NOTES PAGE(S) SLIDE 17
Heart Failure
1.Heart failure is a complex syndrome in which the heart is unable to pump enough blood to meet the metabolic demands of the body. As a result of this inability, cardiac output falls and tissue perfusion decreases.
2.It is often the result of structural and inflammatory disorders, but can also result from excessive demands on a normal heart.
3.As the heart begins to fail, compensatory mechanisms are activated. Primary compensatory mechanisms are the Frank-Starling mechanism, neuroendocrine responses, and myocardial hypertrophy.
4.As heart failure progresses, the compensatory mechanisms begin to be detrimental to muscle function. Heart function continues to deteriorate.
5.The client with heart failure has little or no cardiac reserve and does not tolerate physical or psychologic stress.
6.Systolic failure occurs when the ventricle does not contract adequately and manifests as weakness, fatigue, and decreased exercise tolerance. Diastolic failure occurs when the heart does not relax completely, which impairs its filling ability. It manifests as shortness of breath, tachypnea, respiratory crackles, distended neck veins, liver enlargement, anorexia, and nausea. Many clients have components of both systolic and diastolic failure.
7.Left-sided failure is often caused by coronary heart disease and manifests as fatigue and activity intolerance, dizziness, syncope, dyspnea, shortness of breath, cough, orthopnea, cyanosis, presence of inspiratory crackles and wheezes, and presence of an S3 gallop.
8.Right-sided failure is often caused by factors that restrict blood flow to the lungs. It manifests as congestion of abdominal organs and development of peripheral edema, especially in dependent tissues.
9.Low-output failure occurs when the cardiac output drops due to structural or inflammatory disorders of the heart muscle. In this case, supply is low.
10.High-output failure occurs when demand is increased as when the client is in a hypermetabolic state. In this case, demand is high.
11.Acute failure is abrupt in onset, which results in suddenly decreased cardiac function and output. Chronic failure is a progressive deterioration of the heart muscle.
Pulmonary Edema
12.Pulmonary edema is an abnormal accumulation of fluid in the interstitial tissue and alveoli of the lung, caused by both cardiac and noncardiac disorders. Cardiogenic pulmonary edema is a sign of severe cardiac decompensation.
13.This is a true medical emergency because the client is literally drowning in the fluid in the lungs. Immediate treatment is necessary.
14.As contractility of the left ventricle decreases, pulmonary hydrostatic pressure increases, which forces fluid into interstitial tissues. Eventually this increase in pressure causes fluid to enter the alveoli. Ventilation and gas exchange are severely disrupted.
15.Manifestations include dyspnea; shortness of breath; orthopnea; cyanosis, cool, clammy, diaphoretic skin; productive cough with pink, frothy sputum; crackles in lung fields; restlessness; and confusion.
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Infective Endocarditis
20.Endocarditis is inflammation of the endocardium. It is generally infectious in nature and results in colonization of the cardiac structures by a pathogen.
21.Prosthetic valve endocarditis (PVE) occurs in clients who have undergone valve replacement. PVE may develop early in the postoperative course due to contamination of the prosthetic valve during surgery or perioperative bacteriemia and usually has a rapid course with high mortality. Late PVE has a course more like subacute endocarditis.
22.Development of endocarditis requires entry of pathogens into the bloodstream. Vegetations of pathogens form on the cardiac structures, most commonly the valve leaflets. As these vegetations grow, they interfere with the normal movement of blood through the heart. The vegetations may also fracture and embolize.
23.Classifications of endocarditis are: acute infectious endocarditis which has an abrupt onset and a rapidly progressive course; and subacute infective endocarditis which has a more gradual onset.
24.Manifestations of endocarditis can be nonspecific and flu-like with presence of chills, fever, general malaise, fatigue, cough, dyspnea, and joint pain. There is also often presence of a heart murmur. Anorexia and abdominal pain may develop with splenomegaly. Peripheral manifestations occur from microemboli or circulating immune complexes and include petechiae, splinter hemorrhages of the nails, Osler’s nodes on finger and toe pads, Janeway lesions on the palms and soles of the feet, and Roth’s spots on the retina.
25.Common complications of endocarditis are embolization of vegetative fragments, heart failure, abscess, and aneurysm. Without treatment, endocarditis is almost universally fatal. Antibiotic therapy is generally effective in treating the disease.
Myocarditis
26.Myocarditis is inflammation of the heart muscle, and usually results from infection, most commonly viral in nature.
27.The extent of muscle damage ultimately determines the long-term outcome of the disease. Severe myocarditis may result in cardiomyopathy and heart failure.
28.Myocarditis is often preceded by a nonspecific febrile illness or upper respiratory illness and manifestations often appear similar to those illnesses. Muffling of S1, presence of S3, murmur, or pericardial friction rub may be heard. Chest pain may also be present.
Pericarditis
29.Pericarditis is inflammation of the pericardium and may be a primary disorder or develop secondary to another disorder. It is usually viral, but affects 40–50% of clients with ESRD and uremia. MI and cardiac surgery are also common causes.
30.Inflammation of the pericardium may result in pericardial effusion, fibrosis, or scarring. These changes restrict cardiac function.
31.Classic manifestations include chest pain, a pericardial friction rub, and fever. Dyspnea and tachycardia are common.
32.Common complications are pericardial effusion, cardiac tamponade, and constrictive pericarditis.
Valvular Heart Disease
33.Valvular heart disease interferes with blood flow to and from the heart. Acquired valvular disease may be a result of an acute condition such as infective endocarditis or from a chronic condition such as rheumatic heart disease or MI. Congenital heart defects may also affect heart valve function.
34.Two major types of heart disease are stenosis and regurgitation. Stenosis is when the valve opening narrows and becomes rigid. Regurgitation occurs when valves are insufficient or incompetent and do not close.
Mitral Stenosis
35.Mitral stenosis is a narrowing of the mitral valve and obstructs blood flow from the left atrium into the left ventricle. It is usually caused by rheumatic heart disease or bacterial endocarditis.
36.Manifestations depend upon cardiac output and pulmonary vascular pressures. Dyspnea on exertion is typically the earliest symptom. Other manifestations are cough, hemoptysis, frequent pulmonary infections, paroxysmal nocturnal dyspnea, orthopnea, weakness, fatigue, and palpitations. As stenosis worsens, manifestations of right heart failure, jugular venous distension, hepatomegaly, ascites, and peripheral edema develop. Cyanosis of the face and extremities may occur with severe mitral stenosis. Heart sounds may reveal a loud S1, split S2, a mitral opening snap, and a low-pitched, rumbling, crescendo-decrescendo murmur.
37.Complications include atrial dysrhythmias with resulting thrombi and emboli production.
Shock: Compensated vs Uncompensated
1.-Trust your gut: “he/she does not look right”, “the vital signs don’t look too bad”
2.-Compensated: SBP low end of normal 100’s, HR increasing t 110-120’s, respirations increasing, urine output decreasing. ABG’s-Metbolic acidosis
3-Uncompensated: hypotensive SBP in the 80’s, tachycardic 160’s, tachypneic 30’s, HC03 less than 20, lactic acid increasing due to increased workload. Treatment: vasopressors and IV fluid.
4-Unreversible Shock: SPB in the 30’s, HR in the 200’s, microvascular and organ damage..death is imminent