PART 2: ECG INTERPRETATIONS AND COMMENTS
186.
Ectopic atrial rhythm, rate 69, high left ventricular voltage, abnormal Q-waves in lateral leads suggestive of hypertrophic cardiomyopathy (HCM). The inverted P-wave in lead III suggests a non-sinus node origin. The PR-interval is >0·12 seconds, indicating that the P-waves originate from an ectopic atrial focus rather than an AV junctional focus. The large-amplitude QRS complexes are typical of HCM, as are the deep narrow Q-waves in the lateral leads. In this case, the abnormal Q-waves are most notable in leads I and aVL. HCM Q-waves tend to be narrower than MI Q-waves, which usually are ≥0·04 seconds wide. This patient had been evaluated on two other occasions for exertional syncope. During both of those physician visits, ECGs were obtained and demonstrated similar findings. However, the ECG abnormalities went unrecognized until his current visit.
187.
SR with second degree AV block and 2:1 AV conduction, rate 46, acute inferior MI. Regular P-waves at a rate of 92/minute are found easily in the inferior leads. There is a 2:1 ratio of P-waves:QRS complexes, and the PR-interval remains constant, consistent with second degree AV block. When second degree AV block occurs with 2:1 AV conduction, the diagnosis of Mobitz I versus Mobitz II cannot be certain, although the narrow QRS complexes favors Mobitz I. Q-waves with ST-segment elevation is present in the inferior leads. Reciprocal ST-segment depression is found in I, aVL, and V2–4.
188.
SB with frequent non-conducted PACs in a pattern of atrial bigeminy, rate 45, bifascicular block (RBBB and LAFB). The rhythm was initially misdiagnosed as second degree AV block with 2:1 AV conduction because there are two P-waves for every QRS complex, similar to the previous example (#187). Unlike the previous example, however, the P-waves do not occur regularly. Therefore, second degree AV block is essentially ruled out. The first P-wave in each cycle is a sinus P-wave. This is followed by a QRS complex, then a non-conducted P-wave (a non-conducted PAC). One will note that the PACs have a slightly different morphology to the sinus P-waves. PACs that occur too early in the cycle (before the ventricle has “reset”) do not produce ventricular depolarization. Instead, they are followed by a pause before the next atrial beat occurs. This can easily lead to a misdiagnosis of second degree AV block.
189.
SR, rate 75, T-wave abnormality consistent with anteroseptal ischemia. Although cardiac ischemia is a common cause of T-wave inversions, other conditions are associated with this abnormality as well: persistent juvenile T-wave patterns, left ventricular hypertrophy, acute myocarditis, WPW syndrome, cerebrovascular accident, bundle branch block, later stages of pericarditis, and acute pulmonary embolism. T-wave inversions in the right precordial leads are especially common in pulmonary embolism, with sensitivities for this finding as high as 50%. In this case, the physician initiated treatment for acute cardiac ischemia. However, neither the T-wave inversions nor the chest pain resolved with the administration of nitroglycerin or heparin. At that point, computerized tomography of the lungs with intravenous contrast was performed and demonstrated three pulmonary emboli. Acute pulmonary embolism should always be considered when the ECG demonstrates new T-wave inversions, especially when they are present in the right precordial leads.
190.
Atrial tachycardia with variable AV block, rate 72, lateral MI of uncertain age, non-specific intraventricular conduction delay, rhythm suggestive of digoxin toxicity. The atrial rate, best noted in lead V1, is 200/minute. Atrial tachycardia with variable AV block (“PAT with block”) is highly specific for digoxin toxicity. The serum digoxin level in this case was 4·7 ng/ml (normal 0·5–2·2 ng/ml).
191.
SR, rate 82, RAE, non-specific T-wave flattening in inferior leads, abnormal precordial T-wave balance. The normal ECG has an inverted, flat, or small upright T-wave in lead V1. The T-wave usually is upright in lead V2 and becomes larger in the other precordial leads in normal ECGs. In this case, however, the T-wave in lead V1 is not only upright, but it is larger than the T-waves in the lateral leads. Marriott has referred to this abnormality as “abnormal T-wave balance.”5 Marriott and other others6,7 have suggested that when the T-wave in lead V1 is upright and large (more specifically, when the T-wave in lead V1 is larger than the T-wave in lead V6), it suggests underlying cardiac disease. This patient did prove to have a 90% obstructing lesion of the LAD.
149