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Instruction: Answer the following questions briefly. 1. Explain the process of pulmonary and systemic circulation. Pathway of blood flow through the heart. Answer. The right side of the heart pumps blood into the pulmonary circuit; the left side of the heart pumps blood into the systemic circuit. 2. Explain and enumerate the different classifications of Cardiovascular Disease. Answer. Classifications: Conduction disorders (Dysthymias) † Supraventricular Rhythms † Ventricular Dysrhythmias † Atrioventricular Conduction Blocks † Ventricular Conduction Blocks Myocardial disorders (Coronary Heart Disease) Angina pectoris Acute Myocardial Infarction Sudden Cardiac Death Structural Disorders Valvular Hearth Diseases Cardiomyopathy Infectious Disorder 3. Give the pathophysiology, sign / symptoms and nursing care for the following disorders. Inflammatory Heart Disease Pathophysiology Sign and Symptoms Nursing Care Rheumatic Fever/ Rheumatic Heart Disease Rheumatic Fever +recurrent infection -> Cross immune response between host and streptococcal antigens -> Abnormal reactionautoimmunity disease -> rheumatic pancarditis and Endocarditis in valves -> erosion of valve leaflets -> fibrous thickening and thickened valves -> stenos is and regurgitation. -Fever -Painful and tender joints - most often in the knees, ankles, elbows and wrists -Pain in one joint that migrates to another joint -Red, hot or swollen joints Small, painless bumps (nodules) beneath the skin -Chest pain -Fatigue -Jerky, uncontrollable body movement s- most often in the hands, feet and face. -Monitor vital signs Such as: blood pressure, apical pulse and peripheral pulse. -Monitor cardiac rhythm and frequency. -Semi fowler bed rest in a position that is 45 degrees. -Encourage the patient to stress management techniques (quiet environment, meditation). - Medical collaboration in terms of oxygen delivery and therapy. Endocarditis structural abnormalities of the cardiac valve for bacterial adherence, the adhesion of circulating bacteria to the valvular surface, and the ability of the adherent bacteria to survive on the surface and propagate as vegetation or systemic emboli. Certain bacteria, if present in the bloodstream, may colonize the initially sterile vegetation composed of fibrin and platelets; bacterial growth enlarges the vegetation, further impeding blood flow and inciting inflammation that involves the vegetation and adjacent endothelium. The true incidence of endocarditis complicating each the bacterial species -Fever and chills -Fatigue -Night sweats -Shortness of breath -Paleness -Persistent cough -welling in your feet, legs or abdomen -Unexplained weight loss -Blood in your urine -Monitor vital signs Such as: blood pressure, apical pulse and peripheral pulse. -Monitor cardiac rhythm and frequency. - Medical collaboration in terms of oxygen delivery and therapy. Myocarditis The term myocarditis refers to an inflammatory response within the myocardium that is not secondary to ischemic events or cardiac rejection in the setting of transplantation. The presence of myocyte necrosis is required for certain types of myocarditis — specifically, lymphocytic myocarditis that is triggered by viruses and augmented by autoimmunity — and the myocyte damage is believed to be mediated both by direct invasion of the myocardium and by immune insult. Pericarditis develops quickly, causing inflammation of the pericardial sac and often a -Shortness of breath during exercise, Fatigue, Palpitations light headedness, Irregular heartbeat, Sudden loss of consciousness, Fever, Bluish or Grayish discoloration of the skin, Fluid retention with swelling of legs, Ankles and feet, Headache, Body aches, Sudden breath. -Monitor vital signs Such as: blood pressure, apical pulse and peripheral pulse. -Give a comfortable position (semi-fowler position). -Monitor pain characteristics and administer analgesics as needed and use salicylates around the clock. -Give O2 supplement and ensure saturation ˃90%. -Chest pain - dyspnea - Night sweats, and weight loss -Monitor vital signs Such as: blood pressure, apical pulse and peripheral pulse. Pericarditis pericardial effusion. Inflammation can extend to the epicardial myocardium (myopericarditis). Adverse hemodynamic effects and rhythm disturbance are rare, although cardiac tamponade is possible. Valvular Heart Disease are commonly noted. -Place the patient in upright position to relieve dyspnea and chest pain. -Provide analgesics to relieve pain and oxygen to prevent tissue hypoxia. -Assess the patient’s cardiovascular status frequently, watching for signs of cardiac tamponade. Pathophysiology Sign and Symptoms Nursing Care Mitral Stenosis Mitral stenosis prompts a series of hemodynamic changes that frequently cause deterioration of the patient's clinical status. A reduction in cardiac output, associated with acceleration of heart rate and shortening of the diastolic time, frequently leads to congestive heart failure. In addition, when AF sets in, systemic embolization becomes a real danger. -Place the patient in an upright position to relieve dyspnea, if needed. - Teach the patient about diet restrictions. - Watch closely for signs of pulmonary dysfunction caused by pulmonary hypertension, tissue ischemia caused by emboli, and adverse reactions to drug therapy. -Explain all tests and treatments to the patient. Mitral Regurgitation MR can be caused by organic -Cough, possibly with bloody phlegm -Difficulty breathing during or after exercise (This is the most common symptom.) -Waking up due to breathing problems or when lying in a flat position -Fatigue -Frequent respiratory infections, such as bronchitis -Feeling of pounding heart beat (palpitations) -Swelling of feet or ankles. -Dyspnea -Check vital signs (heart rate Mitral Valve Prolapse disease (e.g., rheumatic fever, ruptured chordae tendineae, myxomatous degeneration, leaflet perforation) or a functional abnormality (i.e., a normal valve may regurgitate [leak] because of mitral annular dilatation, focal myocardial dysfunction, or both). Congenital MR is rare but is commonly associated with myxomatous mitral valve disease. Alternatively, it can be associated with cleft of the mitral valve, as occurs in persons with Down syndrome, or a ostium primum atrial septal defect. -Fatigue -Orthopnea -Pulmonary edema (often the initial manifestation) and blood pressure). -Assess heart sounds, noting gallops, S3, S4. -Assess manually peripheral pulses (with weak rate, rhythm indicated low cardiac output). - Explain diet restrictions (fluid, sodium). - Routinely Assess skin color and temperature (Cold, clammy skin is secondary to compensatory increase in sympathetic nervous system stimulation and low cardiac output and desideration). Mitral valve prolapse (MVP) is characterized primarily by myxomatous degeneration of the mitral valve leaflets. In younger populations, there is gross redundancy of both the anterior and posterior leaflets and chordal apparatus. This is the extreme form of myoxomatous degeneration, known as Barlow’s syndrome. In older populations, however, MVP is characterized by fibroelastic deficiency, sometimes with superimposed chordal rupture due to a lack of connective tissue support. These anatomic abnormalities result in -Shortness of breath, Weakness or dizziness, Wheezing and heavy coughing, Physical exertion, Palpitations mild chest pain, Fever, Rapid weight gain, Swelling of the ankles, feet or abdomen. -Check vital signs (heart rate and blood pressure). -Assess heart sounds, noting gallops, S3, S4. -Assess manually peripheral pulses (with weak rate, rhythm indicated low cardiac output). - Explain diet restrictions (fluid, sodium). - Routinely Assess skin color and temperature (Cold, clammy skin is secondary to compensatory increase in sympathetic nervous system stimulation and low cardiac output and desideration). -Explain all tests and treatments to the patient. malcoaptation of mitral valve leaflets during systole, resulting in regurgitation. Mitral annular dilatation may also develop over time, resulting in further progression of mitral regurgitation (MR). Acute severe MR results in congestive heart failure symptoms without left ventricular dilatation. Conversely, chronic or progressively severe MR can lead to ventricular dilatation and dysfunction, neurohormonal activation, and heart failure. Elevation in left atrial pressures can result in left atrial enlargement, atrial fibrillation, pulmonary congestion, and pulmonary hypertension. Aortic Stenosis When the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. This outflow obstruction leads to an increase in left ventricular (LV) systolic pressure. As a compensatory mechanism to normalize LV wall stress, LV wall thickness increases by parallel replication of sarcomeres, producing concentric hypertrophy. At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance is reduced. -Chest pain (angina) or tightness -Feeling faint or fainting with exertion -Shortness of breath, especially with exertion -Fatigue, especially during times of increased activity -Heart palpitations — sensations of a rapid, fluttering heartbeat -Heart murmur -Place the patient in an upright position to relieve dyspnea. -Administer oxygen as needed to prevent tissue hypoxia. -Keep the patient in a low sodium diet. - Evaluate patient’s activity tolerance and degree of fatigue. -Monitor the patient for chest pain that may indicate cardiac ischemia. -Explain all tests and treatments to the patient. Eventually, however, LV enddiastolic pressure (LVEDP) rises, which causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in cardiac output due to diastolic dysfunction. The contractility of the myocardium may also diminish, which leads to a decrease in cardiac output due to systolic dysfunction. Aortic Regurgitation Incompetent closure of the aortic valve can result from intrinsic disease of the leaflets, cusp, diseases of the aorta, or trauma. Diastolic reflux through the aortic valve can lead to left ventricular volume overload. An increase in systolic stroke volume and low diastolic aortic pressure produces an increased pulse pressure. The clinical signs of AR are caused by the forward and backward flow of blood across the aortic valve, leading to increased stroke volume. The severity of AR is dependent on the diastolic regurgitate valve -Fatigue and weakness, especially when you increase your activity level -Shortness of breath with exertion or when you lie down -Swollen ankles and feet (edema) -Chest pain (angina), discomfort or tightness, often increasing during exercise -Lightheadedness or fainting Irregular pulse (arrhythmia) -Heart murmur Sensations of a rapid, fluttering heartbeat (palpitations) -Place the patient in an upright position to relieve dyspnea. -Administer oxygen as needed to prevent tissue hypoxia. - Observe the patient for complications and adverse reactions to drug therapy. - Monitor the patient for chest pain that may indicate cardiac ischemia. -Regularly assess the patient’s cardiopulmonary function. area, the diastolic pressure gradient between the aorta and LV, and the duration of diastole. Tricuspid Stenosis Tricuspid stenosis results from alterations in the structure of the tricuspid valve that precipitate inadequate excursion of the valve leaflets. The most common etiology is rheumatic fever, and tricuspid valve involvement occurs universally with mitral and aortic valve involvement. With rheumatic tricuspid stenosis, the valve leaflets become thickened and sclerotic as the chordae tendineae become shortened. The restricted valve opening hampers blood flow into the right ventricle and, subsequently, to the pulmonary vasculature. Right atrial enlargement is observed as a consequence. The obstructed venous return results in hepatic enlargement decreased pulmonary blood flow, and peripheral edema. -Tired and lethargic -Fragility -A quivering feeling in the neck -A rapid, irregular heartbeat called a palpitation -Place the patient in an upright position to relieve dyspnea. -Administer oxygen as needed to prevent tissue hypoxia. -Keep the patient in a low sodium diet. - Evaluate patient’s activity tolerance and degree of fatigue. -Monitor the patient for chest pain that may indicate cardiac ischemia. -Explain all tests and treatments to the patient. Tricuspid Regurgitation Tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetence can result from primary structural abnormalities of the leaflets and chordae or, more often, be secondary to myocardial dysfunction and dilatation. -Fatigue -Declining exercise capacity -Swelling in your abdomen, legs or veins in your neck -Abnormal heart rhythms -Pulsing in your neck -An enlarged liver -Shortness of breath with activity -Check vital signs (heart rate and blood pressure). -Explain all tests and treatments to the patient. - Evaluate patient’s activity tolerance and degree of fatigue. -Monitor the patient for chest pain that may indicate cardiac ischemia. Pulmonic Stenosis PS can be due to isolated valvular (90%), subvalvular, or -Heart murmur — an abnormal whooshing sound heard using a -Alternate periods of rest to prevent extreme fatigue and peripheral (supravalvular) obstruction, or it may be found in association with more complicated congenital heart disorders. The characteristics of the various types of PS are described in this section. stethoscope, caused by turbulent blood flow -Shortness of breath, especially during exertion -Chest pain -Loss of consciousness (fainting) -Fatigue dyspnea. -To reduce anxiety, allow the patient to express his concerns about the effects of activity restrictions on his responsibilities and routine. -Check vital signs (heart rate and blood pressure). Pulmonic Regurgitation Incompetence of the pulmonic valve occurs by 1 of 3 basic pathologic processes: dilatation of the pulmonic valve ring, acquired alteration of pulmonic valve leaflet morphology, or congenital absence or malformation of the valve. -Fatigue -Shortness of breath, especially during exertion -Chest pain -Assess mental status -Check vital signs (heart rate and blood pressure). -Routinely Assess skin color and temperature (Cold, clammy skin is secondary to compensatory increase in sympathetic nervous system stimulation and low cardiac output and desideration) -Assess lung sounds and determine any occurrence of Paroxysmal Nocturnal Dyspnea (PND) or orthopnea. -Explain drug regimen, purpose, dose, and side effects Cardiomyopathy Dilated cardiomyopathy is characterized by ventricular chamber enlargement and systolic dysfunction with greater left ventricular (LV) cavity size with little or no wall hypertrophy. Hypertrophy can be judged as the ratio of LV mass to cavity size; this ratio is decreased in persons with dilated cardiomyopathies. The enlargement of the remaining heart chambers is primarily due to LV failure, but it may be secondary to the primary cardiomyopathic process. Dilated cardiomyopathies are associated -Fatigue -Dyspnea on exertion, shortness of breath, cough -Orthopnea, paroxysmal nocturnal dyspnea -Increasing edema, weight, or abdominal girth -Assess mental status -Check vital signs (heart rate and blood pressure). -Routinely Assess skin color and temperature (Cold, clammy skin is secondary to compensatory increase in sympathetic nervous system stimulation and low cardiac output and desideration) -Explain drug regimen, purpose, dose, and side effects with both systolic and diastolic dysfunction. The decrease in systolic function is by far the primary abnormality due to adverse myocardial remodeling that eventually leads to an increase in the end-diastolic and end-systolic volumes. Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further diminish the cardiac output and increase end-systolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction.