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HEART SPEACIALISTS IN BANGALORE Stress echocardiography Ischaemic areas of myocardium are known to have reduced contraction compared with normal areas. This can be demonstrated by high-quality echocardiograms. A number of standard views of the heart are obtained and the wall is divided into regions that are assessed for reduced motion. The echo equipment must be designed to store rest images and to present them next to stress images on a split screen so that direct comparison can be made. The stress can be provided by exercise or dobutamine infusion. Exercise echocardiography is difficult to perform because of movement problems and there is quite high inter-reporter variability, but both techniques can approach the accuracy of sestamibi testing in experienced hands. It is not possible to obtain images of adequate quality in all patients.
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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 HYPERDYNAMIC STATE. MI with hyperdynamic state—that is, elevation of sinus rate, arterial pressure, and cardiac index, occurring singly or together in the presence of a normal or low left ventricular filling pressure—and if other causes of tachycardia such as fever, infection, and pericarditis can be excluded, treatment with beta blockers is indicated. Presumably, the increased heart rate and blood pressure are the result of inappropriate activation of the sympathetic nervous system, possibly secondary to augmented release of catecholamines, pain and anxiety, or some combination of these.
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin . Right ventricular hypertrophy The main criteria fSAor detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QRS) In congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
CARDIOLOGY DOCTORS IN HOSUR ROAD Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours.