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HEART SPEACIALIST IN BANGALORE HYPERTENTION By definition, sinus tachycardia is a heart rate ≥ 100/minute and sinus bradycardia is a heart rate ≤ 50/minute.3 To calculate the heart rate from the ECG, the R-R interval in mm can be divided into 1500. For example, an R-R interval of 20 mm gives a rate of 75/minute and an R-R interval of 15 mm gives a rate of 100. Similarly, large 5 mm squares can be divided into 300; thus three squares give a rate of 100/minute. In regular rhythms, any two congruous points of the P-QRS-T sequence can be used to estimate the rate. An ECG ruler has a scale that enables rapid rate measurement and calculation of other intervals. With practice, the rate can be estimated at a glance.
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)
THE CARDIOLOGISTS IN HSR LAYOUT Atrial fibrillation Atrial fibrillation is the most common sustained arrhythmia. The atrial activity consists of chaotic, small fibrillatory f waves at 400–700/minute. The ventricular response is usually 130–160/minute and is irregular. The ventricular response rate is slower if the patient has been treated with anti-arrhythmic drugs or if there is intrinsic AV nodal disease. When the response rate is slow, the AF is often reported as ‘controlled’ . very rapid ventricular response—more than 200/minute—may be seen in the presence of a bypass tract, like the bundle of Kent in WPW syndrome (Fig 3.24) or James fibres in LGL syndrome . The AF itself should never be reported as ‘fast’ because it always
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 BEST CARDIOLOGISTS IN VIDHYARANYAPURA Ambulatory blood pressure measurement Ambulatory blood pressure measurement (ABPM) is now available in some centres. This auto-­ matic device takes the blood pressure regularly over a 24-hour period and charts the results. It can be helpful when there is continuing doubt about other readings, although the results can be difficult to interpret. Average ambulatory measurements have been shown to be up to 25/10 mmHg lower than those made in the surgery. ABPM adds to the assessment of blood pressure. The absence of diurnal variations in blood pressure is strongly associated with increased CVD risk. Patients quite often feel that they can tell when their blood pressure is high and that they only need anti-hypertensive treatment intermittently. This approach should be strongly
HEART SPECIALISTS IN SILKBOARD Complex congenital heart disease: conduits Anatomy and physiology Babies with a very abnormal right ventricular outflow tract such as pulmonary atresia can have a conduit fashioned to direct blood from the systemic veins more directly to the pulmonary arterial circulation or from a systemic artery to the pulmonary circulation. These conduits are made from veins or occasionally from Gortex. 368 PRACTICAL CARDIOLOGY Complications Conduits of all types have a limited life and tend to deteriorate after 10 years. These patients are also at risk of ventricular arrhythmias and heart block. Follow-up Patients need regular expert echocardiography to assess the conduit function. The conduit may deteriorate significantly before symptoms occur. Further treatment Conduit deterioration is usually an indication for further surgery although it can occasionally be treated with balloon dilatation. Pregnancy and contraception Pregnancy is well tolerated in patients with good conduit function. There are no particular problems with contraception. Sports Patients should avoid competitive and contact sports.
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
DIABETIC SPECIALIST IN YALAHANKA Syncope and dizziness The history Syncope is a transient loss of consciousness resulting from cerebral anoxia, usually due to inadequate blood flow. Syncope may represent a simple faint or be a symptom of cardiac or neurological disease. Establish whether the patient actually loses consciousness and under what circumstances the syncope occurs—for example, on standing for prolonged periods or standing up suddenly (postural syncope), while passing urine (micturition syncope), on coughing (tussive syncope) or with sudden emotional stress (vasovagal syncope). Find out whether there is any warning such as dizziness or palpitations, and how long the episodes last. Recovery may be spontaneous or require attention from bystanders. Bystanders may also have noticed abnormal movements if the patient has epilepsy, but these can also occur in primary syncope. If the patient’s symptoms appear to be postural, enquire about the use of anti-hypertensive or anti-anginal drugs and other medications that may induce postural hypotension. If the episode is vasovagal, it may be precipitated by something unpleasant like the sight of blood, or it may occur in a hot crowded room; patients often feel nauseated and sweaty before fainting and may have had prior similar episodes, especially during adolescence and young adulthood. The diagnosis of this relatively benign and very common cause of syncope can usually be made from the history. Patients with very typical symptoms rarely require extensive investigations. If syncope is due to an arrhythmia there is often sudden loss of consciousness regardless of the patient’s posture. A history of rapid and irregular palpitations or a diagnosis of atrial fibrillation in the past suggests the possibility of sick sinus syndrome. These patients have intermittent tachycardia, usually due to atrial fibrillation, and episodes of profound bradycardia, often due to complete heart block. Chest pain may also occur if the patient has aortic stenosis or hypertrophic cardiomyopathy. Exertional syncope may occur in these patients because of obstruction to left ventricular outflow by aortic stenosis or septal hypertrophy . Dizziness that occurs even when the patient is lying down or that is made worse by movements of the head is more likely to be of neurological origin (vertigo), although recurrent tachyarrhythmias may occasionally cause dizziness in any position. Try to decide whether the dizziness is really vertiginous (there is a sensation of movement or spinning of the surroundings or the patient’s head), or whether it is a presyncopal feeling. A family history of syncope or sudden death raises the possibility of an ion channel abnormality (long QT syndrome, Brugada syndrome or hypertrophic cardiomyopathy). Attempts should be made to find out what the diagnosis was for the affected relatives. A past history of severe structural heart disease, especially heart failure,
HEART SPECIALISTS IN H S R LAYOUT BANGALORE A systematic description of ECGs The following eight short steps will enable most ECGs to be described correctly: 1 Check the paper speed and calibration markers. 2 Measure or estimate the heart rate. 3 Estimate the rhythm. 4 Look for P waves. 5 Measure the PR interval. 6 Examine the QRS complex. 7 Check the ST segment. 8 Measure the T wave. ECG interpretation should always be as restrained as practicable, taking into account the clinical context where known and comparison with previous tracings where possible. The possibility of Prinzmetal’s electrocardiographic heart disease must always be borne in mind—that is, do not assume that an abnormal ECG always means heart disease.2 Paper speed and calibration markers The standard paper speed is 25 mm/second. This means that 1 mm (small square) = 0.04 seconds and 5 mm (large square) = 0.20 seconds. Provided that the grid is shown, this gives the time scale regardless of the actual image magnification used. Voltage is measured on the vertical axis: 10 mm = 1 mV, as shown in the calibration artefact Leads are often described in groups that correspond approximately to the area of the heart they represent. n Leads 1 and aVL are (high) lateral leads. n Leads 2, 3 and aVF are inferior leads. n Leads 1, 2, 3, aVL, aVF and aVR are collectively called limb or frontal plane leads. Leads 1, 2 and 3 are standard limb leads, while leads aVL, aVF and aVR are augmented limb leads. n Leads V1 and V2 are anteroseptal leads. n Leads V3 and V4 are anterior leads. n Leads V5 and V6 are anterolateral leads. n Leads V1–V6 are collectively called chest, precordial or horizontal plane leads. 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 49 Heart rate By definition, sinus tachycardia is a heart rate ≥ 100/minute and sinus bradycardia is a heart rate ≤ 50/minute.3 To calculate the heart rate from the ECG, the R-R interval in mm can be divided into 1500. For example, an R-R interval of 20 mm gives a rate of 75/minute and an R-R interval of 15 mm gives a rate of 100. Similarly, large 5 mm squares can be divided into 300; thus three squares give a rate of 100/minute. In regular rhythms, any two congruous points of the P-QRS-T sequence can be used to estimate the rate. An ECG ruler has a scale that enables rapid rate measurement and calculation of other intervals. With practice, the rate can be estimated at a glance. Rhythm Begin by looking for P waves. They are best seen in lead 2 (L2) (which is calculated electrocardiographically as the arithmetic sum of leads 1 and 3), aVR (where everything including the P waves
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