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'aortic regurgitation'
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THE BEST CARDIOLOGISTS IN YELAHANKA Aortic regurgitation The incompetent aortic valve allows regurgitation of blood from the aorta to the left ventricle during diastole for as long as the aortic diastolic pressure exceeds the left ventricular diastolic pressure. Symptoms: Occur in the late stages of disease and include exertional dyspnoea, fatigue, palpitations (hyperdynamic circulation) and exertional angina. General signs: Marfan’s syndrome may be obvious. The pulse and blood pressure: The pulse is characteristically collapsing; there may be a wide pulse pressure. The neck: Prominent carotid pulsations (Corrigan’s sign). Palpation: The apex beat is characteristically displaced and hyperkinetic. A diastolic thrill may be felt at the left sternal edge when the patient sits up and breathes out. Auscultation): A2 (the aortic component of the second heart sound) may be soft; a decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and extending for a variable time into diastole—it is loudest at the third and fourth left intercostal spaces; a systolic ejection murmur is usually present (due to associated aortic stenosis or to torrential flow across a normal diameter aortic valve). Signs indicating severe chronic aortic regurgitation: Collapsing pulse; wide pulse pressure; long decrescendo diastolic murmur; left ventricular S3 (third heart sound); soft A2; signs of left ventricular failure. Causes of chronic aortic regurgitation: (i) Rheumatic (rarely the only murmur in this case), congenital; (ii) aortic root dilatation—Marfan’s syndrome, dissecting aneurysm. 8• THE PATIENT WITH A MURMUR 305 a b Valve cusps often thickened and calcified Left ventricle may be hypertrophied Ascending aorta may be dilated Systole Diastole S1 A2 P2 S1 Ejection click (Suggests congenital AS) Normal Mild S1 S1 Moderate S1 P2 A2 S1 Severe Reversed S2 Single (S2)
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.
SAMIKSHA HEART AND DIABETIC CARE IN YELAHANKA Echocardiographic findings in certain cardiac abnormalities It is important to be aware that modern colour flow mapping is so sensitive that small amounts of regurgitation are often detected from quite normal valves. Deciding whether these jets are significant can be difficult and requires experience. Mitral stenosis Thickening and doming of the mitral valve leaflets is visible on M mode and 2D scanning , It may be possible to measure the valve area by planimetry . Secondary changes such as left atrial size and the presence of rheumatic disease of other valves can be seen. Doppler interrogation of the jet of blood entering the left ventricle through the mitral valve will enable estimation of the valve area by a formula called the pressure half-time equation This will usually give accurate and consistent estimates of the valve area and is especially useful for serial measurements over months or years. It will also be possible to detect associated mitral regurgitation with Doppler. Mitral regurgitation and mitral valve prolapse Here the mitral valve may appear normal and abnormal co-aptation of the leaflets is not usually visible . The left atrium will appear enlarged if significant chronic MR is present, and if this is severe left ventricular dilatation will be present. If the MR is due to mitral valve
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
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...
The use of invasive hemodynamic monitoring is based on the following principal factors: 1. Difficulty in interpreting clinical and radiographic findings of pulmonary congestion even after a thorough review of noninvasive studies such as an echo-cardiogram. 2. Need for identifying noncardiac causes of arterial hypotension, particularly hypovolemia. 3. Possible contribution of reduced ventricular compliance to impaired hemodynamics, requiring judicious adjustment of intravascular volume to optimize left ventricular filling pressure. 4. Difficulty in assessing the severity and sometimes even determining the presence of lesions such as mitral regurgitation and ventricular septal defect when the cardiac output or the systemic pressures are depressed. 5. Establishing a baseline of hemodynamic measurements and guiding therapy in patients with clinically apparent pulmonary edema or cardiogenic shock. 6. Underestimation of systemic arterial pressure by the cuff method in patients with intense vasoconstriction. The prognosis and the clinical status of patients with STEMI relate to both the cardiac output and the pulmonary artery wedge pressure. Patients
The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality
The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality HEART SPECIALIST IN YELAHANKA
CARDIOLOGIST IN SAHAKARANAGAR The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis.
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