A 42-year-old morbidly obese female presents to your ED with intermittent, exertional chest pain for three days. The presenting EKG shows diffuse low QRS voltage, and inferior-lateral T-wave flattening (II, III, aVF, V5, V6). Her Troponin was not elevated and she was admitted to the chest pain observation unit. A dobutamine stress test was inconclusive. Next, an echocardiogram was read as a technically difficult study with inconclusive findings. Subsequently, the patient had a normal cardiac catheterization.
According to the center for disease control, in 1991 only four states had obesity prevalence rates exceeding 15%. Unfortunately, by 2005 only four states had obesity prevalence rates less than 20%! Diagnostic evaluation of overweight and obese patients represents an inevitable clinical challenge in today’s ED. Recognition of normal obese-related variants may prevent inefficient testing and prolonged ED length-of-stay. The EKG evaluation of chest pain represents one such clinical conundrum and was first reported in the medical literature in 1931.
Obese patients have been shown to have changes in the morphology of the myocardium such as eccentric left ventricular hypertrophy, left ventricular enlargement, and right ventricular hypertrophy. These structural changes are expected to alter the electrocardiogram in one way or the other.
The resting heart rate in obese patients is usually normal, although tachycardia has been reported in up to 0.5%. Abnormal heart rates should prompt evaluation for precipitants of bradycardia or tachycardia, just as they would in any other patient. The P-wave, QRS, and T-wave axis are shifted leftward in obese subjects, but still within normal limits. Presence of diffuse low voltage (11%), voltage criteria for left ventricular hypertrophy (66%), non-specific ST and T-wave abnormalities (11%), flattened T-waves in the inferior (58%) and lateral (29%) leads should all be noted as common variants among normotensive obese patients. Not surprisingly, when obese patients lose weight the T-wave flattening, leftward axis deviation, and low voltage all disappear. Most importantly, obesity is not associated with T-wave inversion which should prompt immediate evaluation for acute coronary syndrome if present in the appropriate clinical scenario.
An increasing body of literature suggests that central obesity is associated with QT prolongation and potential ventricular dysrhythmias, though bundle branch blocks do not occur more frequently in the obese. Ventricular premature beats occur 30 times more frequently in obese patients than in lean cohorts. In addition, sleep apnea syndrome, associated with atrial and ventricular dysrhythmias, is present in almost half of morbidly obese patients. One small autopsy series of young obese adults with sudden death revealed that all had cardiac hypertrophy with fat infiltration into the sinus node and conduction system.
Facing the obesity epidemic of the early 21st century, overweight chest pain patients will undoubtedly be arriving in your ED in the near future. Recognition of obesity-related normal ECG variants, along with their reversal if weight loss attempts are successful, may assist more accurate triage and risk stratification of these difficult patients. As always, ECG interpretation should occur concurrently with the clinical presentation. The science of obese emergency medicine is still young, so stay tuned for additional research reports to assist you with your diagnostic, prognostic, and therapeutic management of these complicated, disease-laden patients.
Ademola Adewale, MD, Dept. of Emergency Medicine, Florida Hospital, OrlandoChristopher R. Carpenter, MD, MSc. Division of Emergency Medicine, Washington University in St. Louis