Chapter 19 Common Cardiovascular Disorders

Layers of the Heart

Pericarditis Pericardium surrounds the external surface of the heart and the roots of the great vessels. Two layers: outer tough fibrous pericardium; inner serous layer Serous pericardium has two layers: The parietal layer lines the internal surface of the fibrous membrane. It extends to the great vessels, where it then folds over on itself to form the inner visceral layer (epicardium). 10 to 50 mL of clear serous fluid lies between these layers and acts as a lubricant. The pericardium helps restrain the heart and isolate it from infections in the surrounding structures. Pericarditis is inflammation of the pericardium.

Question Which of the following confirms the diagnosis of pericarditis? A. Pain on inspiration B. Chest pain C. Pericardial friction rub D. Low-grade fever

Answer C. Pericardial friction rub Rationale: There may also be general symptoms of an infection, such as a low-grade fever, tachycardia, or malaise. The presence of a pericardial friction rub confirms the diagnosis; however, absence of a rub does not rule out pericarditis. The classic friction rub produces a rasping or scraping, high-pitched sound that varies with the cardiac cycle. The rub may wax and wane and may even transiently disappear during the course of the illness. It is best heard with the diaphragm of the stethoscope placed over the lower to middle left sternal edge.

Assessment—Pericarditis Thorough history and physical examination Chest pain is the primary symptom. Pain is worse with breathing deeply or lying supine; relieved by sitting up, leaning forward, and taking shallow breaths. S & S of infection Pericardial friction rub confirms the diagnosis. Friction rub produces a rasping or scraping, high-pitched sound that varies with the cardiac cycle. Best heard over the lower to middle left sternal edge

Assessment—Pericarditis (cont.) Diffuse ST-segment elevation with an upward concavity and PR-segment depression Laboratory tests include CBC, cardiac enzyme levels, rheumatoid factors, and antinuclear antibody titers Blood cultures may be indicated if there is evidence of infection. Viral studies may be obtained if the rest of the diagnostic workup is negative.

Management—Pericarditis Relieve symptoms, eliminate any possible causative agents, and monitor for complications. NSAIDs, such as aspirin or ibuprofen Steroids may be indicated in resistant cases. Anticoagulants must be avoided in the patient recovering from MI. Abates over 2 to 6 weeks Rare to have recurrent episodes

Question Which of the following is a cause of sudden death in athletes? A. Pericarditis B. Myocarditis C. Endocarditis D. Cardiomyopathy

Answer B. Myocarditis Rationale: Myocarditis can be a devastating illness that evolves into a chronic, progressive disease with a poor prognosis. The disorder may result in dysrhythmias, congestive heart failure, or death. It is also recognized as a cause of sudden death in young athletes.

Myocarditis Inflammation of the myocardium Primary myocarditis is believed to be related to an acute viral infection or an autoimmune response to the infection. Secondary myocarditis is inflammation related to a specific organism. May result in dysrhythmias, congestive heart failure, or death Cause of sudden death in young athletes

Assessment—Myocarditis With viral myocarditis, there is a delay before the onset of cardiac symptoms, such as congestive heart failure or dysrhythmias. S & S: Fatigue, dyspnea, palpitations, and precordial discomfort Slight rise in serum enzyme levels Nonspecific ST-T wave changes Definitive diagnosis requires a positive endomyocardial biopsy. Lack of a positive biopsy does not rule out myocarditis.

Management—Myocarditis Treatment is supportive. Treatment with corticosteroids or immunosuppressive agents has not been shown effective. Myocarditis may resolve without further sequelae. Subacute disease may develop with persistent laboratory findings of inflammation. Athletes with myocarditis should withdraw from competitive sports for a period of at least 6 months. Return to training and competition depends on normalization of cardiac function and absence of any significant clinical findings, such as dysrhythmias.

Endocarditis Endocarditis is an infection of the endocardial surface of the heart (IE), including the valves, caused by bacterial, viral, or fungal agents. Children with congenital heart disease are at risk. Adults with mitral valve prolapse, rheumatic heart disease, illicit intravenous drugs, and patients with prosthetic valves or long-term indwelling devices Common infectious organisms include streptococci, enterococci, and Staphylococcus aureus.

Endocarditis (cont.) The development of IE is a complex process that requires the occurrence of several critical elements: Endothelial damage exposes the basement membrane of the valve to turbulent blood flow. This exposure leads to the development of a platelet and fibrin clot on the valve leaflet. The clots, or vegetations, are exposed to bacteria by way of the bloodstream, such as occurs after dental manipulations or urological procedures. Bacterial proliferation takes place. The infected vegetation eventually damages the valve structure. The incompetent valves eventually lead to severe heart failure.

Assessment—Endocarditis Symptoms of endocarditis usually occur within 2 weeks of the precipitating bacteremia. Four underlying processes: bacteremia or fungemia, valvulitis, immunologic response, and peripheral emboli S & S: nonspecific, general malaise, anorexia, fatigue, weight loss, and night sweats Careful history focusing on risk factors for IE and a physical examination Fever and a new or changed heart murmur are present in almost all patients. Definitive diagnosis of IE includes persistent bacteremia and evidence of myocardial involvement such as echocardiographic visualization of a vegetation or new or worsening murmur (Duke criteria). Blood is usually drawn for three separate sets of cultures.

Management—Endocarditis Early identification of complications is key to good patient outcomes. Antibiotic therapy is based on the results and the clinical setting. Treatment should not be delayed while waiting for identification of the specific organism. Immediate surgical intervention is indicated in the presence of severe congestive heart failure secondary to valve dysfunction, uncontrolled infections, and prosthetic valve dysfunction or dehiscence. Usually requires a prolonged course of antibiotic therapy

Cardiomyopathies Cardiomyopathies are diseases of the heart muscle that cause cardiac dysfunction resulting in heart failure, dysrhythmias, or sudden death. Current theories under investigation suggest that ischemic, immune, mechanical, and neurohormonal effects on the pericardium, myocardium, and endothelium lead to structural changes that result in functional changes. Structural changes at the cellular level leads to stiffness of the ventricles and smooth muscle layers in the arteries. Both stiffness and spherical remodeling may occur in the same heart, leading to a compromised cardiac output from impaired relaxation and impaired emptying.

Dilated Cardiomyopathy Increased myocardial cavity size in the presence of normal or reduced left ventricular wall thickness and impaired systolic function Ischemia, alcohol abuse, endocrine disorders, pregnancy, viral infections, and valvular disease may cause a decrease in contractility. Decreased contractility (ejection fraction <40%) results in an increased end- systolic volume. Over time, the ventricle dilates to accommodate the increased intraventricular volumes (preload). In the dilated heart, the increased volume leads to a decreased stroke volume. Mitral and tricuspid insufficiency develop as the valve leaflets are stretched and separated. Dysrhythmias and conduction defects commonly occur. DCM is the third most common cause of heart failure and the most frequent cause of heart transplantation. In most cases, the specific cause is unknown.

Ischemic Cardiomyopathy Result of oxygen levels that are inadequate to meet the metabolic demands of the myocardial cells Caused by obstruction in the coronary arteries; may be acute or chronic Severe, persistent ischemia causes the muscle tissue to die (MI). Dead muscle is replaced with scar tissue. The larger the scar, the greater the dysfunction. Decreased muscle mass leads to decreased energy for pumping blood and decreased cardiac output. Cardiogenic shock results. Left ventricular end-diastolic pressure increases, pulmonary artery pressures increase, and pulmonary edema results. End-organ damage occurs.

Nonischemic Cardiomyopathy Several causes: Idiopathic cardiomyopathy: heart dilates, remodels, and becomes ineffective to pump. Myocarditis May result from pregnancy, heavy alcohol use, hypertension, and tachycardia May be acute or chronic

Question Is the following statement true or false? In dilated cardiomyopathy, the presence of right-sided heart failure is a poor prognosis.

Answer True Rationale: The natural history of DCM is not well defined. Some patients remain asymptomatic or have minimal clinical findings. Symptoms usually develop gradually and are typically related to left ventricular heart failure. The presence of right-sided heart failure is associated with poor prognosis.

Assessment—DCM Some patients remain asymptomatic or have minimal clinical findings. Symptoms develop gradually and are typically related to left ventricular heart failure. The presence of right-sided heart failure is associated with poor prognosis. Laboratory tests include screening for potentially reversible causes, including human immunodeficiency virus. The echocardiogram differentiates the primary abnormality and determines ejection fraction. Cardiac catheterization to rule out coronary artery disease

Management—DCM Identify and eliminate potential causes of DCM. Myocardial damage related to ingesting alcohol is reversible if detected early and the patient abstains from further drinking. Control of heart failure, dysrhythmias, or intracoronary thrombus Biventricular for severe symptomatic heart failure, prolonged QRS, dilated left ventricle, and poor ejection fraction Implantable cardioverter–defibrillators (ICDs) to prevent sudden death associated with lethal dysrhythmias Heart transplantation and some medical therapies have been shown to prolong life.

Hypertrophic Cardiomyopathy (HCM) Hypertrophied, nondilated left ventricle not related to any obvious cause (ie, hypertension or aortic valve stenosis) Diastolic dysfunction is a characteristic feature. The heart can contract but cannot relax and remains abnormally stiff in diastole. Septal wall hypertrophy may occur, leading to a left ventricular outflow tract obstruction during systole. Sudden death, usually from a ventricular dysrhythmia, in asymptomatic or mildly symptomatic people of any age group

Assessment—HCM Often found unexpectedly during investigation of heart murmurs or family screening The most common symptom is dyspnea. Presyncope and syncope also frequently occur. Left ventricular hypertrophy (LVH) present on the echocardiogram confirms the diagnosis. Borderline LVH may be a normal finding in competitive athletes.

Management—HCM Control symptoms. Prevent complications and reduce the risk for sudden death. Genetic screening and counseling Most symptomatic patients can be medically managed. ICD Percutaneous ablation with ethanol or surgery to remove a portion of the septum may be necessary.

Peripheral Vascular Disease A group of distinct disorders involving the arteries, veins, and lymphatic vessels of the peripheral circulation Noncardiac diseases that affect the circulation as a whole Peripheral arterial disease (PAD) Venous disease

Peripheral Arterial Disease Processes that obstruct the blood supply of the lower or upper extremities Symptomatic PAD is a disease of the elderly found more commonly in men aged 70 years and older. Patients of any age with risk factors for atherosclerosis, such as smoking or diabetes Other risk factors: hypertension, lipid disorders, family history, postmenopausal state, and hyperhomocysteinemia The disease develops in major bifurcations and areas of acute angulations.

Question Which of the following is a classic symptom of PAD? A. Intermittent claudication B. Hair loss on extremities C. Thick nails D. Dry skin

Answer A. Intermittent claudication Rationale: The classic symptom of PAD is intermittent claudication, experienced as a cramping, burning, or aching pain in the legs or buttocks that is relieved with rest.

Assessment—PAD The classic symptom of PAD is intermittent claudication. Trophic changes, such as hair loss on the extremities, thickening of the nails, and drying of the skin Sudden onset of extreme pain indicates acute arterial obstruction. Careful vascular examination of the extremities and assessment of all peripheral pulses ABI is the ratio of ankle to brachial systolic blood pressure. Normal—1.0 or greater Critical limb ischemia—less than 0.518

Management—PAD Modifying or eliminating risk factors Smoking cessation, aggressive treatment of hypertension, diabetes, and lipid disorders Antiplatelets (aspirin or clopidogrel [Plavix]) to reduce the risk for MI and stroke and cilostazol (Pletal) to increase walking distance Peripheral balloon angioplasty Surgical bypass in severe obstruction

Venous Disease Phlebitis is inflammation of the vessel wall occurring as the result of direct injury to the vein or as a complication of varicose veins. Can lead to the formation of a thrombus (VTE) Factors that predispose a patient to thrombus formation are vessel wall injury, stasis of blood, and increased blood coagulability (Virchow’s triad).

Assessment—Venous Disease DVT is characterized by pain, swelling, tenderness, and increased temperature over the affected area. Positive Homans’ sign (pain in the calf with passive dorsiflexion of the foot) Accurate diagnosis requires diagnostic testing such as compression ultrasonography.

Management—Venous Disease Relieve symptoms, increase blood flow, and prevent complications. Patients with DVT are at high risk for pulmonary embolism. Treatment: Anticoagulant, long-term warfarin Assess for bleeding. Patient education to decrease recurrence of DVT

Aortic Disease Longest and strongest artery in the body Congenital, degenerative, hemodynamic, and mechanical factors stress the vessel’s elasticity. Dilation of the aortic wall may lead to aortic dissection or rupture.

Abdominal Aortic Aneurysm More common than thoracic aortic aneurysms Men > women Risk factors: smoking, age, hypertension, lipid disorders, atherosclerosis, genetic and environmental influences The major risk from AAAs is rupture, which is associated with a high rate of mortality. Typically identified during health screening for another problem. Abdominal or back pain is the most common complaint. Worsening of symptoms is usually related to expansion or rupture of the aneurysm. Abdominal ultrasonography is the most practical method of confirming the diagnosis.

Management—AAA Control of hypertension and elimination of risk factors Follow with serial noninvasive tests, such as ultrasonography. Treatment involves surgical repair (AAA>5.5 cm). Minimally invasive approach using an endovascular graft has become the treatment of choice for high-risk patients.

Thoracic Aortic Aneurysm Occur infrequently and are classified by the involved segment of the aorta (root, ascending, arch, or descending) Etiology, natural history, and treatment differ for each segment involved. Most ascending thoracic aortic aneurysms are due to cystic medial degeneration. Ascending thoracic aortic aneurysms are also associated with connective tissue disorders, genetic disorders, bicuspid aortic valve, infections, inflammatory diseases, chronic aortic dissection, and trauma.

Assessment—Thoracic Aortic Aneurysm Most are asymptomatic at the time of diagnosis. Symptoms are related to the size and location of the aneurysm; these include aortic insufficiency and signs of pericardial tamponade if the aneurysm involves the aortic root. Rupture or acute dissection of a thoracic aneurysm can be fatal. Fewer than half of patients with rupture survive until they are hospitalized, and by 24 hours, mortality is almost 80%. Management: Surgical repair is indicated at a diameter of 5.5 cm or more. Repair of descending thoracic aneurysms is recommended when the diameter is 6 cm or more.

Aortic Dissection Acute aortic dissection is the most common and the most lethal process involving the aorta. Mortality rates are very high, approaching 1% per hour. Death usually occurs from rupture of the aorta. Pathophysiology Dissection involves a longitudinal separation of the medial layers of the aorta by a column of blood. The dissection begins at a tear in the aortic wall, usually at the proximal end of the dissection.

Assessment—Aortic Dissection Sudden, intense chest pain; “ripping” or “tearing” Careful history and physical examination Assess for aortic regurgitation or alteration of peripheral pulses. Widened mediastinum on CXR Ischemia, tamponade, elevated serum creatinine, decreased urine output, severe hypertension Transesophageal echo or CT with contrast confirms diagnosis.

Management—Aortic Dissection Timely diagnosis Blood pressure control Pain management Surgery for dissection of ascending aorta

Classification of Blood Pressure for Adults

Hypertensive Crisis Pathophysiology Marked rapid increase in BP Compensatory intense vasoconstriction May lead to hypertensive encephalopathy

Assessment—Hypertensive Crisis S & S: headache, visual disturbances, confusion, nausea, vomiting Cotton-wool exudate and hemorrhages of eyes Chest pain Decreased urine output or azotemia Management Reduce BP by not more than 25% within 1 hour. Continuous monitoring Identify the cause.