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PAPULAR CARDIOLOGISTS IN SAHAKARANAGAR Myocardial infarction and ischaemia Recognition of ischaemic changes has gained in importance from the recent increase in percutaneous coronary interventions. It still retains its established importance in other aspects of the management of acute coronary syndromes. Decisions on the immediate treatment of patients with chest pain are made according to findings on the ECG. This is a cheap test that can be performed quickly at the bedside and interpreted without delay
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
CARDIOLOGISTS IN BANGALORE Arrhythmias during pregnancy Women with congenital heart disease are at increased risk of supraventricular arrhythmias during pregnancy. Anti-arrhythmic drug treatment may be necessary for recurrent episodes. Digoxin may be useful for the control of heart rate but is often not effective. Beta-blockers and verapamil have been used for these patients and appear to be free of teratogenic effects.27 Amiodarone is a more effective anti-arrhythmic drug than these but should be reserved for intractable cases and used at the lowest useful dose.28 Sustained tachycardias (atrial flutter is the most common) are not well tolerated in pregnancy and DC cardioversion should be performed without delay for these patients.
THE BEST DIABETIC CENTERS IN YELAHANKA NEW TOWN BANGALORE Treatment of dyslipidaemia The important components of a treatment program for dyslipidaemia are as follows: 1 calculate the patient’s total risk 2 reduce the patient’s weight (reduces triglycerides, cholesterol) 3 increase the patient’s exercise activity (increases HDL, aids weight management) 4 modify the patient’s diet, as follows: • ensure maximum of 30% kJ from fat • ensure maximum of 30% fat as saturated fat • increase plant and fish sources of fat • increase anti-oxidant nutrients from food • reduce alcohol intake if triglyceride level or blood pressure is high 5 treat secondary causes (drugs, diabetes, hypothyroidism) 6 modify other risk factors (e.g. smoking) to reduce overall risk 7 consider drug treatment. By ranking patients according to their risk of future coronary events it is possible to tailor treatment (especially drug treatment) appropriately. This is the basis for the current recommendations for lipid management in the Pharmaceutical Benefits Schedule. This rather complicated schedule tries to take into account the importance of combinations of risk factors . Drug treatment should be delayed in most patients without existing coronary disease until after six weeks to three months of dietary and lifestyle intervention, with the possible exception of those at very high risk. At present, the following drugs are used in the treatment of dyslipidaemia: n statins (HMGcoA reductase inhibitors) n absorption inhibitors n resins
HEART SPECIALISTS IN GANGAMMA CIRCLE BANGALORE Assessment of patients with hypertension A patient with definite or possible newly diagnosed hypertension needs at least a basic clinical assessment to look for possible aetiology, severity and signs of complications. The history Questioning should be directed towards the following areas. 1 Past history. Has hypertension been diagnosed before? What treatment was instituted? Why was it stopped? 2 Secondary causes. Important questions relate to: • a history of renal disease in the patient or his or her family, recurrent urinary tract infec-­ tions, heavy analgesic use or conditions leading to renal disease (e.g. systemic lupus erythematosus (SLE)) • symptoms suggesting phaeochromocytoma (flushing, sweats, palpitations) • symptoms suggesting sleep apnoea • muscle weakness suggesting the hypokalaemia of hyperaldosteronism • Cushing’s syndrome (weight gain, skin changes) • family history of hypertension. 3 Aggravating factors: • high salt intake • high alcohol intake • lack of exercise • use of medications: NSAIDs, appetite suppressants, nasal decongestants, monoamine oxidase inhibitors, ergotamine, cyclosporin, oestrogen-containing contraceptive pills • other: use of cocaine, liquorice, amphetamines. 4 Target organ damage: • stroke or transient ischaemic attack (TIA) • angina, dyspnoea • fatigue, oliguria • visual disturbance • claudication. 5 Coexisting risk factors: • smoking • diabetes • lipid levels, if known • existing vascular disease • family history of ischaemic heart disease. 2• HYPERTENSION 6 Factors affecting choice of treatment: • diabetes (problems with thiazides and beta-blockers) • gout (problems with thiazides) • asthma (problems with beta-blockers) • heart failure (problems with verapamil, diltiazem, some beta-blockers, monoxidine) • severe peripheral arterial disease (problems with beta-blockers) • bradycardia or heart block (problems with beta-blockers, verapamil, diltiazem) • renovascular disease (problems with ACE inhibitors, angiotensin receptor antagonists (ARAs)) • problems with previous anti-hypertensive agents • allergies • likelihood of pregnancy (ACE inhibitors, diuretics and some calcium antagonists are contraindicated). The examination The physical examination should be undertaken with a view to establishing severity. 1 Measure the blood pressure. 2 Look for secondary causes. • Check the appearance for Cushing’s syndrome (central obesity, striae, muscle wasting), acromegaly, polycythaemia and uraemia. • Undertake abdominal palpation for renal masses (polycystic kidneys), occasionally adrenal mass, and auscultation for renal bruit (heard to the left or right of the mid-line above the umbilicus, often into the flanks). • Assess radiofemoral pulse delay and listen for mid
the best cardiologists in yelahanka new town bangalore Miscellaneous conditions Chamber hypertrophy 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 for 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. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
the best cardiologists in yelahanka new town bangalore Miscellaneous conditions Chamber hypertrophy 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 for 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. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
heart doctors in Kattigenahalli, Bangalore • Impulse conduction Sinoatrial block Some instances of apparent sinus bradycardia are due to sinoatrial (SA) block; this can be ascertained only by observing variations in conduction ratios or characteristic periodicity, The sinoatrial node beats (yes, beats) continuously, 7 but some impulses are blocked from entering the atria. The pauses are often termed ‘sinoatrial block’ or ‘sinus arrest’; it is probably permissible to call them ‘sinus pauses’ for convenience. The upper strip shows typical Wenckebach (see below) grouping, with slight acceleration in the last two groups prior to pauses that themselves are shorter than two sinus cycles. The most likely interpretation is 3:2 and 4:3 SA exit block in this patient with known sick sinus syndrome . The lower strip, taken later, shows only sinus arrhythmia (waxing and waning of the sinus rate with respiration—a normal occurrence). Interatrial block The term LAA, of which abnormal interatrial conduction (block) is a major cause, has replaced the more elegant term P mitrale because mitral valve disease is only one cause of the condition. The P wave is prolonged to or beyond 0.10 seconds and is often notched ); the significant notching should have an inter-peak distance of at least 1 mm (0.04 seconds). It is thought to represent a lesion in Bachman’s bundle, the interatrial tract. Atrioventricular blocks Atrioventricular (AV) blocks delay (first-degree) or prevent some (second-degree) or all (third-degree) of the supraventricular impulses from reaching the ventricles. The blocks may be congenital or acquired, transient or permanent. The most clinically useful classification is based on their anatomical cause and their ECG manifestations. This classification also helps in
heart doctors in Kattigenahalli, Bangalore • Impulse conduction Sinoatrial block Some instances of apparent sinus bradycardia are due to sinoatrial (SA) block; this can be ascertained only by observing variations in conduction ratios or characteristic periodicity, The sinoatrial node beats (yes, beats) continuously, 7 but some impulses are blocked from entering the atria. The pauses are often termed ‘sinoatrial block’ or ‘sinus arrest’; it is probably permissible to call them ‘sinus pauses’ for convenience. The upper strip shows typical Wenckebach (see below) grouping, with slight acceleration in the last two groups prior to pauses that themselves are shorter than two sinus cycles. The most likely interpretation is 3:2 and 4:3 SA exit block in this patient with known sick sinus syndrome . The lower strip, taken later, shows only sinus arrhythmia (waxing and waning of the sinus rate with respiration—a normal occurrence). Interatrial block The term LAA, of which abnormal interatrial conduction (block) is a major cause, has replaced the more elegant term P mitrale because mitral valve disease is only one cause of the condition. The P wave is prolonged to or beyond 0.10 seconds and is often notched ); the significant notching should have an inter-peak distance of at least 1 mm (0.04 seconds). It is thought to represent a lesion in Bachman’s bundle, the interatrial tract. Atrioventricular blocks Atrioventricular (AV) blocks delay (first-degree) or prevent some (second-degree) or all (third-degree) of the supraventricular impulses from reaching the ventricles. The blocks may be congenital or acquired, transient or permanent. The most clinically useful classification is based on their anatomical cause and their ECG manifestations. This classification also helps in
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