The Physiology of HBOT
Most oxygen carried in the blood is bound to hemoglobin, which is 97% saturated at standard pressure. Some oxygen, however, is carried in solution, and this portion is increased under hyperbaric conditions due to Henry’s law. Tissues at rest extract 5-6 mL of oxygen per deciliter of blood, assuming normal perfusion. Administering 100% oxygen at normobaric pressure increases the amount of oxygen dissolved in the blood to 1.5 mL/dL; at 3 atmospheres, the dissolved-oxygen content is approximately 6 mL/dL, which is more than enough to meet resting cellular requirements without any contribution from hemoglobin. Because the oxygen is in solution, it can reach areas where red blood cells may not be able to pass and can also provide tissue oxygenation in the setting of impaired hemoglobin concentration or function. Hyperoxia in normal tissues causes vasoconstriction, but this is compensated by increased plasma oxygen content and micro vascular blood flow. This Vasoconstrictive effect does, however, reduce post traumatic tissue edema, which contributes to the treatment of crush injuries, compartment syndromes, and burns. HBOT increases the generation of oxygen free radicals, which oxidize proteins and membrane lipids, damage DNA, and inhibit bacterial metabolic functions. HBO is particularly effective against anaerobes and facilitates the oxygen-dependent Peroxidase system by which leukocytes kill bacteria. Additionally, evidence is growing that HBOT alters the levels of pro-inflammatory mediators and may blunt the inflammatory cascade. More studies are needed to further elucidate this complex interaction. As HBOT is known to decrease heart rate while maintaining stroke volume, it has the potential to decrease cardiac output. At the same time, through systemic vasoconstriction, HBOT increases afterload. This combined effect can exacerbate congestive heart failure in patients with severe disease; however, clinically significant worsening of congestive heart failure is rare.