VEBs & U Waves: Hypokalæmia

Report

Sinus rhythm.

Sinus arrhythmia.

VEBs, bigeminy.

Prominent U waves consistent with hypokalæmia.

Comment:

The ECG monitor alarmed at the heart rate 34/min. This need not be merely spurious bradycardia, a mistake in the first place, due to negative VEB polarity: the pulse produced by the VEBs may be unrecordable as well.

"Renal" patients not infrequently become hypokalæmic due to the (not entirely unfounded) belief that potassium supplementation may be hazardous. This patient's ectopic activity disappeared with 10 mEq/hour of KCL over 2 hours; the serum potassium rose from 3.1 to 3.9 mEq/L. ICU interventions to suppress ventricular ectopic activity as a rule remain confined to correcting electrolytes, hypoxæmia, pH and the hæmodynamics; they are less frequent but more successful than those relying on antiarrhythmic drugs elsewhere.

In the top strip one can map out the nadir of the P waves throughout. It produces a negative notch in the ST segment of the VEBs.

The single VEB in the bottom trace follows the longest sinus cycle, illustrating the tendency of VEBs to follow long cycles. That may be why bigeminy begets bigeminy – the rule of bigeminy. It does not always hold: this VEB (probably) failed to evoke another in its wake.

Speaking of elsewhere, below is a strip from CCU (Fig 268a). Shallow inverted T wave merging into an upright U wave. Here the appearance was due to combination of digoxin and quinidine. The potassium, checked prior to cardioversion, was normal (4.2 mEq/L). There is no substitute for measuring the potassium level.

Hypokalæmia mimicry by digoxin - quinidine combination was stressed by Marriott201. Quinidine is becoming a rarely used drug nowadays; the strip may not survive more than a few more years in this Library.