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THE BEST HEART SPECIALIST S IN YELAHANKA ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG . ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation. hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated
CARDIAC CENTERS IN YELAHANKA NEW TOWN BANGALORE ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG . ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation. hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction . A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated U inversion is a specific but insensitive sign of coronary disease. 54 PRACTICAL CARDIOLOGY ECG reports Reports should be short and stereotyped, with the description clearly separated from the comment. It is a good general strategy to under-report, especially for a beginner. It is generally wiser to state ‘inferior Q waves noted’ or ‘non-specific ST/T changes’ than to indulge in speculation on possible or probable infarction or ischaemia. ECG labels tend to have serious employment and insurance implications. On the other hand, specific questions on the request form must be addressed, since they constitute the reason for taking the ECG in the first place.
THE BEST CARDIOLOGISTS IN YELAHANKA NEWTOWN BANGALORE ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation . hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs ) or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated U inversion
Popular Cardiologist in yelahanka New Town, Bangalore• Duke treadmill score Exercise time in minutes n mm ST depression × 5 –n Angina (not limiting) –4 Angina (limiting) –8 Risk 1-year mortality Low risk > 5 0.25% Intermediate risk 4 to –10 1.25% High risk < –11 5.25% For example, a patient who exercised for 5 minutes but stopped because of limiting angina and had 2 mm of ST depression in the leads with maximum changes would have a score of –13 (that is, 5 [exercise time in minutes] – 2 × 5 [mm of ST depression × 5] – 8 [limiting angina] = –13). This represents a high risk of death
Popular Cardiologist in yelahanka New Town, Bangalore• Duke treadmill score Exercise time in minutes n mm ST depression × 5 –n Angina (not limiting) –4 Angina (limiting) –8 Risk 1-year mortality Low risk > 5 0.25% Intermediate risk 4 to –10 1.25% High risk < –11 5.25% For example, a patient who exercised for 5 minutes but stopped because of limiting angina and had 2 mm of ST depression in the leads with maximum changes would have a score of –13 (that is, 5 [exercise time in minutes] – 2 × 5 [mm of ST depression × 5] – 8 [limiting angina] = –13). This represents a high risk of death
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.
Cardiologist in Chikkajala, Bangalore • Electronic pacemakers Pacemakers come as temporary or permanent, fixed-rate (although only if they are faulty these days), demand or rate-responsive, atrial, ventricular, biventricular or dual chamber, unipolar or bipolar and as a combination of many of these features. In routine ECG reporting the pacemaker’s exact programming is not usually known, but it is still possible to diagnose the pacemaker type Acute inferolateral infarction with LBBB. Although ST elevation and depression in the limb leads are suggestive, the more discrete elevation in V6 proves the diagnosis (arrows). Within hours, it disappeared and all that was left were primary T wave changes in the inferior leads ). The same patient as in , showing residual primary T wave changes in the inferior leads 90 PRACTICAL CARDIOLOGY Pathological Q waves in all the LV leads in a 90-year-old man with known old anterior infarction Table 3.1 The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) generic (NBG) pacemaker codes Position I II III IV V Category Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate modulation Anti- tachyarrhythmia function(s) O = none A = atrium V = ventricle D = dual (A + V) O = none A = atrium V = ventricle D = dual (A + V) O = none T = triggered I = inhibited D = dual (D + I) O = none P = simple programmable M = multiprogrammable C = communicating R = rate modulation O = none P = pacing (antitachyarrhythmia) S = shock D = dual (P + S) Manufacturers’ designation only S = single (A or V) S = single (A or V) Note: positions I–III are used exclusively for anti-bradyarrhythmia function. Source: and the all-important capacity to sense the native complexes and pace the appropriate chambers. An international letter code has evolved for describing pacemaker types, shown in Table 3.1. Thus: n VVI = ventricular pacing and sensing, inhibition (in response to sensing)—the pacemaker is inhibited and produces no impulse when it senses a ventricular impulse n AAI = atrial pacing and sensing 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 91 n VOO = fixed-rate (asynchronous) ventricular pacing, no sensing—this is used for pacemaker testing and is the usual response of a pacemaker when a magnet is placed over it; modern pacemakers are always demand (inhibited) devices n DDD = atrial and ventricular (dual) sensing and pacing n DDDR = same as universal (DDD) pacemaker, with rate-responsiveness—the device will change its pacing rate in response to the patient’s physical activity n VDD = ventricular pacing with dual-chamber sensing (through a single lead). The above codes include the implantable cardioverter-defibrillators. ‘Failed pacemaker’ is not a proper or complete diagnosis. Failure may be intermittent or complete and involve sensing or capture (pacing), or both. A few examples are shown in More examples and details of the pacemaker syndrome and arrhythmias 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 QR congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
Popular Cardiologist in Rajanukunte, Bangalore • Coexisting disease and patient risk profile LVH: Choose ACE inhibitors, ARAs, alpha-blockers, beta-blockers, calcium antagonists. Previous acute myocardial infarction (AMI): Choose beta-blockers, ACE inhibitors in left ventricular dysfunction (LVD). Angina: Choose beta-blockers, verapamil, diltiazem. Cardiac failure or LVD: ACE inhibitors (and ARAs) and beta-blockers (carvedilol, bisoprolol and slow-release metoprolol) reduce symptoms and mortality. Monoxi-­ dine is contraindicated. Diuretics reduce symptoms, but loop diuretics (frusemide) are too short-acting to be useful for hypertension. Diabetes: ACE inhibitors and ARAs protect renal function in patients with pro-­ teinuria.16 Aortic stenosis: Vasodilators should be used with caution. Renovascular disease: ACE inhibitors and ARAs are effective but can lead to deterioration of renal function. Potassium and creatinine levels should be monitored. ACE inhibitors and ARAs are contraindicated in bilateral renal artery stenosis, or where there is a single functioning kidney. PVD: Beta-blockers are relatively contraindicated. Stroke: ARAs and low-dose thiazides are more effective for prevention than beta-blockers. Diabetes: Diuretics have an adverse effect on glucose metabolism. ACE inhibitors and ARAs are of value in reducing the development of diabetic nephropathy. Dyslipidaemia: Alpha-blockers have a mild beneficial effect on serum lipids. ACE inhibi-­ tors and calcium antagonists have a neutral effect. Gout: Diuretics inhibit uric acid excretion and are relatively contraindicated. Asthma and chronic obstructive pulmonary disease (COPD): Beta-blockers are usually contraindicated. Depression: Methyldopa, calcium antagonists and clonidine may aggravate.
Cardiologist in Chikkajala, Bangalore • Electronic pacemakers Pacemakers come as temporary or permanent, fixed-rate (although only if they are faulty these days), demand or rate-responsive, atrial, ventricular, biventricular or dual chamber, unipolar or bipolar and as a combination of many of these features. In routine ECG reporting the pacemaker’s exact programming is not usually known, but it is still possible to diagnose the pacemaker type Acute inferolateral infarction with LBBB. Although ST elevation and depression in the limb leads are suggestive, the more discrete elevation in V6 proves the diagnosis (arrows). Within hours, it disappeared and all that was left were primary T wave changes in the inferior leads ). The same patient as in , showing residual primary T wave changes in the inferior leads 90 PRACTICAL CARDIOLOGY Pathological Q waves in all the LV leads in a 90-year-old man with known old anterior infarction Table 3.1 The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) generic (NBG) pacemaker codes Position I II III IV V Category Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate modulation Anti- tachyarrhythmia function(s) O = none A = atrium V = ventricle D = dual (A + V) O = none A = atrium V = ventricle D = dual (A + V) O = none T = triggered I = inhibited D = dual (D + I) O = none P = simple programmable M = multiprogrammable C = communicating R = rate modulation O = none P = pacing (antitachyarrhythmia) S = shock D = dual (P + S) Manufacturers’ designation only S = single (A or V) S = single (A or V) Note: positions I–III are used exclusively for anti-bradyarrhythmia function. Source: and the all-important capacity to sense the native complexes and pace the appropriate chambers. An international letter code has evolved for describing pacemaker types, shown in Table 3.1. Thus: n VVI = ventricular pacing and sensing, inhibition (in response to sensing)—the pacemaker is inhibited and produces no impulse when it senses a ventricular impulse n AAI = atrial pacing and sensing 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 91 n VOO = fixed-rate (asynchronous) ventricular pacing, no sensing—this is used for pacemaker testing and is the usual response of a pacemaker when a magnet is placed over it; modern pacemakers are always demand (inhibited) devices n DDD = atrial and ventricular (dual) sensing and pacing n DDDR = same as universal (DDD) pacemaker, with rate-responsiveness—the device will change its pacing rate in response to the patient’s physical activity n VDD = ventricular pacing with dual-chamber sensing (through a single lead). The above codes include the implantable cardioverter-defibrillators. ‘Failed pacemaker’ is not a proper or complete diagnosis. Failure may be intermittent or complete and involve sensing or capture (pacing), or both. A few examples are shown in More examples and details of the pacemaker syndrome and arrhythmias 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 QR congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
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