There are two premature beats seen in this rhythm tracing (#4 and #7). Although they appear similar in morphology to supraventricular beats, both are PVCs by criteria that define the difference between PVC and PAC.

Both beats are followed by a pause – in these beats, a compensatory pause, which implies that the next P wave was undisturbed by the premature beat. Another way of saying the same thing is that the sinus P waves “march through” the premature beat, or that the sinus metronome marked by regular P and QRS complexes is undisturbed. Each of these descriptions say the same thing – these premature beats are both PVCs!

This bradycardic rhythm is wide-complex and regular at 22/minute. There are no discernible P waves. Without further information this rhythm is best described as a slow junctional rhythm.

However, we do have more information. This young woman has SLE with renal failure requiring dialysis. Even if she has not missed a dialysis session, one must assume this bradycardic wide-complex rhythm is due to hyperkalemia.

Hyperkalemia has several predictable effects on the EKG. The P-wave, QRS-complex, and T-wave are all targets of this “poison” that effects normal depolarization and repolarization. These effects occur in a predictable sequence. The first sign seen is increased amplitude of the T waves – a peaked, narrow-based T wave. As the level of potassium continues to rise, the next changes are prolongation of the QRS complex and then diminution of the P wave. With further QRS prolongation, the EKG complex begins to resemble the pre-terminal sin wave of critically severe hyperkalemia.

After treatment with Ca++ gluconate