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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.
SAMIKSHA HEART AND DIABETIC CARE ''CONNECTIVE TISSUE DISORDERS'' ''Marfan Syndrome'' Marfan syndrome is a systemic connective tissue disorder with a frequency of 2 to 3 in 10, 000. The disorder is characterized by manifestations involving the cardiovascular, skeletal, and ocular systems. Current diagnostic criteria are based on involvement of above organ systems and family history. Cardiovascular manifestations include mitral valve prolapse, progressive aortic root enlargement, and ascending aortic aneurisms, possibly leading to aortic regurgitation, dissection, or rupture. Some characteristic skeletal manifestations of this syndrome include disproportional increase of linear bone growth resulting in malformations of the digits (arachnodactyly), craniofacial abnormalities, pectus excavatum/carinatum, and scoliosis. A common ocular involvement is severe myopia and lens dislocation in one or both eyes (ectopia lentis). Marfan syndrome is an autosomal dominant disorder caused by fibrillin-1 gene mutations encoding for the extracellular matrix protein fibrillin (Fbn-1). Fibrillin is an integral component of both elastic and nonelastic connective tissue. The mechanism of fibrillin mutation in Marfan syndrome remains unclear. However, animal models of Fbn-1 have demonstrated a role of TGF-beta signaling. In some patients with phenotypes similar to Marfan syndrome but without fibrillin- 1 gene mutations, TGF-beta receptor mutations have been identified, suggesting a significant role of TGF-beta pathway in the pathogenesis of Marfan syndrome features. Aortic root involvement remains the leading cause of death in patients with Marfan syndrome. Echocardiography is recommended to routinely screen and to follow aortic root dilation. In addition, all first-degree relatives of the family should have screening echocardiography. Patients should be advised against strenuous exercises. Medical therapy for Marfan syndrome includes beta-blockers to reduce myocardial contractility and pulse pressure. Animal models of Marfan syndrome have demonstrated a possible benefit of losartan in preventing progression of the disease by inhibiting the TGF-beta pathway, and this therapy is the subject of an active clinical trial. Elective aortic root replacement remains the therapy of choice once the aortic root becomes significantly enlarged. Marfan patients who become pregnant need to be counseled not only about the 50% chance of transmitting the disease but also the substantially increased risk of aortic rupture/dissection during and after pregnancy. Important components of Marfan syndrome counseling are consideration of contraception and pregnancy management. Loeys-Dietz Syndrome Recently, an aortic aneurysm syndrome has been identified with TGF-beta receptor mutations. Loeys-Dietz syndrome is an autosomal dominant condition with a characteristic triad of arterial tortuosity/aneurysm, hypertelorism, and bifid uvula or cleft palate. There is significant overlap with Marfan syndrome, and the management is similar in terms of cardiovascular manifestation. Early, elective, surgical intervention should be considered in patients with significant aneurysmal dilation of the aorta. Some clinicians have argued for much earlier surgical intervention for the dilated aorta in this condition, compared with Marfan syndrome, since there appears to be a much greater risk of rupture and dissection at earlier ages and smaller aortic sizes. Pregnancy counseling is also an integral part of therapy. Ehlers-Danlos Syndrome Ehlers-Danlos syndrome is a group of disorders that affect connective tissue development due to defects in collagen and connective tissue biosynthesis. Prevalence of the disease is about 1 in 400, 000 people in the United States. Cardiac manifestations include spontaneous rupture of medium to large sized arteries including the aorta. Frequently, extracardiac presentations include hyperextensible skin and hypermobile joints. To date, 11 types of the disorder have been recognized, but collagen defects have been described in only 6 types. Although all types of Ehlers-Danlos syndrome affect the joints and the skin, clinical features vary by type. Different features characterize each type of the syndrome. Type IV carries the poorest prognosis, especially due to spontaneous ruptures of arteries and organs. Extreme caution needs to be taken if surgical intervention is needed due to weakened connective tissue structures. Many genes, including ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2, PLOD1, and TNXB, have been implicated in the pathogenesis of Ehlers- Danlos syndrome, but the predominant cardiovascular concern exists in the Type IV vascular form of Ehlers-Danlos associated with mutations in the COL3A1 gene and aortic dilation/aneurysms. Other less commonly associated anomalies include ventricular septal defect, patent ductus arteriosus, bicuspid pulmonic valve, and Ebstein’s anomaly. Bicuspid aortic valve has been shown to demonstrate familial clustering. However, identifying culprit genes have been difficult due to variable penetrance and the common nature of the disorder.
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.
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