INFLUENCE OF PROPHYLACTIC ADMINISTRATION OF N-ACETYLCYSTEINE ON THE CLINICAL INDICATORS OF TISSUE OXYGENATION DURING HYPEROXIC VENTILATION IN CARDIAC RISK PATIENTS

Hyperoxic ventilation, used to prevent hypoxia during potential period s of hypoventilation, has been reported to paradoxically decrease whol e-body oxygen consumption (VO2). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigat ed whether pretreatment with the sulfhydryl group donor and O-2 radica l scavenger N-acetylcysteine (NAC) would preserve VO2 and other clinic al indicators of tissue oxygenation in cardiac risk patients. Methods. Thirty patients, requiring hemodynamic monitoring (radial and pulmona ry artery catheters) because of cardiac risk factors, were included in this randomized investigation. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, F(1)0(2)<0.5) . Cardiac output was determined by thermodilution and VO2 by cardiovas cular Fick. After baseline measurements, patients randomly received ei ther 150 mg kg(-1) NAC (n=15) or placebo (n=15) in 250 ml 5% dextrose i.v. over a period of 30 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (F1O 2=1.0), and 30 min after resetting the original F1O2. Results. There w ere no significant differences between groups in any of the measuremen ts before treatment and after the return to baseline F1O2 at the end o f the study, respectively. NAC, but not placebo infusion, caused a sli ght but not significant increase in cardiac index (CI), left ventricul ar stroke work index (LVSWI) and a decrease in systemic vascular resis tance. Significant differences between groups during hyperoxia were: V O2 (NAC: 108 +/- 38 ml min(-1)m(-2) vs placebo: 79 +/- 22 ml min(-1)m( -2), P less than or equal to 0.05, CI (NAC: 4.6 +/- 1.0 vs placebo: 3. 7 +/- 1/11 min(-1)m(-2), P less than or equal to 0.05) and LVSWI (NAC: 47 +/- 12 vs placebo: 38 +/- 9 P less than or equal to 0.05). The mea n decrease of VO2 was 22% in the NAC group vs 47% in the placebo group (P less than or equal to 0.05) and the mean difference between groups in venoarterial carbon dioxide gradient (PvaCO(2)) was 14% (P less th an or equal to 0.05). ST segment depression (>0.2 mV) was significantl y less marked in the NAC group (NAC: -0.02 +/- 0.17 vs placebo: -0.23 +/- 0.15; P less than or equal to 0.05). Conclusions. NAC helped prese rve VO2 oxygen delivery, CT, LVSWI and PvaCO(2) during brief hyperoxia in cardiac risk patients. Clinical signs of myocardial ischemia did n ot occur such as ST-depression if patients were prophylactically treat ed with NAC. This suggests that pretreatment with NAC could be conside red to attenuate impaired tissue oxygenation and to preserve myocardia l performance better in cardiac risk patients during hyperoxia.