You shouldn't! There are subtle but real ST elevations inferiorly (II,III and aVF) and in V5 and V6. Cath showed postero-basal hypokinesis and he underwent circumflex/obtuse marginal angioplasty after ruling in for a small MI. ST depressions here in aVL are reciprocal to primary ST elevations infero-laterally. Whenever you see ST depressions, always look in contralateral leads for ST elevations and remember that you do not get reciprocal ST elevations with acute ischemia.
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Be careful here. This may look superficially like sinus but if you look in V1, you can see P waves just before the QRS (there is right bundle branch block (RBBB) and also P waves in the T wave (halfway in between) which are partly hidden. Atrial rate is about 150, ventricular rate 75. This is an atrial tachycardia with 2:1 block (paroxysmal atrial tachycardia or "PAT with block" if it occurs paroxysmally) which may be due to digoxin toxicity, atrial disease, etc. If you got this right, PAT yourself on back; if you choked on it, a more forceful interscapular blow may be indicated. (Note that "PAT" is often a misnomer since the tachycardia may be sustained. So the term "atrial tachycardia with block" is most accurate here.)
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The ECG shows sinus tachycardia with an indeterminate (not "indeterminant") axis and prominent T wave inversions in V1-V4 with delayed precordial transition zone (R=S in V6). QT is at upper normal limits and there is an S wave in lead I with a minuscule R in III, aVF. P waves are peaked (well, almost) in II. Obviously it doesn't take an Oslerian wizard to think of anterior ischemia when you see poor wave progression and T wave inversions. But you should always think about acute right ventricular (RV) overload ("strain") due to pulmonary embolus, etc. That's what this patient with history of deep vein thrombosis (DVT) had. Contrary to common wisdom, there is no diagnostic ECG in pulmonary embolus, but there are suggestive ones. Unfortunately, most of the time the ECG is non-specific; although, with a large PE, sinus tachcardia is usual. Possible other findings include: T wave inversions in the right to mid chest leads; Poor R wave progression--due to acute RV dilation; the latter may also lead to S1Q3 pattern simulating inferior myocardial infarction (MI); P pulmonale; RV conduction delays; right axis shift.
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Sinus rhythm with left atrial abnormality. Most striking are tall right precordial R waves with pathologic inferior and lateral Q waves giving a "reverse" type R wave progression. There are also ST-T abnormalities in I, aVL, V6. Thus the patient has coronary artery disease (CAD), s/p large infero-(postero)-lateral myocardial infarction (MI) accounting for congestive heart failure (CHF) findings. Recall that differential diagnosis of tall right precordial R waves includes: 1) Normal/positional variants, 2) Right ventricular hypertrophy (RVH) (look for right axis deviation, P pulmonale), 3) Posterior/lateral MI (usually signs of inferior MI, too), 4) hypertrophic cardiomyopathy/idiopathic hypertrophic subaortic stenosis (HCM/IHSS), 5) right bundle branch block (RBBB), 6) Wolff-Parkinson-White (WPW ) variants with posterior/lateral pre-excitation 7) Duchenne muscular dystrophy (young men with myopathy).
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The ECG shows sinus rhythm with normal axis and intervals. The two notable findings are 1) inferior Q-wave myocardial infarction (MI) of indeterminate age and 2) diffuse ST elevations in anterior and lateral leads, with PR deviations (up in aVR, down laterally) c/w with pericarditis. The story was of prior MI with pericarditis post-coronary artery bypass graft (CABG) surgery. If you know anyone who got this right (the first time), drop us a line so we can sign them up for a Cardiology Fellowship!
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