EFFECTS OF BUFFER AGENTS ON POSTRESUSCITATION MYOCARDIAL DYSFUNCTION

Objectives: Earlier studies demonstrated that hypertonic buffer agents administered during cardiopulmonary resuscitation (CPR) altered neith er myocardial pH nor cardiac resuscitability. The rationale for the ro utine use of buffer agents for CPR has therefore been challenged. Howe ver, when these buffer agents are administered during CPR, they may ha ve favorable effects on the postresuscitation course. Postresuscitatio n myocardial dysfunction has more recently emerged as a potentially fa tal complication after successful cardiac resuscitation. Options for p revention and management of this complication have prompted the presen t stud ies, in which the effects of buffer agents administered during CPR are evaluated as to their effects on postresuscitation myocardial function and survival. Design: Prospective, randomized, controlled ani mal study. Setting: University animal laboratory. Subjects: Forty male Sprague-Dawley rats (450 to 570 g). Interventions: Ventricular fibril lation was induced electrically. Mechanical Ventilation and precordial compression were initiated after either a 4- or an 8-min interval of untreated cardiac arrest. Sodium bicarbonate as a CO2-generating buffe r, Carbicarb(R) and tromethamine as CO2 consuming buffers, or hyperton ic saline placebo were injected as a bolus into the right atrium durin g CPR. Defibrillation after 10 mins of cardiac arrest and CPR was succ essful in each instance. No differences in the electric power required for successful resuscitation were documented. Left ventricular pressu re, rate of left Ventricular pressure increase measured at a left vent ricular pressure of 40 mm Hg (dP/dt(40)), rate of left ventricular pre ssure decline (-dP/dt), and end-tidal PCO2 were continuously measured for 240 mins after successful resuscitation. Measurements and Main Res ults: Decreases in coronary per fusion pressure were observed after ea ch buffer or placebo injection. As anticipated, end-tidal PCO2 increas ed after bicarbonate and decreased after Carbicarb or tromethamine. Po stresuscitation left Ventricular function was significantly decreased in all animals. However, there was significantly less depression in ra te of left Ventricular pressure increase measured at a left ventricula r pressure of 40 mm Hg (dP/dt(40)), rate of left ventricular pressure decline (-dP/dt), and a lower left Ventricular diastolic pressure with both Carbicarb and tromethamine in association with significant incre ases in postresuscitation survival rate. When the duration of untreate d cardiac arrest was increased to 8 mins, the severity of postresuscit ation left ventricular dysfunction was magnified and postresuscitation myocardial function and survival were significantly improved with bot h CO2-generating and CO2-consuming buffer agents. Conclusion: Although buffer agents may not improve the success of resuscitation when admin istered during CPR, they may ameliorate postresuscitation myocardial d ysfunction and thereby improve postresuscitation survival.