Predominantly negative QRS in at least two out of four leads (I, II, V1 and V6, with either Lead I or V6 included) diagnosed VT in 89.2% of cases, SVT in 100% of cases. Thus 94.5% of all cases were correctly diagnosed. Presented for the first time, they can be used as a simple approximate tool to differentiate wide complex tachycardia in critical care settings and may help avoid misdiagnosis with its therapeutic risks.
A plethora of ECG criteria have been developed over the last few years to distinguish between VT and aberrantly conducted SVT (1-10). Most of these criteria are full of details such as precise measurement of waveform intervals in milliseconds recorded from specific leads. Therefore it is not surprising that recently advanced cardiac life support do not recommend using these criteria to distinguish between VT and aberrantly conducted SVT because this distinction is too difficult and time consuming in the immediate care setting. In these guidelines, clinicians are urged to treat patients and not the cardiac monitor (11).
Unfortunately, clinical findings such as patients blood pressure or level of consciousness, have not proven reliable in distinguishing SVT from VT. In fact recent reports (12-14) confirm that when patients signs and symptoms are used to make the diagnosis, wide QRS tachycardia are frequently misdiagnosed and patients suffer disastrous outcome. For example, in two recent reports (12-14) when patients with haemodynamically stable VT were misdiagnosed as having SVT with aberration and treated with IV verapamil, outcome included acute severe hypotension requiring vasopressor, acceleration of the tachycardia, degeneration of VT into VF requiring defibrillation, and a systole following cardioversion. More recently, the danger of administrating verapamil in these patients have been appreciated and adenosine has been recommended (11). Adenosine can provide important diagnostic information regarding the tachycardia mechanism, however it may not be as safe as originally thought in the immediate care setting. For example, adenosine has triggered torsades de points in the presence of long Q-T syndrome (15), has caused atrial fibrillation and dangerous acceleration of ventricular rate in patients with atrial fibrillation or flutter (16-20).
In 1978 Wellens published his morphologic criteria to diagnose wide complex tachycardia based on retrospective analysis of hundreds of ECG tracings, other published criteria were all based on complicated analysis of QRS morphology, duration and relative relation of r/s in different leads which was rather non practical in the critical care setting. We are hereby presenting a new simplified approach for wide QRS complex tachycardia especially in the critical care settings based on the polarity of QRS in both limb leads (I, II) and chest leads (V1, V6). These leads were chosen in particular because they represent the principal deflection in bundle branch block (BBB).
METHODS
We retrospectively and prospectively analyzed the 12-lead ECG of 81 monomorphic wide (>120 ms) QRS tachycardias records from 81 patients who underwent cardiac electrophysiological study (EPS) at the critical care department of Cairo University. (61 male, 20 female, mean age 47.8+13.9 years) clinical diagnosis included ischemic HD in 28 patients, dilated CM in 13 pts, congenital HD in 3 patients, HTN in 7 pts. and rheumatic HD in 6 pts. In all pts. the site of origin of the tachycardia was diagnosed by EPS (VT vs SVT).
Analysis: QRS morphology of the four chosen leads (I, II, V1 and V6) were introduced in computer guided software and analysis proceeded so as to find the commonest morphology (rS, QS, R … etc) among ECG tracings in each of these leads among different group (VT, SVT) and the commonest combination of predominantly negative complex using two leads at a time, and also these tracings were subjected to analysis using both Brugada algorithm 1991 (8) and A-John Camm criteria 1994 (21).
RESULTS
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