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

It is commonly believed that during hyperbaric oxygen (HBO) treatment, in spite of the vasoconstriction induced by the increased O₂ content in the breathing gas, the elevated carrying capacity of O₂ in the arterial blood results in augmented O₂ delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in delivering O₂ to poorly perfused tissues if the vasoconstriction induced by elevated O₂ could be abolished or attenuated by adding CO₂ to the breathing gas. Organ blood flow (Q̇OBF), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O₂ (group 1) or 300 kPa O₂ with 2 kPa CO₂ (group 2), in awake, instrumented rats. During the HBO exposure the respiratory frequency (f(b)) fell (4 breaths·min^-1·100 kPa O₂^-1), with no changes in arterial CO₂ tension (P(a)CO₂), but when CO₂ was added, f(b) and P(a)CO₂ increased. The left ventricular pressure (LVP) and the systolic arterial pressure (SBP) increased. The maximum velocity of LVP (+ dP/dt) rose linearly with LVP whether CO₂ was added or not (r² = 0.72 and 0.75 respectively). Similarly, the cardiac output (Q̇(c)) and heart rate (f(c)) fell, while the stroke volume (SV) was unaltered, independent of P(a)CO₂. There was a general vasoconstriction in most organs in both groups, with the exception of the central nervous system (CNS), eyes, and respiratory muscles. HBO reduced the blood flow to the CNS by 30%, but this vasoconstriction was diminished or eliminated when CO₂ was added. In group 2, the blood flow to the CNS rose linearly with increased P(a)CO₂ and decreased pH. After decompression f(c) and SBP stayed high, while Q̇(c) returned to control values by reducing the SV; 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), Q̇(c), LVP, dP/dt, SBP and most Q̇OBF values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HBO treatment at a constant P(a)CO₂. Hypercapnia prevented this decline. Elevated P(a)CO₂ augmented O₂ delivery to the CNS and eyes, but increased the susceptibility to O₂ poisoning. A prolonged suppression of O₂ supply to the CNS 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 to the breathing gas.