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best cardiologists in bangalore Murmurs Murmurs are produced by turbulent blood flow, and are described according to their location, intensity, timing, frequency, and radiation (Tables 15.1 to 15.3 and Figure 15.1). Innocent murmurs are due to pulmonary flow and can be heard in children, pregnancy, and high-flow states, such as hyperthyroidism and anaemia. They are heard over the left sternal edge and are ejection systolic, and there are no added sounds or thrill. The cervical venous hum is a continuous murmur, common in children and typically reduced by turning the head laterally or bending the elbows back. The mammary soufflé is a continuous murmur that may be heard in pregnancy. Dynamic auscultation manoeuvres may help bedside diagnosis of systolic murmurs (Table 15.2). 4, 5 Murmurs originating within the right-sided chambers of the heart can be differentiated from all other murmurs by augmentation of their intensity with inspiration and diminution with expiration. The murmur of hypertrophic cardiomyopathy is distinguished from all other systolic murmurs by an increase in intensity with the Valsalva manoeuvre and during squatting-to-standing, and by a decrease in intensity during standing-to-squatting action, passive leg elevation, and handgrip. The murmurs of MR and VSD have similar responses but can be differentiated from other systolic murmurs by augmentation of their intensity with handgrip and during transient arterial occlusion.
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
A risk factor is a demographic characteristic associated with an increased risk of ischaemic heart disease when other variables have been controlled. The presence of a risk factor in an individual increases his or her relative risk of a coronary event (angina, infarction or death). The absolute risk of a coronary event depends on the individual’s total number of risk factors and theirseverity (total risk). Important coronary risk factors are shown in Table 1.1. Risk assessment charts have been developed to estimate a patient’s cardiac risk over a number of years using easily identified risk factors. There are charts for different populations. The charts can be used to predict cardiovascular events or mortality (as in the NHF chart in Fig 1.1 on p. 4) or cardiac risk (systematic coronary risk evaluation system or SCORE charts). These charts can be very helpful in deciding when intervention to reduce risk is warranted; for example, when anti-hypertensive treatment should be commenced for a patient with mild blood pressure elevation. Risk factor reduction involves assessing the presence, severity and importance of risk factors for a
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.
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Cardiomyopathies and valvular heart disease Regardless of the status of the coronary arterial tree, both primary and secondary heart muscle disease can produce anginal pain through the imbalance of the oxygen demand and supply. Hypertrophic cardiomyopathy is a relatively common cause of angina in the presence of normal coronary arteries. Aortic stenosis is the most common valvular cause of exertional chest tightness, which is probably due to myocardial ischaemia Exertional chest pain, which may be due to right ventricular angina, is a feature of pulmonary hypertension . Syndrome X There is some confusion regarding the ‘metabolic’ and ‘cardiac’ varieties. The former is a combination of insulin resistance, obesity, pro-inflammatory state and so on, leading to raised cardiovascular risk in the sufferers. The latter is, or should be, a form of stable effort angina that can be ascribed to coronary microvascular malfunction.23 The epicardial coronary tree is normal and the diagnosis is rather difficult to make except by exclusion. Acute coronary syndromes The terminology used to describe acute coronary syndromes (ACSs) continues to evolve as clinicians attempt to adjust to the accumulating evidence of the usefulness of modern cardiac markers and the treatment implications of different results. The most recent terminology is designed to help with treatment decisions based on the earliest clinical information from the patient. This comes from the history and the ECG. When the patient’s symptoms suggest an acute coronary syndrome, the first decisions about diagnosis and treatment are based on the ECG. If there is ST elevation present in a pattern to suggest myocardial infarction, the diagnosis is of ‘ST elevation myocardial infarction’ (STEMI). If there is no ST elevation, the initial diagnosis is of ‘non-ST elevation acute coronary syndrome’ (NSTEACS).24 This elegant phrase has replaced ‘non-ST elevation myocardial infarction’ (non- STEMI). The reason is that the diagnosis of infarction cannot be made in the absence of ST elevation until cardiac marker estimations are available. The decisions about treatment, however, need to be made immediately and are based on symptoms and ECG changes.