In healthy individuals breathing air the volume of oxygen bound with hemoglobin at normobaric pressure is adequate to meet normal tissue metabolic requirements. The inspired oxygen essentially saturates the hemoglobin. Only an insignificant amount of oxygen is carried in physical solution in plasma. Oxygen diffusion across the blood-gas barrier is a passive process and any disruption to the oxygen pathway can have significant impact on tissue oxygenation.
Oxygen is a critical nutrient and plays an important part in wound repair (Niinikoski, 1977). Wound healing is an oxygen-dependent mechanism which is rate limited by its availability (Sheffield, 1988). The impairment of tissue oxygen delivery causes an energy crisis and can lead to the development of chronic, infected, non-healing wounds (Hunt et al, 1977). The formation of edema increases the diffusion distance, and significantly disrupts tissue oxygenation. The migration of inflammatory cells also raises wound oxygen requirements. All ischemic wounds are hypoxic but not all hypoxic wounds are ischemic. Even adequately perfused wounds may become hypoxic as the presence of infection raises oxygen requirements (Davis & Hunt, 1988). Thus, the common denominator in chronic wounds is profound tissue hypoxia.
Hyperbaric oxygen is used to promote oxygen transport to tissues in certain conditions where the normal oxygen pathway has been compromised by infection, traumatic injury, ischemia, hypoxia, inflammation and edema, and tissue poisoning. The primary actions are as follows:
HBO2 increases oxygen delivery to the tissue:
Since hemoglobin is normally saturated the only way that oxygen delivery to the tissues can be increased is by significantly elevating the partial pressure of respired oxygen. A normal level of oxygen in arterial blood does not ensure that tissue oxygen levels are normal. The volume of oxygen normally delivered to tissue when breathing air is the sum of the amount (19.5ml/100mls) bound to hemoglobin plus the amount (0.3ml/100mls) which remains in physical solution in plasma. When breathing 100% oxygen at atmospheric pressure, the amount in physical solution is increased to approximately 2.0ml/100mls for each atmosphere (760mmHg) of pressure. The availability of oxygen to tissue depends on its distance from functioning capillaries, the oxygen requirements of that tissue and the partial pressure of oxygen in the capillary.
Hyperbaric oxygen therapy works by elevating the plasma oxygen level in proportion to the partial pressure of inspired oxygen (Henry's Law). At 3 atm abs, the maximum pressure used in clinical hyperbaric oxygen therapy, the volume of oxygen carried in physical solution in plasma increases to approximately 6vol% while the amount bound on hemoglobin remains essentially constant. Studies have shown that at 3 atm abs, the average metabolic oxygen requirements of the body can be met by the oxygen dissolved in plasma and that oxyhemoglobin will pass unchanged from the arterial to the venous side since the oxygen in solution in plasma will be used more readily than that bound with hemoglobin (Bassett & Bennett, 1977, Boerema et al 1960).
HBO2 reduces edema:
Hyperbaric oxygen reduces cardiac output by some 20%, which is primarily due to bradycardia rather than a reduction in stroke volume (Jain & Fischer, 1989). In addition, increased arterial PO2 causes vasoconstriction that produces a reduction in capillary blood pressure. Data show that hypoxic tissue does not vasoconstrict (Hammarlund, 2002). These actions, in turn, facilitate a reduction in transcapillary fluid flow and encourage extravascular fluid to be reabsorbed into the circulation while paradoxically improving oxygen delivery to the tissue (Strauss et al 1986; Nylander et al 1985).
HBO2 helps to protect the microcirculation:
Increased arterial PO2 prevents neutrophil adherence and so helps to maintain the microcirculation by protecting it from physical blockage and damage to the post-capillary endothelium, and chemically mediated arterial vasoconstriction (Zamboni et al 1989, 1992, 1993).
HBO2 promotes neovascularization:
In the compromised host impairment of the microcirculation causes hypoxia. The partial pressure of oxygen may be as low as a few mmHg in some hypoxic zones. While fibroblasts can survive they become inactive at this low PO2. Elevating the partial pressure of oxygen increases the rate and distance oxygen will diffuse from patent capillaries across the barriers created by edema and poor perfusion. When the tissue PO2 is elevated, using hyperbaric oxygen, to 40 mmHg, healing is facilitated by the enhancement of macrophage function, fibroblast proliferation and collagen synthesis, angiogenesis, and epithelialization (Knighton 1981; Hunt TK, 1988; Uhl et al 1994; Tompach et al 1997; Hehenberger et al 1997).
HBO2 enhances the killing power of leukocytes:
Phagocytic leukocytes are the primary defense against infection in injured tissue and it is generally assumed that granulocyte function is normal. However, data show that both the degranulation and oxidative killing functions of leukocytes depend largely on the degree to which molecular oxygen is available, and this is significantly reduced at the low PO2's in chronic wounds. Their activity, and thus, killing ability is significantly enhanced when oxygen levels are elevated with hyperbaric oxygen (Hohn et al 1976; Mader et al 1978; Rabkin & Hunt 1988; Allen et al 1997; Hopf et al 1997).
HBO2 has a direct effect on anaerobic bacteria:
In addition to enhancing host defenses, hyperbaric oxygen at 2-3 atm abs acts directly against, and significantly reduces the proliferation of anaerobic bacteria (Kaye, 1967; Demello, 1970; Demello, 1973 Hill & Osterhout, 1972). In gas gangrene, HBO2 has also been shown to inhibit the production of clostridial alpha toxin, which destroys cell membranes and increases capillary permeability (Van Unnik, 1965; Hill & Osterhout, 1966).
Copyright Life Support Technologies Group Inc, Sept 2012