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Cardiologist in Bettahalasur, Bangalore • Aortic dissection and aneurysms A dissecting haematoma of the aortic root will cause severe chest and back pain but leads to ECG changes only if the coronary ostia are involved. The right coronary ostium is more often affected. Dissection into the coronary ostium usually causes its occlusion and results in an acute myocardial infarction. The diagnosis of dissection cannot be made from the ECG.27 There may, however, be evidence of pre-existing LVH in a high proportion of cases. Haemopericardium (tracking of blood from the dissection into the pericardial sac) is often the terminal event for these patients, but pericarditis-type ST elevation occurs only rarely. Thyroid disease Hyperthyroidism is characterised by a resting sinus tachycardia, sometimes associated with RAA. The QRS complexes and ST segments and T waves are generally unaffected but marked changes may occur, especially in acute exacerbations and ‘thyroid storms’.28 A significant proportion of patients develop AF with a rapid response, increasing with age (as Sinus tachycardia may be so marked as to be mistaken for atrial tachycardia or flutter, with potentially dangerous consequences In myxoedema there may be sinus bradycardia, sometimes with first-degree AV block, but less often than commonly thought (Fig 3.109). The most constant features are a small voltage (regardless of the presence of a pericardial effusion) and T wave flattening or shallow inversion. The QTc is prolonged. Both thyrotoxicosis and hypothyroidism can be induced by one of the most commonly used anti-arrhythmic drugs: amiodarone.29 The QT prolongation in myxoedema is unrelated to amiodarone therapy. Cardiomyopathies No distinctive ECG markers are present in myocardial disease although some patterns may be typical of the conditions in which they occur. An exception is the occurrence of LBBB with RAD in congestive (including ischaemic) cardiomyopathy , a combination not seen
Cardiologist in Bettahalasur, Bangalore • Aortic dissection and aneurysms A dissecting haematoma of the aortic root will cause severe chest and back pain but leads to ECG changes only if the coronary ostia are involved. The right coronary ostium is more often affected. Dissection into the coronary ostium usually causes its occlusion and results in an acute myocardial infarction. The diagnosis of dissection cannot be made from the ECG.27 There may, however, be evidence of pre-existing LVH in a high proportion of cases. Haemopericardium (tracking of blood from the dissection into the pericardial sac) is often the terminal event for these patients, but pericarditis-type ST elevation occurs only rarely. Thyroid disease Hyperthyroidism is characterised by a resting sinus tachycardia, sometimes associated with RAA. The QRS complexes and ST segments and T waves are generally unaffected but marked changes may occur, especially in acute exacerbations and ‘thyroid storms’.28 A significant proportion of patients develop AF with a rapid response, increasing with age (as Sinus tachycardia may be so marked as to be mistaken for atrial tachycardia or flutter, with potentially dangerous consequences In myxoedema there may be sinus bradycardia, sometimes with first-degree AV block, but less often than commonly thought (Fig 3.109). The most constant features are a small voltage (regardless of the presence of a pericardial effusion) and T wave flattening or shallow inversion. The QTc is prolonged. Both thyrotoxicosis and hypothyroidism can be induced by one of the most commonly used anti-arrhythmic drugs: amiodarone.29 The QT prolongation in myxoedema is unrelated to amiodarone therapy. Cardiomyopathies No distinctive ECG markers are present in myocardial disease although some patterns may be typical of the conditions in which they occur. An exception is the occurrence of LBBB with RAD in congestive (including ischaemic) cardiomyopathy , a combination not seen
HEART DOCTORS IN CHIKKAJALA, BANGALORE; Pulmonary hypertension Pulmonary hypertension is an uncommon but important cause of dyspnoea. Many patients with this chronic and often severe illness will have raised pulmonary artery pressures as a result of a cardiac or respiratory illness. Other patients may present with increasing dyspnoea without an obvious cardiac or respiratory problem. Idiopathic (primary) pulmonary hypertension (IPH) is diagnosed only when other causes of pulmonary hypertension have been excluded. By definition, pulmonary hypertension is present when the mean pulmonary artery pressure (PAP) exceeds 25 mmHg at rest or 30 mmHg during exercise. The classification of pulmonary hypertension has been revised. The Venice classification was released in 2003. The term ‘primary pulmonary hypertension’ has been replaced with ‘idiopathic pulmonary hypertension’ . Patients may have used fenfluramine or phenermine (appetite-suppressing drugs), or both. Use of these drugs for long periods has been associated with the greatest risk of developing pulmonary hypertension. In cases of IPH there may be a family history (6%; autosomal dominant condition with incomplete penetrance, 20–80%). The majority of familial cases are associates with a mutation on the BMPR2 gene. There may be associated symptoms including fatigue, chest pain, syncope and oedema. Cough and haemoptysis can be present.
HEART DOCTORS IN BETTAHALASUR, BANGALIREHypertension and pregnancy Hypertension is the most common complication of pregnancy and remains an important cause of maternal and fetal mortality and morbidity. Hypertension in pregnancy can be classified as follows: 1 Chronic: existing hypertension with or without proteinuria. 2 Pre-eclampsia or eclampsia: proteinuria (> 300 mg/day) as well as new hypertension. Note that oedema is no longer part of the definition. 3 Pre-eclampsia in the context of existing hypertension: blood pressure higher than before pregnancy. 4 Gestational hypertension: new hypertension > 140/90 at least twice and after week 20 of pregnancy; no proteinuria. For most patients with existing hypertension the problem is just the blood pressure elevation. Pre-eclampsia, on the other hand, is a serious systemic disorder. It seems related to endothelial dysfunction due to failure of normal placental perfusion and the release of an unknown endothelial toxin. This causes vasospasm, reduced organ perfusion and eventually activation of the coagulation cascade. Superimposed pre-eclampsia occurs in up to 35% of women with pre-existing hypertension. These women are also at risk of abruptio placentae and cerebral haemorrhage. The fetus may also be affected by prematurity and there is an increased risk of still birth. Gestational hypertension does not involve proteinuria and if blood pressure returns to normal within 12 weeks of delivery, it is called
THE BEST CARDIOLOGISTS IN YELAHANKA Pulmonary hypertension Pulmonary hypertension is an uncommon but important cause of dyspnoea. Many patients with this chronic and often severe illness will have raised pulmonary artery pressures as a result of a cardiac or respiratory illness. Other patients may present with increasing dyspnoea without an obvious cardiac or respiratory problem. Idiopathic (primary) pulmonary hypertension (IPH) is diagnosed only when other causes of pulmonary hypertension have been excluded. By definition, pulmonary hypertension is present when the mean pulmonary artery pressure (PAP) exceeds 25 mmHg at rest or 30 mmHg during exercise. The classification of pulmonary hypertension has been revised. The Venice classification was released in 2003. The term ‘primary pulmonary hypertension’ has been replaced with ‘idiopathic pulmonary hypertension’ Patients may have used fenfluramine or phenermine (appetite-suppressing drugs), or both. Use of these drugs for long periods has been associated with the greatest risk of developing pulmonary hypertension. In cases of IPH there may be a family history (6%; autosomal dominant condition with incomplete penetrance, 20–80%). The majority of familial cases are associates with a mutation on the BMPR2 gene. There may be associated symptoms including fatigue, chest pain, syncope and oedema. Cough and haemoptysis can be present. 270 PRACTICAL CARDIOLOGY The examination may help in assessing the severity of the patient’s dyspnoea as he or she undresses. Try to work out the patient’s functional class from the history and examination (p. 256) (NYHA I–IIII, often called the NYHA–WHO class when related to pulmonary hypertension). There may be signs of chronic lung disease or congenital heart disease, or specific signs of pulmonary hypertension and right heart failure (p. 257). Investigations are directed at finding an underlying reason for pulmonary hypertension— idiopathic pulmonary hypertension is a diagnosis of exclusion—and at assessing its severity and potential reversibility. The chest X-ray is abnormal in 90% of IPH patients. It may show pulmonary fibrosis or an abnormal cardiac silhouette—RV dilatation. There may be large proximal pulmonary arteries that appear ‘pruned’ in the periphery, and the heart may appear enlarged because of right ventricle dilatation) Respiratory function tests may show a normal, restrictive or obstructive pattern. Moderate pulmonary hypertension itself is associated with a reduction in the diffusing capacity for the carbon monoxide test (DLCO) to about 50% of predicted. On the ECG look for signs of right heart strain or hypertrophy, which are present in up to 90% of patients The blood gas measurements may show hypercapnia—elevated pCO2 in hypoventilation syndromes—but hypocapnia is more common in IPH because of increased alveolar ventilation. Mild hypoxia (reduction in pO2) may be present in IPH, and is more severe when pulmonary hypertension is secondary to lung disease. On CT pulmonary angiogram (CTPA), ventilation/perfusion (V/Q) lung scan or Doppler venograms look for a deep venous thrombosis (DVT) and PE and assess the extent of involvement of the pulmonary bed. A high-resolution CT scan of the lungs is the best way of looking for interstitial lung disease. The six-minute walking test predicts survival and correlates with the NYHA–WHO class. Reduction in arterial oxygen concentration of more than 10% during this test predicts an almost threefold mortality risk over 29 months. Patients unable to manage 332 m in six minutes also have an adverse prognosis.
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