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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.
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.
PAPULAR CARDIOLOGISTS IN HEBBALA 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.
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 BEST CARDIOLOGISTS IN YELAHANKA Aortic regurgitation The incompetent aortic valve allows regurgitation of blood from the aorta to the left ventricle during diastole for as long as the aortic diastolic pressure exceeds the left ventricular diastolic pressure. Symptoms: Occur in the late stages of disease and include exertional dyspnoea, fatigue, palpitations (hyperdynamic circulation) and exertional angina. General signs: Marfan’s syndrome may be obvious. The pulse and blood pressure: The pulse is characteristically collapsing; there may be a wide pulse pressure. The neck: Prominent carotid pulsations (Corrigan’s sign). Palpation: The apex beat is characteristically displaced and hyperkinetic. A diastolic thrill may be felt at the left sternal edge when the patient sits up and breathes out. Auscultation): A2 (the aortic component of the second heart sound) may be soft; a decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and extending for a variable time into diastole—it is loudest at the third and fourth left intercostal spaces; a systolic ejection murmur is usually present (due to associated aortic stenosis or to torrential flow across a normal diameter aortic valve). Signs indicating severe chronic aortic regurgitation: Collapsing pulse; wide pulse pressure; long decrescendo diastolic murmur; left ventricular S3 (third heart sound); soft A2; signs of left ventricular failure. Causes of chronic aortic regurgitation: (i) Rheumatic (rarely the only murmur in this case), congenital; (ii) aortic root dilatation—Marfan’s syndrome, dissecting aneurysm. 8• THE PATIENT WITH A MURMUR 305 a b Valve cusps often thickened and calcified Left ventricle may be hypertrophied Ascending aorta may be dilated Systole Diastole S1 A2 P2 S1 Ejection click (Suggests congenital AS) Normal Mild S1 S1 Moderate S1 P2 A2 S1 Severe Reversed S2 Single (S2)
HEART DOCTORS IN YELAHANKA NEWTOWN, BANGALORE Management of ACS (NSTEACS) Patients with this diagnosis represent a rather heterogeneous group. Some have had the recent onset of angina at the extremes of exercise, others have angina at rest associated with ECG changes. This variation has made attempts to study the effects of different treatment rather difficult. Although the majority of patients with myocardial infarction have a preceding period of unstable angina, only about 5% of all patients admitted to hospital with a diagnosis of an ACS go on to infarct during that admission. The in-hospital mortality for these patients is low. Mortality rates of less than 2% are usual. Nevertheless, there is a real short-term and longerterm risk of infarction, recurrent admission with unstable symptoms and death which is higher than that of patients with stable angina. The diagnosis should therefore lead to admission to a CCU. The cardiac enzymes are, by definition, not elevated in these patients but the newer, more sensitive tests for troponin T and troponin I may be abnormal and indicate a worse prognosis . In the CCU, bed rest, oxygen and ECG monitoring are routinely enforced and any mobile phones taken away (allegedly to protect the monitoring equipment). Recurrence of chest pain can be assessed quickly and ECGs performed to look for changes suggesting infarction. The cardiac biomarkers can be checked regularly. All patients should receive aspirin (300 mg) unless there is a contraindication. Patients with an intermediate or a higher risk should also be given clopidogrel (usually a 300–600 mg loading dose). The use of intravenous heparin has become standard treatment. A typical starting dose is 5000 units as a bolus followed by 24, 000 units over 24 hours. The activated partial thromboplastin time (APPT) should be measured after about six hours of treatment and the infusion rate of heparin adjusted to maintain this at about twice normal. Heparin is generally safe when used in this way. Bleeding problems may sometimes occur and the platelet count should be checked every few days so that heparin-induced thrombocytopenia (HITS), a rare but serious complication, can be detected early. Low molecular weight heparins are at least as effective as unfractionated heparin. These drugs have some advantages over heparin. Their dose response effect is more predictable and they cause less thrombocytopenia. They are effective given subcutaneously without APPT monitoring and are now cheaper than IV heparin when savings on APPT monitoring and the use of infusion sets are considered. A standard twice-daily dose is given according to the patient’s weight—1 mg/kg for enoxaparin (Clexane). The dose is reduced by half for those with moderate or severe renal impairment and for those over the age of 75. Additional treatment should include beta-blockers unless these are contraindicated. These drugs reduce the number of ischaemic episodes and probably the risk of myocardial infarction. Nitrates can be a useful adjunctive treatment. They may be given orally, topically or intravenously. The IV dose can be titrated up or down depending on the amount of pain the patient is experiencing and the severity of side effects such as hypotension and headache. The problem of tachyphylaxis with nitrates can be overcome by steady increases in the IV dose if necessary. Calcium antagonists are appropriate treatment for patients intolerant of beta-blockers and may sometimes be added to beta-blockers. Nifedipine, especially in its short-acting form, should not be used for patients with acute coronary syndromes unless they are already taking beta-blockers. Thrombolytic drugs have been disappointing when used for NSTEACS. In trials where they have been used for patients with ischaemic chest pain but without ST elevation there has been a trend towards an adverse outcome. This may be related to the rebound hypercoagulable state that can occur after their use. In general they should not be used for the treatment of NSTEACS. Glycoprotein IIb/IIIa inhibitors (p. 198) should be given for high-risk patients,
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 DEVARABESANAHALLI BANGALORE Complex congenital heart disease: Fontan repair Anatomy and physiology Babies with a single ventricle or equivalent defect are often treated during childhood with a palliative operation to connect venous return directly to the pulmonary arteries—a Fontan repair. The prognosis is usually good: 75% of these patients survive at least 20 years. Complications Problems develop because of failure of the systemic ventricle, obstruction of the venous to pulmonary connection, atrial enlargement and AV valve regurgitation. Atrial arrhythmias become increasingly common. Sinus node dysfunction may necessitate pacing, which requires an epicardial electrode in most cases. Follow-up Echocardiography allows assessment of ventricular function and the AV valve. Obstruction in the Fontan connections can be examined with Doppler. MRI is increasingly useful for this assessment. Treatment Severe AV valve regurgitation, cyanosis and ventricular dysfunction are indications for intervention, including transplant or revision of the Fontan. Atrial arrhythmias can be treated with radiofrequency ablation. Pregnancy and contraception Pregnancy is possible in some patients with excellent Fontan function, good LV function and minimal AV valve regurgitation. Maternal risk is high if the Fontan is failing. There may be problems with the need to withdraw ACE inhibitors and with anticoagulation.
HEART SPECIALISTS IN YELAHANKA NEW TOWN BANGALORE Mitral stenosis Rheumatic mitral stenosis is rare in developed countries but is an important cause of maternal and fetal morbidity and mortality in many parts of the world. Mitral stenosis is often poorly tolerated because of the shortened diastolic filling period that occurs during pregnancy. A mitral valve area of less than 1.5 cm2) means a considerable risk to the mother of pulmonary oedema as pregnancy proceeds. Even previously asymptomatic patients are at risk. Close follow-up and regular echocardiograms are indicated. Treatment to slow the heart and increase the length of diastole (beta-blockers) should be commenced if symptoms (dyspnoea) appear or the Doppler echo measurement of pulmonary artery pressure exceeds 50 mmHg Diuretics may improve symptoms but for severe stenosis balloon valvotomy can be performed during pregnancy.30 There are risks to the mother and fetus associated with the procedure, which should be performed only at an experienced centre and only for severe stenosis. Aortic stenosis Delivery is usually well tolerated by women with aortic stenosis unless they are very symptomatic. If heart failure has developed, balloon valvotomy of the valve is safer than surgical replacement. The procedure provides temporary relief of symptoms. Mechanical prosthetic valves and pregnancy
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