Physics of Hyperbaric Medicine
Adapted from - https://emedicine.medscape.com/article/1464149-overview#a2

The physics behind hyperbaric oxygen therapy (HBOT) lies within the ideal gas laws.
  • The application of Boyle’s law (p1 v1 = p2 v2) is seen in many aspects of HBOT. This can be useful with embolic phenomena such as decompression sickness (DCS) or arterial gas emboli (AGE). As the pressure is increased, the volume of the concerning bubble decreases. This also becomes important with chamber decompression; if a patient holds her breath, the volume of the gas trapped in the lungs overexpands and causes a pneumothorax.
  • Charles’ law ([p1 v1]/T1 = [p2 v2]/T2) explains the temperature increase when the vessel is pressurized and the decrease in temperature with depressurization. This is important to remember when treating children or patients who are very sick or are intubated.
  • Henry’s law states that the amount of gas dissolved in a liquid is equal to the partial pressure of the gas exerted on the surface of the liquid. By increasing the atmospheric pressure in the chamber, more oxygen can be dissolved into the plasma than would be seen at surface pressure.

The clinician must be able to calculate how much oxygen a patient is receiving. In order to standardize this amount, atmospheres absolute (ATA) are used. This can be calculated from the percentage of oxygen in the gas mixture (usually 100% in HBOT; 21% if using air) and multiplied by the pressure. The pressure is expressed in feet of seawater (fsw), which is the pressure experienced if one were descending to that depth while in seawater. Depth and pressure can be measured in many ways; some common conversions are 1 atmosphere (atm) = 33 feet of seawater (fsw) = 10 meters of sea water (msw) = 14.7 pounds per square inch (psi) = 1.01 bar.


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

Hyperbaric Physiology Table 1 below summarizes the physiologic mechanisms of HBOT. Each of these is discussed in the context of the indications for HBOT.What is the physiology of hyperbaric oxygen therapy (HBOT)?  

Mechanism

References

Clinical Application

Hyperoxygenation*

Boerema I[5]



Bassett BE[6]



Bird AD[7]



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's law

Air or gas embolism

Vasoconstriction †

Nylander G[8]



Sukoff MH[9]



Crush injury/compartment syndrome



Thermal burns



Angiogenesis

Knighton DR[10]

Problem wounds



Compromised grafts and flaps



Delayed radiation injury



Fibroblast proliferation/collagen synthesis

Hunt TK[11]

Problem wounds



Delayed radiation injury

Leukocyte oxidative killing ‡

Mader JT[12]



Park MK[13]



Mandell GL[14]



Necrotizing soft tissue infections



Refractory osteomyelitis



Problem wounds

Reduces intravascular leukocyte adherence

Zamboni WA[15]



Thom SR[16, 17]



Crush injury/compartment syndrome

Reduces lipid peroxidation

Thom SR[18]

CO poisoning



Crush injury/compartment syndrome

Toxin inhibition

Van Unnik A[19]

Clostridial myonecrosis

Antibiotic synergy

Mirhij NJ[20]



Keck PE[21]



Mendel V[22]



Muhvich KH[23]



Necrotizing soft tissue infections



Refractory osteomyelitis

*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 microvascular blood flow. This vasoconstrictive effect does, however, reduce posttraumatic 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 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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