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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.
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.
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.
HEART DOCTORS IN YELAHANKA NEWTOWN, BANGALORE Management of ACS (NSTEACS) Patients with this diagnosis represent a rather heterogeneous group. Some have had the recent onset of angina at the extremes of exercise, others have angina at rest associated with ECG changes. This variation has made attempts to study the effects of different treatment rather difficult. Although the majority of patients with myocardial infarction have a preceding period of unstable angina, only about 5% of all patients admitted to hospital with a diagnosis of an ACS go on to infarct during that admission. The in-hospital mortality for these patients is low. Mortality rates of less than 2% are usual. Nevertheless, there is a real short-term and longerterm risk of infarction, recurrent admission with unstable symptoms and death which is higher than that of patients with stable angina. The diagnosis should therefore lead to admission to a CCU. The cardiac enzymes are, by definition, not elevated in these patients but the newer, more sensitive tests for troponin T and troponin I may be abnormal and indicate a worse prognosis . In the CCU, bed rest, oxygen and ECG monitoring are routinely enforced and any mobile phones taken away (allegedly to protect the monitoring equipment). Recurrence of chest pain can be assessed quickly and ECGs performed to look for changes suggesting infarction. The cardiac biomarkers can be checked regularly. All patients should receive aspirin (300 mg) unless there is a contraindication. Patients with an intermediate or a higher risk should also be given clopidogrel (usually a 300–600 mg loading dose). The use of intravenous heparin has become standard treatment. A typical starting dose is 5000 units as a bolus followed by 24, 000 units over 24 hours. The activated partial thromboplastin time (APPT) should be measured after about six hours of treatment and the infusion rate of heparin adjusted to maintain this at about twice normal. Heparin is generally safe when used in this way. Bleeding problems may sometimes occur and the platelet count should be checked every few days so that heparin-induced thrombocytopenia (HITS), a rare but serious complication, can be detected early. Low molecular weight heparins are at least as effective as unfractionated heparin. These drugs have some advantages over heparin. Their dose response effect is more predictable and they cause less thrombocytopenia. They are effective given subcutaneously without APPT monitoring and are now cheaper than IV heparin when savings on APPT monitoring and the use of infusion sets are considered. A standard twice-daily dose is given according to the patient’s weight—1 mg/kg for enoxaparin (Clexane). The dose is reduced by half for those with moderate or severe renal impairment and for those over the age of 75. Additional treatment should include beta-blockers unless these are contraindicated. These drugs reduce the number of ischaemic episodes and probably the risk of myocardial infarction. Nitrates can be a useful adjunctive treatment. They may be given orally, topically or intravenously. The IV dose can be titrated up or down depending on the amount of pain the patient is experiencing and the severity of side effects such as hypotension and headache. The problem of tachyphylaxis with nitrates can be overcome by steady increases in the IV dose if necessary. Calcium antagonists are appropriate treatment for patients intolerant of beta-blockers and may sometimes be added to beta-blockers. Nifedipine, especially in its short-acting form, should not be used for patients with acute coronary syndromes unless they are already taking beta-blockers. Thrombolytic drugs have been disappointing when used for NSTEACS. In trials where they have been used for patients with ischaemic chest pain but without ST elevation there has been a trend towards an adverse outcome. This may be related to the rebound hypercoagulable state that can occur after their use. In general they should not be used for the treatment of NSTEACS. Glycoprotein IIb/IIIa inhibitors (p. 198) should be given for high-risk 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.
cardiologists in yelahanka At our center we conduct echo cardiograms both adult and pediatric, TMT, ECG, PFT, HOLTER, AMBULATORY BP
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 YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
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.