74 year old male with a history of hypertension presented one week after his total knee replacement complaining on a generalized weakness. The patient admitted to a low oral intake due to nausea. He continued taking his antihypertensive medications including ACE-inhibitor.

His initial work-up in the Emergency Department revealed potassium of 9.6mmol/L (normal<5.1mmol/L) and creatinine of 4.6mg/dl (normal<1.2mg/dl). The patient was also hypotensive with blood pressures in the 70’s systolic despite IVF boluses.

His EKG (see the image above) demonstrated severe QRS prolongation and absent P-waves consistent with hyperkalemia. The patient was admitted to ICU.

The etiology of the renal failure and hyperkalemia in this case is volume depletion and ATN (acute tubular necrosis) in addition to taking ACE-inhibitor.

The electrocardiographic manifestations of early hyperkalemia include peaked T-waves. Subsequently, PR interval lengthens and QRS duration increases. A variety of conduction blocks may occur at this point (left/right bundle and bifascicular blocks).

Later, the P wave disappears and the QRS widens further and may become a sine wave with subsequent cardiac arrest.

Surprisingly, the patient above did not require emergent dialysis. His potassium and creatinine improved with aggressive medical therapy.