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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)
ECHOCARDIOLOGIST IN GANGAMMA CIRCLE Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia.
THE BEST CARDIOLOGIST IN YELAHANKA Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia. Mitral valve prolapse (systolic-click murmur syndrome) This syndrome can cause a systolic murmur or click, or both, at the apex. The presence of the murmur indicates that there is some mitral regurgitation present. Auscultation: Systolic click or clicks at a variable time (usually mid-systolic) may be the only abnormality audible, but a click is not always audible; systolic
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 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,
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