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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.
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.
CARDIOLOGY DOCTORS IN HOSUR ROAD Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours.
THE HEARTDOCTORS IN BANGALORE Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours. 7
CARDIOLOGISTS IN H S R LAYOUT BANGALORE Cyanotic congenital heart disease Some of the more common cyanotic lesions are discussed below. There are, however, a number of problems common to patients with cyanotic heart disease. 1 Erythrocytosis. Chronic cyanosis causes an increase in red cell numbers as a way of increasing oxygen carrying capacity. The platelet count is sometimes reduced and the white cell count normal. The increased blood viscosity associated with the high red cell mass causes a slight increase in the risk of stroke.37 Most patients have a stable elevated haemoglobin level, but venesection is recommended if this is greater than 20 g/dL and the haematocrit is greater than 65%. Levels as high as this can be associated with the hyperviscosity syndrome: headache, fatigue and difficulty concentrating. Recurrent venesection can cause iron depletion and the production of microcytic red cells, which are stiffer than normal cells and so increase viscosity further. 2 Bleeding. Reduced platelet numbers, abnormal platelet function and clotting factor deficiencies mean these patients have an increased risk of haemorrhage. The most dangerous problem is pulmonary haemorrhage but bleeding from the gums and menorrhagia are more common. The use of anticoagulation must be restricted to those with a strong indication for treatment. 3 Gallstones. Chronic cyanosis and increased haem turnover are associated with an increased incidence of pigment gallstones. 4 Renal dysfunction and gout. Congestion of the renal glomeruli is associated with a reduced glomerular filtration rate and proteinuria. This and the increased turnover of red cells lead to urate accumulation and gout. 5 Pulmonary hypertension. Lesions associated with increased flow through the pulmonary circulation (e.g. a large atrial septal defect) can lead to a reactive rise in pulmonary arterial resistance. This is more likely to occur if the left to right shunt is large. Eventually these pulmonary vascular changes become irreversible, pulmonary pressures equal or exceed systemic pressures, and central cyanosis occurs because the intra-cardiac shunt reverses (Eisenmenger’s syndrome). Flow is now from right to left. There is then no benefit in attempting to correct the underlying cardiac abnormality. Earlier and more successful treatment of children with congenital heart disease has reduced the number of patients with this inexorable disease. Careful management of these conditions can nevertheless improve patients’ symptoms and survival. Reasonable exercise tolerance is usually maintained into adult life for most patients but progressive deterioration then occurs. Haemorrhagic complications, especially haemoptysis, are common. Thrombotic stroke, cerebral abscess and pulmonary infarction can also occur. 364 PRACTICAL CARDIOLOGY In a recent European survey, survival for patients with simple defects and Eisenmenger’s was to 32.5 years, but only 25.8 years for those with Eisenmenger’s resulting from complex abnormalities.38 There is a 50% maternal mortality risk with pregnancy. Quite minor surgical procedures are associated with high risk. Trials with endothelin antagonists are being conducted and continuous oxygen treatment can provide symptomatic relief. Lung and heart lung transplant should be considered for some of these patients. 6 Endocarditis. Most patients with congenital heart disease have a lifelong risk of infective endocarditis. Constant reminders of this risk should be given to the patients and their usual doctors. As well as appropriate antibiotic prophylaxis . before procedures, a high index of suspicion is very important. A febrile illness should not be treated with antibiotics until at least two sets of blood cultures have been taken. Early referral
heart doctors in Kattigenahalli, Bangalore • Atrial tachycardia The diagnosis of atrial tachycardia is based on the presence of P waves different from sinus P waves and from retrograde junctional ones; if the P waves are identical to sinus ones, it is called sinoatrial tachycardia. Most atrial tachycardias represent autonomous focal discharge rather than re-entry. The onset of AV block (as a result of drug treatment or carotid sinus massage) will reduce the ventricular rate without affecting the atrial rate Atrial tachycardia with block Atrial tachycardia with block (paroxysmal atrial tachycardia (PAT) with block) is also an autonomous (automatic, ectopic) atrial tachycardia but its P waves are usually smaller (often discernible only in lead V1) and faster. As a result of this high rate, AV block—mostly 2:1, but often variable—is usually present prior to any exposure to drugs or vagal manoeuvres . In the past this was one of the classic manifestations of digoxin toxicity. It can be difficult to distinguish from other atrial rhythms such as AF, flutter and even sinus rhythm ). Multifocal atrial tachycardia At rates below 100/minute multifocal atrial tachycardia (MAT) is called chaotic atrial rhythm. Although it is traditionally associated with hypoxaemic respiratory failure, it can complicate any advanced cardiac disease. The criteria distinguishing MAT from multiple SVEBs are: There are at least three different P wave morphologies visible in the same lead. There is no dominant single pacemaker. The rate and PR intervals are variable. There is no significant AV block (Fig 3.30).
heart doctors in Kattigenahalli, Bangalore • Atrial tachycardia The diagnosis of atrial tachycardia is based on the presence of P waves different from sinus P waves and from retrograde junctional ones; if the P waves are identical to sinus ones, it is called sinoatrial tachycardia. Most atrial tachycardias represent autonomous focal discharge rather than re-entry. The onset of AV block (as a result of drug treatment or carotid sinus massage) will reduce the ventricular rate without affecting the atrial rate Atrial tachycardia with block Atrial tachycardia with block (paroxysmal atrial tachycardia (PAT) with block) is also an autonomous (automatic, ectopic) atrial tachycardia but its P waves are usually smaller (often discernible only in lead V1) and faster. As a result of this high rate, AV block—mostly 2:1, but often variable—is usually present prior to any exposure to drugs or vagal manoeuvres . In the past this was one of the classic manifestations of digoxin toxicity. It can be difficult to distinguish from other atrial rhythms such as AF, flutter and even sinus rhythm ). Multifocal atrial tachycardia At rates below 100/minute multifocal atrial tachycardia (MAT) is called chaotic atrial rhythm. Although it is traditionally associated with hypoxaemic respiratory failure, it can complicate any advanced cardiac disease. The criteria distinguishing MAT from multiple SVEBs are: There are at least three different P wave morphologies visible in the same lead. There is no dominant single pacemaker. The rate and PR intervals are variable. There is no significant AV block (Fig 3.30).
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.
Cardiologist in Bettahalasur, Bangalore • Causes of dyspnoea Cardiac Left ventricular failure (ischaemia, cardiomyopathy, valvular disease) Angina Mitral valve disease Tachyarrhythmia Pericardial effusion or constrictive pericarditis Intra-cardiac shunting (e.g. atrial septal defect) Non-cardiac Respiratory Airways disease (asthma, COPD, bronchiectasis) Parenchymal disease (pneumonia, pulmonary fibrosis, pneumoconiosis, pneumothorax, infiltrating carcinoma) Pulmonary circulation (pulmonary embolism, pulmonary hypertension) Chest wall and pleura (effusion, pleural tumour, fractured ribs, kyphoscoliosis) Anaemia Other Psychogenic Obesity and lack of physical fitness Acidosis (
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