A patient presents with a history of fatigue and dyspnea. He is found to have hepatomegaly, ascites, and an elevated jugular venous pulse. Heart sounds are normal, no murmurs are present, and the heart is of normal size. The pulse pressure is decreased by palpation. Electrocardiography (ECG) is normal except for low voltage. The most likely diagnosis is:
Classic physical examination findings include jugular venous distention with Kussmaul sign, diminished cardiac apical impulses, peripheral edema, ascites, pulsatile liver, a pericardia! knock, and, in advanced disease, signs of liver dysfunction, such as jaundice or cachexia. The "pericardia! knock" is an early diastolic sound that reflects a sudden impediment to ventricular filling, similar to an s3 but of higher pitch.
Several findings are characteristic on noninvasive and invasive testing. Central venoud pressure ( CVP) is often elevated 15 to 20 mm Hg or higher. ECG commonly demonstrates nonspecific low voltage QRS complexes and isolated repolarization abnormalities. Chest X-ray may demonstrate calcification of the pericardium, which is highly suggestive of constrictive pericarditis in patients with heart failure, but this is present in only 25% of cases. Cardiac CT or MRI ( cMRI) typically demonstrate increased pericardia! thickness (>4 mm) and calcification, dilation of the inferior vena cava, deformed ventricular contours, and flattening or leftward shift of the ventricular septum. Pericardia! adhesions may also be seen on tagged cine MRI studies.
As discussed, it is most important to distinguish pericardia! constriction from restrictive cardiomyopathy, which is best done with either echocardiography or right heart catheterization. Findings favoring constriction on echocardiography include respiratory variation of ventricular septal motion and mitral inflow velocity, preserved or increased mitral annulus early diastolic filling velocity, and increased hepatic vein flow reversal with expiration. Cardiac catheterization will show increased atrial pressures, equalization of end-diastolic pressure, and early ventricular diastolic filling with a subsequent plateau, called the square-root sign. Additional findings upon catheterization that would favor constriction include respiratory variation in ventricular filling and increased ventricular interdependence, manifest as a discordant change in the total area of the LV and RV systolic pressure curve with respiration.
Each of the following effects is anticipated after insertion of an intra-aortic balloon pump EXCEPT:
The intra-aortic balloon pump (IABP) is the most commonly used device for mechanical circulatory support, and it may be easily deployed in the catheterization laboratory, in the operating room or at the bedside. The device is inserted percutaneously through the femoral artery into the thoracic aorta. It is synchronized so that the balloon is inflated during diastole and deflated during systole, resulting in augmentation of diastolic perfusion of the coronary arteries and decreased afterload. Typically, this improves cardiac index and decreases both preload and myocardial oxygen consumption.
Pericarditis is usually treated with:
The preferred treatment depends on the underlying cause of the pericarditis. The disease usually follows a self-limited and benign course and can be successfully treated with a short course of nonsteroidal anti-inflammatory drugs (NSAIDs). Some patients may require judicious use of steroids or IV antibiotics. In cases of purulent pyogenic pericarditis, surgical exploration and drainage are occasionally necessary. Rarely, accumulation of fluid in the pericardium may lead to tamponade, requiring prompt evacuation of the pericardia! space. While pericardiocentesis will typically suffice, surgical drainage may be required for thick, viscous, or clotted fluid or in patients with significant scarring from previous surgeries. More commonly, surgical intervention is required to manage recurrent disease.
The most common cause of isolated aortic in AI sufficiency in patients undergoing AVR is:
The most common cause of isolated AI in patients undergoing AVR is aortic root disease, and represents over 50% of such patients in some studies. Other common causes of AI include congenital abnormalities of the aortic valve, such as bicuspid aortic valve, calcific degeneration, rheumatic disease, infective endocarditis, systemic hypertension, myxomatous degeneration, dissection of the ascending aorta, and Marfan syndrome. Less common causes of AI include traumatic injuries to the aortic valve, ankylosing spondylitis, syphilitic aortitis, rheumatoid arthritis, osteogenesis imperfecta, giant cell aortitis, Ehlers-Danlos syndrome, Reiter syndrome, discrete subaortic stenosis, and ventricular septal defects with prolapse of an aortic cusp. Although most of these lesions produce chronic aortic insufficiency, rarely acute severe aortic regurgitation can result, often with devastating consequences.
During cardiopulmonary bypass (CPB) anticoagulation, the range ofheparin needed to increase the activated clotting time to greater than 450 seconds is:
The basic cardiopulmonary bypass (CPB) circuit consists of the venous cannulae, a venous reservoir, pump, oxygenator, filter, and the arterial cannula. Anticoagulation is required during CPB, and 300 to 400 units/kg of heparin is given to increase the activated clotting time (ACT) to greater than 450 seconds. Once adequate anticoagulation is achieved, arterial cannulation is performed through a purse-string suture, or through a side graft which is sewn on to the native artery.
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