A 62 year old man with ischemic cardiomyopathy (EF 35%) and CKD
(baseline Cr ~3 mg/dl) had a witnessed out-of-hospital cardiac arrest. EMS arrived within 3 minutes. He received CPR and was shocked out of ventricular
fibrillation (VF). He was intubated and
therapeutic hypothermia was initiated in the field. He was admitted to the CCU,
where therapeutic hypothermia was continued for 24 hours. He received aggressive KCl repletion for
hypokalemia (see graph below) and supraventricular arrhythmias. On the second hospital day the patient was
rewarmed, developed severe DIC (INR 10), worsening shock requiring 3 pressors,
and renal was consulted for hyperkalemia and oliguric AKI on CKD.
(baseline Cr ~3 mg/dl) had a witnessed out-of-hospital cardiac arrest. EMS arrived within 3 minutes. He received CPR and was shocked out of ventricular
fibrillation (VF). He was intubated and
therapeutic hypothermia was initiated in the field. He was admitted to the CCU,
where therapeutic hypothermia was continued for 24 hours. He received aggressive KCl repletion for
hypokalemia (see graph below) and supraventricular arrhythmias. On the second hospital day the patient was
rewarmed, developed severe DIC (INR 10), worsening shock requiring 3 pressors,
and renal was consulted for hyperkalemia and oliguric AKI on CKD.
Clinical pearls: Hypokalemia
is a frequent complication of hypothermia for two major reasons:
is a frequent complication of hypothermia for two major reasons:
1) cold
diuresis, which is believed to result from peripheral vasoconstriction,
increased venous return, and increased ANP;
diuresis, which is believed to result from peripheral vasoconstriction,
increased venous return, and increased ANP;
2) catecholamine-induced shift of
KCl into cells.
KCl into cells.
Interestingly, the latter
seems to depend on the type of protocol used to induce hypothermia. Core cooling increases norephinephrine but not epinephrine, and therefore does not cause
a shift of K into cells. In contrast, external cooling (which was used in this case, with the application of cooling pads)
increases epinephrine disproportionately to norepinephrine. The B2
agonist actions of epinephrine cause a shift of K into cells. It is therefore critically important to avoid KCl repletion during
rewarming due to the risk of rebound hyperkalemia, particularly in oliguric
patients such as this one who are unable to deal with the excess potassium load once it moves back out of the cells during rewarming.
seems to depend on the type of protocol used to induce hypothermia. Core cooling increases norephinephrine but not epinephrine, and therefore does not cause
a shift of K into cells. In contrast, external cooling (which was used in this case, with the application of cooling pads)
increases epinephrine disproportionately to norepinephrine. The B2
agonist actions of epinephrine cause a shift of K into cells. It is therefore critically important to avoid KCl repletion during
rewarming due to the risk of rebound hyperkalemia, particularly in oliguric
patients such as this one who are unable to deal with the excess potassium load once it moves back out of the cells during rewarming.
Posted by David Leaf
Interesting case David. Thanks for sharing. Do you think use of epinephrine and norepinephrine as vasopressor in this pt ( as he had 3 vasopressor) contribute to the problem?