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THE BEST CARDIOLOGISTS IN YELAHANKA A systematic description of ECGs The following eight short steps will enable most ECGs to be described correctly: 1 Check the paper speed and calibration markers. 2 Measure or estimate the heart rate. 3 Estimate the rhythm. 4 Look for P waves. 5 Measure the PR interval. 6 Examine the QRS complex. 7 Check the ST segment. 8 Measure the T wave. ECG interpretation should always be as restrained as practicable, taking into account the clinical context where known and comparison with previous tracings where possible. The possibility of Prinzmetal’s electrocardiographic heart disease must always be borne in mind—that is, do not assume that an abnormal ECG always means heart disease.2.
This ordinarily consists of monitoring of  is suspected. heart rate and rhythm,  repeated measurement of systemic arterial pressure by cuff,  obtaining chest radiographs to detect heart failure,  repeated auscultation of the lung fields for pulmonary congestion,  measurement of urine flow,  examination of the skin and mucous membranes for evidence of the adequacy of perfusion, and
PAPULAR CARDIOLOGISTS IN HEBBALA ECG interpretation: points to remember 1 ECG reports should be short and based on clinical information where possible. 2 Check that the patient’s name is on the ECG and that the paper speed and calibration markers are correct. 3 Measure or estimate the heart rate—3 large squares = 100/minute. 4 Establish the rhythm. Look for P waves (best seen in L2). Are the P waves followed by QRS complexes? Look for anomalously conducted or ectopic beats. 5 Measure the intervals: PR, QRS duration and QT interval (for the latter, consult tables, but normal is less than 50% of the RR interval). 6 If the QRS complex is wide (> 3 small squares) consider the possibilities: LBBB, RBBB, WPW or ventricular rhythm or beats. If the pattern is of LBBB, there is no need in most cases to attempt further interpretation. 7 Estimate the QRS axis. In LAD, L1 and aVF diverge and L2 is predominantly negative. In RAD, L1 and aVF converge, while L2 matters little. Indeterminate axis is diagnosed when all six frontal leads are (more or less) equiphasic. 8 Check whether the criteria for LAHB or LAFB have been met. 9 Look for pathological Q waves. In general these are longer than 0.04 seconds and are more than 25% of the size of the following R wave.
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...
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
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
HEART SPEACIALIST IN BANGALORE HYPERTENTION By definition, sinus tachycardia is a heart rate ≥ 100/minute and sinus bradycardia is a heart rate ≤ 50/minute.3 To calculate the heart rate from the ECG, the R-R interval in mm can be divided into 1500. For example, an R-R interval of 20 mm gives a rate of 75/minute and an R-R interval of 15 mm gives a rate of 100. Similarly, large 5 mm squares can be divided into 300; thus three squares give a rate of 100/minute. In regular rhythms, any two congruous points of the P-QRS-T sequence can be used to estimate the rate. An ECG ruler has a scale that enables rapid rate measurement and calculation of other intervals. With practice, the rate can be estimated at a glance.
THE BEST CARDIOLOGISTS IN YELAHANKAMedical treatment of stable angina Treatment of any disease must begin with a thorough explanation of the likely diagnosis, severity and prognosis. The possible investigations required and steps to be taken if symptoms persist despite treatment should be outlined. A warning (firm, but not alarming) should be given that a prolonged episode of chest pain (more than about 15 minutes) should prompt the patient to get to a hospital without delay. This may also be the first opportunity to speak to the patient about the control of risk factors (e.g. smoking, hyperlipidaemia) that will be important for the long-term prognosis. Risk factor assessment should form part of this initial consultation and include a request for measurement of the serum lipids . a b (a) An MDCT scan of a diseased right coronary artery and the corresponding coronary angiogram (b) An MDCT reconstructed image of the heart and great vessels 140 PRACTICAL CARDIOLOGY A patient with symptoms typical of angina but who seems stable enough not to need admission to hospital should be started on treatment while awaiting investigations to confirm the diagnosis (usually stress testing). Treatment should aim to improve symptoms and, if possible, improve the prognosis (i.e. reduce the risk of unstable angina, infarction or death). Some drugs that help control the symptoms of angina may also improve the prognosis; other treatment may help the longer-term outlook by improving risk factors. Anti-platelet
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.
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