Key result
In a canine model of cardiac arrest, serum potassium increased significantly from baseline during closed-chest CPR (p<0.001) and returned to baseline by 15 minutes post-resuscitation.
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May caution potassium interpretation during CPR; leaves open translation to human resuscitation protocols.
Although recent clinical reports have noted hypokalemia after resuscitation from cardiac arrest, extensive animal work indicates that potassium is released from cells during ischemia. This study was undertaken to define the changes that occur in serum potassium ion during cardiac arrest and resuscitation in a canine model. Fourteen dogs were subjected to 5 min of cardiac arrest followed by 30 min of closed-chest CPR (CCPR). Resuscitation was performed according to a standardized protocol. Serum potassium increased significantly (p less than .001) from baseline, remained elevated 5 min after return of spontaneous circulation (ROSC), but declined to baseline levels at 15 min post-ROSC. Increases in interstitial potassium would be expected to be even greater due to the poor exchange between interstitial and intravascular compartments during CCPR. Interstitial hyperkalemia may play a role in the genesis of wide-complex electromechanical dissociation and may explain the reported success of calcium chloride in treating this problem.
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Martin et al. (1986) studied Cardiac arrest and resuscitation (n=14). Cardiac arrest and closed-chest CPR vs. Baseline was evaluated on Changes in serum potassium ion (p=<0.001). In a canine model of cardiac arrest, serum potassium increased significantly from baseline during closed-chest CPR (p<0.001) and returned to baseline by 15 minutes post-resuscitation.
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