THE EFFECT OF ACIDOSIS ON CATECHOLAMINE RESPONSIVENESS IN ISOLATED INFANT RABBIT HEART. † 260

Current management of respiratory failure involves permissive hypercapnia to minimize lung trauma, producing respiratory acidosis. Catecholamine infusions are frequently required for hemodynamic support, current debate centers around the need for correction of acidosis based on hemodynamic performance and catecholamine responsiveness. Therefore, the effects of systemic acidosis on myocardial epinephrine responsiveness was studied in an isolated perfused infant rabbit heart model.

METHODS: Isolated Hearts from 4 day-old New Zealand white rabbits were perfused with Hepes buffer at 37°C with LVEDP maintained at 10 mmHg. Following a 60 min baseline period, hearts were perfused with epinephrine (10^-6M) for 60 min and then with epinephrine (10^-5 M) for 60 min. Control hearts (n=8) were perfused with pH 7.4, experimental hearts (n=8) at pH 7.2. Isovolumic LV function was measured as rate-pressure-product, (RPP = HR X LV developed pressure). O₂ consumption (MVO₂) was measured with YSI microoxygen probes. Myocardial efficiency was MVO₂/RPP. Data are Mean±SEM with significance defined as P<0.05 (ANOVA).

RESULTS: Baseline results were similar for RPP, MVO₂ and myocardial efficiency at pH 7.4 and 7.2. Epinephrine infusion increased RPP to 153±14% and 144±8, MVO₂ 163±15 and 141±6 at pH 7.4 and 7.2 respectively. Myocardial efficiency was unchanged during all experiments. No significant differences were noted comparing pH 7.4 to pH 7.2.

CONCLUSIONS: Perfusion of isolated infant hearts at pH similar to that noted during permissive hypoventilation (7.2) did not result in changes in cardiac output or myocardial oxygen consumption at baseline or during catecholamine infusion. By using the isolated heart model, this study was able to focus on cardiac performance with preload (LVEDP) fixed and without effects due to alterations in peripheral vascular resistance. These data imply that correction of acidosis (pH 7.2) noted with permissive hypoventilation is not necessary to optimize myocardial performance, including during catecholamine infusions.