What is the physiology of hyperbaric oxygen therapy (HBOT)?

Updated: Nov 16, 2020
  • Author: Emi Latham, MD, FACEP, FAAEM, UHM; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Answer

Answer

Table 1 below summarizes the physiologic mechanisms of HBOT. Each of these is discussed in the context of the indications for HBOT later in this article.

Table 1. Physiologic Mechanisms of Hyperbaric Oxygen Therapy (Open Table in a new window)

Mechanism

References

Clinical Application

Hyperoxygenationa

Boerema I [6]

Bassett BE [7]

Bird AD [8]

DCS/AGE

CO poisoning

Central retinal artery occlusion

Crush injury/compartment syndrome

Compromised grafts and flaps

Severe blood loss anemia

Decrease gas bubble size

Boyle law

Air or gas embolism

Vasoconstrictionb

Nylander G [9]

Sukoff MH [10]

Crush injury/compartment syndrome

Thermal burns

Angiogenesis

Knighton DR [11]

Tal S [12]

Problem wounds

Compromised grafts and flaps

Delayed radiation injury

Fibroblast proliferation/collagen synthesis

Hunt TK [13]

Problem wounds

Delayed radiation injury

Leukocyte oxidative killingc

Mader JT [14]

Park MK [15]

Mandell GL [16]

Necrotizing soft tissue infections

Refractory osteomyelitis

Problem wounds

Reduces intravascular leukocyte adherence

Zamboni WA [17]

Thom SR [18, 19]

Crush injury/compartment syndrome

Reduces lipid peroxidation

Thom SR [20]

CO poisoning

Crush injury/compartment syndrome

Toxin inhibition

Van Unnik A [21]

Clostridial myonecrosis

Antibiotic synergy

Mirhij NJ [22]

Keck PE [23]

Mendel V [24]

Muhvich KH [25]

Necrotizing soft tissue infections

Refractory osteomyelitis

aMost 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.

bHyperoxia in normal tissues causes vasoconstriction, but this is compensated by increased plasma oxygen content and microvascular blood flow. This vasoconstrictive effect does, however, reduce posttraumatic tissue edema, which contributes to the treatment of crush injuries, compartment syndromes, and burns.

cHBOT 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 proinflammatory 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.


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