Saturation Diving; Physiology and Pathophysiology

Abstract

In saturation diving, divers stay under pressure until most of their tissues are saturated with breathing gas. Divers spend a long time in isolation exposed to increased partial pressure of oxygen, potentially toxic gases, bacteria, and bubble formation during decompression combined with shift work and long periods of relative inactivity. Hyperoxia may lead to the production of reactive oxygen species (ROS) that interact with cell structures, causing damage to proteins, lipids, and nucleic acid. Vascular gas-bubble formation and hyperoxia may lead to dysfunction of the endothelium. The antioxidant status of the diver is an important mechanism in the protection against injury and is influenced both by diet and genetic factors. The factors mentioned above may lead to production of heat shock proteins (HSP) that also may have a negative effect on endothelial function. On the other hand, there is a great deal of evidence that HSPs may also have a "conditioning" effect, thus protecting against injury. As people age, their ability to produce antioxidants decreases. We do not currently know the capacity for antioxidant defense, but it is reasonable to assume that it has a limit. Many studies have linked ROS to disease states such as cancer, insulin resistance, diabetes mellitus, cardiovascular diseases, and atherosclerosis as well as to old age. However, ROS are also involved in a number of protective mechanisms, for instance immune defense, antibacterial action, vascular tone, and signal transduction. Low-grade oxidative stress can increase antioxidant production. While under pressure, divers change depth frequently. After such changes and at the end of the dive, divers must follow procedures to decompress safely. Decompression sickness (DCS) used to be one of the major causes of injury in saturation diving. Improved decompression procedures have significantly reduced the number of reported incidents; however, data indicate considerable underreporting of injuries. Furthermore, divers who are required to return to the surface quickly are under higher risk of serious injury as no adequate decompression procedures for such situations are available. Decompression also leads to the production of endothelial microparticles that may reduce endothelial function. As good endothelial function is a documented indicator of health that can be influenced by regular exercise, regular physical exercise is recommended for saturation divers. Nowadays, saturation diving is a reasonably safe and well controlled method for working under water. Until now, no long-term impact on health due to diving has been documented. However, we still have limited knowledge about the pathophysiologic mechanisms involved. In particular we know little about the effect of long exposure to hyperoxia and microparticles on the endothelium.

Wearable Current-Based ECG Monitoring System with Non-Insulated Electrodes for Underwater Application

“…The results of the heart rate variability study endorse the physiological response to immersion showing an initial reflex bradycardia resulting from a restriction of blood flow to the peripheries and to venoconstriction due to hydrostatic forces, typically known as the mammalian diving reflex [29]. In general, immersion results in an increase of venous return, increased stroke volume and bradycardia as a modest increase in cardiac output [30].…”

The Impact of Repetitive Long-duration Water Immersion on Vascular Function

“…This is evidenced by the significant increase in the number of endothelial microparticles (a marker of endothelial damage) observed following compressed gas dives at 283 kPa [21]. This notion is supported by research showing that the production of reactive oxygen species (ROS) causes a reduction in endothelial function by inhibition of NO-mediated vasoregulation [22,23,24,25], and both ROS and intravascular bubble formation can result in physical endothelial cell damage [21,23,26,27,28,29].…”

Comments on unresponsive decompression illness case

“…In fact, need for decompression stops may be more with shorter bottom times at certain depths. Also, relating bubble formation only to gas density would be inadequate as many other factors such as solubility, diffusion coefficient, tissue circulation, or surface tension of the bubble are important [6, 7]. …”