PHYSIOLOGICAL BASIS OF HYPERBARIC OXYGEN THERAPY
The effects of HBOT are based on Boyle’s, Dalton’s and Henry’s gas laws and the physiologic effects of hyperoxia.
Most oxygen carried in blood is bound to hemoglobin which is 97% saturated at normal atmospheric pressure (1 ATM). A small percentage of oxygen is carried in solution when breathing normobaric air. The percentage of oxygen in solution can be increased significantly when the inspired oxygen is increased in concentration and pressure i.e. hyperbaric oxygen (Henry’s gas law). At 1 ATM the arterial oxygen tension is near 100mmHg and tissue oxygen tension near 55mmHg. Providing 100% inspired oxygen at 3 ATA can increase arterial oxygen tension and tissue oxygen tension to 2,000mmHg and 500mmHg, respectively, solely by increasing the amount of oxygen carried in solution. (Clinically, treatments do not exceed 2ATM to avoid potential oxygen toxicity).
This will increase oxygen delivery to the tissues significantly and is sufficient to support the cellular functions of the tissues in the absence of hemoglobin in blood. The elevated oxygen level in solution can reach tissues that have limited RBC transportation due to disease or in cases of decreased oxygen carrying capacity,of blood/hemoglobin (anemia or carbon monoxide toxicity).
HBOT MECHANISMS OF ACTION
HBOT damages bacterial cellular DNA and enhances the oxygen dependent peroxidase system leukocytes used to kill bacteria. The transport of certain antibiotics into tissues that use oxygen-dependent transport mechanisms is increased, thereby, enhancing their efficacy. This is most effective for aminoglycosides and trimethoprim sulfa. Flouroquinolones are less effective in a hypoxic environment and HBOT will restore their effectiveness.
Creating a large oxygen gradient at the periphery of ischemic or poorly healing wounds enhances fibroblast function and the oxygen dependent matrix formation needed for angiogenesis, enhances wound healing.
During reperfusion injuries, leukocytes adhere to damaged/ischemic tissues releasing oxygen free radicals and proteases, further damaging tissues and causing further vasoconstriction. HBOT will reduce leukocyte adherence and post-ischemic vasoconstriction thereby providing a beneficial effect on reperfusion injuries (crush injuries, compartment syndromes, edematous skin grafts). HBOT protects tissue from oxygen free radicals and prevents the sequestration of neutrophils on damaged endothelium during ischemia so when reperfusion occurs the damage from neutrophils, inflammatory mediators and oxygen free radicals is reduced.
Increased oxygen tension in blood will lead to vasoconstriction, however; this is offset by the increased diffusion of oxygen down a pressure gradient. In posttraumatic edematous tissue, this vasoconstriction will reduce edema and the increased oxygen in solution will reduce tissue hypoxia significantly.
HBOT promotes angiogenesis in injured tissues.
Beneficial effects are evident when treating at 1.5 to 2.0 ATM for 45 to 60 minutes. There is little need for treating at higher ATM or for more prolonged periods of time. This can potentiate deleterious effects of increased pressure and hyperoxia (oxygen toxicity). Treatments can be repeated every four hours after completing decompression. Most patients will benefit from a series of treatment sessions, not a single session.
CLINICAL INDICATIONS FOR HBOT IN VETERINARY PATIENTS
COMPLICATIONS OF HBOT
CONTRAINDICATIONS FOR HBOT