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Hyperkalemia and ionized hypocalcemia during cardiac arrest and resuscitation: possible culprits for postcountershock
1UCLA School of Medicine, and the Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, CA, USA. jniemann@ucla.edu
Insights
During prolonged resuscitation efforts, increased serum potassium and decreased ionized calcium were observed in dogs. These electrolyte shifts may contribute to refractory postcountershock rhythm disturbances like asystole or PEA.
Area of Science:
- Cardiology
- Emergency Medicine
- Physiology
Background:
- Early defibrillation improves outcomes in out-of-hospital cardiac arrest.
- Prolonged ventricular fibrillation (VF) countershock often leads to asystole or pulseless electrical activity (PEA).
- The mechanisms behind post-countershock rhythm disturbances are not fully understood, potentially involving myocardial electrical injury or metabolic abnormalities.
Purpose of the Study:
- To investigate changes in serum potassium and ionized calcium homeostasis during cardiac arrest and advanced cardiac life support (ACLS).
Main Methods:
- Ventricular fibrillation (VF) was induced in 13 dogs.
- After 7.5 minutes of VF, animals underwent countershock, cardiopulmonary resuscitation (CPR), and epinephrine administration.
- Serum electrolytes were monitored throughout the resuscitation period.
Main Results:
- Animals that could not be resuscitated showed a significant increase in serum potassium (4.3 to 6.0 mEq/L) and a decrease in ionized calcium (4.95 to 3.44 mg/dL) during ACLS.
- These electrolyte changes occurred within 5-10 minutes of initiating resuscitation.
- Nine of ten non-resuscitated animals developed asystole or PEA.
Conclusions:
- Hypocalcemia and hyperkalemia develop during prolonged resuscitation efforts.
- These ionic shifts may result from impaired transcellular transport mechanisms.
- Electrolyte imbalances may contribute to refractory post-countershock rhythm disturbances, impacting cardiac function.
Study Objective:
Early countershock of ventricular fibrillation (VF) has been shown to improve immediate and long-term outcome of out-of-hospital cardiac arrest. However, studies indicate that countershock of prolonged VF most commonly results in asystole or a nonperfusing bradyarrhythmia (pulseless electrical activity [PEA]), which rarely respond to current therapy. The cause of these postcountershock rhythm disturbances is not well understood but may be related to electrical injury of the globally ischemic myocardium or to local metabolic abnormalities that impair impulse formation and cardiac contraction. The purpose of this study was to evaluate changes in serum potassium and free calcium homeostasis during cardiac arrest and advanced cardiac life support (ACLS) interventions.
Methods:
After sedation, intubation, anesthesia, and instrumentation, VF was induced in 13 dogs. After 7.5 minutes of VF, animals were immediately countershocked, standard closed-chest CPR was initiated, and epinephrine was administered (1 mg in repeated doses if necessary).
Results:
Ten animals could not be resuscitated despite 20 minutes of ACLS interventions. In these animals, a progressive increase in serum potassium was observed from the onset of ACLS to the termination of resuscitation efforts (4.3+/-.6 to 6.0+/-.8 mEq/L, P<.01). A significant increase was observed within 10 minutes of beginning ACLS measures. This was accompanied by a decrease in ionized calcium concentration over the same period (4.95+/-.40 to 3.44 mg/dL, P<.01). The decrease in ionized calcium was significant within 5 minutes of ACLS interventions. Nine of these 10 animals had either postcountershock asystole or PEA at the termination of resuscitative efforts. The increase in potassium was not related to acidemia. Successfully resuscitated animals did not demonstrate these electrolyte changes.
Conclusion:
Ionized hypocalcemia and hyperkalemia occur during prolonged resuscitative efforts and may be related to dysfunctional transcellular ionic transport mechanisms. These cations play important roles in cardiac electrical and contractile activity and may play a role in refractory postcountershock rhythm disturbances.