The ECG in the figure below was obtained from a previously healthy 43-year-old woman who presented to the ED with chest pressure and shortness of breath over the past day. She was alert but hypotensive at the time this ECG was recorded. How would you interpret this tracing? What entities should be considered in your differential diagnosis?
This ECG is markedly abnormal. The rhythm is sinus tachycardia at a rate just > 100/minute. The PR and QRS intervals are normal, but the QT interval appears to be markedly prolonged. The axis is normal. There is no chamber enlargement.
When it comes to QRST changes, Q waves are present in leads III and aVF. There is poor R wave progression in the chest leads, with late transition to a predominant R wave not occurring until between lead V5 to V6. But the most remarkable finding is deep symmetric T wave inversion that is most pronounced in leads V1, V2, and V3. Several additional leads show ST segment coving with a lesser degree of T wave inversion.
Clinical correlation is essential for optimal interpretation of this tracing. Deep, symmetric T wave inversion may clearly be a manifestation of ischemia and/or an acute coronary event. Hypertrophic cardiomyopathy (especially when there is apical hypertrophy) is also known to produce deep symmetric T wave inversion in multiple leads. The markedly prolonged QT interval in association with the pronounced ST-T wave changes seen here could be consistent with a central nervous system event such as stroke, intracerebral or subarachnoid bleed, coma, seizure, or trauma. That said, the clinical scenario of hypotension, plus new-onset dyspnea in a previously healthy young adult with this ECG, is most suggestive of acute pulmonary embolism (PE) as the diagnosis. Massive PE was confirmed on further evaluation.
ECG diagnosis of acute PE is difficult because there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of supportive ECG findings that occur in a patient with either unexplained dyspnea, syncope, or shock. Although deep symmetric anterior T wave inversion should suggest the possibility of coronary ischemia, this finding is also a manifestation of right ventricular “strain,” as is commonly seen in patients with acute hemodynamically significant PE. Other ECG findings consistent with the diagnosis of a large acute PE include sinus tachycardia, the presence of an S1Q3T3 pattern, a positive pointed P wave in leads V2, V3 (a subtle sign of right atrial abnormality), poor R wave progression with persistence of S waves through to lead V6, ST elevation in right-sided lead aVR, and subtle ST segment coving and T wave inversion in leads III and aVF (as may also be seen with right ventricular “strain”). Taken together in the clinical context presented here, the diagnosis of acute hemodynamically significant PE should be presumed until proven otherwise.
Please see http://tinyurl.com/KG-Blog-119 for additional discussion on this case.
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