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ECHOCARDIOLOGIST IN GANGAMMA CIRCLE Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia.
THE BEST CARDIOLOGIST IN YELAHANKA Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia. Mitral valve prolapse (systolic-click murmur syndrome) This syndrome can cause a systolic murmur or click, or both, at the apex. The presence of the murmur indicates that there is some mitral regurgitation present. Auscultation: Systolic click or clicks at a variable time (usually mid-systolic) may be the only abnormality audible, but a click is not always audible; systolic
THE BEST CARDIOLOGISTS NEAR HSR LAYOUT Coronary angiography (cardiac catheterisation) This procedure enables the cardiologist to visualise the coronary arteries . It is the standard against which other less-invasive investigations are assessed. Selective catheterisation of the right and left coronary ostia is performed. Contrast is then injected into the vessels and digital tape or disc storage of the images obtained. In most hospitals the patient is admitted on the morning of the test and allowed to go home that afternoon. The procedure is most often performed through the femoral artery (Judkins technique) . This artery can be punctured through the skin under local anaesthetic. A fine softtipped guide wire is then advanced into the artery and the needle withdrawn (Seldinger method). A short guiding sheath can then be placed over the wire and long cardiac catheters advanced through this sheath along a long guide wire into the femoral artery and up via the aorta to the aortic arch. The catheter and wire are advanced under X-ray control. Usually one catheter with a curved tip (pig-tail catheter; is advanced across the aortic valve into the left ventricle where left ventricular pressures are measured via a pressure transducer connected to the other end of the catheter. Measurement of the left ventricular end-diastolic pressure gives an indication of left ventricular function. Raised end-diastolic pressure (over 15 mmHg) suggests left ventricular dysfunction . The catheter is then connected to a pressure injector. This enables injection of a large volume of contrast over a few seconds; for example, 35 mL at 15 mL/second. X-ray recording during injection produces a left ventriculogram , Here left ventricular contraction can be assessed and the ejection fraction (percentage of end-diastolic volume ejected with each systole) estimated. The normal is 60% or more. The figure obtained by this method tends to be higher than that produced by the nuclear imaging method—gated blood pool scanning. The guide wire is reintroduced and the catheter withdrawn to be replaced by one shaped to fit into the right or left coronary orifice...
POPULAR CARDIOLOGIST IN KATTIGENAHALLI, BANGALORE Cyanotic congenital heart disease Some of the more common cyanotic lesions are discussed below. There are, however, a number of problems common to patients with cyanotic heart disease. 1 Erythrocytosis. Chronic cyanosis causes an increase in red cell numbers as a way of increasing oxygen carrying capacity. The platelet count is sometimes reduced and the white cell count normal. The increased blood viscosity associated with the high red cell mass causes a slight increase in the risk of stroke.37 Most patients have a stable elevated haemoglobin level, but venesection is recommended if this is greater than 20 g/dL and the haematocrit is greater than 65%. Levels as high as this can be associated with the hyperviscosity syndrome: headache, fatigue and difficulty concentrating. Recurrent venesection can cause iron depletion and the production of microcytic red cells, which are stiffer than normal cells and so increase viscosity further. 2 Bleeding. Reduced platelet numbers, abnormal platelet function and clotting factor deficiencies mean these patients have an increased risk of haemorrhage. The most dangerous problem is pulmonary haemorrhage but bleeding from the gums and menorrhagia are more common. The use of anticoagulation must be restricted to those with a strong indication for treatment. 3 Gallstones. Chronic cyanosis and increased haem turnover are associated with an increased incidence of pigment gallstones. 4 Renal dysfunction and gout. Congestion of the renal glomeruli is associated with a reduced glomerular filtration rate and proteinuria. This and the increased turnover of red cells lead to urate accumulation and gout. 5 Pulmonary hypertension. Lesions associated with increased flow through the pulmonary circulation (e.g. a large atrial septal defect) can lead to a reactive rise in pulmonary arterial resistance. This is more likely to occur if the left to right shunt is large. Eventually these pulmonary vascular changes become irreversible, pulmonary pressures equal or exceed systemic pressures, and central cyanosis occurs because the intra-cardiac shunt reverses (Eisenmenger’s syndrome). Flow is now from right to left. There is then no benefit in attempting to correct the underlying cardiac abnormality. Earlier and more successful treatment of children with congenital heart disease has reduced the number of patients with this inexorable disease. Careful management of these conditions can nevertheless improve patients’ symptoms and survival. Reasonable exercise tolerance is usually maintained into adult life for most patients but progressive deterioration then occurs. Haemorrhagic complications, especially haemoptysis, are common. Thrombotic stroke, cerebral abscess and pulmonary infarction can also occur.
Indications for Hemodynamic Monitoring in Patients with STEMI Management of complicated acute myocardial infarction Hypovolemia versus cardiogenic shock Ventricular septal rupture versus acute mitral regurgitation Severe left ventricular failure Right ventricular failure Refractory ventricular tachycadia Differentiating severe pulmonary disease from left ventricular failure Assessment of cardiac tamponade Assessment of therapy in selected individuals Afterload reduction in patients with severe left ventricular failure Inotropic agent therapy Beta-blocker therapy Temporary pacing (ventricular versus atrioventricular) Intraaortic balloon counterpulsation Mechanical ventilation
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