Understanding Hyperbaric Oxygen Therapy
Since hyperbaric oxygen therapy (HBOT) involves the application of oxygen (a gas) under pressure, a short lesson in physics is needed to understand the basic principles.
“Normal” atmospheric pressure that we live under every day exerts approximately 14.7 pounds per square inch (psi), or 760 millimeters of mercury (mmHg) on our skin and on the air that we breathe. This atmospheric air is approximately 79% nitrogen and 21% oxygen, resulting in an oxygen pressure of about 160 mmHg.
Dalton’s law states that the component gas exerts a pressure equivalent to its percentage composition of the mixture. HBOT is talked about in terms of atmospheres absolute (ATA). Normal atmospheric pressure at sea level of 14.7 psi or 760 mmHg is equal to 1 ATA. Anyone with scuba diving experience may remember that as you dive you experience an increase in pressure with increasing depth.
Each 33 feet of sea water provides an equivalent increase of 1 ATA of pressure. Therefore, at 33 feet under water you are at 2 ATA. 2 ATA is equivalent to 29.4 psi.
Normal circumstances of oxygen delivery in the body are dependent on the following:
- Proportion of oxygen in the air that we breathe
- Lung function
- The amount of hemoglobin in the blood
- The body’s normal circulation processes (blood pressure)
The hemoglobin molecule is the primary carrier of oxygen to the tissues under normal atmospheric circumstances. Hemoglobin is approximately 97% saturated with oxygen and there is a smaller amount of oxygen dissolved in the plasma. Increasing the inspired oxygen cannot improve delivery by hemoglobin, and breathing 100% oxygen at normal atmospheric pressure will only increase the amount of oxygen dissolved in the plasma by a small amount. The amount of oxygen dissolved in the plasma is referred to as the partial pressure of oxygen and is designated as pO2.
The atmosphere and the mitochondria in the cells is a complicated transport system along which the pO2 is reduced; this determines the rate at which oxygen can be delivered to the tissues. The succession of diminishing pO2 is called the “Oxygen Cascade”. The oxygen cascade involves a successive decrease in the partial pressure of oxygen as blood flow leaves the lungs and progresses to the cellular level, such that the capillary pO2 is less than 50 mmHg at the capillary level and even lower at the intracellular level.
If you calculate the increase in partial pressure of oxygen obtained in the gas breathed in during HBOT you will see that it is dramatically increased. At 2 ATA with 100% oxygen:
2 x 760 mmHg = 1,520 mmHg of oxygen.
Breathing air (21% oxygen or 160 mmHg per ATA) would result in a pO2 of 320 mmHg. Therein lies the essence of hyperbaric oxygen therapy, the ability to dramatically increase the inspired oxygen and thus the amount of dissolved oxygen in the plasma. Most therapeutic applications of HBOT involve 3 ATA or less.
Physiology of Tissue Injury
The body has a complicated set of reactions to injury that result in a cascade of biochemical mediators described clinically as inflammation. Most of these processes revolve around the blood vessels. The classic components of inflammation include the following:
- Loss of function
The role of blood vessels in injury is the reason for the above mentioned factors. All tissues have a certain density of capillary vessels. With injury, these vessels expand and become leaky, losing some of the plasma components into the surrounding tissue. This effect results in tissue swelling post injury. In certain circumstances, the swelling is severe enough and the distance for oxygen diffusion is too far.
In other situations, clotting of the blood vessels may occur resulting in complete loss of blood flow (ischemia). The result of either is tissue necrosis. The distance oxygen can diffuse is partly related to the concentration gradient. Increasing this gradient with hyperbaric oxygen therapy can increase the distance that oxygen can diffuse into these tissues.
Another mechanism of the effect of hyperoxygenation on tissue injury is vasoconstriction. This acts to reduce the hydrostatic pressure that forces fluid out of the capillaries into the tissues and therefore reduces tissue swelling.
Beyond inflammation is the issue of the reparative response of the body’s tissues. A wound defect is filled with blood components that progress to a clot that covers the defect. As time passes, the connective tissue cells (fibroblasts) become activated and begin to produce new connective tissue (collagen) to fill the defect.
Concurrently, new blood vessel ingrowth begins to provide nutrients and oxygen in order for this process to proceed. In addition, the epithelium begins to spread out and divide to cover the defect. Appropriate nutrients and oxygen are required for this concert of healing to work.
In certain injuries, the process is delayed as a result of the extent of the tissue injury, which impairs the delivery of oxygen and nutrients to the area. HBOT decreases tissue swelling and therefore allows improved oxygen and nutrient delivery to the area. HBOT also assists the epithelium covering the wound and stimulates fibroblast production of collagen.