Tromethamine buffer modifies the depressant effect of permissive hypercapnia on myocardial contractility in patients with acute respiratory distress syndrome

In patients with acute respiratory distress syndrome (ARDS), permissive hyp ercapnia Is a strategy to decrease airway pressures to prevent ventilator-i nduced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. However, in experimental studies hypercapnia Impai rs myocardial contractility and hemodynamic function. We investigated the e ffect of short-term permissive hypercapnia on myocardial contractility and hemodynamics in patients with ARDS. We hypothesized that the administration of tromethamine (THAM), a buffer which does not increase carbon dioxide pr oduction, would modify these changes. In 12 patients with ARDS, permissive hypercapnia was implemented for 2 h with a target Pa-CO2 of 80 mm Hg. Patie nts were randomized to have respiratory acidosis corrected by THAM (pH-corr ected group), or not corrected (pH-uncorrected group). Hemodynamic response s were measured, and transesophageal echocardiography (TEE) was used to det ermine myocardial contractility. Permissive hypercapnia resulted in signifi cant decreases in systemic vascular resistance (SVR) and increases in cardi ac output ((Q) over dot). Myocardial contractility decreased in both groups but significantly less in the pH-corrected group (approximately 10%) than in the pH-uncorrected group (approximately 18%, p < 0.05). Mean arterial pr essure decreased and mean pulmonary arterial pressure increased significant ly only in the pH-uncorrected group. All values returned to baseline condit ions 1 h after permissive hypercapnia was terminated. Our study demonstrate s a reversible depression of myocardial contractility and hemodynamic alter ations during rapid permissive hypercapnia which were attenuated by bufferi ng with THAM. This may have applicability to the clinical strategy of permi ssive hypercapnia and allow the benefit of decreased airway pressures to be realized while minimizing the adverse hemodynamic effects of hypercapnic a cidosis.