Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

It is commonly believed that during hyperbaric oxygen (HBO) treatment, in s pite of the vasoconstriction induced by the increased O-2 content in the br eathing gas, the elevated carrying capacity of O-2 in the arterial blood re sults in augmented O-2 delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in deliver ing O-2 to poorly perfused tissues if the vasoconstriction induced by eleva ted O-2 could be abolished or attenuated by adding CO2 to the breathing gas . Organ blood flow ((Q)over dot (OBF)), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O-2 (group 1) or 300 kPa O-2 with 2 kPa CO2 (group 2), in awake, instru mented rats. During the HBO exposure the respiratory frequency (f(b)) fell (4 breaths . min(-1) . 100 kPa O-2(-1)), with no changes in arterial CO2 te nsion (PaCO2), but when CO2 was added, f(b) and PaCO2 increased. The left v entricular pressure (LVP) and the systolic arterial pressure (SBP) increase d. The maximum velocity of LVP (+dP/dt) rose linearly with LVP whether CO2 was added or not (r(2) = 0.72 and 0.75 respectively). Similarly, the cardia c output ((Q)over dot (c)) and heart rate (f(c)) fell, while the stroke vol ume (SV) was unaltered, independent of PaCO2. There was a general vasoconst riction in most organs in both groups, with the exception of the central ne rvous system (CNS), eyes, and respiratory muscles. HBO reduced the blood fl ow to the CNS by 30%, but this vasoconstriction was diminished or eliminate d when CO2 was added. In group 2, the blood flow to the CNS rose linearly w ith increased PaCO2 and decreased pH. After decompression f(c) and SEP stay ed high, while (Q)over dot (c) returned to control values by reducing the S V; CNS blood flow remained markedly elevated in group 2, while in group 1, it returned to control levels. We conclude that the changes in f(c), (Q)ove r dot (c), LVP, dP/dt, SBP and most (Q)over dot (OBF) values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HB O treatment at a constant PaCO2. Hypercapnia prevented this decline. Elevat ed PaCO2 augmented O-2 delivery to the CNS and eyes, but increased the susc eptibility to O-2 poisoning. A prolonged suppression of O-2 supply to the C NS occurred during the HBO exposure and in air following the decompression in the absence of CO2. This suppression was offset by the addition of CO2 t o the breathing gas.