Cardiomyopathies, myocarditis and inflammatory disorders gas used in ww1


Systolic dysfunction is manifested by decreased shortening and ejection fractions which leads to increased end-diastolic volume and pressure. The blood flow to kidneys is diminished with resultant salt and water retention and worsening of CHF. Myocardial fibrosis may lead to ventricular arrhythmias secondary to the development of reentry circuits in the ventricles.

• Echocardiography shows decreased shortening fraction (the percentage of decrease in LV dimensions between diastole and systole gas bubble retinal detachment.) The origin of the coronary arteries should be delineated to rule out coronary anomalies. Pericardial effusion may be present. Cardiac catheterization and myocardial biopsy are useful in confirming the diagnosis and evaluating the patient for potential cardiac transplantation.

If cardiac decompensation is present, intravenous inotropic agents, such as dobutamine and dopamine (in renal doses), may be useful. Amrinone and milrinone also have positive inotropic effect and also reduce the afterload. When the patient is clinically stable, oral digoxin, ACE inhibitors and B-blockers (carvedilol) may be started. Diuretic therapy is useful for removing excess fluid. Patients with acute and severe decompensation may require ventricular assist devices or extracorporeal membrane oxygenation. Heart transplantation may be considered if all other measures fail. Constrictive Pericarditis

Constrictive pericarditis occurs when a scarred, thickened, and calcified pericardium impairs cardiac filling. The pathophysiological hallmark of pericardial constriction is equalization of the end-diastolic pressures in all four cardiac chambers. This occurs because the filling is determined by the limited pericardial volume, not the electricity in india travel compliance of the chambers themselves.

Initial ventricular filling occurs rapidly in early diastole as blood moves from the atria to the ventricles without much change in the total cardiac volume. However, once the pericardial constraining volume is reached, diastolic filling stops abruptly. The stiff pericardium also isolates the cardiac chambers from respiratory changes in intrathoracic pressures, resulting in Kussmaul’s sign.

Patients with pericardial constriction typically present with manifestations of elevated systemic venous electricity distribution companies pressures and low cardiac output. Typically, there will be marked jugular venous distension, hepatic congestion, ascites, and peripheral edema. The limited cardiac output typically presents as exercise intolerance. Patients with pericardial constriction are much more likely to have left-sided or bilateral pleural effusions.

• Doppler echocardiography is important in the evaluation of patients with suspected pericardial constriction. The echocardiogram may demonstrate pericardial thickening and calcification. However, increased pericardial thickness can be missed on a transthoracic echocardiogram. Transesophageal echocardiography is more sensitive and accurate ideal gas questions in determining pericardial thickness. Doppler echocardiography frequently demonstrates restricted filling of both ventricles.

Restrictive cardiomyopathy (RCM) is a rare form of myocardial disease that is characterized by restrictive filling of the ventricles. In this disease the contractile function of the heart and wall thicknesses are usually normal, but the filling phase of the heart is abnormal. This occurs because the cardiac muscle is stiff and poorly compliant and does not allow ventricular filling. This inability to relax and fill with blood results in a backup of blood into the atria. RCM is the least common in children, accounting for 2.5-5% of the diagnosed cardiomyopathies. The average age of diagnosis is 5 to 6 years old and it appears to affect girls somewhat more often than boys. There is a family history of cardiomyopathy 66 gas station near me in approximately 30% of cases. In most cases the cause of the disease is unknown (idiopathic), although a genetic cause is suspected in most cases of pediatric RCM.

Hypertrophic obstructive cardiomyopathy (HOCM) is the most common cause of sudden death in the young. The most important predictors of sudden death are a family history of sudden death and recurrent syncope. Mortality in children with HOCM is twice as high as adults. The condition is usually progressive and the symptoms depend on the age and mode of presentation.

HOCM is an inherited disorder of the cardiac muscle characterized by a hypertrophied, non-dilated left ventricle. The condition is associated with abnormal relaxation of the LV and sometimes with outflow tract obstruction. The mode of inheritance is most often autosomal dominant with variable penetrance and several genetic defects have been described.

The hallmark of HOCM is left ventricular hypertrophy (LVH) which is characteristically asymmetric with more involvement of the ventricular septum. This asymmetric septal hypertrophy often produces sub-aortic obstruction that is exaggerated by systolic anterior movement (SAM) of the anterior mitral valve leaflet and its apposition to the bulging septum. Histologically, there is extensive myocardial fiber disarray. The myocardial cells are disorganized and are separated by loose connective tissue. The coronary arteries sometimes run within the myocardium (intramural) and gas bloating show increased intimal and medial thickening causing luminal narrowing.

• A systolic ejection murmur may be present due to LV outflow tract obstruction (LVOTO). The murmur is intensified by maneuvers that decrease the LV volume and increase the systolic anterior movement of the mitral valve leaflet such as standing or performing the Valsalva maneuver. Its intensity decreases by squatting or assuming a supine position. These maneuvers have the opposite effect of an aortic stenosis murmur.

Beta-blockers are helpful in the medical management by reducing the contractility and the heart rate; thereby prolonging the diastolic time. However, these agents have no effect on the degree of LVOTO obstruction or sudden death. Digoxin, other inotropic agents, and ACE inhibitors are contraindicated in HOCM as they worsen the obstruction, though they may have a role in the end-stage dilated thin-walled HOCM hearts with impaired LV systolic function static electricity definition physics. Diuretics are also usually contraindicated as they reduce the preload and enhance the LVOTO.