EKG interpretation:
Sinus at 70/minute
Axis normal (10°)
PR and QRS intervals normal, QT is prolonged in many leads (eg aVL)
No chamber enlargement
A U wave is present after the T wave in several leads (leads V2-3)

The important features to recognize in this EKG is the appearance of a U wave and the diminution of the T-waves, leaving the appearance of a prolonged QT in several leads. The differential of a prolonged QT interval, besides offending medications, are hypokalemia (seen with increasing U waves and diminishing T waves), hypomagnesemia, and hypocalcemia. Alcoholics are already prone to hypomagnesemia, and the addition of several days of gastroenteritis may quickly deplete other electrolytes and cations.

While the patient was being monitored during the initial stages of her evaluation, she suddenly became unresponsive and the following rhythm was captured on the monitor:

She regained consciousness with sinus rhythm on the monitor and stable VS without intervention. Soon thereafter labs resulted:

K – 2.3 mEq/L (3.6 – 5.2)
Mg – 0.6 mEq/L (1.3 – 1.9)
iCa – 0.96 mmol/L (1.1 – 1.3)

Remember that alcoholics who become sick are at risk for prolonged QT, torsade de pointe, and syncope or sudden death!

EKG interpretation
Sinus at 100/minute
Axis is normal
Intervals are normal
Ischemia/infarct – T wave inversion V1-4 with loss R waves (deep Q waves) in the same leads

T-wave inversion in the anterior leads has a broad differential. Deep, or giant, T-wave inversion has it’s own differential including CNS changes (see full differential under Impressive T-wave Inversion on TorreyEKG.com). More minor T-wave inversion can be seen with ischemia, acute PE, evolving or subacute STEMI, and many other causes.

These T-wave inversions in leads with well-formed Q waves suggest a subacute MI, possibly days to weeks old (the Q’s have formed, the ST-segments are back close to baseline, but the T-wave inversion can persist for weeks).

And what is the connection between a recent anterior MI and his presentation with a stroke? Once anticoagulated on heparin, a transesophageal ultrasound showed a large mural thrombus in a dyskinetic wall of his left ventricle.

His level of hypotension seemed unusual for an acute septal MI, especially in an otherwise fairly healthy young man. He had no chest pain, just some shortness of breath.

78/46   110   28   O₂sat 92% on RA   afebrile
lungs – clear bilaterally
cor – regular, no murmur appreciated
extremities – no edema, diminished distal pulses

RUSH (Rapid US in Shock) exam revealed a massively dilated right ventricle. When asked about leg pain, he described significant pain in his right calf for 2 days. Ultrasound of the right popliteal area revealed a non-compressible vein with intramural clot. STAT CT angiogram revealed large bilateral pulmonary emboli. This patient received TPA in the ED and has done well.

While PE has no definite EKG findings, it is a great masquerader…it can present with T-wave inversion anteriorly (small or giant T-wave inversion) and with ST-segment elevation on occasion. Keep PE on many differentials, especially when the EKG findings don’t quite fit with the clinical presentation.