Abstract

NM-289

Suspension of Disbelief . . . Abrupt Cessation of Isoproterenol Resulting in Hyperkalemia in a Pacemaker-Dependent Patient

Schwartz R, Henson S
The Children's Hospital at OU Health Sciences Center, Oklahoma City, OK, USA

Severe hyperkalemia can result in life-threatening arrhythmia if not treated promptly. Laboratory confirmation, characteristic ECG changes, and a recognized clinical etiology are factors that in the aggregate enable a clinician to diagnose and treat this condition in a timely manner. We present a case in which the absence of several of these factors resulted in a delay in diagnosis and treatment.
A 17-year-old male presented to the emergency department complaining of fatigue. He was noted to have junctional bradycardia at 40 beats per minute. His medical history was significant for complete heart block and pacemaker-dependency after Fontan completion as a child for double-inlet left ventricle and L-transposition of the great arteries.
An isoproterenol infusion was started at 0.05 mcg/kg/min due to pacemaker failure. The heart rate increased marginally and symptoms improved. He was taken to the operating room the next day for pacemaker replacement. The isoproterenol infusion was discontinued after new lead placement. He was extubated and transported to the CVICU.
Routine postoperative iSTAT was notable for K+ of 7.4 mEq/dL. This was thought to be erroneous since K+ was normal preoperatively and there was no clear etiology to account for an acute change. Elevated K+ was confirmed again by iSTAT from a central venous sample. Since the patient’s ventricles were being paced, classic “peaked T waves” were not readily identifiable. Only after a 3rd confirmation of elevated K+ by a serum sample sent to the laboratory did treatment begin with aerosolized albuterol, furosemide and calcium chloride. K+ corrected to normal within the hour and the patient was transferred to the floor on the following day.
-receptor agonists (-2-receptor in particular) are known to cause intracellular shifting of K+ through stimulation of active sodium-potassium transport across the cellular membrane. While non-selective -blockers are known to result in an increase in K+ in the setting of a large K+ load or during exercise, severe hyperkalemia due to an abrupt withdrawal of a potent -agonist is a previously reported but not widely-known phenomenon. The sudden discontinuation of Isoproterenol in this case was the most likely etiology for hyperkalemia.
A hemodynamically stable patient without an obvious reason for severe, acute hyperkalemia coupled with the absence of more commonly recognized ECG changes resulted in a significant delay in treating a potentially life-threatening condition. In presenting this case we hope to increase awareness of the potential for significant hyperkalemia due to the abrupt cessation of a potent -agonist infusion. Moreover, in the absence of an apparent etiology for hyperkalemia, we recommend the suspension of one’s disbelief in favor of early treatment.
Alfonzo, AV, et al. (2006).Potassium disorders—clinical spectrum and emergency management. Resuscitation, 70(1), 10-25.
Lundborg, P. (1983) The effect of adrenergic blockade on potassium concentrations in different conditions. Acta Medica Scandinavica, 213(S672), 121-126.
Veerbhadran, S., et al. (2016). Slow Down to Brake: Effects of Tapering Epinephrine on Potassium. The Annals of Thoracic Surgery, 102(1), e37-e38.