Ran Arieli1. 1. Israel Naval Medical Institute, Haifa, Israel. rarieli@netvision.net.il
Abstract
INTRODUCTION: Clinical hyperbaric oxygen (HBO) therapy and the use of pure oxygen or gases having a high partial pressure of oxygen in diving carry a risk of central nervous system (CNS) oxygen toxicity. Previously, we solved the power equation K = t2(PO2/101.3)C for humans, where t is the exposure time, PO2 is the oxygen pressure, and K is the cumulative oxygen toxicity index. The value of c was 6.76, and a symptom may appear when K reaches a threshold value Kc = 2.31 X 10(8) (Arieli et al. J Appl Physiol 2002; 92:248-56). METHODS AND RESULTS: The calculation of K for a complex exposure profile made it possible to estimate risk from the normal distribution for a metabolic rate of 1.28 L x min(-1), Z = [ln(K0.5)-9.63]/2.02 and for 0.9 L x min(-1), Z = [ln(K0.5)-11.19]/1.35. The predicted risk was in agreement with the reported risk in composite exposures. The parameters c and ln(Kc) in the power equation are linearly related to metabolic rate (M) and inspired CO2 in rats. Due to the assumed similar relationship between the data from rats and humans, the mean time to CNS oxygen toxicity (tc(M)) as a function of metabolic rate may be calculated for humans as follows: tc(M) = [(e(-2.85 M + 31.8))/(PO2/101.3)(-7.45 M + 39.6)]0.5, where M is metabolic rate in units of resting metabolic rate. A parallel equation for the mean time to toxicity as a function of PCO2 was derived for the rat. This equation can be transformed to express the latency in humans, once the parameters for humans are known. CONCLUSIONS: The power equation that predicts oxygen toxicity in humans was extended to include a complex diving profile as well as the effects of metabolic rate and CO2.
INTRODUCTION: Clinical hyperbaric oxygen (HBO) therapy and the use of pure oxygen or gases having a high partial pressure of oxygen in diving carry a risk of central nervous system (CNS) oxygentoxicity. Previously, we solved the power equation K = t2(PO2/101.3)C for humans, where t is the exposure time, PO2 is the oxygen pressure, and K is the cumulative oxygentoxicity index. The value of c was 6.76, and a symptom may appear when K reaches a threshold value Kc = 2.31 X 10(8) (Arieli et al. J Appl Physiol 2002; 92:248-56). METHODS AND RESULTS: The calculation of K for a complex exposure profile made it possible to estimate risk from the normal distribution for a metabolic rate of 1.28 L x min(-1), Z = [ln(K0.5)-9.63]/2.02 and for 0.9 L x min(-1), Z = [ln(K0.5)-11.19]/1.35. The predicted risk was in agreement with the reported risk in composite exposures. The parameters c and ln(Kc) in the power equation are linearly related to metabolic rate (M) and inspired CO2 in rats. Due to the assumed similar relationship between the data from rats and humans, the mean time to CNS oxygentoxicity (tc(M)) as a function of metabolic rate may be calculated for humans as follows: tc(M) = [(e(-2.85 M + 31.8))/(PO2/101.3)(-7.45 M + 39.6)]0.5, where M is metabolic rate in units of resting metabolic rate. A parallel equation for the mean time to toxicity as a function of PCO2 was derived for the rat. This equation can be transformed to express the latency in humans, once the parameters for humans are known. CONCLUSIONS: The power equation that predicts oxygentoxicity in humans was extended to include a complex diving profile as well as the effects of metabolic rate and CO2.