN; C courtesy Baxter Healthcare Corporation, Edwards CVS Division, Santa Ana, CA.)

Fi gure 3 5 – 2 Examples of prosthetic (synthetic) heart valves.

A, Medtronic Hall, a tilting-disk valve.

B, St. Jude Medical mechanical heart valve.

C, Monostrat mechanical heart valve.

D, Starr-Edwards Silastic ball valve.

(A courtesy Medtronic, Inc., Minneapolis, MN; B courtesy St. Jude Medical, Inc. All rights reserved. St. Jude Medical is a registered trademark of St. Jude Medical, Inc.; C courtesy Alliance Medical Products, Irvine, CA; D courtesy Baxter Healthcare Corporation, Edwards CVS Division, Santa Ana, CA.)

 

The mitral valve should be replaced if the leaflets are calcified and immobile. The surgeon excises the valve during cardiopulmonary bypass surgery, and the new biologic or prosthetic valve is sutured into place.

An aortic valve is replaced for most symptomatic adults with aortic stenosis and aortic insufficiency. As with mitral valve replacement, the surgeon excises the aortic valve during cardiopulmonary bypass surgery and sutures the new valve into place.

 

PREOPERATIVE CARE.

Clients undergoing valve surgery have open heart surgery similar to the procedure for a coronary artery bypass graft (CABG). Ideally, surgery is an elective and planned procedure. Therefore the nurse can assist in preparing the client by instructing the client and fam­ily members or a significant other about the management of postoperative pain, incision care, and strategies to prevent res­piratory complications.

The nurse may also introduce the client and the family or significant other to the staff and the environment of the surgi­cal critical care unit (where the client will be transferred after surgery). Clients receiving oral anticoagulants stop taking them at least 72 hours before the procedure.

 

POSTOPERATIVE CARE.

Nursing interventions for clients undergoing open heart surgery for valve disorders are similar to those for a CABG (see Chapter 38). However, a few significant differences depend in part on the type of valvular surgery. Clients with mitral stenosis often have pulmonary hypertension and stiff lungs. The nurse monitors respiratory status and watches the client closely during weaning from the ventilator. Aortic valve replacements pose a higher risk for postoperative hemorrhage, and the nurse is especially vigilant for indications of bleeding.

Clients with valve replacements are also more likely to ex­perience significant reductions in cardiac output after surgery, especially those with aortic stenosis or left ventricular failure from mitral valve disease. The nurse is particularly attentive in monitoring the client’s cardiac output and identifying any indications of pump failure. High filling pressures (pul­monary artery wedge pressure greater than 18 mm Hg) may be required to maintain an acceptable cardiac output in the immediate postoperative period. The physician may prescribe digoxin (Lanoxin, Novodigoxin) for 3 to 6 months postop­eratively to maintain cardiac output and prevent atrial fibrilla­tion. Clients who have had valve replacements with prosthetic valves require lifetime prophylactic anticoagulation therapy to prevent thrombus formation.

 

Community-Based Care

 

The client with valvular heart disease may be discharged home on medical therapy or postoperatively after valve repair or replacement. Because fatigue is a common problem for clients with valve disorders, the nurse helps the client and family ensure that the home environment is conducive to pro­viding rest. Older clients with aortic stenosis may reside in long-term care.

 

HEALTH TEACHING

 

The teaching plan for the client with valvular heart disease in­cludes the following:

–                   The disease process

–                   Medications, including diuretics, vasodilators, cardiac glycosides, antibiotics, and anticoagulants

–                   The prophylactic use of antibiotics

–                   A plan of work, activity, and rest to conserve energy

–                   The purpose and nature of surgical intervention, if appropriate

Because clients with defective or repaired valves are at risk for infective endocarditis, the nurse teaches them to adhere to the precautions described for endocarditis. The nurse instructs clients to inform all health care providers of the valvular heart disease history; they are also told that they require antibiotic administration before all invasive procedures and tests. In­structions for the client are described in Chart 35-10.

 

 

The nurse teaches clients taking anticoagulants how to manage their drug therapy successfully, including dietary considerations (if taking warfarin) and prevention of bleed­ing. For example, the client should be taught to avoid foods high in vitamin K and to use an electric razor to avoid skin cuts. The client should report any bleeding or excessive bruis­ing to the health care provider. (See Chapter 38 for more in­formation on anticoagulants.)

The nurse teaches clients who have undergone valve sur­gery how to care for the sternal incision and instructs them to watch for and report any fever or drainage or redness at the site. Clients can usually return to normal activity after 6 weeks but should avoid heavy physical labor with their upper extremities for 3 to 6 months to allow the sternotomy incision to heal. Clients who have had valvular surgery should also avoid any dental procedures for 6 months because of the po­tential for endocarditis. Those with prosthetic valves need to avoid any procedure using magnetic resonance technology.

Clients with valvular heart disease may have complicated medication schedules as well as long-term antibiotic or anticoagulant therapy. These circumstances may potentially lead to noncompliance. The nurse provides clear, concise instructions about medication schedules.

The psychologic response to valve surgery is similar to that following coronary artery bypass surgery. Clients may experience an altered self-image as a result of the required lifestyle changes or the visible medial sternotomy incision. In addition, clients with prosthetic valves may need to adjust to a soft but audible clicking sound of the prosthetic valve. The nurse encourages them to verbalize their feelings about the sternotomy incision and the prosthetic heart valve.

HOME CARE MANAGEMENT

A home care nurse may be needed to help the client adhere to medication and activity schedules and to detect any problems, particularly with anticoagulant therapy. Clients who have un­dergone surgery may require a nurse for assistance with inci­sion care. A home care aide may assist with activities of daily living.

HEALTH CARE RESOURCES

The American Heart Association is a community resource that provides information about valvular heart disease. A wallet- sized card can be obtained to identify the client as needing prophylactic antibiotics. The nurse advises clients receiving anticoagulants to obtain an identification bracelet that states the name of the drug they are taking.

INFLAMMATIONS AND INFECTIONS

Inflammations and infections of the heart often follow sys­temic infections. Recovery from these infections is often prolonged, and clients are at great risk for future heart problems. Inflammation and infection may involve the endocardium (endocarditis), pericardium (pericarditis), or entire heart (rheu­matic carditis).

 

 

 

Infective Endocarditis

OVERVIEW

Pathophysiology

Infective endocarditis (previously called bacterial endocarditis) refers to a microbial infection involving the endocardium. A defective or prosthetic valve is most commonly affected, but infection may also occur in apparently healthy endocardium or in septal defects. Current classification of in­fective endocarditis is by site of involvement, type of pathogen, and definitiveness of the diagnosis.

Etiology

 

Infective endocarditis occurs primarily in clients who abuse IV drugs, have had valve replacements, or have structural car­diac defects.

With a cardiac defect, blood may flow rapidly from a high-pressure area to a low-pressure zone, eroding a section of endocardium. Platelets and fibrin adhere to the denuded endocardium, forming a vegetative lesion. During bac-teremia, bacteria become trapped in the low-pressure “sinkhole” and are deposited in the vegetation. Additional platelets and fibrin are deposited, which causes the vegetative lesion to grow; the endocardium and valve are destroyed. Valvular insufficiency may result when the lesion interferes with normal alignment of the valve. If vegetations become so large that blood flow through the valve is obstructed, the valve appears stenotic.

Possible ports of entry for infecting organisms include the following:

Ø                The oral cavity (especially if dental procedures have been performed)

Ø                Skin rashes, lesions, or abscesses

Ø                Infections (cutaneous, genitourinary, or gastrointestinal)

Ø                Surgery  or invasive procedures,  including IV line placement

Incidence/Prevalence

The incidence of infective endocarditis is estimated to be 5 out of every 100,000 people, with men having a higher inci­dence than women. Mortality rates for infective endocarditis have remained high—12% to 15% despite antibiotic therapy. In 1995 approximately 2000 people died from endocarditis, and 16,000 people were discharged from hospitals with the primary diagnosis of endocarditis (AHA, 1998).

 COLLABORATIVE MANAGEMENT

Assessment

Because mortality remains high, early detection of infective endocarditis is essential. Unfortunately, many clients (espe­cially older adults) are misdiagnosed. Clinical manifestations usually occur within 2 weeks of a bacteremia. Assessment usually reveals a recurrent fever. Most clients have temperatures from 99° to 103° F (37.2° to 39.4° C). Many older adults remain afebrile. The severity of symptoms may depend on the virulence of the infecting organism.

 

MANIFESTATIONS

 

CARDIOVASCULAR MANIFESTATIONS

The nurse assesses the client’s cardiovascular status. More than 90% of clients with infective endocarditis develop mur­murs. The nurse carefully auscultates the precordium, noting and documenting any new murmurs (usually regurgitant iature) or any changes in the intensity or quality of an old murmur. An S₃ or S₄ heart sound may also be heard.

Heart failure is the most common complication of infective endocarditis. The nurse assesses for right-sided heart failure (as evidenced by peripheral edema, weight gain, and anorexia) and left-sided heart failure (as evidenced by fatigue, shortness of breath, and crackles on auscultation of breath sounds).

 

EMBOLIC COMPLICATIONS

 

Arterial embolization is a major complication in up to 50% of clients with infective endocarditis. Fragments of vegetation break loose and travel randomly through the circulation. When the left side of the heart is involved, vegetation frag­ments are carried to the spleen, kidneys, gastrointestinal (GI) tract, brain, and extremities. When the right side of the heart is involved, emboli enter the pulmonary circulation.

Clients with splenic infarction describe sudden abdominal pain with radiation to the left shoulder. When performing an abdominal assessment, the nurse notes rebound tenderness on palpation. The classic pain described with renal infarction is flank pain that radiates to the groin and is accompanied by hematuria or pyuria. Mesenteric emboli may result in the client complaining of diffuse abdominal pain, often after eat­ing, and abdominal distention.

Emboli to the central nervous system cause either transient ischemic attacks (TIAs) or a stroke. The client may appear confused, experience reduced concentration and aphasia, or have dysphagia. Pleuritic chest pain, dyspnea, and cough are often described by the client who is experiencing pulmonary infarction related to embolization.

 

PERIPHERAL MANIFESTATIONS

Petechiae (pinpoint red spots) occur in up to 40% of clients with endocarditis. The nurse examines the mucous mem­branes, the palate, the conjunctivae, and the skin above the clavicles for small, red, flat lesions. The nurse also examines the distal third of the nail bed for splinter hemorrhages, which appear as black longitudinal lines or small red streaks (Figure 35-4).

Osier’s nodes and Janeway’s lesions are considered clas­sic manifestations of endocarditis but may occur with other conditions. The nurse inspects the pads of the fingers, hands, and toes for Osier’s nodes, a late sign, which are reddish ten­der lesions with a white center. Janeway’s lesions, an early sign (Figure 35-5), are nontender, hemorrhagic lesions on the fingers, toes, nose, or earlobes. Splenomegaly and clubbing of the fingers may occur in clients who have had infective endo­carditis for longer than 6 weeks.

 

DIAGNOSTIC ASSESSMENT

 

A positive blood culture is of prime diagnostic and therapeutic importance. Both aerobic and anaerobic specimens are obtained for culture. Some slow-growing organisms may take 3 weeks and require a specialized medium to isolate. Therefore cultures should be monitored by the laboratory for 3 to 4 weeks. Low he­moglobin and hematocrit levels may also be found.

Echocardiography has improved the ability to accurately diagnose infective endocarditis. Transesophageal echocardi­ography (TEE) allows visualization of cardiac structures that are difficult to see with transthoracic echocardiography (TTE). TEE provides good resolution and is very sensitive for discovering valvular abnormalities, thereby enabling the cli­nician to diagnose infective endocarditis more accurately.

The most reliable criteria for diagnosing endocarditis in­clude positive blood cultures, a new regurgitant murmur, and evidence of endocardial involvement by echocardiography.

Interventions

 

Care of the client with endocarditis usually includes antibi­otics, rest, and supportive therapy for heart failure. If these in­terventions are successful, surgery is usually not required.

NONSURGICAL MANAGEMENT.

The major component of treatment for endocarditis is drug therapy. Other interven­tions help to prevent the life-threatening complications.

DRUG THERAPY.

Antibiotics are the mainstay of treat­ment, with the choice of antibiotics depending on the specific organism involved. Because vegetations surround and protect the bacteria, an appropriate antibiotic must be given in a suf­ficiently high dose to ensure a bactericidal effect. Antibiotics are most often given intravenously, with the course of treat­ment lasting 4 to 6 weeks. In most cases, the ideal antibiotic is one of the penicillins.

Until recently, clients with endocarditis were hospitalized for up to 6 weeks for IV antibiotic therapy. Now they are hos­pitalized for 5 to 7 days to institute IV therapy and then are discharged for continued IV therapy at home. During hospitalization, the nurse assesses the client’s response to therapy. Clients are responding to antimicrobial therapy and may be considered for home therapy when they have been afebrile for 3 to 4 days, have negative blood cultures, and have no signs of heart failure or embolization.

Anticoagulants are of no value in preventing embolization from vegetations. Because they may result in bleeding, they are avoided unless they are required to prevent thrombus for­mation on a prosthetic valve.

OTHER INTERVENTIONS.

Complete bedrest need not be enforced unless clients have fever or signs of heart failure.

However, activities are monitored to allow adequate rest. The nurse explains proper oral and general body hygiene and consistently uses appropriate aseptic technique to protect the client from contact with potentially infective organisms. Nursing assessment for signs of heart failure (including rapid pulse, fatigue, cough, and dyspnea; new heart murmurs; and early signs of embolization) continues throughout the antibi­otic regimen.

SURGICAL MANAGEMENT.

The cardiac surgeon may be consulted if antibiotic therapy is ineffective in sterilizing a valve, if refractory heart failure develops secondary to a de­fective valve, if large valvular vegetations are present, or if multiple embolic events occur. Current surgical interventions for infective endocarditis include the following:

Ø                Removing the infected valve (either biologic or pros­thetic)

Ø                Repairing or removing congenital shunts

Ø                Repairing injured valves and chordae tendineae

Ø                Draining abscesses in the heart or elsewhere

Preoperative and postoperative care of clients having sur­gery involving the valves is similar to that described earlier for valve replacement.

Community-Based Care

Community-based care for clients with infective endocarditis is essential to resolve the problem and avoid complications. Clients and families need to be motivated and have the knowl­edge, physical ability, and resources to administer IV antibi­otics at home. The home care nurse may be contacted to com­plete teaching started in the acute care institution and to monitor client compliance and health status.

The home care nurse and pharmacist arrange for appropri­ate supplies to be available to the client at home. Supplies in­clude the prepared antibiotic, IV pump with tubing, alcohol wipes, IV access device, normal saline solution, and a heparin or saline lock flush solution drawn up in syringes. A heparin or saline lock, peripherally inserted central catheter (PICC line), or central catheter is positioned at a new venous site that is easily accessible to the client or a family member.

The nurse teaches the client, family members, or a signifi­cant other how to administer the antibiotic and care for the in­fusion site while maintaining aseptic technique. The client or family member demonstrates this technique before the client is discharged from the hospital. The nurse emphasizes the importance of maintaining a blood level of the antibiotic by ad­ministering the antibiotics as scheduled. After stabilization at home, the health care provider contacts the client every 3 to 7 days to determine if he or she is able to comply with and ben­efit from the IV antibiotic therapy.

The nurse encourages proper hygiene, particularly oral hy­giene. Clients are advised to use a soft toothbrush, to brush their teeth at least twice a day, and to rinse the mouth with wa­ter after brushing. They should not use irrigation devices or floss the teeth because bacteremia may result. The nurse in­structs clients to wash lacerations well and apply an antibiotic ointment.

Clients must remind health care providers (including their dentists) of their endocarditis and request prophylactic antibi­otic coverage for every invasive procedure, including dental care (Table 35-3). This protection is essential because studies have documented low compliance with prophylaxis regimens by health care providers.

 

The nurse teaches clients self-monitoring for the manifesta­tions of endocarditis, including the complications of heart fail­ure and embolic phenomena. They are instructed to monitor their temperature daily and record it for up to 6 weeks. They are also taught to report fever, chills, malaise, weight loss, in­creased fatigue, or dyspnea to their primary care provider.

 

Pericarditis

OVERVIEW

Pericarditis is an inflammation or alteration of the peri­cardium, the membranous sac that encloses the heart. There are two general types of pericarditis: acute pericarditis and chronic constrictive pericarditis.

Acute pericarditis may be fibrous, serous, hemorrhagic, purulent, or neoplastic. Acute pericarditis is most commonly associated with the following:

Ø                Malignant neoplasms

Ø                Idiopathic causes

Ø                Infective organisms (bacteria, viruses, or fungi)

Ø                Postmyocardial infarction (MI) syndrome (Dressler’s syndrome)

Ø                Postpericardiotomy syndrome

Ø                Systemic connective tissue disease

Ø                Renal failure

The cause of the pericarditis determines its presentation. Acute viral pericarditis commonly follows a respiratory infec­tion and is more common in men between 20 and 50 years of  age. In 5% to 15% of clients who experience an MI, Dressler’s syndrome occurs from 1 to 12 weeks after the infarction. This syndrome is characterized by pericarditis, fever, and pericardial and pleural effusions. Postpericardiotomy syndrome oc­curs in 10% to 40% of clients after cardiac surgery.

Chronic constrictive pericarditis occurs when chronic pericardial inflammation causes a fibrous thickening of the pericardium. It is caused by tuberculosis, radiation therapy, trauma, renal failure, or metastatic cancer. In chronic constrictive pericarditis, the pericardium becomes rigid, preventing adequate filling of the ventricles and eventually resulting in cardiac failure.

COLLABORATIVE MANAGEMENT

Assessment

Assessment findings include substernal precordial pain that radiates to the left side of the neck, the shoulder, or the back. Pain is classically grating and oppressive and is aggravated by breathing (mainly on inspiration), coughing, and swallowing. The pain is worse when the client is in the supine position and may be relieved by sitting up and leaning forward. The nurse asks all of the questions to evaluate chest discomfort because it is important that the pain of pericarditis be differentiated from that of an acute MI.

The nurse may hear a pericardial friction rub with the di­aphragm of the stethoscope positioned at the left lower ster­nal border. This scratchy, high-pitched sound is produced when the inflamed, roughened pericardial layers create fric­tion as their surfaces rub together.

Clients with acute pericarditis may have an elevated white blood cell count. Electrocardiogram (ECG) changes consist­ing of an ST-T wave elevation in all leads develop concur­rently with the onset of the chest pain. Later with treatment and as the pain diminishes and after ST segments return to baseline, the T waves become inverted in most leads. Clients with infectious pericarditis usually have fever. Blood speci­mens for culture may be obtained to assess for possible bac­terial infection. Echocardiograms may demonstrate a pericar­dial effusion.

Clients with chronic constrictive pericarditis show signs of right-sided heart failure, elevated systemic venous pressure with jugular distention, hepatic engorgement, and dependent edema. Exertional fatigue and dyspnea are common compli­cations. These clients may have thickening of the pericardium on echocardiography or a computed tomography (CT) scan. ECG changes include inverted or flat T waves. Atrial fibrilla­tion is common.

Interventions

MEDICAL THERAPY.

The client with acute pericarditis may be hospitalized for diagnostic evaluation, observation for complications, and symptom relief. The health care provider usually prescribes nonsteroidal anti-inflammatory drugs for the relief of pain. Clients who do not obtain pain relief within 48 to 96 hours and who do not have bacterial pericarditis may receive corticosteroid therapy. The nurse assesses for pain re­lief and assists the client to assume positions of comfort— usually sitting upright and leaning slightly forward. If the pain is not relieved within 24 to 48 hours, the nurse notifies the pri­mary care provider.

 

 

The various causes of pericarditis require specific thera­pies. For example, bacterial pericarditis (acute) usually re­quires antibiotics and pericardial drainage. The usual clinical course of acute pericarditis is short term (2 to 6 weeks), but episodes may recur. Chronic pericarditis caused by malignant disease may be treated with radiation or chemotherapy, whereas uremic pericarditis is treated by hemodialysis.

The definitive treatment for chronic constrictive pericardi­tis is surgical excision of the pericardium (pericardiectomy).

 

MONITORING FOR COMPLICATIONS OF PERI­CARDITIS.

A significant complication of pericarditis is peri­cardial effusion, which occurs when the space between the parietal and visceral layers of the pericardium fills with fluid. Pericardial effusion puts the client at risk for cardiac tampon­ade, or excessive fluid within the pericardial cavity. Tampon­ade, which occurs in 15% of clients with acute pericarditis, restricts diastolic ventricular filling, and cardiac output drops. Findings of cardiac tamponade include the following:

Ø                Jugular venous distention

Ø                Paradoxical pulse (systolic blood pressure 10 mm Hg higher or more on expiration than on inspiration)

Ø                Decreased cardiac output

Ø                Muffled heart sounds

Ø               

 

MANAGEMENT OF ACUTE CARDIAC TAMPONADE.

 

Acute cardiac tamponade may occur when small volumes (20 to 50 mL) of fluid accumulate rapidly in the pericardium. If the fluid accumulates slowly, the pericardium may stretch to accommodate several hundred milliliters of fluid. The nurse reports any suspicion of this complication to the physi­cian immediately. The physician may initially manage the de­creased cardiac output with increased fluid volume adminis­tration while awaiting a chest x-ray study or echocardiogram  to confirm the diagnosis. Unfortunately, these tests are not al­ways helpful because the fluid volume around the heart may be too small to visualize. Hemodynamic monitoring in a spe­cialized critical care unit usually demonstrates compression of the heart, with all pressures (right atrial, pulmonary artery, and wedge) being similar and elevated (plateau pressures).

The physician may elect to perform a pericardiocentesis to relieve the pressure on the heart. Under echocardiographic or fluoroscopic and hemodynamic monitoring, the cardiologist inserts an 8-inch (20.3-cm), 16- or 18-gauge pericardial needle into the pericardial space. The physician and the nurse moni­tor the needle’s position, recognizing that ST-wave and T-wave changes indicate myocardial injury and that the needle must be withdrawn slightly. When the needle is properly positioned, a catheter is inserted and all available pericardial fluid is with­drawn. The nurse monitors the pulmonary artery, wedge, and right atrial pressures during the procedure. The pressures should return to normal as the fluid compressing the heart is removed, and the clinical manifestations of tamponade should resolve. In situations in which the cause of the effusion is un­known, pericardial fluid specimens may be sent to the labora­tory for cell count, culture and sensitivity tests, and cytology.

After the pericardiocentesis, the nurse closely monitors for the recurrence of tamponade. Pericardiocentesis alone often does not resolve acute tamponade. The nurse should be pre­pared to provide adequate fluid volumes to increase cardiac output and to prepare the client for emergency sternotomy if tamponade recurs.

If the client experiences a recurrence of tamponade or re­current effusions or adhesions from chronic pericarditis, a portion or all of the pericardium may need to be removed to allow adequate ventricular filling and contraction. The sur­geon may perform a pericardial window, which involves re­moving a portion of the pericardium to permit excessive peri­cardial fluid to drain into the pleural space. In more severe cases, removal of the toughened encasing pericardium (pericardiectomy) may be necessary.

 

Rheumatic Carditis

OVERVIEW

 

Rheumatic carditis occurs in about 40% of clients with rheu­matic fever and affects more than 1 million Americans. It is a sensitivity response that develops after an upper respiratory tract infection with group A beta-hemolytic streptococci. The precise mechanism by which the infection causes inflamma­tory lesions in the heart is not established. However, inflam­mation is evident in all layers of the heart. The inflammation results in impaired contractile function of the myocardium, thickening of the pericardium, and valvular damage.

Rheumatic carditis is characterized by the formation of Aschoff’s bodies, small nodules in the myocardium that are replaced by scar tissue. A diffuse cellular infiltrate also devel­ops and appears to be responsible for the heart failure. The pericardium becomes thickened and covered with exudate, and a serosanguineous pleural effusion may develop. The most serious damage occurs to the endocardium, with inflam­mation of the valve leaflets developing. Hemorrhagic and fi­brous lesions form along the inflamed surfaces of the valves, resulting in stenosis or regurgitation primarily of the mitral and aortic valves.

Rheumatic fever may be a complication of 3% of group A beta-hemolytic throat infections. Although the primary attacks occur most often in childhood, rheumatic fever may occur in adulthood. The incidence of rheumatic carditis had been de­creasing consistently until the mid-1980s. At that time, a resur­gence of rheumatic fever began in both the United States and Europe.

COLLABORATIVE MANAGEMENT

Rheumatic carditis is one of the major indicators of rheumatic fever. The following are common clinical manifestations:

Ø                Tachycardia

Ø                Cardiomegaly

Ø                Development of a new murmur or a change in an existing murmur

Ø                Pericardial friction rub

Ø                Precordial pain

Ø                Electrocardiogram (ECG) changes (prolonged PR interval)

Ø                Indications of heart failure

Ø                Evidence of an existing streptococcal infection

Primary prevention is extremely important. The nurse teaches all clients to consult their health care providers and re­ceive appropriate antibiotic therapy if they develop the follow­ing indications of streptococcal pharyngitis: moderate to high fever, abrupt onset of a sore throat, a reddened throat with ex­udate, and enlarged and tender lymph nodes. Penicillin is the antibiotic of choice for treatment. Erythromycin (Eryc, Erythromid) is the alternative for penicillin-sensitive clients.

The signs of rheumatic carditis must be recognized promptly, and antibiotic therapy must be instituted immediately for secondary prevention. The client is urged to continue the antibiotic administration for the full 10 days to prevent re­infection. The nurse suggests ways to manage the fever, such as maintaining hydration and administering antipyretics. The nurse encourages the client to obtain adequate rest.

The nurse emphasizes tertiary prevention in client educa­tion, explaining that a recurrence of rheumatic carditis is probable with reinfection by a streptococcal organism. Thus antibiotic therapy is essential for streptococcal infection. The nurse also informs the client that antibiotic prophylaxis is necessary for the rest of his or her life to prevent infective en­docarditis.

 

CARDIOMYOPATHY

OVERVIEW

Cardiomyopathy is a subacute or chronic enlargement of cardiac muscle. It is not common, occurring in only 10 to 20 per 100,000 population and resulting in about 27,000 deaths each year in the United States. The cause is usually unknown.

Treatment is usually palliative, not curative, and approxi­mately 50% of clients die within 5 years of diagnosis. Clients need to deal with a shortened life span along with numerous lifestyle changes.

Cardiomyopathies are classified into three categories on the basis of abnormalities in structure and function: dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy .

 

 

Dilated Cardiomyopathy

Dilated cardiomyopathy (DCM) is the structural abnormality in 87% of cardiomyopathy cases. DCM involves extensive damage to the myofibrils and interference with myocar-dial metabolism. There is normal ventricular wall thickness but a dilation of both ventricles and impairment of systolic function. Decreased cardiac output from inadequate pump­ing of the heart causes the client to experience dyspnea on exertion, decreased exercise capacity, fatigue, and palpita­tions. With the exception of peripartum cardiomyopathy, DCM is twice as common in men as in women and occurs most often in middle age. Causes may include alcohol abuse and chemotherapy.

 

Hypertrophic Cardiomyopathy

 

The cardinal features of hypertrophic cardiomyopathy (HCM) are asymmetric ventricular hypertrophy of the left ventricle and disarray of the myocardial fibers. Left ventricular hypertrophy leads to a hypercontractile left ventricle with rigid ven­tricular walls.

Obstruction in the left ventricular outflow tract is seen in 75% to 80% of clients with HCM. The abnormal stiffness of the ventricle in HCM results in diastolic filling abnormalities. In approximately 50% of clients, HCM is transmitted as a single-gene autosomal dominant trait. The American Heart Association (1998) reports that approxi­mately 36% of young athletes who die suddenly probably had hypertrophic cardiomyopathy.

 

Restrictive Cardiomyopathy

 

Restrictive cardiomyopathy, the rarest of the three cardiomyopathies, results in restriction of filling of the ventricles. It is caused by endocardial and/or myocardial disease and produces a clinical picture similar to that of constrictive pericarditis.

 

COLLABORATIVE MANAGEMENT

Assessment

Findings in cardiomyopathy depend on the structural and functional abnormalities. Left ventricular or biventricular fail­ure is characteristic of dilated cardiomyopathy (DCM). Some clients with DCM are asymptomatic for months to years and have left ventricular dilation identified on x-ray examination. Other clients experience sudden, pronounced symptoms of left ventricular failure, such as progressive dyspnea on exer­tion, orthopnea, palpitations, and activity intolerance. Right-sided heart failure develops late in the disease and is associ­ated with a poor prognosis. Atrial fibrillation occurs in 25% of clients and is associated with embolism.

The clinical picture of hypertrophic cardiomyopathy (HCM) results from the hypertrophied septum, which in 80% of cases causes a mechanical obstruction and thereby reduces stroke volume and cardiac output. Most clients are asympto­matic until late adolescence or early adulthood. The primary symptoms of HCM are exertional dyspnea (90% of clients), angina (75% of clients), and syncope. The chest pain is atyp­ical in that it usually occurs at rest, is prolonged, has no rela­tion to exertion, and is not relieved by the administration of nitrates. A high incidence of ventricular dysrhythmias is asso­ciated with HCM. Sudden death occurs and may be the first manifestation of the disease.

The earliest clinical finding in restrictive cardiomyopathy is exertional dyspnea. Cardiac output cannot increase during periods of exertion because of the fixed ventricular volume. The client also reports weakness, exercise intolerance, palpitations, and syncope.

Echocardiography, radionuclide imaging, and angiocardiography during cardiac catheterization are performed to diagnose and differentiate cardiomyopathies.

Interventions

The treatment of choice for the client with cardiomyopathy varies with the type of cardiomyopathy and may include both medical and surgical interventions.

NONSURGICAL MANAGEMENT.

The care of clients with dilated or restrictive cardiomyopathy is initially the same as for heart failure. Drug therapy includes the use of diuretics, vasodilating agents, and cardiac glycosides to increase car­diac output. Because clients are at risk for sudden death, the nurse urges them to report any palpitations, dizziness, or fainting, which might indicate a dysrhythmia.

Antidysrhythmic drugs or implantable cardiac defibrillators may be used to control life-threatening dysrhythmias. Beta blockers (e.g., metoprolol) are used experimentally for clients with excessive sympathetic stimulation and resting tachycardia. If cardiomyopathy has developed in response to a toxin, clients are in­structed to avoid further exposure to that toxin. The nurse teaches all clients with cardiomyopathy to abstain from alco­hol ingestion because of its cardiac depressant effects.

Management of obstructive HCM includes administering negative inotropic agents such as beta-adrenergic blocking agents (carvedilol) and calcium antagonists (diltiazem). They decrease the outflow obstruction that accompanies exercise and also decrease heart rate, resulting in less angina, dyspnea, and syncope. Vasodilators and cardiac glycosides are con-traindicated in clients with obstructive HCM because vasodilating and positive inotropic effects may augment the ob­struction. Strenuous exercise is also prohibited because it can increase the risk of sudden death.

SURGICAL MANAGEMENT.

The type of surgery performed depends on the type of cardiomyopathy.

EXCISION OF HYPERTROPHIED SEPTUM.

Surgery may be considered for the small percentage of clients with ob­structive HCM who do not respond to medical therapy. The most commonly used surgical treatment (ventriculomyomectomy) includes excising a portion of the hypertrophied ven­tricular septum to create a widened outflow tract. Surgery re­sults in long-term improvement in exercise tolerance in most clients with HCM.

CARDIOMYOPLASTY.

Cardiomyoplasty is used for some clients with DCM who cannot undergo cardiac trans­plantation and are asymptomatic at rest. The latissimus dor-sum muscle is dissected free of its distal insertion and is wrapped around the heart. For the next 2 months, the muscle is stimulated with increasing frequency until it can contract in synchrony with each heartbeat. Six months after surgery, the client should begin to feel the effects of an enhanced cardiac output.

HEART TRANSPLANTATION.

 Heart transplantation is the treatment of choice for clients with severe DCM and may be considered for clients with restrictive cardiomyopathy. Each year about 2300 clients in the United States receive car­diac transplants—most for DCM. Criteria for candidate selection include the following:

Ø                Life expectancy less than 1 year

Ø                Age generally less than 65 years

Ø                New York Heart Association (NYHA) class III or IV

Ø                Normal or only slightly increased pulmonary vascular resistance

Ø                Absence of active infection

Ø                Stable psychosocial status

Ø                No evidence of drug or alcohol abuse

The surgeon transplants a heart from a donor with a comparable body weight and ABO compatibility into a recipient less than 6 hours after procurement. In the most common procedure (orthotopic transplantation), the surgeon removes the diseased heart and leaves the posterior walls of the client’s atria. The remnant atria serve as the anchor for the donor heart. Anastomoses are made between the recipient and donor atria, aorta, and pulmonary arteries (Figure 35-6). Because the remaining remnant of the recipient’s atria contains the sinoatrial node, two unrelated P waves are visible on the ECG.

 

The postoperative care of the heart transplant recipient is similar to that for conventional cardiac surgery. However, the nurse must be especially vigilant to identify occult bleeding into the pericardial sac with the potential for tamponade. The recipient’s pericardium has usually stretched considerably to accommodate the diseased, hypertrophied heart. This predis­poses the client to concealed postoperative bleeding.

The transplanted heart is denervated and is unresponsive to vagal stimulation. The client’s heart rate approximates 100 beats/min, responding slowly to exercise, stress, or position change with increases in heart rate, contractility, and cardiac output. In the early postoperative phase, the nurse may titrate isoproterenol (Isuprel) to support the heart rate and maintain cardiac output. Atropine, digitalis, and carotid sinus pressure are not used because they do not have their usual effects on the denervated heart. Denervation of the heart may cause pro­nounced orthostatic hypotension in the immediate postopera­tive phase, and the nurse cautions the client to change position slowly.

To suppress natural defense mechanisms and prevent transplant rejection, clients require immunosuppressant therapy for the rest of their lives. Most commonly, the physician prescribes therapy with cyclosporine (Sandimmune) and azathioprine (Imuran). Nurses must be vigilant about handwash-ing and aseptic technique because clients are immunosuppressed and infection is the major cause of death. Infection usually develops in the immediate post-transplant period or during treatment for acute rejection.

Most clients experience their initial episode of acute rejec­tion in the first 3 months after heart transplantation. Symp­toms of rejection are nonspecific and occur late in the rejec­tion process. They include cardiac dysrhythmias (especially atrial dysrhythmias), hypotension, weakness, fatigue, and dizziness. To detect rejection, the surgeon performs right en-domyocardial biopsies at regularly scheduled intervals and whenever symptoms occur.

Approximately 75% of clients survive 3 years after trans­plantation; most return to NYHA class I or II status (AHA, 1998). Five years after transplantation, many of the surviving clients (20% to 40%) have evidence of coronary artery dis­ease (CAD) presenting as diffuse plaque in the arteries of the donor heart. Because the heart is denervated, clients do not usually experience angina, and regularly scheduled exercise tolerance tests and angiography are required to identify CAD.

To delay the development of CAD, clients are encouraged to follow a prudent lifestyle similar to clients with CAD. The physician may prescribe a calcium channel blocker such as diltiazem (Cardizem) to decrease the rate of coronary artery narrowing. The nurse stresses the importance of compliance with dietary modifications and medication reg­imens. The client is encouraged to participate in a regular ex­ercise program but is cautioned to allow at least 10 minutes of warm up and cool down for the denervated heart to adjust to changes in activity level.

DECREASED CARDIAC OUTPUT

PLANNING: EXPECTED OUTCOMES. The client with heart failure is expected to resume and maintain an ade­quate cardiac output, as indicated by (1) a heart rate in ex­pected range (IER), (2) a cardiac index IER, (3) dysrhythmia not present, (4) abnormal heart sounds not present, and (5) pe­ripheral pulses strong.

INTERVENTIONS. The purpose of care is to optimize afterload, preload, and contractility, thus improving cardiac output. Therapy may be directed toward optimizing the two major components of cardiac output: stroke volume (deter­mined by preload, afterload, and contractility) and heart rate (see Chart 35-3). (See Chapter 33 for a further explanation of these concepts.)

HEMODYNAMIC REGULATION. Interventions to opti­mize stroke volume include reducing afterload, reducing preload, and improving cardiac muscle contractility.

REDUCING AFTERLOAD. By relaxing the arterioles, arterial vasodilators can reduce the resistance to left ventricular ejection (afterload) and improve cardiac output. These drugs do not cause excessive vasodilation but reverse some of the inappropriate or excessive vasoconstriction common in heart failure.

Clients with even mild heart failure resulting from left ventricular dysfunction should be given a trial of angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors are a group of arterial vasodilators such as enalapril (Vasotec), moexipril (Univasc), and captopril (Capoten). In general, these drugs prolong and improve the quality of life for clients with heart failure (Chart 35-4). They enhance functional sta­tus, with 40% to 80% of clients showing an improvement in the New York Heart Association (NYHA) class.

ACE inhibitors suppress the renin-angiotensin-aldosterone system, which is activated in response to decreased renal blood flow. ACE inhibitors benefit clients by reducing arterial resistance, decreasing pulmonary artery wedge pressure, and increasing stroke volume and cardiac output.

The health care provider usually starts doses of ACE in­hibitors slowly and cautiously. The first dose of an ACE in­hibitor is sometimes associated with a rapid drop in blood pressure. Clients at risk for hypotension following ACE in­hibitor administration have initial systolic blood pressures less than 100 mm Hg, are older than 75 years of age, have a serum sodium level less than 135 mEq/L, or are volume de­pleted. Blood pressure is monitored for several hours after the initial dose and each time the dose is increased.

The nurse clarifies with the health care provider the guidelines for administering the vasodilator. For example, many clinicians maintain clients with heart failure at sys­tolic blood pressures ranging from 90 to 110 mm Hg. When such a blood pressure is the maintenance level, the client is assessed for orthostatic hypotension, confusion, poor pe­ipheral perfusion, and reduced urine output. While the client is receiving ACE inhibitors, the nurse monitors serum potassium levels for hyperkalemia, serum creatinine for re­nal dysfunction, and the client for development of a cough.

REDUCING PRELOAD.

Ventricular fibers contract less forcefully when they are overstretched, such as in a failing heart. Interventions aimed at reducing preload attempt to de­crease volume and pressure in the left ventricle, optimizing ventricular muscle stretch and contraction. Preload reduction is appropriate for heart failure accompanied by congestion with total body sodium and water overload.

Diet Therapy. In heart failure, diet therapy is aimed at re­ducing sodium and water retention.

Sodium Restriction. In collaboration with the dietitian, the health care provider may restrict sodium intake in an attempt to decrease fluid retention. Many clients with heart failure need to omit only table salt (ingest no added salt) from their diet, thus reducing sodium intake to approximately 3 g/day.

If salt intake must be reduced further, the client may need to eliminate all salt in cooking as well as high-sodium foods, thus reducing sodium intake to 2.0 g/day. A dietitian is essen­tial in helping to select foods that meet such a restricted ther­apeutic diet. Approximately 25% of hospital admissions for clients with heart failure are due to excessive sodium intake. Therefore all clients must be advised to maintain an appropri­ate sodium restriction and avoid bingeing on high sodium foods (e.g., pickles). Table 11-6 lists the sodium contents of some common foods.

Fluid Volume Restriction.

Few clients are placed on severe fluid restrictions. However, clients with excessive aldosterone secretion may experience thirst and drink 3 to 5 L of fluid each day. As a result, their fluid intake may be limited to a more normal 2 L/day. Compliance with these simple strate­gies may be high, especially if the client experiences relief of any of the symptoms of volume excess. When a fluid restric­tion is imposed on the hospitalized client, the nurse adjusts oral and IV therapy accordingly.

The nurse or assistive nursing personnel weighs the client daily (1 kg of weight gain or loss equals 1 L of retained or lost fluid, respectively) and keeps accurate records of fluid intake and output. The same scale should be used every morning be­fore breakfast for the most accurate assessment of weight.

Drug Therapy. Common drugs prescribed to reduce pre­load are diuretics and venous vasodilators.

Diuretics. The health care provider adds diuretics to the regimen when diet and fluid restriction have not been effec­tive in managing the symptoms of systemic or pulmonary congestion associated with heart failure. Diuretics enhance the renal excretion of sodium and water by reducing circulating blood volume, decreasing preload, and reducing systemic and pulmonary congestion.

The type and dosage of diuretic prescribed depend on the degree of heart failure and renal function. High-ceiling (loop) diuretics, such as furosemide (Lasix, Furoside^), torsemide (De-madex), and ethacrynic acid (Edecrin), are most effective for treating fluid volume overload. The practitioner may initially use a thiazide diuretic, such as hydrochlorothiazide (Hydro-DIURIL, Urozidc+O and metolazone (Zaroxolyn), for older clients with mild volume overload. The action of thiazide di­uretics is self-limiting (i.e., diuresis decreases after edema fluid is lost), thus the excessive diuresis and dehydration that may oc­cur with loop diuretics are uncommon occurrences with thiazide diuretics. Clients often prefer thiazide diuretics because of the gradual onset of diuresis. However, loop diuretics are needed to ensure effective diuresis for many clients in heart failure.

As heart failure progresses, many clients develop diuretic resistance with refractory edema. The health care provider may choose to treat this problem by administering two types of diuretics, most commonly a loop diuretic and a thiazide diuretic such as metolazone.

The nurse also needs to monitor for and prevent potassium deficiency (hypokalemia) from diuretic therapy. The signs of hypokalemia are nonspecific neurologic and muscular com­plaints such as generalized weakness, depressed reflexes, and irregular heart rate. Therefore the physician, nurse, and dieti­tian monitor serum potassium levels to accurately identify hypokalemia.

If the client’s serum potassium level is less than 4.0 mEq/L, the health care provider has several alternatives:

* Add a potassium-sparing diuretic to the regimen

* Request that clients increase their dietary intake of potassium-rich foods

* Prescribe a potassium supplement

Clients being treated simultaneously with ACE inhibitors and diuretics may not experience hypokalemia. If their kid­neys are not functioning well, they may develop hyperkalemia (elevated serum potassium level). The nurse should review the client’s serum creatinine level. If the creatinine is greater than 1.8, the nurse should notify the health care provider before ad­ministering supplemental potassium.

 

Venous Vasodilators.

The health care provider may pre­scribe venous vasodilators, (e.g., nitrates) for the client with heart failure and persistent dyspnea. Significant constriction of venous and arterial blood vessels occurs to compensate for reduced cardiac output. This reduces the volume of fluid that the vascular bed can hold and increases preload.

Venous va­sodilators may benefit by:

§                   Returning venous vasculature to a more normal capacity

§                   Decreasing the volume of blood returning to the heart

§                   Improving left ventricular function

 

 

 

Nitrates may be administered intravenously, orally, or top­ically. These drugs cause primarily venous vasodilation but also a significant amount of arteriolar vasodilation. It is essential for the nurse to monitor the client’s blood pressure when initiating nitrate therapy or increasing the dosage. Clients may initially report headache, but they are assured that they will develop a tolerance to this effect and that the headache will cease or diminish.

Unfortunately, clients may develop tolerance to the vasodilating effects wheitrates are uniformly administered during 24 hours. To prevent such tolerance, the health care provider may order at least one 12-hour nitrate-free period out of every 24 hours (usually overnight). Clients whose major complaint is nocturnal dyspnea may experience relief when nitroglycerin ointment is applied at bedtime and removed dur­ing the day.

ENHANCING CONTRACTILITY.

 

Contractility of the heart can also be enhanced with drug therapy. The preferred drug is digitalis.

Digitalis. Digoxin (Lanoxin), a cardiac glycoside, has been demonstrated to provide benefits for clients in heart fail­ure with sinus rhythm and atrial fibrillation. “Dig” therapy re­duces exacerbations of heart failure and hospitalizations, re­sulting in an estimated annual savings of $406 million. When added to a regimen of angiotensin-converting enzyme (ACE) inhibitors and diuretics, digoxin increases functional capacity and improves hemodynamic parameters in clients with New York Heart Association (NYHA) class III and IV heart failure resulting from left systolic dysfunction.

The potential benefits of digitalis derivatives include an in­crease in contractility, a reduction in heart rate, a slowing of conduction through the atrioventricular node, and an inhibi­tion of sympathetic activity while enhancing parasympathetic activity. Digitalis also may have a mild diuretic effect. In­creased automaticity occurs with toxic digitalis levels or in the presence of hypokalemia (which increases sensitivity to digitalis), and ectopic beats (premature ventricular contrac­tions [PVCs]) may result.

The most commonly prescribed cardiac glycoside is digoxin (Lanoxin, Novodigoxin^). Digoxin is erratically ab­sorbed from the gastrointestinal tract. Many medications, es­pecially antacids, interfere with its absorption. It is eliminated primarily by renal excretion.

Digitalis Toxicity.

The presentation of digitalis toxicity is often vague and nonspecific and includes anorexia, fatigue, and mental status changes. Toxicity may cause nearly any dysrhythmia, but premature ventricular contractions (PVCs) are most commonly noted. The nurse or nursing staff member carefully monitors the apical pulse rate and heart rhythm of clients receiving digoxin. A resting heart rate of less than 60 beats/min or greater than 100 beats/min is reported to the health care provider. It is equally important to report the de­velopment of either an irregular rhythm in a client with a pre­viously regular rhythm or a regular rhythm in a client with a previously irregular one. The nurse also monitors serum digoxin and potassium levels (hypokalemia potentiates digi­talis toxicity) to identify toxicity.

Any medication that increases the workload of the failing heart also increases its oxygen requirement. The nurse should be alert for the possibility that the client may experience angina (chest pain) in response to digoxin.

 

Beta-Adrenergic Blockade.

Although it is not completely clear how they accomplish their effect, beta blockers improve the condition of some clients in heart failure. It ap­pears that prolonged exposure to increased levels of sympathetic stimulation and catecholamines worsens cardiac function. Beta-adrenergic blockade reverses this effect, improving morbidity, mortality, and quality of life for clients in heart failure.

Beta blockers must be started and used with great caution for heart failure. In most cases, clients in heart failure should not be started on a beta blocker until their ACE inhibitor and diuretic doses have been stabilized for 2 weeks. Carvedilol (Coreg) is the only beta blocker approved for treatment of heart failure, but metoprolol (Lopressor, Betaloc, Novometoprol) is also often used. The first dose is extremely low,  and the client is monitored either in the hospital or the health care provider’s office to detect bradycardia or hypotension.

The nurse instructs the client to weigh daily while taking the beta blocker and to report any signs of worsening heart failure immediately. The health care provider gradually titrates the drug dose upward, and the client is evaluated at least weekly for changes in blood pressure, pulse, activity tol­erance, and orthopnea. A modest drop in blood pressure is ac­ceptable if the client remains asymptomatic and can stand without experiencing dizziness or a further drop in blood pressure. The resting heart rate should remain between 55 and 60 and increase slightly with exercise. The client’s activity tolerance should improve, and he or she should not experi­ence orthopnea. Most clients with mild and moderate heart failure demonstrate improved ejection fraction, decreased hospital admissions, and improvement in symptoms when beta blockers are added to their treatment regimens. Clients should be advised that the benefits of beta-blocker therapy ac­crue over a long period, not immediately.

ACTIVITY INTOLERANCE

 

PLANNING: EXPECTED OUTCOMES.

The client with heart failure is expected to (1) perform activities of daily living, (2) walk at least two blocks without experiencing dyspnea or excessive fatigue, (3) have energy restored after rest, and (4) perform usual routine.

 

INTERVENTIONS.

The purpose of interdisciplinary interventions is to regulate energy to prevent fatigue and optimize function .

ENERGY MANAGEMENT.

The client in severe heart fail­ure initially requires physical and emotional rest. On the first day of hospitalization, he or she may sit up in a chair for meals and perform basic leg exercises while out of bed. Nurs­ing care should be organized to allow periods of rest. The in­terdisciplinary team observes and documents the client’s physiologic response to activity.

As the condition improves, the physical therapist (PT) ini­tiates ambulation, usually on hospital day 2. The nurse checks the blood pressure, pulse, and oxygen saturation before and after the activity. A blood pressure change of more than 20 mm Hg or a pulse increase of more than 20 beats/min may in­dicate that the activity is too stressful. Other indications of activity intolerance include dyspnea, fatigue, and chest pain. A client displaying any of these symptoms is asked to rate how hard he or she has been working on a scale of 1 to 20, with 20 being the maximum perceived exertion. If the client rates the exertion higher than 12, the nurse counsels him or her to slow down. If the client tolerates the activity, the PT steadily in­creases the activity level until the client is ambulating 200 to 400 feet several times a day.

If the client is able, the PT (or assistive nursing or PT per­sonnel) might time him or her for 6 minutes while walking at a comfortable pace. The distance the client can walk can be used to determine his or her functional level and activity plan.

POTENTIAL FOR PULMONARY EDEMA

PLANNING: EXPECTED OUTCOMES.

The client with heart failure is expected to be free of pulmonary edema.

INTERVENTIONS.

The nurse monitors for acute pul­monary edema, a life-threatening event that can result from severe heart failure. In pulmonary edema, the left ventricle fails to eject sufficient blood, and pressure increases in the lungs because of the accumulated blood. The increased pres­sure causes fluid to leak across the pulmonary capillaries and into the pulmonary interstitium.

The nurse assesses for early signs and symptoms of pul­monary edema (e.g., crackles in the lung bases, dyspnea at rest, disorientation, and confusion), especially in older clients. Documentation of the precise location of the crackles is cru­cial, because the level of the fluid ascends as the pulmonary edema worsens. The client in acute pulmonary edema is also extremely anxious, tachycardiac, and struggling for air. As pulmonary edema becomes more severe, he or she may have a moist cough productive of frothy, blood-tinged sputum, and his or her skin may be cold, clammy, or cyanotic.