http://WWW.HEARTDIABETESCARE.COM
SAMIKSHAHEARTCARE 57698d5b9ec66b0b6cfb5b6b False 536 1
OK
background image not found
Found Update results for
'broad giant inversion'
5
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
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
heart Doctor in Sahakaranagar Cor pulmonale Cor pulmonale is simply heart disease secondary to lung disease. In a sense, the example in is cor pulmonale too: RVH (heart disease) from pulmonary hypertension (lung disease) from mitral stenosis (heart disease again). The term tends to be used mostly for heart disease due to primary lung disease, which may be vascular or parenchymal. It is often described as acute or chronic, but the distinction is more clinical than electrocardiographic. shows an ECG taken on the ward for a patient with stable COPD, yet the V1 morphology shows acute right ventricular ‘strain’. A 61-year-old man with ‘cardiac asthma’ due to mitral stenosis. His LAA is a real P mitrale. He had proven RVH from pulmonary hypertension and eventually came to mitral valve replacement. The frontal plane axis is about +160°, but should perhaps be best described as indeterminate, with all six leads more or less equiphasic. A 76-year-old woman with obvious cor pulmonale with RVH of uncertain age. The lack of sinus tachycardia suggests that it is chronic, but the patient may have chronotropic incompetence (the sinus node is diseased and unable to increase its rate when required). RAA is diagnosed because the P wave axis is +78° and there is a qR complex in V1, even though the actual P wave looks like LAA. The QRS LAD (–60°) is due to the position of the heart rather than to LAHB. The S wave in L2 is larger than the S wave in L3, which is the opposite to what is seen in LAHB and is typical of COPD. This hypotensive, hypoxic and breathless 39-year-old man had extensive thrombophlebitis and a clear chest X-ray. He would easily have been diagnosed with pulmonary embolism even without the typical ECG shown. The pattern can be caused by any acute respiratory failure and the clinical context remains paramount. Note the superficial resemblance to acute inferior myocardial infarction, including the slight ST elevation in L3. However, there are no reciprocal changes and L2 shows ST depression, partly produced by a marked shift of the atrial repolarisation often seen in sinus tachycardia of this magnitude. The same patient in a day later. The original S1Q3T3 pattern has almost resolved. The right precordial T inversion implies extensive embolism, but this was obvious from the patient’s clinical course. The clinical picture also rules out anteroseptal ischaemia as the cause of the ECG changes. The prototype acute cor pulmonale is pulmonary embolism that classically produces the S1Q3T3 (McGinn-White) pattern—a deep S wave in L1, and Q wave and T wave inversion in L3—followed by right precordial T wave inversion ). Electrocardiographically, cor pulmonale is quite pleomorphic. As expected, the effects are mostly right-sided (new or chronic RAA, RBBB, rightward axis shift), but the coexistence of hypoxaemia and acidosis may cause left ventricular ST/T changes suggesting severe ischaemia. Massive embolism may cause bradycardia rather than tachycardia. Atrial tachyarrhythmias may impose a haemodynamic burden of their own and mask the ‘causal’ underlying condition.
heart Doctor in Sahakaranagar Cor pulmonale Cor pulmonale is simply heart disease secondary to lung disease. In a sense, the example in is cor pulmonale too: RVH (heart disease) from pulmonary hypertension (lung disease) from mitral stenosis (heart disease again). The term tends to be used mostly for heart disease due to primary lung disease, which may be vascular or parenchymal. It is often described as acute or chronic, but the distinction is more clinical than electrocardiographic. shows an ECG taken on the ward for a patient with stable COPD, yet the V1 morphology shows acute right ventricular ‘strain’. A 61-year-old man with ‘cardiac asthma’ due to mitral stenosis. His LAA is a real P mitrale. He had proven RVH from pulmonary hypertension and eventually came to mitral valve replacement. The frontal plane axis is about +160°, but should perhaps be best described as indeterminate, with all six leads more or less equiphasic. A 76-year-old woman with obvious cor pulmonale with RVH of uncertain age. The lack of sinus tachycardia suggests that it is chronic, but the patient may have chronotropic incompetence (the sinus node is diseased and unable to increase its rate when required). RAA is diagnosed because the P wave axis is +78° and there is a qR complex in V1, even though the actual P wave looks like LAA. The QRS LAD (–60°) is due to the position of the heart rather than to LAHB. The S wave in L2 is larger than the S wave in L3, which is the opposite to what is seen in LAHB and is typical of COPD. This hypotensive, hypoxic and breathless 39-year-old man had extensive thrombophlebitis and a clear chest X-ray. He would easily have been diagnosed with pulmonary embolism even without the typical ECG shown. The pattern can be caused by any acute respiratory failure and the clinical context remains paramount. Note the superficial resemblance to acute inferior myocardial infarction, including the slight ST elevation in L3. However, there are no reciprocal changes and L2 shows ST depression, partly produced by a marked shift of the atrial repolarisation often seen in sinus tachycardia of this magnitude. The same patient in a day later. The original S1Q3T3 pattern has almost resolved. The right precordial T inversion implies extensive embolism, but this was obvious from the patient’s clinical course. The clinical picture also rules out anteroseptal ischaemia as the cause of the ECG changes. The prototype acute cor pulmonale is pulmonary embolism that classically produces the S1Q3T3 (McGinn-White) pattern—a deep S wave in L1, and Q wave and T wave inversion in L3—followed by right precordial T wave inversion ). Electrocardiographically, cor pulmonale is quite pleomorphic. As expected, the effects are mostly right-sided (new or chronic RAA, RBBB, rightward axis shift), but the coexistence of hypoxaemia and acidosis may cause left ventricular ST/T changes suggesting severe ischaemia. Massive embolism may cause bradycardia rather than tachycardia. Atrial tachyarrhythmias may impose a haemodynamic burden of their own and mask the ‘causal’ underlying condition.
1
false