http://WWW.HEARTDIABETESCARE.COM
SAMIKSHAHEARTCARE 57698d5b9ec66b0b6cfb5b6b False 536 1
OK
background image not found
Found Update results for
'regular pulsations'
5
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
1
false