Pathophysiologic and therapeutic implications of acid-base changes during CPR

Area of Science:

• Cardiology
• Emergency Medicine
• Physiology

Background:

• Cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) induce complex acid-base disturbances.
• These changes are linked to a low-perfusion state with hypercarbic and lactic acidosis.
• The dynamic nature of this state depends on arrest-to-CPR and CPR-to-circulation restoration intervals.

Purpose of the Study:

• To review experimental data on the role of buffer agents in managing acid-base changes during CPR.
• To evaluate the controversial use of sodium bicarbonate and other buffers in cardiac arrest scenarios.
• To determine if buffer therapy improves neurologically intact survival post-CPR.

Main Methods:

• Review of experimental studies on acid-base balance during CA and CPR.
• Analysis of data regarding the efficacy of CO2-generating and CO2-consuming buffers.
• Assessment of the impact of ventilation and chest compressions on acid-base status.

Main Results:

• Experimental data suggest that very low pH may be compatible with neurologically intact survival.
• No conclusive evidence shows that CO2-generating or CO2-consuming buffers improve long-term neurologically intact survival after CPR.
• Adequate ventilation and effective chest compressions are crucial for counterbalancing acidemia during CPR.

Conclusions:

• The primary treatment for acid-base changes during CPR relies on airway management, adequate ventilation, effective chest compressions, and early defibrillation.
• Buffer therapy, particularly sodium bicarbonate, remains controversial due to a lack of controlled clinical studies.
• Buffer therapy may be considered in cases of prolonged cardiac arrest or pre-existing metabolic acidosis.