Chapter 16: Nursing Management: Patients with Structural, Inflammatory and Infectious Cardiac Disorders

Clinical manifestations of mitral stenosis

Although patients with MS can remain asymptomatic, symptoms usually develop when the pressure in the LA becomes greater than that of the LV, after the valve opening is reduced by one third to one half its usual size. Dyspnea on exertion (DOE) results from pulmonary congestion. Patients become progressively fatigued as a result of low CO. Palpitations Chest pain Paroxysmal nocturnal dyspnea (PND) Premature beats AF Paroxysmal atrial tachycardia Dyspnea at rest is likely with severe MS. Cough, sometimes with hemoptysis from ruptured pulmonary veins Hoarseness from the dilated atrium impinging on the left recurrent laryngeal nerve Orthopnea Recurrent respiratory infections. Later, symptoms of right heart failure, including peripheral edema and ascites, occur. A loud S1 and an opening snap can be heard because of the elevated left atrial pressure

Bioprosthetic valves

Bioprosthetic valves are less durable than mechanical valves because of the structural degeneration that occurs over time. This can lead to the need for reoperation. Generally, older patients have shorter anticipated survival, so the risk of reoperation is less than it would be for a younger person. Because long-term anticoagulation generally is not recommended for bioprosthetic valves after the first 3 months of implantation, these valves are used when anticoagulation is contraindicated or should be avoided, such as in women of childbearing age, patients who are noncompliant with medications and follow-up, patients with a history of bleeding disorders, and others who cannot tolerate long-term anticoagulation. The major disadvantage of tissue valves is that they lack longevity. Types of bioprosthetic valves include homograft (preserved human cadaver), pericardial, and xenograft (bovine, porcine, or equine). Generally homografts are used for the treatment of valve endocarditis. Newer tissue valves demonstrate improved hemodynamics compared with older models.

Risk factors for aortic regurgitation

Calcific valve disease and bicuspid aortic valve are the most common risk factors for AR. Because they affect the valve leaflets, rheumatic heart disease and infective endocarditis can cause AR. Disorders affecting the aortic root, such as Marfan syndrome and dissecting aortic aneurysms, can lead to AR, as can chronic hypertension

Diagnostic tests for mitral regurgitation

Chest x-ray may reveal left ventricular and left atrial enlargement. An echocardiogram provides information regarding left ventricular size and function, left atrial size, and pulmonary artery pressures as well as the anatomy of the valve. Also, echocardiography is used to monitor the severity and progression of MR. Cardiac catheterization may be used if there is a discrepancy between clinical and noninvasive findings to determine the severity of MR.

Risk factors for mitral valve prolapse

Female gender family history Marfan syndrome

Nursing management for valvuloplasty

Symptoms of the backward heart failure resolve in hours to days. With valve replacement for a regurgitant valve, it may take months for the chamber into which blood had been regurgitating to achieve its optimal postoperative function Patients with percutaneous valvuloplasty procedures must be assessed for signs and symptoms of emboli and heart failure. Attention is given to hemodynamic stabilization: augmenting preload, reducing afterload, and enhancing contractility, recognizing that the heart is adjusting to improved function. Patients are at risk for postoperative complications, including thromboembolism, bleeding, infective endocarditis, arrhythmias, structural deterioration (bioprosthetic valves), and hemolytic anemia. Thromboembolism is the most common complication of prosthetic valves and can lead to hemodynamic compromise by occluding the valve orifice. Long-term anticoagulation with warfarin, a vitamin K antagonist, is indicated after mechanical valve replacement. Heparin is used as a "bridge" until an acceptable level of anticoagulation is achieved with warfarin. Frequently low-dose aspirin is used with warfarin Usually low-dose (75 to 100 mg daily) aspirin is recommended. For patients with additional thrombotic risk factors, such as concurrent AF, anticoagulation with warfarin generally is prescribed for 3 months postoperatively. The nurse educates the patient about long-term anticoagulant therapy, including the risks associated with it as well as the need for frequent follow-up appointments and blood laboratory studies. Patients receiving warfarin will have individualized target international normalized ratios (INRs), typically between 2 and 3.5 seconds, and will vary based upon the type of valve. Prosthetic valve endocarditis occurs more often with tissue valves. It can occur early, within the first 60 days after surgery, or later. Signs include fever, heart failure, embolic events, and new murmur. In general, for a patient with a prosthetic heart valve, if the temperature is higher than 100°F, endocarditis must be excluded by blood culture; whereas for fever with signs of sepsis, broad-spectrum antibiotics must be begun while awaiting culture results Hemolytic anemia results from the destruction of red blood cells by the movement of the prosthetic valve disk or caged ball. Conduction disturbances and atrial arrhythmias occur frequently following valve surgery, likely due to circulating catecholamines, myocardial inflammation, and electrolyte imbalances. Digoxin, BBs, and CCBs may be used for the treatment of arrhythmias. The nurse provides teaching about all prescribed medications: Patients with prosthetic valves require education to prevent infective endocarditis with antibiotic prophylaxis. The American Heart Association (AHA) recommends antibiotic prophylaxis for dental procedures that involve manipulation of gingival tissue, the periapical region of teeth, or perforation of the oral mucosa, not for routine cleaning

Nursing management of cardiomyopathies

The echocardiogram is used in the evaluation of cardiomyopathy because it allows assessment of both the structure and function of the ventricles, including valvular abnormalities and EF. A chest x-ray can identify the extent of cardiac enlargement and the presence of pulmonary congestion, an electrocardiogram (ECG) can confirm the presence of arrhythmias, and cardiac catheterization can detect the presence of coronary artery disease. Endomyocardial biopsy may be performed; analysis of myocardial tissue may be used to guide therapy or to establish a precipitating cause, if unknown. Because genetic factors may be involved, detailed and careful family history, should be obtained. Supportive care with standard heart failure therapy, including ACE inhibitors, aldosterone receptor antagonists (ARBs), BB and diuretics, should be administered for all cardiomyopathies. BBs and CCBs reduce catecholamine response and decrease heart rate. ACE inhibitors are prescribed to reduce preload, afterload, and hypertension by causing vasodilation. ARBs reduce afterload by blocking the action of Angiotensin II, resulting in vasodilation, which subsequently decreases preload and helps regulate fluid and electrolyte balance. Diuretics remove excess sodium and fluid to reduce pulmonary congestion. Nitrates and dehydration should be avoided in HCM to maintain CO. Systemic anticoagulation may be needed to prevent thromboembolic events. Because mural thrombi (a thrombus formed on and attached to a diseased patch of endocardium, not on a valve or on one side of a large blood vessel) are also a risk, the patient's neurologic status should be monitored carefully. Often antiarrhythmic medications are initiated to prevent and treat arrhythmias. For stress-induced cardiomyopathy, accurate diagnosis and differentiation from STEMI is critical to avoid unnecessary treatments, such as administration of thrombolytics, which can cause harm to the patient. Unstable patients may require positive inotropic medications, vasopressors and intra-aortic balloon pumps (IABPs), implantable devices, or surgery. Pacemakers are used to correct conduction abnormalities and control heart rate when tachyarrhythmias or bradyarrythmias are present. Cardiac resynchronization therapy with biventricular pacing can resynchronize the ventricles to improve contractility. ICDs are recommended when there is a high risk for life-threatening arrhythmias, particularly with ARVC/D. IABP, septal myectomy (removal of hypertrophied portion of the septum that is obstructing the flow of blood from the LV to the aorta) or alcohol septal ablation, left ventricular assist devices (VADs), and heart transplantation may be necessary in the most severe cases. Nursing management of cardiomyopathy includes careful cardiovascular assessment for signs of worsening heart failure, particularly dyspnea, congested lungs, peripheral edema, and the presence of abnormal heart sounds. Bed rest is maintained to decrease cardiac workload. Physical activity is increased slowly, and the patient is asked to report symptoms that occur with increasing activity.

Clinical manifestations of mitral valve prolapse

Commonly asymptomatic fatigue dyspnea palpitations chest pain Shortness of breath (SOB) Cardiac auscultation may reveal a mitral midsystolic click

Nursing management of myocarditis

ACE-Is, ARBs, BBs, and diuretics may be prescribed to treat heart failure symptoms. Self-limiting, mild cases may resolve with bed rest and supplemental oxygen, while more severe cases will require hemodynamic support. Surgical options, such as the placement of a VAD or TAH or heart transplantation, should be considered when there is no improvement in symptoms or hemodynamic status despite maximal medical therapy. In addition to monitoring vital signs, heart sounds, lung sounds, and peripheral perfusion, the nurse must assess hemodynamic, oxygenation, and fluid status

Clinical manifestations of aortic regurgitation

AR is asymptomatic for years Palpitations, particularly when lying down, and visible neck vein pulsations are a result of the increased force and volume of the blood ejected from the hypertrophied LV. dyspnea fatigue angina orthopnea pulmonary congestion Pulse pressure, the widens, resulting in high systolic and low diastolic blood pressure. Another characteristic sign of AR is the water-hammer pulse, in which the pulse has a rapid upstroke and collapses. Systolic blood pressure in the lower extremities is higher than in the upper extremities. A decrescendo diastolic murmur is heard as a high-pitched blowing sound at the 3rd or (4th) intercostal space (ICS) at the left sternal border with the patient sitting up and leaning forward. If the AR is severe, the murmur may be holodiastolic (throughout the S2) and radiate widely along the left sternal border.

Clinical manifestations of aortic stenosis

AS can be asymptomatic for decades. Exertional dyspnea or decreased exercise tolerance can be early signs. The triad of symptoms associated with AS includes angina due to LV hypertrophy and diminished coronary blood flow; dyspnea due to increased pulmonary venous pressure from LV failure; and syncope, usually with exertion, due to a reduction in cerebral blood flow that occurs when vasodilation leads to a decrease in arterial pressure in the setting of fixed CO. With AS, the heart rate will increase in an attempt to increase CO, but CO does not improve. Symptomatic AS has a poor prognosis if untreated. On physical examination, a thrill, or a vibration, may be felt. A loud, systolic ejection murmur may be heard over the aortic area (second intercostal space, right sternal border) and may radiate into the neck The patient should be instructed to lean forward during auscultation, especially upon exhalation, to accentuate the murmur. An S4 gallop may be heard.

Pathophysiology of acute mitral regurgitation

An acute MI can damage the ventricular wall and disrupt the attachment of the papillary muscle or the chordae tendineae Without a normally functioning valve to direct the flow of blood forward, a large amount of blood from the LV flows backward into the LA. This compromises forward flow of blood and CO is diminished, which can lead to cardiogenic shock. Compensatory mechanisms lead to an increase in systemic vascular resistance (SVR), which can worsen regurgitation.

Diagnostic tests for dilated cardiomyopathy

An echocardiogram is the preferred diagnostic tool as it can evaluate LV function and size, as well as valvular abnormalities. Cardiac catheterization is important to exclude coronary artery disease.

Clinical manifestations of mitral regurgitation

As the LV becomes progressively impaired and CO diminishes, fatigue, tachycardia, and weakness can occur. As left atrial pressure increases, orthopnea, DOE, and PND result from pulmonary congestion. Palpitations are related to a hyperdynamic LV and/or AF. Peripheral edema and ascites occur when the RV fails Patients may report a sudden inability to breathe accompanied by chest pain. a hyperdynamic point of maximal impulse A holosystolic (pansystolic) murmur is heard as a high-pitched, blowing sound at the apex; radiation to the axilla is possible. An S3 may be present because of increased, rapid blood flow into the ventricle during diastole.

restrictive cardiomyopathy

Characterized by diastolic dysfunction that negatively affects or "restricts" the heart's ability to fill with blood Uncommon cardiomyopathy Frequently idiopathic Associated with amyloidosis and endomyocardial fibrosis (scarring of the heart) Often occurs after a heart transplant Stiff ventricular walls lack ventricular stretch (flexibility to expand as they fill with blood). This impairs diastolic filling, resulting in diastolic HF. Normal, or slightly increased, ventricular wall thickness and atrial enlargement with normal systolic function are characteristic. Atrioventricular block and symptomatic bradycardia can occur.

Symptoms of stress-induced cardiomyopathy

Clinical presentation is identical to that of acute ST-segment elevation MI: acute substernal pain and shortness of breath following an emotionally or physically stressful trigger. ST-segment elevation may be present on ECG, and cardiac enzymes may be mildly elevated, disproportionate to levels seen with acute MI. Acute presentation may be severe; arrhythmias, HF, pulmonary edema, and cardiogenic shock have been reported in the absence of significant coronary artery disease. Ballooning of the LV, with rapid and complete recovery, is the hallmark feature.

Valvular disease

Common causes include degenerative disease, rheumatic heart disease, and infective endocarditis (inflammation of the inner lining of the heart, the endocardium). Progression of valvular heart disease can result in heart failure, arrhythmias, stroke, and sudden death

Postoperative transplant care

Commonly, patients receive cyclosporine or tacrolimus, azathioprine or mycophenolate mofetil (CellCept), and corticosteroids to minimize rejection. Patients must gradually increase and decrease their exercise (i.e., extended warm-up and cool-down periods), because 20 to 30 minutes may be required to achieve the desired heart rate. Rejection is most common in the first 3 to 6 months following transplant, although the risk of infection continues to be a significant risk even after the first year because of the immunosuppressant medications. In addition to rejection and infection, other complications include posttransplant lymphoproliferative disease and the development of allograft vasculopathy or rapidly progressing atherosclerosis in the arteries of the transplanted heart. Osteoporosis frequently occurs as a side effect of the anti-rejection medications and pretransplantation dietary insufficiency and long-term sedentary lifestyle. Immunosuppressants and corticosteroids can cause weight gain, diabetes, dyslipidemia, kidney failure, and disturbances of the central nervous and gastrointestinal systems, and toxicity from immunosuppressants can occur.

Diagnostic tests for mitral stenosis

Echocardiography is the most sensitive and specific noninvasive method to diagnose MS and is used to evaluate valve morphology and to measure cardiac pressures

Diagnostic tests for aortic stenosis

Echocardiography is used to diagnose and monitor the progression of AS and will demonstrate calcification of the valve or decreased mobility of valve cusps, as well as size and function of LV. Cardiac catheterization can measure the severity of AS when noninvasive testing is inconclusive.

Diagnosis of myocarditis

Echocardiography is widely used when myocarditis is suspected and may show nonspecific findings or demonstrate impaired heart muscle function or pericardial effusion. Endomyocardial biopsy is used to confirm diagnosis.

Hypertrophic cardiomyopathy

Hypertrophied, nondilated LV leads to obstruction of left ventricular outflow, without cardiac or systemic disease HCM is an inherited autosomal dominant heart muscle disorder and one of the most common types of cardiomyopathy. It is the most common cause of sudden cardiac death (SCD) in young athletes. Heart muscle asymmetrically increases in mass, especially along the septum, and increased thickness reduces the size of the ventricular cavities, taking longer to relax after systole. During diastole, ventricular filling is impaired; atrial contraction at the end of diastole becomes critical for filling and systolic contraction. Smaller-than-normal LV cavity creates high-velocity blood flow from the LV into the aorta. Left ventricular outflow tract obstruction causes high systolic pressure in the LV that leads to prolonged ventricular relaxation and diminished cardiac output, resulting in diastolic dysfunction. Systolic function is normal or high, resulting in an above-normal ejection fraction.

Clinical manifestations of dilated cardiomyopathy

Initial presentation is often with heart failure dyspnea fatigue weight gain volume overload Arrhythmias and SCD frequently occur Altered valve function, usually regurgitation, can result from an enlarged stretched ventricle. Poor blood flow through the ventricle also may cause ventricular or atrial thrombi, which can embolize to other locations in the body. A persistent gallop rhythm, JVD, and a holosystolic murmur due to severe MR may be present

Transcatheter mitral valve repair

may be used in people with severe degenerative MR who are not candidates for surgery. Patients who are older, symptomatic, and very high risk or not surgical candidates may benefit from a minimally invasive procedure.

Clinical manifestations of hypertrophic cardiomyopathy

Most patients with HCM are asymptomatic, but some present with ventricular arrhythmias, SCD, or other symptoms: syncope, dyspnea, or chest pain. Atrial fibrillation commonly occurs from atrial enlargement. Systolic ejection murmurs (heard on S1) do not radiate to the neck. Mitral murmurs result from regurgitation.

Nursing management for valvular diseases

No treatment is required for asymptomatic patients with valvular pathology. The goal of medical therapy is not curative; it is symptom relief Beta-blockers (BBs) and calcium channel blockers (CCBs) may be used for rate control, to treat palpitations, for chest discomfort, and for anxiety, and are particularly useful when there is concomitant coronary artery disease. Less commonly, digoxin is given to increase contractility and slow rapid rates to allow for improved ventricular filling. Antiarrhythmics and electrical cardioversion are utilized to restore sinus rhythm, and anticoagulation is indicated if AF is persistent. Diuretics, vasodilators, and sodium restriction may be used to reduce preload and pulmonary congestion. Because patients with severe AS are dependent on preload to maintain CO, diuretics should be used with caution. Angiotensin-converting enzyme inhibitors (ACE-Is) are prescribed to reduce preload, afterload, and hypertension by causing vasodilation. ACE-Is are commonly prescribed for patients with concomitant hypertension but may be avoided in patients with AS because the vasodilation reduces pressure distal to the obstruction without increasing CO and may cause syncope. Afterload reduction may be managed with angiotensin blockers (ARBs), nitrates, or hydralazine. In acute cases of decompensation, intravenous nitroprusside is the vasodilator used most commonly for afterload reduction, but nitrates should be used with great caution with AS because their use can result in reduced CO. Daily aspirin is recommended for people who have had documented TIA, even when they are in sinus rhythm. Elimination of caffeine and alcohol may control or reduce symptoms, and the nurse encourages the patient to read labels on over-the-counter products, such as cough medicine, because these products may contain alcohol, caffeine, ephedrine, and epinephrine, which may produce arrhythmias and other symptoms. Symptoms may appear or worsen when the heart rate increases, such as during exercise, and also may be triggered by pregnancy or other stress on the body, such as a pulmonary infection. Strenuous activity is avoided since it increases workload of the heart. Intra-aortic balloon counterpulsation may be considered as it aids afterload reduction until surgery is performed; however, it is contraindicated in AR because it increases regurgitation.

Nursing management of pericarditis

Nonsteroidal anti-inflammatory medications (NSAIDs) and aspirin constitute first-line treatment Colchicine is used to treat recurrent pericarditis cases of constrictive pericarditis, surgical removal of the pericardium (pericardectomy) may be necessary to provide relief from restrictive inflammation and scarring. In addition to pain management, patients with acute pericarditis benefit from positioning: sitting upright and leaning forward will relieve pressure on the pericardium. Patients with chest pain often benefit from psychological support, education, and reassurance that the chest pain they are experiencing is not a heart attack.

Stenosis

Occurs when the opening of the valve is narrowed, valve leaflets fail to open properly and the forward flow of blood through the valve is reduced The increase in resistance results in turbulent blood flow. The volume of blood in the chamber increases and the heart is forced to work harder to eject blood through the narrowed valve, resulting in increased afterload and eventually, decreased CO.

Pathophysiology of mitral stenosis

Over time as fibrous tissue replaces normal valve tissue, the leaflets begin to thicken and fuse Left atrial pressure increases because of the resistance caused by slowed blood flow into the LV through the narrowed orifice. The LA dilates and hypertrophies because of the increased blood volume. Sluggish atrial blood flow can lead to clot formation and thromboembolism. Because there is no functional valve to protect the pulmonary veins from the backward flow of blood from the atrium, pulmonary venous pressure rises and circulation becomes congested. As a result, the right ventricle (RV) must contract against an abnormally high pulmonary pressure. Pulmonary hypertension increases the work of the RV, and the RV and right atrium become enlarged. Eventually, this results in right-sided heart failure.

Diagnostic tests for infective endocarditis

Positive blood cultures are highly sensitive for diagnosis; however, negative blood cultures do not definitely rule out infective endocarditis, especially if a patient has received antibiotics or if slow-growing bacteria are present. Three sets of blood cultures should be obtained 24 hours apart before administration of any antimicrobial agents. The modified Duke Criteria are used to aid in the diagnosis of IE. Major clinical criteria are positive blood cultures and evidence of endocardial involvement. When these are supplemented by minor clinical criteria, such as predisposing cardiac conditions or IVDU, persistent fever without an alternative cause, systemic or pulmonary embolism, Osler nodes, or Roth spots, a diagnosis of IE can be made. A diagnosis of IE is established with two major criteria or one major and three minor criteria, or five minor criteria. A possible diagnosis of IE is made when one major and one minor or three minor criteria are present Echocardiography can detect the presence of vegetations or abscesses, prosthetic valve dehiscence, new regurgitation, or heart failure, and is recommended for all patients with suspected IE. Other abnormal findings include anemia, elevated white blood cell (WBC) count, elevated sedimentation rate (ESR), and elevated C-reactive protein. Abnormal electrocardiographic (ECG) findings include atrioventricular blocks, bundle branch blocks, and fascicular blocks.

Risk factors for infective endocarditis

Pre-existing heart disease increases the risk of developing IE. A cardiac valve with epithelial damage will attract bacteria to its surface, and this can result in endocardial infection. This injury may be the result of rheumatic heart disease, previous endocarditis, a prosthetic valve, a congenital abnormality such as a bicuspid aortic valve, a structural abnormality such as MVP, or it may be age-related, degenerative valvular changes. Central venous access devices and long-term indwelling catheters, such as those used for hemodialysis, are associated with the hospital-acquired IE. IVDU and body piercing are risk factors for IE

Arrhythmogenic right ventricular cardiomyopathy

Rare but increasingly recognized condition ARVC/D should be suspected in patients with ventricular tachycardia originating in the right ventricle (i.e., left bundle branch block on ECG) or SCD, especially among previously symptom-free athletes. Familial in more than 50% of patients and usually occurs in early adulthood ARVC/D occurs when the right ventricle is progressively infiltrated and replaced with fibrous scar and adipose tissue. Initially, only localized areas of the right ventricle are affected, but, as the disease progresses, the entire heart is affected. Eventually, the right ventricle dilates and develops poor contractility, and arrhythmias occur.

Risk factors for mitral stenosis

Rheumatic fever (RF) or endocarditis, which gradually causes the mitral valve leaflets to thicken and can result in leaflet fusion. Radiation therapy to the chest area

Clinical manifestations of arrhythmogenic right ventricular cardiomyopathy

Symptoms are consistent with right HF. Supraventricular arrhythmias may occur. Ventricular arrhythmias and SCD may be the initial presentation, and often diagnosis is made postmortem. Family history, ECG, and a history of arrhythmias can help establish a diagnosis of ARVC/D.

Clinical manifestations of restricted cardiomyopathy

Symptoms are similar to constrictive pericarditis: dyspnea, nonproductive cough, chest pain, and exercise intolerance. Signs may include jugular venous distention, edema, ascites, anasarca, pulmonary edema, and an S3 and S4 can be heard with auscultation.

Stress-induced (takotsubo) cardiomyopathy

Syndrome of transient LV dysfunction. Ventricular function fully returns within weeks. LV morphology, seen with echocardiography or ventriculogram, demonstrates apical akinesis (absence of or decreased movement) with sparing of the base and resultant ballooning of the ventricle. It has been identified predominantly in white, postmenopausal women. Noncardiac comorbidities, such as anxiety, chronic pulmonary disease, and thyroid disease are associated. Precipitated by emotional or physical distress The pathophysiology of stress-induced cardiomyopathy remains unclear. One theory gaining acceptance is catecholamine excess triggered by activation of the sympathetic system.

Intracardiac septal defects

The atrial or ventricular septum may have an abnormal opening between the right and left sides of the heart, causing oxygenated blood to be shunted from the left side of the heart, which is under greater pressure, to the right. A small septal defect will be asymptomatic and have minimal effect on heart function, but larger ones may require repair to prevent problems related to excess blood volume in the right side of the heart. Over time, a large defect can cause pulmonary congestion, which can cause elevated right heart pressure; eventually this may cause right heart failure and pulmonary hypertension. With an atrial septal wall defect there is a risk that the clot could bypass the lungs and travel directly to the brain, causing a TIA or stroke. AF is common in patients with ASDs and further increases risk of stroke. Closure of the PFO is usually a percutaneous procedure to implant a device to plug the opening. Often anticoagulation with aspirin is prescribed. Small ventricular septal defects (VSDs) are rarely closed in adults unless there is evidence of endocarditis or if valve function is compromised due to the location of the defect. A stitch or pericardial or synthetic patch is used to close the opening.

Risk factors for aortic stenosis

The buildup of calcium deposits on heart valves is the most common cause of AS Acquired AS is common in those over 70 years of age, particularly in males. Besides degeneration of the valve, rheumatic heart disease also can lead to AS. Having a congenital malformation, such as a bicuspid aortic valve, is another risk factor.

orthotopic transplantation

The recipient's heart is removed, leaving a portion of the recipient's atria with the vena cava and pulmonary veins in place. The donor heart, which usually has been preserved in ice, is prepared for implant by cutting away a small section of the atria that corresponds with the sections of the recipient's heart that were left in place. The donor heart is implanted by suturing the donor atria to the residual atrial tissue of the recipient's heart. After the venous or atrial anastomoses are complete, the recipient's pulmonary artery and aorta are sutured to those of the donor heart.

Complications of pericarditis

The two major complications of pericarditis are pericardial effusion, the accumulation of fluid in the pericardial sac, and cardiac tamponade, compression of the heart from excessive fluid buildup

Mitral stenosis

The valve opening is narrowed, and blood flow from the LA into the LV is slowed during diastole. MS is slow and progressive. Symptoms may take decades to appear. Timing: diastole (S2) Low-pitched, rumbling, decrescendo Auscultation site: Apex

Mechanical valves

Three major types of mechanical valves exist: (a) bi-leaflet valve, (b) tilting disk, and (c) caged-ball. The age and life expectancy of the patient determine the need for durability of a bioprosthetic valve. Mechanical valves are more durable than bioprosthetic valves and may be more likely to be used in a younger patient. However, patients with mechanical valves require lifelong anticoagulation due to the risk of thromboembolism and valve thrombosis, and with this comes the additional risk of bleeding complications.

Nursing management of rheumatic fever

Throat cultures are necessary to diagnose the presence of a GAS infection. If group A beta-hemolytic streptococcus (GAS) is identified, aggressive treatment with penicillin for a 10-day course of therapy is prescribed. Clarithromycin or clindamycin may be prescribed for patients who are penicillin-allergic. Aspirin, or other anti-inflammatory medicines, is usually prescribed. Long-term antibiotic prophylaxis against group A strep is indicated in cases of known RF or rheumatic heart disease because recurrent RF is associated with worsening rheumatic heart disease People who have recovered from RF should have annual cardiac evaluations to identify the presence of new heart murmurs, which suggest the presence of rheumatic heart disease. Echocardiograms should be done to determine whether rheumatic valvular disease is developing. When a new murmur is detected in a patient with a systemic infection, endocarditis should be suspected. The nurse monitors the patient for signs and symptoms of valvular disease, heart failure, thromboemboli, and arrhythmias.

Nursing management of infective endocarditis

Treatment with long-term intravenous antibiotic therapy is targeted to the pathogen identified by the blood cultures. It is administered for a significant period, often up to 6 weeks, in doses that produce a high serum concentration to ensure eradication of the infection Invasive lines and wounds must be assessed for erythema (redness), tenderness, warmth, swelling, drainage, or other signs of infection. Blood cultures are taken periodically to monitor the effect of therapy, and serum levels of the selected antibiotic are monitored to ensure the serum demonstrates bactericidal activity. Nurses should be alert for complications such as persistent infection, heart failure, kidney failure, or emboli. A new or worsening murmur may indicate dehiscence of a prosthetic valve, rupture of an abscess, or injury to valve leaflets. When IE is complicated by persistent or recurrent infection, heart failure, systemic emboli, neurologic complication, myocardial abscess, or fungal endocarditis, surgery is indicated. Most patients who have prosthetic valve endocarditis require valve replacement.

Tricuspid regurgitation

Usually occurs with mitral stenosis because of the increased volume and pressure load on the right side of the heart but also can result from infective endocarditis.

Regurgitation

Valvular insufficiency Occurs when valves do not close completely and blood flows backward through the valve If the aortic valve is affected, blood will flow backward into the left ventricle (LV) during diastole, and if the mitral valve is affected, blood will flow back into the left atrium (LA) during systole. Preload is increased.

Pathophysiology of aortic regurgitation

When the aortic valve is incompetent, blood from the aorta returns to the LV during diastole in addition to the blood normally delivered by the LA. The LV dilates in an attempt to accommodate blood volume overload, causing hypertrophy. Dilatation and hypertrophy allow the LV to expel more blood with above-normal force, increasing afterload and, as a result, systolic blood pressure, while maintaining a normal ejection fraction (EF). The arteries attempt to compensate for the higher pressures by reflex vasodilation; the peripheral arterioles relax, reducing peripheral resistance and diastolic blood pressure. Although compensatory mechanisms allow patients to remain asymptomatic for some time despite pressure and volume overload, when left ventricular dysfunction develops, symptoms appear.

Pathophysiology of mitral regurgitation

When the mitral valve leaflets thicken, fibrose, and contract, they cannot close completely. With each heartbeat, blood is forced backward into the LA during systole. Regurgitation of blood into the LA causes left atrial pressure to rise. The LA stretches to accommodate the increased volume, and left atrial dilation occurs. During diastole, regurgitant blood from the LV increases volume load in the LA. Over time, compensatory left ventricular dilation and hypertrophy occur to maintain a normal CO. Eventually this leads to left ventricular failure. The backward flow of blood from the LV reduces blood volume flowing into the atrium from the lungs, and pulmonary venous pressure increases. Pulmonary congestion results, elevating pulmonary artery pressure; this adds further strain on the RV, causing enlargement and right ventricular failure.

Infective endocarditis

a serious infection of the endocardium, the membrane that lines the interior chambers of the heart and forms the valves. Certain factors, such as the presence of a prosthetic heart valve, a structural cardiac defect, an implantable device, or a previous episode of endocarditis, account for the majority of infectious endocarditis (IE). Other conditions, such as immunosuppression, neutropenia, malignancy, intravenous drug use (IVDU), and nosocomial hospital exposures, such as the presence of an indwelling central venous catheter, can predispose the patient to IE because they can introduce bacteria into the bloodstream. Acute IE has a rapid onset, occurring within days to weeks, and often is accompanied by high fever and chills. Subacute IE occurs gradually and is notable by low-grade fever, malaise, and lethargy, and its course is prolonged. Often, the onset of IE is insidious, and signs and symptoms slowly develop from inflammation, destruction of the heart valves, and embolization of the vegetative growths on the heart.

rheumatic fever

a systemic inflammatory condition that is a complication of Group A beta-hemolytic streptococcal (GAS) pharyngitis, commonly known as strep throat results in damage to connective tissues, especially in the heart, brain, joints, and skin.

Aortic regurgitation

also referred to as aortic insufficiency the backward flow of blood into the LV from the aorta during diastole. This occurs when the valve leaflets do not close completely.

Mitral regurgitation

also termed mitral insufficiency is the backward flow of blood from the LV into the LA during systole because the valve fails to close completely. Timing: Systole (S1) Description: high-pitched, loud rumbling Auscultation site: Apex

Myocarditis

an inflammation of the heart muscle (myocardium), commonly resulting from viral infection. It also may be caused by bacterial infections, immune-mediated mechanisms, and toxic agents. Cardiac muscle inflammation that results in myocyte necrosis (e.g., cardiac cell death) is the hallmark of myocarditis. Acute myocarditis is characterized by myocyte damage from viral infection, autoimmunity, or other precipitating event. Myocyte antigens and cytokines are released. In the subacute phase (days 4 through 14), T and B lymphocytes infiltrate the myocardium, and the virus is cleared. The immune response continues, and infected myocytes are lysed. Myocyte necrosis results in fibrosis. During the chronic phase, myocyte injury continues and can lead to DCM, left ventricular failure, and ventricular arrhythmias.

Pericarditis

an inflammation of the pericardium, the membranous sac surrounding the heart. Causes of the less common, noninfectious pericarditis include acute myocardial infarction, chest trauma or cardiac surgery, autoimmune disorders, medications (e.g., isoniazid, hydralazine), and malignancy Acute pericarditis develops rapidly, occurring when the pericardial sac becomes inflamed. Pericarditis may lead to an accumulation of fluid in this space, called pericardial effusion. This may result in increased pressure on the heart, leading to cardiac tamponade Pericarditis that reappears 4 to 6 weeks after an episode of acute pericarditis is termed recurrent pericarditis. In chronic effusive pericarditis, fluid slowly accumulates in the pericardial space, between the two layers of the pericardium. Frequent or prolonged episodes of pericarditis can lead to thickening and decreased elasticity of the pericardium, and scarring may fuse the visceral and parietal pericardium. This compresses the heart and restricts its ability to fill with blood. Over time, the pericardium may become calcified, further restricting ventricular expansion during diastole. With less filling, the ventricles pump less blood, leading to decreased CO and signs and symptoms of heart failure. Because higher pressure is required to fill the compressed heart, pressure increases in the veins that return blood to the heart. This increased systemic venous pressure will lead to peripheral edema and liver failure.

Clinical manifestations of infective endocarditis

anorexia myalgias fever chills weight loss back and joint pain night sweats. Fever is common, but may be intermittent or absent, especially in patients who are receiving antibiotics or corticosteroids, in the elderly, or in those who have heart failure or kidney failure. A heart murmur may be absent initially but develops in almost all patients. Murmurs that worsen over time are indicative of progressive damage from vegetations or perforation of the valve or chordae tendineae. Osler nodes, Janeway lesions, and Roth spots are distinguishing signs of IE, and are the result of microembolization Osler nodes are painful, erythematous nodules present on the pads of fingers or toes. Janeway lesions are painless, red or purple macules found on the palms and soles. Roth spots, seen on fundoscopic exam, are oval retinal hemorrhages with pale centers. Splinter hemorrhages may be seen under the fingernails and toenails, and petechiae may appear on the neck, chest, abdomen, conjunctiva, and mucous membranes. Central nervous system manifestations of IE include headache, transient cerebral ischemia, and strokes, which may be caused by emboli to the cerebral arteries. Embolization may be a presenting symptom; it may occur at any time and may involve other organ systems. Cardiomegaly, heart failure, tachycardia, or splenomegaly may occur. Abdominal discomfort, particularly in the left upper quadrant, is suggestive of splenic embolization or infarction

Infectious endocarditis prophylaxis

antibiotic prophylaxis is recommended prior to dental procedures for only the subset of patients who are at highest risk of adverse outcomes. For patients with a (1) prosthetic cardiac valve, (2) history of infective endocarditis, (3) congenital heart disease with persistent risk of IE, and (4) heart transplantation with valvular disease, antibiotic prophylaxis is warranted for dental procedures that involve manipulation of gingival tissue, the periapical region of teeth, or perforation of the oral mucosa. Antibiotic prophylaxis is not recommended for (1) routine anesthetic injections through noninfected tissue, (2) taking dental radiographs, or (3) placement or adjustment of removable prosthodontic or orthodontic appliances

Leaflet repair

includes removal of excess leaflet tissue and the repair of leaflet damage from stretching or tearing by using pericardial or synthetic patches.

Diagnostic tests for pericarditis

can be made if two of the following are present: pleuritic chest pain, pericardial friction rub, 12-lead ECG demonstrating widespread ST elevation without reciprocal changes or T-wave inversion, and pericardial effusion. Echocardiography is done to assess for pericardial effusion or tamponade, but the absence of effusion does not exclude pericarditis.

transcatheter aortic valve replacement (TAVR)

can be performed for aortic valve pathology. A collapsible artificial valve is inserted into the stenotic aortic valve through a catheter that is inserted either into the femoral artery (transcatheter) or through a small incision in the chest wall allowing insertion through the LV (transapical). Then the replacement valve is positioned in the damaged valve, and, as it expands, it pushes the damaged valve leaflets aside and becomes the functional valve

Ventricular assist device (VAD)

can support a failing heart by generating blood flow to the systemic circulation and unloading the ventricle. Most patients receive a left VAD, but some may receive a biventricular device (BiVAD) or a total artificial heart (TAH) Nondurable (temporary) support indications include cardiogenic shock, acute myocarditis (discussed shortly), and acute, reversible heart failure. Another nondurable indication is the use of a VAD as a bridge to the decision regarding candidacy for transplantation or to a more permanent VAD when the patient becomes more clinically stable. Durable or long-term indications include using a VAD as a bridge to transplantation, to sustain life until a donor heart becomes available, or as destination therapy (DT) in patients with end-stage heart failure who are ineligible for transplantation and for whom ventricular recovery is not possible. Increasingly, VADs are being used as DT. Long-term indications include using a VAD as a bridge to transplant (BTT) in patients failing on maximal medical therapy, or for DT in patients with end-stage heart failure who are not transplant candidates. These devices can have pumps that are outside the body (extracorporeal) or implantable and can be broadly classified as pulsatile volume displacement or continuous flow (axial flow, centrifugal). Most are surgically inserted via sternotomy, but some short-term use VADs can be inserted percutaneously.

Diagnosis of aortic regurgitation

confirmed by echocardiography valve morphology, degree of LV hypertrophy, and functional capacity are determined Patients with symptoms usually have echocardiograms every 4 to 6 months, and those without symptoms have annual echocardiograms. Exercise stress testing will assess functional capacity and symptom response.

Intra-aortic balloon pump (IABP)

decreases the workload of the heart by reducing left ventricular afterload. Additionally, it improves coronary artery blood flow by increasing coronary artery perfusion pressure. The IABP is used pre- and postoperatively in patients with severely compromised left ventricular function, in patients with myocardial ischemia undergoing complex percutaneous coronary interventions, and for patients with complications resulting from acute myocardial infarction, such as papillary muscle rupture, awaiting surgical repair. Bleeding, limb ischemia, infection, and vascular injury are potential complications of IABP, and monitoring the patient for compromised circulation and hemodynamic instability is a priority for nursing management.

total artificial heart (TAH)

designed to replace both ventricles Complications of VADs and TAHs include infection, ventricular arrhythmias, thrombus, thromboemboli, hemolysis, hemorrhage, right heart failure, multisystem failure, and mechanical failure of the device.

Cardiomyopathies

diseases of the myocardium (heart muscle) characterized by mechanical and electrical dysfunction and structural abnormalities Cardiomyopathy results from various etiologies that are most frequently genetic and is characterized by abnormal hypertrophy or dilatation of the ventricles. Other causes include autoimmune disorders, excessive alcohol intake, pregnancy, chemotherapeutic agents, or infection (usually viral). Regardless of cause, cardiomyopathy results in impaired CO. Decreased stroke volume stimulates the sympathetic nervous system and the renin-angiotensin-aldosterone response, resulting in increased SVR and increased sodium and fluid retention, which places an increased workload on the heart. These alterations lead to severe heart failure, lethal arrhythmias, myocardial destruction, and death.

Clinical manifestations of myocarditis

fever myalgias fatigue dyspnea ventricular arrhythmias cardiogenic shock DCM S3 gallop tachycardia tachypnea JVD edema ECG abnormalities orthopnea palpitations Fulminant heart failure or SCD can develop quickly. A minority of patients will have elevated cardiac enzymes and WBC count

Septal Myectomy

generally is used for younger patients with obstructive HCM and severe symptoms refractory to medical management. Removing part of the thickened septum that is bulging into the LV improves blood flow through the heart and out to the body.

peripheral intravenous line

give the health care team access the vascular system in case of emergency; a potential site for blood sampling; and the ability to provide fluids, medications, and nutrition. Contraindications to specific placements (right vs. left side) will include history of mastectomy, arterial-venous shunt placement, peripherally inserted central catheter (PICC) line placement, thrombus, trauma, and other device placements, such as splints and casts Potential complications include bruising, infection, extravasation of fluids and medications, and air embolus. An arterial line is a peripheral IV in the arterial system used for frequent blood pressure monitoring when a patient requires vasoactive medications (such as nitroprusside) and frequent blood sampling. It is not for administration of fluids or medications. Potential complications include ischemia, thrombosis, infiltration, and exsanguination

Risk factors for mitral regurgitation

more common in older adults and can result over time from normal aging. Having MVP or mitral valve stenosis can lead to the development of chronic primary MR Rheumatic heart disease can result in a thick, rigid mitral valve that does not open and close completely, leading to MR.

Aortic stenosis

narrowing of the valve opening between the LV and the aorta, resulting in obstruction of blood flow across the valve Progressive narrowing of the valve orifice develops gradually over several years to several decades, increasing afterload. Because the narrowing occurs slowly, the LV is able to adapt by contracting more slowly and stronger than normal, forcibly squeezing the blood through the smaller opening. Normal blood volume in the LV is maintained for a while, but, eventually, left ventricular pressure increases, causing the ventricular wall to hypertrophy to maintain CO. Diastolic dysfunction leads to increased work of the heart, which results in left ventricular failure. This results in elevated left atrial pressure, pulmonary congestion, and, ultimately, heart failure. Timing: Midsystolic (S1) Description: Loud, crescendo-decrescendo Auscultation site: 2nd ICS right sternal border; may radiate into the neck

Acute mitral regurgitation

occurs abruptly, when papillary muscle rupture occurs as a complication of myocardial infarction (MI) or if infective endocarditis or trauma leads to rupture of the chordae tendineae.

Mitral valve prolapse

occurs when the mitral valve does not close properly and the valve leaflets balloon back into the LA during systole. Myxomatous degeneration (pathologic weakening of connective tissue) can cause one or both of the valve leaflets to become enlarged and floppy, causing them to billow into the LA during systole. Over time, as the leaflets prolapse, they can stretch to a degree where the leaflet edges do not fully coapt, or close, resulting in MR.

Aortic balloon valvuloplasty

performed by introducing a balloon catheter across the aortic valve and into the LV. As the balloon is inflated, the calcified leaflets are cracked and split open and the valve ring is stretched. Potential complications include AR, emboli, ventricular perforation, rupture of the aortic valve annulus, ventricular arrhythmias, mitral valve damage, and bleeding from the catheter insertion sites.

Annuloplasty

repair of a cardiac valve's outer ring Mitral annuloplasty narrows the diameter of the valve's orifice to treat valvular regurgitation. An annuloplasty ring prosthesis is sutured to the annulus and leaflets, creating an annulus of the desired size

Chordoplasty

repair of the tendinous fibers that connect the edges of the atrioventricular valve leaflets to the papillary muscles

Clinical manifestations of acute mitral regurgitation

severe SOB Pallor tachycardia crackles hypotension peripheral edema jugular venous distention (JVD) ascites. Poor tissue perfusion is common as is acute pulmonary decompensation.

Clinical manifestations of rheumatic fever

sore throat fever headache weakness diaphoresis nausea irritability swollen glands Polyarthritis occurs in 75% of cases, and swollen, tender, painful joints can persist for up to 4 weeks. Erythema marginatum is a nonitchy macular rash on the trunk and proximal extremities that blanches with pressure, is not indurated, and does not scar. It often occurs with subcutaneous nodules: round, firm, painless bumps beneath the skin that usually disappear after 1 to 2 weeks. Patients also may develop chorea, which is characterized by spontaneous, purposeless movements of the trunk and extremities. Typically self-limiting, chorea can last for weeks to months. Rheumatic carditis is inflammation of the pericardium, myocardium, or endocardium, separately or in combination. Rheumatic myocarditis can temporarily weaken the pumping ability of the heart and cause conduction abnormalities. Rheumatic pericarditis occurs during the acute illness and may result in accumulation of fluid in the pericardial sac. Myocardial and pericardial inflammation usually resolves without sequelae, but rheumatic endocardial inflammation often results in permanent adverse effects. Heart valves become swollen, and tiny vegetations or growths develop on the valve leaflets. They can lead to thickening of the leaflets, causing them to shorten and preventing them from closing completely. As a result, blood regurgitates backward through the valve. The most common site of valvular regurgitation is the mitral valve, although any of the heart valves may be affected. Heart murmurs characteristic of valvular regurgitation, stenosis, or both become audible on auscultation. Since most patients with rheumatic heart disease develop mitral insufficiency, a blowing, high-pitched holosystolic murmur is frequently heard. Diastolic murmurs are heard if AR occurs. The myocardium compensates for some time, but as the valvular pathology progresses, compensatory mechanisms fail, and heart failure can develop.

open commissurotomy

splitting or separating fused cardiac valve leaflets, which is performed to increase the size of the specific valve orifice when the valve is not calcified. Although some valves can be repaired by commissurotomy, most require replacement because of significant calcification or regurgitation

Blood volume status

the amount of blood circulating in the enclosure of the arterial and venous systems. This fluid exerts or creates a pressure that can be monitored to determine preload: The greater the blood volume, the greater the pressure (assuming no confounding variables, such as severe hypertension). describe the total amount of pressure exerted in the vasculature by a particular volume of fluid

surgical valve replacement

the definitive treatment for symptomatic AS. However, surgical valve replacement for MS is indicated when the valvular problem is not amenable to a percutaneous procedure, percutaneous valvotomy failed, or when there is another indication for surgery, such as coronary artery disease, aortic valve disease, or concomitant mitral or tricuspid regurgitation a decision must be made to use either a mechanical or a bioprosthetic (tissue, biologic) valve

Septal ablation

the destruction of the hypertrophied septum caused by injecting alcohol into the artery that supplies blood to that area. Alcohol septal ablation can improve symptoms, but possible complications with this procedure include permanent heart block, which can occur in as many as 10% of the cases and requires implantation of a pacemaker. Generally this is thought to be an acceptable alternative to myectomy when concomitant cardiac surgery is not necessary, coronary anatomy is appropriate, in older patients at risk for operative morbidity, or for those with a strong desire to avoid surgery

dilated cardiomyopathy

the most common cardiomyopathy and is distinguished by significant irreversible dilation of the ventricles and systolic dysfunction without hypertrophy. It is a common cause of heart failure and the major reason for cardiac transplantation. The ventricles have increased systolic and diastolic volumes with decreased left ventricular function. As the LV becomes dilated (enlarged), contractility is impaired and becomes less forceful. The LV is unable to pump blood out of the heart effectively because of impaired contractility, and this often results in heart failure, ventricular arrhythmias, and sudden cardiac death (SCD). DCM occurs more often in men than in women and is generally seen between 20 and 60 years of age.

Clinical manifestations of pericarditis

the most common symptom is chest pain. Irritation of the pericardium causes pain that is typically persistent, sharp, pleuritic, and retrosternal. Although usually felt in the midchest, it may radiate to the neck, shoulders, or arms, making it difficult to differentiate from chest pain associated with an MI. However, in contrast to myocardial ischemic pain, the discomfort is usually aggravated by deep inspiration, coughing, lying down, or turning. It is characteristically relieved with a forward-leaning or sitting position because that position reduces pressure on the parietal pericardium. Although not heard in all patients with pericarditis, a common finding is a creaky or scratchy friction rub. mild fever increased WBC count anemia an elevated ESR or C-reactive protein level. Patients may have a nonproductive cough. Dyspnea unrelated to exertion is typical of pericarditis SOB occurs as a result of pericardial compression from cardiac tamponade.

Valvuloplasty

the repair of a cardiac valve, can be done percutaneously or surgically. Percutaneous balloon dilatation of stenotic valves is an appropriate alternative to surgical valve replacement or repair in some patients with valvular heart disease. In general, patients do not require continuous anticoagulation when they undergo valvuloplasty.

central intravenous line

used for a number of reasons, including: Failure to obtain or maintain peripheral access Complication of peripheral access The patient requires numerous access sites, parenteral nutrition, or hypertonic fluid administration Treatment failure with IV fluids necessitates the first level of hemodynamic monitoring for readings of central venous pressure (CVP) The patient requires vasoactive medications that place his or her limb at risk if an infiltrate occurs The triple-lumen catheter is a central line that measures the CVP or the amount of fluid returning to the heart at the level of the right atrium

Pulmonary artery catheter

used when previous interventions have not yielded the expected outcome (increased urine output with increased IV fluid administration), or when the patient has a complicating factor, such as kidney or heart failure or pulmonary hypertension, that makes clinical judgments difficult without additional information increase the risk of complications, such as pneumothorax, cardiac arrhythmias, and pulmonary artery rupture allow the medical and nursing team to monitor, intervene upon, and evaluate: Blood volume status Blood flow Tissue oxygenation

Extracorporeal membrane oxygenator

uses a pump to circulate blood through an oxygenator outside the body to provide both cardiac and respiratory support by artificially removing the carbon dioxide and re-oxygenating red blood cells. The purpose of ECMO is to allow time for intrinsic recovery of the lungs and heart; a standard cardiopulmonary bypass provides support during various types of cardiac surgical procedures. Increasingly, MCS is used long term (months to years) for the management of advanced heart failure from causes including cardiomyopathy