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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.
CARDIOLOGIST IN YELAHANKA SECOND DEGREE AV BLICK There are two basic types of second-degree AV block: AV nodal Möbitz type I (Wenckebach) heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (Fig 3.10) (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB (Fig 3.11), since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block (Fig 3.12). There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as
THE BEST CARDIOLOGISTS IN YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
THE BEST CARDIOLOGISTS IN YELAHANKA Indications for coronary angiography 1 Angina not responding to medical treatment in a patient without contraindications (e.g. extreme old age—usually older than about 85 these days—or severe co-morbidities) to cardiac surgery or angioplasty. 2 Continuing chest pain whose cause is not clear despite non-invasive investigations. The procedure may well be worthwhile if it reveals normal coronary arteries and prevents a patient being treated unnecessarily with more and more anti-anginal drugs. Non-invasive investigations are more often equivocal in women, and more women than men are found to have normal coronaries at angiography. 3 Preparation of a patient older than 35 or so for some other cardiac surgery (e.g. valve replacement). The surgeon needs to know whether significant coronary disease is present so that coronary grafting can be performed at the time of valve surgery. Otherwise, patients are at risk of ischaemic problems in the post-operative period. 4 Diagnosis of cardiomyopathy (p. 267) by excluding coronary artery disease and infarction as the cause of angina or cardiac failure. These patients may benefit from revascularisation if significant coronary disease is also present (‘ischaemic cardiomyopathy’). 5 Investigation of patients following myocardial infarction. Routine transfer to a centre with angiographic facilities after successful thrombolytic treatment is a grade D recommendation. There is no proof that a patient without continuing ischaemia has an improved prognosis when angiography and revascularisation are carried out routinely after infarction. The Open Artery Trial results suggest there is no benefit compared with optimal medical treatment for patients without ischaemic symptoms in having an occluded vessel opened five days or more after an infarction. However, spontaneous or induced ischaemia (by modified stress testing or perfusion imaging) leads to a grade B recommendation for angiography and intervention. The management of post-infarct patients is definitely easier if the coronary anatomy is known, and many units adopt the policy of early (within a week) angiography of infarct patients without contraindications to revascularisation. 6 Non-ST elevation acute coronary syndromes (p. 156). 7 Acute myocardial infarction in a unit where primary angioplasty can be performed
POPULAR CARDIOLOGISTS IN H S R LAYOUT Ventricular tachycardia Ventricular tachycardia is defined as three or more ventricular ectopic beats at a rate over 100/minute. It is said to be sustained if it lasts more than 30 seconds. Most broad-complex tachycardias are ventricular (rather than supraventricular with aberrant conduction). The diagnosis of VT is greatly strengthened if there is a history of myocardial infarction or cardiac failure but, oddly enough, the patient’s haemodynamics are of no help. A number of criteria have evolved over the years to help ascertain the diagnosis of VT over aberrancy. These include: evidence of AV dissociation—P waves can be seen unrelated to the QRS complexes (they are usually visible only at relatively slow VT rates) the presence of supraventricular capture or fusion beats visible retrograde conduction with 2:1 block (P waves visible following every second complex) the presence of monophasic R, qR or QR patterns in V1, provided a septal infarction has not modified a RBBB a taller left rabbit ear in RR' or qRR' complexes in V1 n QS complexes in V1 with a slow S descent and sharp upstroke—the opposite of LBBB—or a broad small primary R wave in rS morphology (the Rosenbaum pattern) RAD in the frontal plane with LBBB-like QRS complexes
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