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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 Cardiologist in yelahanka New Town, Bangalore • 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. 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 115 10 Increased QRS voltages suggest LVH if: • the height of the S wave in V1 added to the R wave in V5 or V6 is greater than 35 mm (SV1 + RV5 or RV6 > 35 mm) or • any R + S wave height in the V leads is greater than 45 mm or • the R wave in aVL (RaVL) is greater than 13 mm or • the R wave in L2 (R2) is greater than 15 mm. If the ST segment and T wave are affected, it is reported as LVH with ST/T changes or strain pattern. In RVH, the R wave is larger than the S wave in V1. 11 Look for ST depression or elevation. ST depression may reflect strain pattern rather than ischaemia, and ST elevation may be due to early repolarisation or pericarditis rather than infarction.
Popular Cardiologist in yelahanka New Town, Bangalore • 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. 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 115 10 Increased QRS voltages suggest LVH if: • the height of the S wave in V1 added to the R wave in V5 or V6 is greater than 35 mm (SV1 + RV5 or RV6 > 35 mm) or • any R + S wave height in the V leads is greater than 45 mm or • the R wave in aVL (RaVL) is greater than 13 mm or • the R wave in L2 (R2) is greater than 15 mm. If the ST segment and T wave are affected, it is reported as LVH with ST/T changes or strain pattern. In RVH, the R wave is larger than the S wave in V1. 11 Look for ST depression or elevation. ST depression may reflect strain pattern rather than ischaemia, and ST elevation may be due to early repolarisation or pericarditis rather than infarction.
THE BEST CARDIOLOGIST IN HEBBALA Hypertension as a risk factor Hypertension is a risk factor for coronary disease, but even more so for cerebrovascular disease and left ventricular failure.1 Control of blood pressure reduces this risk. Large randomised trials have shown that every 10–14 mmHg reduction in systolic and 5 mmHg reduction in diastolic blood pressure confers a 29% reduction in CHD risk and a 40% reduction in stroke risk. The risk of a coronary event in a man with blood pressure greater than 160/95 is five times the risk in a man with blood pressure of 140/90 or less. Hypertension can be diagnosed only by blood pressure measurements. There is little evidence that high blood pressure causes symptoms, except for malignant hypertension with cerebral oedema. The symptoms often ascribed to hypertension—epistaxis, dizziness, headache and fainting—are no more common in hypertensives than in normotensives. Anxiety (often about the blood pressure) and hyperventilation may explain some of these symptoms.2 The trials providing the above figures have been carried out using diuretics or beta-­blockers in the treatment of hypertension. Because these drugs may adversely affect lipid profiles and therefore coronary risk, it has been suggested that newer agents may produce a greater reduction in the risk of CHD events. However, this has not been proven. There is evidence from metaanalyses of blood pressure lowering trials that beta-blockers are less protective against stroke than other agents. They are more effective than placebo in providing protection against stroke. The reduction in blood pressure that is achieved is still more important than the choice of drug. The trials have shown that blood pressure reduction in the elderly, including those over the age of 80, is associated with reduced cardiovascular morbidity but not all-cause (overall) mortality. Treatment of isolated systolic hypertension, common in the elderly, has also shown benefit in terms of the reduced risk of stroke, cardiac failure and coronary disease.3 As in the case of other risk factors, the greatest absolute benefit in the treatment of hyper-­ tension is gained in those patients with existing heart disease, diabetes or multiple risk factors. Blood pressure is an important component of the total risk score . The effects of hypertension Cardiovascular Sustained hypertension results in increased left ventricular wall thickness (left ventricular hypertro-­ phy, LVH) and may ultimately lead to left ventricular dilatation and cardiac failure. LVH results in higher oxygen demands by the ventricle, making angina more likely. The mechanism by which hypertension is thought to increase CHD risk is mechanical damage to the endothelium, leading to increased permeability and therefore increased atherogenesis. Elevated blood pressure interacts with other hereditary and acquired risk factors, all of which are associated with endothelial dysfunction; some are probably implicated in the genesis of hypertension in the first place.4 Neurological Hypertension
GOOD AND WELL CARDIOLOGISTS IN SILKBOARD BANGALORE Hypertension as a risk factor Hypertension is a risk factor for coronary disease, but even more so for cerebrovascular disease and left ventricular failure.1 Control of blood pressure reduces this risk. Large randomised trials have shown that every 10–14 mmHg reduction in systolic and 5 mmHg reduction in diastolic blood pressure confers a 29% reduction in CHD risk and a 40% reduction in stroke risk. The risk of a coronary event in a man with blood pressure greater than 160/95 is five times the risk in a man with blood pressure of 140/90 or less. Hypertension can be diagnosed only by blood pressure measurements. There is little evidence that high blood pressure causes symptoms, except for malignant hypertension with cerebral oedema. The symptoms often ascribed to hypertension—epistaxis, dizziness, headache and fainting—are no more common in hypertensives than in normotensives. Anxiety (often about the blood pressure) and hyperventilation may explain some of these symptoms.2 The trials providing the above figures have been carried out using diuretics or beta-­blockers in the treatment of hypertension. Because these drugs may adversely affect lipid profiles and therefore coronary risk, it has been suggested that newer agents may produce a greater reduction in the risk of CHD events. However, this has not been proven. There is evidence from metaanalyses of blood pressure lowering trials that beta-blockers are less protective against stroke than other agents. They are more effective than placebo in providing protection against stroke. The reduction in blood pressure that is achieved is still more important than the choice of drug. The trials have shown that blood pressure reduction in the elderly, including those over the age of 80, is associated with reduced cardiovascular morbidity but not all-cause (overall) mortality. Treatment of isolated systolic hypertension, common in the elderly, has also shown benefit in terms of the reduced risk of stroke, cardiac failure and coronary disease.3 As in the case of other risk factors, the greatest absolute benefit in the treatment of hyper-­ tension is gained in those patients with existing heart disease, diabetes or multiple risk
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