Cardiac effects of carbon dioxide-consuming and carbon dioxide-generating buffers during cardiopulmonary resuscitation

Abstract

Recent studies have demonstrated an increase in carbon dioxide (CO2) tension (PCO2) in both mixed venous and coronary vein blood early in the course of cardiac arrest and cardiopulmonary resuscitation. Because increased PCO2 in the myocardium correlates with both ischemic injury and depression of contractile function, the effects of hypertonic solutions of either the CO2-"generating" sodium bicarbonate (NaHCO3) buffer, a mixture of sodium carbonate (Na2CO3) and sodium bicarbonate (carbicarb) acting as a CO2-"consuming" buffer, or saline placebo (NaCl) were compared during cardiopulmonary resuscitation in 25 healthy minipigs. Both buffer agents significantly increased the pH and HCO3- of arterial, mixed venous and coronary vein blood. Bicarbonate increased whereas carbicarb reduced blood PCO2 in the systemic circuit as anticipated. However, neither the PCO2 nor the lactate content of coronary vein blood was favorably altered by buffer therapy. Four of eight animals treated with bicarbonate, five of eight treated with carbicarb and six of nine placebo-treated animals were successfully resuscitated and had a comparable 24 h survival rate. Coronary perfusion pressure during precordial compression, a critical determinant of resuscitability, was transiently decreased by each of the hypertonic solutions. Accordingly, neither CO2-generating nor CO2-consuming buffers mitigated increases in coronary vein PCO2 or improved the outcome of cardiopulmonary resuscitation under these experimental conditions.

Zoniporide preserves left ventricular compliance during ventricular fibrillation and minimizes postresuscitation myocardial dysfunction through benefits on energy metabolism*

“…During closedchest resuscitation, this level of coronary perfusion pressure is insufficient to reverse myocardial ischemia (2) yet sufficient to enable successful resuscitation (16,31). In the current open-chest model, the coronary perfusion pressure of 10 mm Hg promoted a coronary blood flow corresponding to 50% of baseline.…”

Sodium-Hydrogen Exchange Inhibition During Ventricular Fibrillation

“…The force of compression was gradually increased in an attempt to generate within 3 minutes a coronary perfusion pressure above the minimal resuscitability threshold of 10 mm Hg in pigs. 6 This requirement was met in 8 of 12 pigs randomized to NaCl and in 8 of 13 pigs randomized to cariporide. Only pigs that met this criterion are reported here.…”

“…LV ejection fraction, % NaCl (nϭ8) 60Ϯ6 NHE-1 inhibition using the potent and selective inhibitor cariporide prevented ischemic contracture and enabled chest compression to maintain a coronary perfusion pressure above resuscitability thresholds. 6 In a limited number of experiments in which the left ventricle was well visualized during chest compression, cariporide attenuated reductions in left ventricular cavity size. Thus, preservation of end-of-chest-relaxation ventricular volumes with enhanced forward blood flow probably explained these favorable effects of NHE-1 inhibition.…”

Guidelines for paediatric life support

“…However, increasing the pH of blood in the coronary vein by either carbon dioxide consuming (carbicarb) or carbon dioxide generating buffers (bicarbonate) had no effect on outcome in experimental animals with ventricular fibrillation 51. Indeed, there was evidence that the hyperosmolar solution increased right atrial pressure and therefore could decrease myocardial perfusion pressure 51 52. A particular concern with bicarbonate is that it generates carbon dioxide in its buffering action.…”