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POPULAR CARDIOLOGISTS IN SILK BOARD Atrial tachycardia with block Atrial tachycardia with block (paroxysmal atrial tachycardia (PAT) with block) is also an autonomous (automatic, ectopic) atrial tachycardia but its P waves are usually smaller (often discernible only in lead V1) and faster. As a result of this high rate, AV block—mostly 2:1, but often variable—is usually present prior to any exposure to drugs or vagal manoeuvres ). inthe past this was one of the classic manifestations of digoxin toxicity. It can be difficult to distinguish from other atrial rhythms such as AF, flutter and even sinus rhythm ..
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.
THE BEST CARDIOLOGIST IN YELAHANKA 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. Mitral valve prolapse (systolic-click murmur syndrome) This syndrome can cause a systolic murmur or click, or both, at the apex. The presence of the murmur indicates that there is some mitral regurgitation present. Auscultation: Systolic click or clicks at a variable time (usually mid-systolic) may be the only abnormality audible, but a click is not always audible; systolic
THE CARDIOLOGISTS IN HSR LAYOUT Atrial fibrillation Atrial fibrillation is the most common sustained arrhythmia. The atrial activity consists of chaotic, small fibrillatory f waves at 400–700/minute. The ventricular response is usually 130–160/minute and is irregular. The ventricular response rate is slower if the patient has been treated with anti-arrhythmic drugs or if there is intrinsic AV nodal disease. When the response rate is slow, the AF is often reported as ‘controlled’ . very rapid ventricular response—more than 200/minute—may be seen in the presence of a bypass tract, like the bundle of Kent in WPW syndrome (Fig 3.24) or James fibres in LGL syndrome . The AF itself should never be reported as ‘fast’ because it always
CCARDIOLOGIST IN DODDABOMMASANDRA, BANGALORE ardiac drugs A detailed drug history is essential. Ask about anti-anginal and anti-failure drugs. It is important to attempt to ensure that the patient gets these drugs on the day of the operation. This applies most of all to beta-blockers. Withdrawal of beta-blockers used for angina can precipitate unstable angina or an infarct. There is also evidence that the use of beta-blockers in the peri-operative period reduces the risk of significant ischaemic events.36 This is probably not the case for nitrates and calcium antagonists. Aspirin used for any patient with ischaemic heart disease should be stopped for the shortest possible period before surgery (about three days) . Warfarin, when used for protection against embolic events for atrial fibrillation, can usually be stopped four or five days pre-op and begun again soon afterwards. A possible exception is a patient with atrial fibrillation and a recent embolic event or a left atrial thrombus seen on echo. These patients may need to change to heparin, as detailed below. A history of infective endocarditis, known valvular heart disease (even if mild) or the presence of a prosthetic cardiac valve may be an indication for antibiotic prophylaxis. Patients with a prosthetic heart valve who are taking warfarin need careful management. If the valve is in the aortic position and it is a modern disc valve, it may be safe to allow the INR to fall moderately (to 1.8 or so) by the day of surgery and then to resume warfarin as soon as the patient can swallow. If the surgeon requires the INR to have fallen to normal or the patient has a valve in the mitral position, then cessation of warfarin and use of heparin is necessary. Normally the patient omits a warfarin dose and then is admitted to hospital three or four days before surgery. Intravenous heparin is begun and the APPT adjusted to 2 or 2.5 times normal. The heparin is stopped some hours before surgery and begun as soon afterwards as the surgeon allows. It is now possible, however, to use low molecular weight heparin instead
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
THE BEST CARDIOLOGISTS IN YELAHANKA Second-degree AV block There are two basic types of second-degree AV block: AV nodal Möbitz type I 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 (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 , 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 . 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 Möbitz type
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.
BEST CARDIOLOGY HOSPITALS IN BANGALORE Cardiac failure Cardiac failure is an increasingly common condition affecting about 1% of the population but much higher proportions of older people. It is responsible for an increasing number of hospital admissions. The various aetiologies have been discussed above, but the most common cause is now ischaemic heart disease rather than hypertensive heart disease. This reflects the improved modern management of hypertension in the population. The definition of heart failure has always included reference to the inability of the heart to meet the metabolic needs of the body. The earliest concepts of heart failure were of inadequate cardiac pump function and associated salt and water retention. Treatment was aimed at improving cardiac contractility and removing salt and water from the body. In the 1970s the concept of after-load reduction was introduced. This was based partly on the realisation that vasoconstriction was part of the problem. This has led to the modern neuro-hormonal concept of heart failure. It is clear that many of the features of cardiac failure are a result of stimulation of the renin-angiotensin-aldosterone system and sympathetic stimulation. These responses of the body to the fall in cardiac output temporarily increase cardiac performance and blood pressure by increasing vascular volumes, cardiac contractility and systemic resistance. In the medium and longer term these responses are maladaptive. They increase cardiac work and left ventricular volumes and lead to myocardial fibrosis with further loss of myocytes. Most recently it has become clear that heart failure is also an inflammatory condition, with evidence of cytokine activation. Work is underway to establish a role for treatment of this part of the condition. Current drug treatment has been successful in blocking many of the maladaptive aspects of neuro-hormonal stimulation. Many of these treatments have become established after benefits have been ascertained in large randomised controlled trials. These trials have also led to the abandoning of certain drugs (often those that increase cardiac performance) that were shown to have a detrimental effect on survival (e.g. Milrinone). The principles of treatment of heart failure are as follows: 1 Remove the exacerbating factors. 2 Relieve fluid retention. 3 Improve left ventricular function and reduce cardiac work; improve prognosis. 4 Protect against the adverse effects of drug treatment. 5 Assess for further management (e.g. revascularisation, transplant). 6 Manage complications (e.g. arrhythmias). 7 Protect high-risk patients from sudden death.
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