37 - Acid–base considerations and buffer therapy

Summary

Introduction

Both respiratory (hypercarbic) and metabolic acidosis are important components of cardiac arrest pathophysiology, and resuscitation measures aim to ameliorate or to counteract their potentially harmful effects. The acid–base derangements of cardiac arrest and CPR are exceptionally complicated because of the distinctive kinetics of carbon dioxide during the low-flow state of CPR. On the basis of this physiology, far-reaching hypotheses regarding buffer therapy in general and bicarbonate in particular have been considered and have profoundly affected clinical practice for the past two decades. These hypotheses, however, have not been substantiated by firm published data, resulting in rather ambiguous official recommendations and an atmosphere of uncertainty in the field.

The main objectives of this chapter are to discuss the complicated acid–base derangements of cardiac arrest and CPR and their effects on critical body systems, and to clarify ambiguities regarding buffer therapy.

The discussion in this chapter is limited to acid–base considerations in the context of cardiac arrest and CPR, and not in other contexts of metabolic acidosis, such as hypoxia with adequate tissue perfusion, shock, or ketoacidosis. Despite some similarities, the pathophysiology of these conditions differs markedly from that of cardiac arrest and direct extrapolation might lead to erroneous conclusions.

Historical perspectives

In their original 1961 “Report of Application of External Cardiac Massage in 118 Patients”1 Jude, Kouwenhoven and Knickerbocker wrote: “Continued cardiac arrest, even though the circulation is artificially maintained, will result in metabolic acidosis.