Targeting pH during cardiac arrest and in the postresuscitation period

Cardiac arrest carries high mortality and morbidity, driven in part by a profound mixed respiratory and metabolic acidosis arising from hypoperfusion during cardiopulmonary resuscitation and ischemia-reperfusion injury after return of spontaneous circulation (ROSC). Severe acidosis impairs cardiovascular function, oxygen delivery, CO2 transport, and cellular metabolism, potentially worsening outcomes. This review examines the physiological rationale and current evidence for pH-targeted therapies in cardiac arrest.

Sodium bicarbonate remains the most studied buffer, but randomized trials and observational studies have largely failed to demonstrate improved survival or neurological outcomes. Its efficacy depends critically on adequate ventilation to eliminate generated CO2, a frequently overlooked variable. Sodium lactate has emerged as a promising alternative, offering buffering capacity alongside utility as an oxidizable energy substrate, with encouraging experimental data, though clinical evidence remains preliminary. Key gaps persist regarding optimal timing, dosing, and the interaction between buffer administration and ventilatory strategy.

Despite limited support for routine bicarbonate use, pH-targeted interventions retain strong physiological plausibility, and remains a promising field for future research.