These days, it’s hard to come to the ED and not get an ECG. Sometimes that stubbed toe will have early repol and you’ll wonder why the ECG was done; but some other times a ECG may provide some clues for a diagnosis you may not otherwise have suspected. For today’s pearl I’m going to present some ECG’s that manifest extra-cardiac pathology.
Case 1: 32F no sig pmhx developed sudden onset L sided chest pain, dyspnea 6 hours ago
The ECG shows R ventricle strain pattern: there’s RBBB, significant right axis deviation (+180 degrees), there’s even the famed S1Q3T3 (not sensitive nor specific for PE!), as well as TWI V1-4 indicating R sided strain/ischemia. All this is concerning for PE. Remember that the most common rhythm in non-massive PE is either normal sinus rhythm or sinus tachycardia (depends on study, sinus tachycardia rates ranged from 8-69%, see table from Chan 2001). The most common abnormal ECG finding(s) are T wave or ST segment changes.
Case 2: 31M no sig pmhx had sudden collapse at work; EMS found pt in respiratory arrest, the pt then rapidly regained consciousness, but remains confused and not able to provide much of a history. His vitals are normal as is his exam, aside from the confusion/disorientation.
This pt had a SAH. Up to 80% of pt’s with SAH will have ECG changes; wide, deeply inverted TW (cranial T waves) are frequently found; prolonged QT and bradycardia are also seen. Prolonged QT and ST/TW changes may predict higher in-hospital mortality (Huang et al, 2012)
This is all thought to be due to increased ICP so this can occur with other causes of increased ICP. The physiologic basis of these abnormalities is controversial but may involve CNS mediated increases in sympathetic and vagal tone or actual myocardial necrosis (high ICP patients will commonly make trops but don’t be distracted; MI’s shouldn’t cause respiratory arrest and confusion with a normal pulse and BP…).
Case 3: 57F h/o HTN (on HCTZ, well controlled), presents with worsening weakness the past day; has had copious vomiting the past 2 days.
The ECG shows prolonged PR; the QT appears long because of U wave (ECG below) that is joined/superimposed over the T wave. Compare this to the prolonged QT in hypocalcemia (see 2nd ECG below) where it’s a ‘true’ long QT (due to the long ST, the T wave itself is normal width)
Chan TC, et al. Electrocardiographic manifestations: pulmonary embolism. The Journal of Emergency Medicine. 2001; 21: 263-270.
Stein PD, et al. Clinical Characteristics of Patients with Acute Pulmonary Embolism: Data from PIOPED II, The American Journal of Medicine. 2007; 120:871-879
Huang CC, et al. The 12-lead electrocardiogram in patients with subarachnoid hemorrhage: early risk prognostication. Am J Emerg Med. 2012;30:732-6