Hypoxia (low oxygen levels in tissue) hinders healing. The sooner that tissue hypoxia is corrected the better the outcome. Many hypoxic tissues require hyperbaric pressure to achieve a significant increase in oxygen delivery because of poor oxygen solubility in blood.
Despite thousands of publications, including controlled trials, attesting to the value of higher dosage oxygen, Hyperbaric Oxygen therapy is not widely practiced because:
I Oxygen transport is determined by the percentage respired and the barometric pressure: In normal hospital practice barometric pressure is ignored and it is assumed that patients receiving 100% are being given the same amount. In Denver Colorado which is at an altitude of over 5000 feet, the partial pressure is significantly lower than at sea level and a hyperbaric chamber is needed to give the same amount of oxygen as at sea level.
II Tissue hypoxia may be present in the absence of cyanosis: Oxygen supplementation is accepted in the alleviation of cyanosis, where the absolute level of deoxygenated hemoglobin exceeds 5g /100 ml of blood. However, the presence of cyanosis requires blood to be present in the microcirculation of a tissue and there can be significant hypoxemia without cyanosis when the hematocrit is low or when there is microcirculatory closure.
III Plasma oxygen transport is not limited by the saturation of hemoglobin: It is common for physicians to argue that blood is saturated with oxygen when a normal oxygen partial pressure (0.21 atm abs) is breathed at sea level. However it is not blood that is saturated, it is hemoglobin. The transport of oxygen by hemoglobin is finite as each of the ferrous receptor sites on the molecule can only bind one oxygen molecule. However, the plasma oxygen content increases directly as a function of the inspired partial pressure of oxygen. Breathing pure oxygen at twice atmospheric pressure, the plasma oxygen content is ten times the value of breathing air at sea level and life can be sustained without hemoglobin (continued consciousness may need higher pressure).
IV Oxygen transport to tissue depends on the tension of oxygen in plasma: Severe tissue hypoxia can be present when arterial oxygen tensions are normal if local circulatory factors, such as arterial occlusion, closure of the microcirculation and edema are present. An increase in the water content of tissue limits oxygen transport. If inflammation, edema and the invasion of metabolically active inflammatory cells occur at the same time, we can have hypoxia even when the blood flow per unit volume of tissue is increased, hence hyperemic hypoxia. In hyperbaric conditions the oxygen plasma tension increases from values of 95mm Hg to over 2000 mm Hg increasing the gradient or the transfer of oxygen into tissues by 20 fold.
V Normal blood flow does not ensure normal oxygenation: Oxygen delivery requires blood flow, although blood flow may be normal and the tissue still hypoxic. The only tissue that does not need blood flow for oxygenation is the lung.
Dr. Philip James, Professor Emeritus, Wolfson Hyperbaric Medicine Unit, University of Dundee, Ninewalls Medical School.
Dr. Philip James: trained in general medicine, involved in vascular research before specializing in occupational medicine.
Over the last 40 years he has been involved in the study of acute neurological syndromes associated with decompression sickness. He became interested in the effects on the nervous system after witnessing them first hand in decompression trials and then being involved in the acute treatment of divers working in the North Sea. He worked with Prof. Brian Hills the biomedical scientist now living in Brisbane. In persuing this area in the University of Texas and in Texas A&M University they researched a number of aspects of spinal cord function and pathophysiological mechanisms including microembolism. They also did research into the blood-brain barrier and its stabilization by adsorbed surfactant and mechanisms of disruption. The message is that although blood-brain barrier function is well understood by the drug industry it has been ignored by neurologists who are rarely in a position to do any fundamental research. If tissue barriers are disrupted then the secondary effect is the activation of aseptic inflammation due the extravasation of protein and an immune response – directed at damaged host tissue – the so-called “auto-immune” response. Over the last ten years they have looked at experimental inflammation in a human model and the role of hypoxia and hyperoxia.