Atrial fibrillation with controlled ventricular response of 84/minute, left axis deviation (-50°), QRS slightly prolonged at 100msec, voltage for LVH (with associated changes including left axis, prolongation of the QRS, and repolarization changes of strain pattern laterally, poor R wave progression and ST-elevation V2-3). A good example of the changes of severe LVH.
Atrial flutter with 2:1 block (clue – the rate is exactly 150/min), axis -30°, notice how the QRS in some leads (eg, II, III, aVF) appears prolonged by a portion of the flutter wave inscribed behind the QRS.
2° AV block, Type I (Wenckebach) with rate of 36/minute, with hyperacute T waves inferiorly (II, III, aVF) and ST-segment depression and T wave inversion V1-3 representing acute inferior-posterior infarction.
Sinus at 108/minute, right axis deviation (+120°) and tall R wave in V1 suggest right ventricular hypertrophy in this patient with primary pulmonary HTN.
Sinus at 66/min, axis -30°, PR interval is short (the width of the P wave), widening of the QRS by a delta wave most noticeable in I and aVL – Wolff-Parkinson-White, type B (not LBBB).
Sinus at 84/minute, axis 0°, short PR interval and delta waves – WPW, type A because of the tall R wave in V1.
Sinus at 72/minute, normal axis, PR 200msec (1° AV block), QRS prolonged at 120msec with tall R wave in V1 – RBBB (also note wide terminal S waves in lateral leads).
Sinus at 78/minute, left axis at -60°, tall R waves in V1-2 with associated Q waves in inferior leads – old inferior-lateral MI.
Sinus at 72/minute, left axis, wide QRS at 160msec with tall monophasic R in lateral leads consistent with LBBB, note expected repolarization changes of ST depression and T inversion laterally, and ST-segment elevation and exuberant T waves in anterior leads (V1-3).
Regular rate at 72/minute, no P waves seen, very wide QRS and peaked T waves (V4) – severe hyperkalemia.
Sinus tachycardia at 105/minute, slight prolongation of both QRS and QT intervals, note prominent R in aVR – all consistent with TCA toxicity. 11a has a noticeably prolonged QRS and an R in aVR > 5mm – a severe TCA overdose in a teenager.
Sinus bradycardia at 48/minute, significant QRS prolongation by an additional wave at the end of each QRS, an Osborne wave – this is hypothermia.
2° AV block, type II with overall rate of 72/minute, right axis deviation, wide QRS with tall R in V1 – RBBB, the right axis with a RBBB adds the diagnosis of left posterior hemiblock (a bifascicular block). The 9th and 10th complexes are PVCs because P waves march through the rhythm, and thus these beats are dissociated from sinus activity and are necessarily ventricular in origin.
Sinus tachycardia at 126/minute, right axis deviation and tall R in V1 – RVH, negative terminal deflection of biphasic P wave in V1 diagnostic of LA enlargement – this combination is typical of mitral stenosis.
Sinus tachycardia at 144/minute, tall R wave in V1 coupled with tiny but perceptible Q waves inferiorly diagnose a subacute inferior-posterior MI; the very small complexes in the limb leads suggest tamponade – this elderly woman presented in shock three days after severe chest and back pain following rupture of the myocardium resulting in tamponade.
MAT (multifocal atrial tachycardia) at 180/minute, axis +90, although P waves vary because of MAT they are nearly all tall in the inferior leads suggestive of right atrial enlargement (“P-pulmonale”), and the essentially isoelectric complexes in lead I has been called the “lead I sign” suggestive of COPD. This patient had severe COPD and was actually theophylline toxic causing the rapid MAT.
Sinus at 96/min, axis -30, intervals normal, striking ST-segment elevation in V2-6, I, and aVL with reciprocal changes in the inferior leads consistent with an acute anterolateral STEMI.
100% ventricular paced rhythm at 72/minute, with appropriate “LBBB morphology” of QRS complexes including repolarization changes of ST-segment elevation in V1-3.
Sinus at 90/minute, normal axis and intervals, ST-segment elevation in I, II, V3-6 with PR interval depression in II and PR elevation in aVR – all suggestive of acute pericarditis. 19a additionally has good Spodick’s sign of downsloping T-P segment in lead II rhythm strip.
Sinus at 54/minute, normal axis and intervals, with ST elevation V2-6, notching of J point in same leads, and early transition of R/S – early benign repolarization.
Sinus at 114/minute, ST-segment V1-6 with Q waves in same leads – ventricular aneurysm.
Sinus at 60/minute, PR interval prolonged at 280msec (1° AV block), QT interval prolonged with striking T wave inversion – in this patient with subarachnoid hemorrhage, these changes are consistent with CNS effect.
Sinus at 66/minute, normal axis and intervals, deep T wave inversion in V2-4 – in this patient with prior chest pain, a classic presentation of Wellens’ syndrome.
Sinus at 72/minute, striking T wave inversion and QT intervals – in this middle-aged man it is consistent with Takotsubo cardiomyopathy.
Striking T wave inversion in a young man – Yamaguchi syndrome, or apical hypertrophic cardiomyopathy.
Basic rhythm is atrial fibrillation with two ventricular paced beats, widespread T wave inversion – an example of T-wave inversions due to ventricular pacing or “memory T waves.”
Sinus at 48/minute, normal axis and intervals, biphasic T waves in V2-3 – in a patient with prior chest pain, consistent with a form of Wellens’ syndrome.
Sinus at 78/minute, normal axis and intervals, persistent hyperacute T waves V2-4 with J point depression and upsloping ST in the same leads – de Winters’ sign of proximal LAD occlusion.
Sinus at 84/minute and PAC, impressive ST-segment depression in 9 of 12 leads, and ST-segment elevation in aVR and aVL – this pattern is predictive of critical left main disease.
Sinus at 96/minute with PVC, wide QRS in a LBBB morphology with concordant ST-segment elevation in I and aVL – positive Sgarbossa criteria for acute MI.
Sinus at 60/minute, normal axis and intervals – ST-seg depression in V2-4, an isolated posterior MI due to total occlusion of the circumflex artery.
Ventricular paced rhythm at 78/minute, with ST-segment in multiple leads and ST-segment elevation in aVR, changes not typical of the expected LBBB morphology, and in fact suggestive of critical left main disease.
Sinus tachycardia at 108/minute, left axis at -60°, intervals normal, voltage criteria for LVH with repolarization changes including T wave inversion laterally and ST-segment elevation V1-2.
Sinus at 54/minute, normal axis and intervals, subtle biphasic T waves V1-2 that were new from prior tracing – a Wellens’ syndrome and the patient went on to have a large anterior MI one week later.
Obvious ST-segment elevation in multiple leads (inferior as well as V1-6) – this is not pericarditis; it is an acute STEMI due to a wrap-around LAD with extension of the distal LAD around the apex to the inferior wall.
References Armstrong EJ, Kulkarni AR, et al. Electrocardiographic criteria for ST-elevation myocardial infarction in patients with left ventricular hypertrophy. Am J Cardiol 110:977-983, 2012.
De Winter RJ, et al. A new ECG sign of proximal LAD occlusion. NEJM 359:2071-73, 2008.
Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: classification, differential diagnosis, and caveats. Clev Clin J Med 78: 404-414, 2011.
Hayden GE, Brady WJ, Perron AD, et al. Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. Am J Emerg Med 20:252, 2002.
Lawner BJ, Nable JV, Mattu A. Novel patterns of ischemia and STEMI equivalents. Cardiol Clin 20:591-599, 2012.
LeWinter MM. Percarditis – clinical review. NEJM 371:2410-16, 2014.
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Rhinehart J, Brad WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med 20:638-43, 2002.
Smith SW, Dodd KW, et al. Diagnosis of ST-elevation myocardial infarction in the presence of LBBB with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med 60:766-776, 2012.
Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. NEJM 349:2128-35, 2003.