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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
CARDIOLOGIST IN YELAHANKA SECOND DEGREE AV BLICK There are two basic types of second-degree AV block: AV nodal Möbitz type I (Wenckebach) heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (Fig 3.10) (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB (Fig 3.11), since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block (Fig 3.12). There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as
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.
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