Nursing Management: Inflammatory and Structural Heart Disorders



Nursing Management


Inflammatory and Structural Heart Disorders


Nancy Kupper and De Ann F. Mitchell




Learning Outcomes



1. Differentiate the etiology, pathophysiology, and clinical manifestations of infective endocarditis and pericarditis.


2. Describe the collaborative care and nursing management of the patient with infective endocarditis and pericarditis.


3. Describe the etiology, pathophysiology, and clinical manifestations of myocarditis.


4. Describe the collaborative care and nursing management of the patient with myocarditis.


5. Differentiate the etiology, pathophysiology, and clinical manifestations of rheumatic fever and rheumatic heart disease.


6. Describe the collaborative care and nursing management of the patient with rheumatic fever and rheumatic heart disease.


7. Relate the pathophysiology to the clinical manifestations and diagnostic studies for the various types of valvular heart disease.


8. Describe the collaborative care and nursing management of the patient with valvular heart disease.


9. Relate the pathophysiology to the clinical manifestations and diagnostic studies for the different types of cardiomyopathy.


10. Compare the nursing and collaborative management of patients with different types of cardiomyopathy.



Key Terms


















Reviewed by Katrina Allen, RN, MSN, CCRN, Nursing Instructor, Faulkner State Community College: Division of Nursing, Fairhope and Bay Minette, Alabama; Tracy H. Knoll, RN, MSN, Nursing Instructor, Chamberlain College of Nursing, St. Louis, Missouri; and Tammy Ann Ramon, RN, MSN, Nursing Instructor, Delta College, University Center, Michigan.



image eNursing Care Plan 37-1   Patient With Infective Endocarditis





Patient Goal


Maintains normal body temperature






Patient Goals














Outcomes (NOC) Interventions (NIC) and Rationales








image




Patient Goal


Describes disease process, appropriate treatments, and measures to prevent recurrence of disease



*Nursing diagnoses listed in order of priority.



image eNursing Care Plan 37-2   Patient With Valvular Heart Disease




Patient Goal


Maintains adequate tissue and organ perfusion





Patient Goal


Achieves fluid and electrolyte balance





Patient Goal


Achieves optimal level of activity





Patient Goal


Describes disease process and appropriate measures to prevent complications












Outcomes (NOC) Interventions (NIC) and Rationales





Teaching: Disease Process


• Explain pathophysiology of disease process to ensure knowledge base.


• Describe disease process and possible chronic complications (e.g., heart failure, infective endocarditis) to ensure early reporting and treatment of complications.


• Instruct patient on measures to prevent complications (e.g., importance of notifying dentist, urologist, gynecologist, and other health care providers of valvular disease) so prophylactic antibiotic treatments can be initiated before invasive procedures and to wear Medic Alert bracelet to notify providers of health condition in emergencies.


• Discuss lifestyle changes to prevent complications and/or control the disease (e.g., smoking cessation) to prevent an increased cardiac workload and the oxygen-depleting effect of carbon monoxide.


• Instruct patient and/or caregiver on signs and symptoms to report to health care provider to ensure appropriate interventions.




image


*Nursing diagnoses listed in order of priority.


This chapter describes the pathophysiology and management of patients experiencing select inflammatory and structural heart disorders. In addition, the nursing care required to manage the needs of these patients is presented.



Inflammatory Disorders of Heart


Infective Endocarditis


Infective endocarditis (IE) is an infection of the endocardial layer of the heart. The endocardium is the innermost layer of the heart (Fig. 37-1) and heart valves. Therefore IE affects the valves. Treatment of IE with antibiotic therapy has improved the prognosis of this disease. Though relatively uncommon, an estimated 10,000 to 15,000 new cases of IE are diagnosed in the United States each year.1


image
FIG. 37-1 Layers of the heart muscle and pericardium. The section of the heart wall shows the fibrous pericardium, the parietal and visceral layers of the serous pericardium (with the pericardial sac between them), the myocardium, and the endocardium.



Etiology and Pathophysiology


The most common causative organisms of IE, Staphylococcus aureus and Streptococcus viridans, are bacterial. Other possible pathogens include fungi and viruses.2 IE occurs when blood turbulence within the heart allows the causative organism to infect previously damaged valves or other endothelial surfaces. This can occur in individuals with a variety of underlying cardiac and noncardiac conditions (Table 37-1).



Vegetations, the primary lesions of IE, consist of fibrin, leukocytes, platelets, and microbes that stick to the valve surface or endocardium (Fig. 37-2). The loss of parts of these fragile vegetations into the circulation results in emboli. As many as 50% of patients with IE experience systemic embolization. This occurs from left-sided heart vegetation moving to various organs (e.g., brain, kidneys, spleen) and to the extremities, causing limb infarction. Right-sided heart lesions move to the lungs, resulting in pulmonary emboli.


image
FIG. 37-2 Bacterial endocarditis of the mitral valve. The valve is covered with large, irregular vegetations (arrow).

The infection may spread locally and damage the valves or their supporting structures. This causes dysrhythmias, valve dysfunction, and eventual invasion of the myocardium, leading to heart failure (HF), sepsis, and heart block (Fig. 37-3).


image
FIG. 37-3 Pathogenesis of infective endocarditis.

At one time rheumatic heart disease was the most common cause of IE. However, now it accounts for less than 20% of cases. The main contributing factors to IE include (1) aging (more than 50% of older people have aortic stenosis [AS]), (2) IVDA, (3) use of prosthetic valves, (4) use of intravascular devices resulting in health care–associated infections (e.g., methicillin-resistant S. aureus [MRSA]), and (5) renal dialysis.3



Clinical Manifestations


The clinical manifestations of IE are nonspecific and can involve multiple organ systems. Low-grade fever occurs in more than 90% of patients. Other nonspecific manifestations include chills, weakness, malaise, fatigue, and anorexia. Arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache, and clubbing of fingers may occur in subacute forms of endocarditis.


Vascular manifestations of IE include splinter hemorrhages (black longitudinal streaks) that may occur in the nail beds. Petechiae may result from fragmentation and microembolization of vegetative lesions. They can occur in the conjunctivae, lips, buccal mucosa, and palate and over the ankles, feet, and antecubital and popliteal areas. Osler’s nodes (painful, tender, red or purple, pea-size lesions) may be found on the fingertips or toes. Janeway’s lesions (flat, painless, small, red spots) may be seen on the palms and soles. Funduscopic examination may reveal hemorrhagic retinal lesions called Roth’s spots.


The onset of a new or changing murmur is noted in most patients with IE. The aortic and mitral valves are most often affected. Murmurs are usually absent in tricuspid endocarditis because right-sided heart sounds are too low to be heard. HF occurs in up to 80% of patients with aortic valve endocarditis and in approximately 50% of patients with mitral valve endocarditis.4


Clinical manifestations secondary to embolization may be present in various body organs. Embolization to the spleen may cause sharp, left upper quadrant pain and splenomegaly, local tenderness, and abdominal rigidity. Embolization to the kidneys may cause flank pain, hematuria, and renal failure. Emboli may lodge in small peripheral blood vessels of the arms and legs and may cause ischemia and gangrene. Embolization to the brain may cause neurologic damage resulting in hemiplegia, ataxia, aphasia, visual changes, and change in the level of consciousness. Pulmonary emboli may occur in right-sided endocarditis and cause dyspnea, chest pain, hemoptysis, and respiratory arrest.



Diagnostic Studies


The patient’s recent health history is important in assessing IE. Ask patients if they have had any recent (within the past 3 to 6 months) dental, urologic, surgical, or gynecologic procedures, including normal or abnormal obstetric delivery. Document any previous history of IVDA, heart disease, recent cardiac catheterization, cardiac surgery, intravascular device placement, renal dialysis, or infections (e.g., skin, respiratory, urinary tract).


Two blood cultures drawn 30 minutes apart from two different sites will be positive in more than 90% of patients. Culture-negative endocarditis is often associated with antibiotic usage within the previous 2 weeks, or results from a pathogen not easily detected by standard culture procedures. Negative cultures should be kept for 3 weeks if the clinical diagnosis remains endocarditis because of the possibility of slow-growing organisms. A mild leukocytosis occurs in acute IE (uncommon in subacute). The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels may also be elevated.


Major criteria to diagnose IE include at least two of the following: positive blood cultures, new or changed heart murmur, or intracardiac mass or vegetation noted on echocardiography.5 Echocardiography is valuable in the diagnostic workup for a patient with IE when the blood cultures are negative, or for the patient who is a surgical candidate and has an active infection. Transesophageal echocardiogram and two- or three-dimensional (2-D or 3-D) transthoracic echocardiograms can detect vegetations on the heart valves.6


A chest x-ray is done to detect cardiomegaly (an enlarged heart). An electrocardiogram (ECG) may show first- or second-degree atrioventricular (AV) block. Heart block occurs because the cardiac valves lie close to conductive tissue, especially the AV node. Cardiac catheterization may be used to evaluate valve functioning and to assess the coronary arteries when surgical intervention is being considered.7



Collaborative Care



Prophylactic Treatment.

The situations and conditions requiring antibiotic prophylaxis are presented in Table 37-2.



TABLE 37-2


ANTIBIOTIC PROPHYLAXIS TO PREVENT ENDOCARDITIS
















Target Groups for Prophylactic Antibiotics
People with the following heart conditions should receive prophylactic antibiotics when they have the conditions or procedures listed below.

Conditions or Procedures Requiring Antibiotic Prophylaxis
When the target groups have the following conditions or procedures, they need prophylactic antibiotics.



image


*Except for the conditions listed above, prophylaxis is no longer recommended for any form of CHD.


Source: Habib G, Hoen B, Tornos P, et al: Guidelines on the prevention, diagnosis and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC), Eur Heart J 30:2369, 2009.



Drug Therapy.

Accurate identification of the infecting organism is the key to successful treatment of IE. Long-term treatment is necessary to kill dormant bacteria within the valvular vegetations. Complete elimination of the organism generally takes weeks, and relapses are common.


Initially, patients are hospitalized and IV antibiotic therapy, based on blood cultures, is started. The effectiveness of therapy is assessed with subsequent blood cultures. Cultures that remain positive indicate inadequate or inappropriate selection of antibiotic, aortic root or myocardial abscess, or the wrong diagnosis (e.g., an infection elsewhere).


Fungal endocarditis and PVE respond poorly to antibiotic therapy alone. Early valve replacement followed by prolonged (6 weeks or more) antibiotics is recommended in these situations. Valve replacement (discussed later in this chapter) has become an important adjunct procedure in the management of IE.


Fever may persist for several days after treatment has been started and can be treated with aspirin, acetaminophen (Tylenol), ibuprofen (Motrin), fluids, and rest. Complete bed rest is usually not indicated unless the temperature remains elevated or there are signs of HF. Endocarditis coupled with HF responds poorly to drug therapy and valve replacement and is often life threatening.



Nursing Management Infective Endocarditis


Nursing Assessment


Subjective and objective data that you should obtain from a patient with IE are presented in Table 37-3. Assess vital signs together with heart sounds to detect a murmur, a change in a preexisting murmur, and extra sounds (e.g., S3).



TABLE 37-3


NURSING ASSESSMENT
Infective Endocarditis


Subjective Data


Important Health Information


Past health history: Valvular, congenital, or syphilitic cardiac disease, including valve repair or replacement; previous endocarditis, childbirth, staphylococcal or streptococcal infections, hospital-acquired bacteremia


Medications: Immunosuppressive therapy


Surgery or other treatments: Recent obstetric or gynecologic procedures; invasive techniques, including catheterization, cystoscopy, intravascular procedures; recent dental or surgical procedures; GI procedures (e.g., endoscopy)


Functional Health Patterns


Health perception–health management: IV drug abuse, alcohol abuse; malaise


Nutritional-metabolic: Weight gain or loss; anorexia; chills, diaphoresis


Elimination: Bloody urine


Activity-exercise: Exercise intolerance, generalized weakness, fatigue; cough, dyspnea on exertion, orthopnea; palpitations


Sleep-rest: Night sweats


Cognitive-perceptual: Chest, back, or abdominal pain; headache; joint tenderness, muscle tenderness


Objective Data


General


Fever


Integumentary


Osler’s nodes on extremities; splinter hemorrhages under nail beds; Janeway’s lesions on palms and soles; petechiae of skin, mucous membranes, or conjunctivae; purpura; peripheral edema, finger clubbing


Respiratory


Tachypnea, crackles


Cardiovascular


Dysrhythmia, tachycardia, new murmurs, S3, S4; retinal hemorrhages


Possible Diagnostic Findings


Leukocytosis, anemia, ↑ ESR, ↑ CRP and cardiac enzymes; positive blood cultures; hematuria; echocardiogram showing chamber enlargement, valvular dysfunction, and vegetations; chest x-ray showing cardiomegaly and pulmonary infiltrates; ECG demonstrating ischemia and conduction defects; signs of systemic embolization or pulmonary embolism


CRP, C-reactive protein; ESR, erythrocyte sedimentation rate.


Arthralgia, which is common in IE, may involve multiple joints and be accompanied by myalgias. Assess the patient for joint tenderness, decreased range of motion (ROM), and muscle tenderness. Examine the patient for petechiae, splinter hemorrhages, and Osler’s nodes. Complete a general systems assessment to determine any hemodynamic or embolic complications.





Nursing Implementation


Health Promotion.


The incidence of IE can be decreased by identifying individuals who are at risk for the disease (see Tables 37-1 and 37-2). Assessment of the patient’s history and an understanding of the disease process are crucial for planning and implementing appropriate health promotion strategies.


Teaching the patient at high risk for IE helps reduce the incidence and recurrence of the disease. Teaching is crucial for the patient’s understanding of and adherence to the treatment regimen. Tell the patient to avoid people with infection, especially upper respiratory tract infection, and to report cold, flu, and cough symptoms. Stress the importance of avoiding excessive fatigue and the need to plan rest periods before and after activity. Good oral hygiene, including daily care and regular dental visits, is also important. Instruct the patient to inform health care providers performing certain invasive procedures of the history of IE. Be certain the patient understands the importance of prophylactic antibiotic therapy before certain invasive procedures. Refer the patient with a history of IVDA for drug rehabilitation.



Ambulatory and Home Care.


A patient with IE has many problems that require nursing management (see eNursing Care Plan 37-1 on the website for this chapter). IE generally requires treatment with antibiotics for 4 to 6 weeks. After initial treatment in the hospital, the patient may continue treatment at home if hemodynamically stable and adherent. Assess the home setting for adequate support. Patients who receive outpatient IV antibiotics require vigilant home nursing care.


Assessment findings are often nonspecific (see Table 37-3) but can help with the treatment plan. Fever, chronic or intermittent, is a common early sign. Instruct the patient or caregiver about the importance of monitoring body temperature. Persistent temperature elevations may mean that the drug therapy is ineffective. Patients with IE are at risk for life-threatening complications, such as stroke, pulmonary edema, and HF. Teach patients and caregivers to recognize signs and symptoms of these complications (e.g., change in mental status, dyspnea, chest pain, unexplained weight gain).


The patient with IE needs adequate periods of physical and emotional rest. Bed rest may be necessary when the patient has fever or complications (e.g., heart damage). Otherwise the patient may ambulate and perform moderate activity. To prevent problems related to reduced mobility, tell the patient to wear elastic compression stockings, perform ROM exercises, and deep breathe and cough every 2 hours.


The patient may experience anxiety and fear associated with the illness. You must recognize this and implement strategies to help the patient cope with the illness.


Monitor laboratory data to determine the effectiveness of the antibiotic therapy. Ongoing monitoring of the patient’s blood cultures is necessary to ensure destruction of the infecting organism. Assess IV lines for patency and signs of complications (e.g., phlebitis). Administer antibiotics as scheduled, and monitor the patient for any adverse drug reactions.


Management also focuses on teaching the patient and caregiver the nature of the disease and on reducing the risk of reinfection. Explain to the patient the relationship of follow-up care, good nutrition, and early treatment of common infections (e.g., colds) to maintain health. Instruct the patient about symptoms that may indicate recurrent infection (e.g., fever, fatigue, chills). Tell the patient to notify the health care provider if any of these symptoms occur. Finally, inform the patient about the importance of prophylactic antibiotic therapy before certain invasive procedures (see Table 37-2).




Acute Pericarditis


Pericarditis is a condition caused by inflammation of the pericardial sac (the pericardium).The pericardium is composed of the inner serous membrane (visceral pericardium) and the outer fibrous (parietal) layer (see Fig. 37-1). The pericardial space is the cavity between these two layers. Normally it contains 10 to 15 mL of serous fluid. The pericardium serves an anchoring function, provides lubrication to decrease friction during systolic and diastolic heart movements, and assists in preventing excessive dilation of the heart during diastole. It may be congenitally absent or surgically removed.



Etiology and Pathophysiology


Common causes of acute pericarditis are listed in Table 37-4. Most often the cause of acute pericarditis is idiopathic (unknown), with a variety of suspected viral causes. The coxsackie B virus is the most commonly identified virus.8



Pericarditis in the patient with an MI may be described as two distinct syndromes. The first is acute pericarditis, which may occur within the initial 48 to 72 hours after an MI. The second is Dressler syndrome (late pericarditis), which appears 4 to 6 weeks after an MI (see Chapter 34). An inflammatory response is the characteristic pathologic finding in acute pericarditis. There is an influx of neutrophils, increased pericardial vascularity, and eventually fibrin deposition on the epicardium (Fig. 37-4).


image
FIG. 37-4 Acute pericarditis. Note shaggy coat of fibers covering surface of heart.


Clinical Manifestations


In acute pericarditis, clinical manifestations include progressive, frequently severe, sharp chest pain. The pain is generally worse with deep inspiration and when lying supine. It is relieved by sitting up and leaning forward. The pain may radiate to the neck, arms, or left shoulder, making it difficult to differentiate from angina. One distinction is that the pain from pericarditis can be referred to the trapezius muscle (shoulder, upper back), since the phrenic nerve innervates this region. The dyspnea that accompanies acute pericarditis is related to the patient’s need to breathe in rapid, shallow breaths to avoid chest pain and may be aggravated by fever and anxiety.


The hallmark finding in acute pericarditis is the pericardial friction rub. The rub is a scratching, grating, high-pitched sound believed to result from friction between the roughened pericardial and epicardial surfaces. It is best heard with the stethoscope placed at the lower left sternal border of the chest with the patient leaning forward. Since it is difficult to distinguish a pericardial friction rub from a pleural friction rub, ask the patient to hold his or her breath. If you still hear the rub, then it is cardiac. It may require frequent attempts to identify because pericardial friction rubs are often intermittent and short lived.



Complications


Two major complications that may result from acute pericarditis are pericardial effusion and cardiac tamponade. Pericardial effusion is a build-up of fluid in the pericardium. It can occur rapidly (e.g., chest trauma) or slowly (e.g., tuberculosis pericarditis). Large effusions may compress nearby structures. Pulmonary tissue compression can cause cough, dyspnea, and tachypnea. Phrenic nerve compression can induce hiccups, and compression of the laryngeal nerve may result in hoarseness. Heart sounds are generally distant and muffled, although blood pressure (BP) usually is maintained.


Cardiac tamponade develops as the pericardial effusion increases in volume. This results in compression of the heart. The speed of fluid accumulation affects the severity of clinical manifestations. Cardiac tamponade can occur acutely (e.g., rupture of heart, trauma) or subacutely (e.g., secondary to renal failure, malignancy).


The patient with cardiac tamponade may report chest pain and is often confused, anxious, and restless. As the compression of the heart increases, there is decreased cardiac output (CO), muffled heart sounds, and narrowed pulse pressure. The patient develops tachypnea and tachycardia. Neck veins usually are markedly distended because of increased jugular venous pressure, and pulsus paradoxus is present. Pulsus paradoxus is a decrease in systolic BP during inspiration that is exaggerated in cardiac tamponade. (See Table 37-5 for the measurement technique.) In a patient with a slow onset of a cardiac tamponade, dyspnea may be the only clinical manifestation.




Diagnostic Studies


The ECG is useful in the diagnosis of acute pericarditis, with changes noted in approximately 90% of the cases. The most sensitive ECG changes include diffuse (widespread) ST segment elevations. This reflects the abnormal repolarization that develops secondary to the pericardial inflammation. You need to differentiate these changes from the ST changes seen with MI. (See Chapter 36 for more information on ECG monitoring.)


Echocardiographic findings are most useful in determining the presence of a pericardial effusion or cardiac tamponade. Methods such as Doppler imaging and color M-mode assess diastolic function and diagnose constrictive pericarditis (discussed later in the chapter). Computed tomography (CT) and magnetic resonance imaging (MRI) provide for visualization of the pericardium and pericardial space. Chest x-ray findings are generally normal, but cardiomegaly may be seen in a patient who has a large pericardial effusion (Fig. 37-5).


image
FIG. 37-5 A, X-ray of a normal chest. B, Pericardial effusion is present, and the cardiac silhouette is enlarged with a globular shape (arrows).

Related posts:

  1. Introduction
  2. Nursing Management: Sexually Transmitted Infections
  3. Nursing Management: Integumentary Problems
  4. Nursing Management: Musculoskeletal Problems

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Nov 17, 2016 | Posted by in NURSING | Comments Off on Nursing Management: Inflammatory and Structural Heart Disorders

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