SHALLOW WATER BLACKOUT (Latent hypoxia)

Posted by MoE-Bike on 6:05 AM

Shallow water blackout (SWB)

A shallow water blackout is a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold dive in water typically shallower than five meters (16 feet), when the swimmer does
not necessarily experience an urgent need to breathe and has no other obvious medical condition that might have caused it. Victims are often established practitioners of breath-hold diving, are fit, strong swimmers, and have not experienced problems before.
Many drowning and near drowning events occur among swimmers who black out underwater while free-diving or doing breath-hold pool laps. Blacking out, or greying out, near the end of a breath-hold dive is common. Although the mechanism is well understood, it is not common knowledge among breath-hold divers.
Shallow water blackout is related to, but differs from deep water blackout in its characteristics, mechanism and prevention; deep water blackout is precipitated by depressurization on ascent from depth.

Tips to avoid blackouts :
  • Do not hyperventilate to excess no more than three or four breaths.
  • Reduce exercise at depth.
  • Recognize the danger of focusing.
  • Don't hesitate to drop your weight belt.
  • Avoid endurance dives.
  • Adjust your weight belt so that you will float at 15 feet.
  • Don't practice breath-holding in a swimming pool. Always have an observer standing by to assist.
Still wanna read more !!!!!!
ok go ahead 
Conditions that produce latent hypoxia (Shallow water blackout)
Hyperventilation
Hyperventilation is the practice of excessive breathing with an increase in the rate of respiration or an increase in the depth of respiration, or both. This will not store extra oxygen. On the contrary, if practiced too vigorously, it will actually rob the body of oxygen. The magical benefit of hyperventilation is what it does to carbon dioxide levels in the blood. Rapid or deep breathing reduces carbon dioxide levels rapidly. It is high levels of carbon dioxide, not low levels of oxygen, that stimulate the need to breathe.
The beginning diver is very sensitive to carbon dioxide levels. These levels build even with a breath-hold of 15 seconds, causing the lungs to feel on fire. The trained diver has blown off massive amounts of carbon dioxide with hyperventilation, thus outsmarting the brain's breathing center. Normally metabolizing body tissues, producing carbon dioxide at a regular rate, do not replace enough carbon dioxide to stimulate this breathing center until the body is seriously short of oxygen.  

Hyperventilation causes some central nervous system changes as well. Practiced to excess, it causes decreased cerebral blood flow, dizziness and muscle cramping in the arms and legs. But moderate degrees of hyperventilation can cause a state of euphoria and well-being. This can lead to overconfidence and the dramatic consequence of a body performing too long without a breath: blackout.  

Pressure changes in the free diver's descent-ascent cycle conspire to rob him of oxygen as he nears the surface by the mechanism of partial pressures. Gas levels, namely oxygen and carbon dioxide, are continuously balancing themselves in the body. Gases balance between the lungs and body tissues. The body draws oxygen from the lungs as it requires. The oxygen concentration in the lungs of a descending diver increases because of the increasing water pressure.
As the brain and tissues use oxygen, more oxygen is available from the lungs while he is still descending. This all works well as long as there is oxygen in the lungs and the diver remains at his descended level. The problem is in ascent. The re-expanding lungs of the ascending diver increase in volume as the water pressure decreases, and this results in a rapid decrease of oxygen in the lungs to critical levels. The balance that forced oxygen into the body is now reversed. It is most pronounced in the last 10 to 15 feet below the surface, where the greatest relative lung expansion occurs. This is where unconsciousness frequently happens. The blackout is instantaneous and without warning. It is the result of a critically low level of oxygen, which in effect, switches off the brain.

Well if u r not board yet ,,,,finish this,,,,,it's the physics behind it:
Dalton's Law of partial pressures applies. (Pb - PO2 + PN2 + Pother gases.)
As Pb decreases, the partial pressures of all component gases decrease in the same ratio. The hypoxia of predive hyperventilation is corrected by an increased PO2 during descent.
During descent, the lung volume decreases due to chest compression, resulting in increased lung PO2, PCO2 and PN2.
  • In the lung there is an increased breathing rate and a reduced PCO2. Lung volume is reduced to one-half, lung PO2 is increased, lung PCO2 increases initially, but is followed by lowered PCO2 due to reversed gradient.
  • The blood reacts by developing a respiratory alkalosis and a right shift of the HbO2 (oxyhemoglobin) curve. The reaction is CO2 + H2O - H+ + HCO3.
  • Carotid body chemoreceptors cause a slow-down of the heart and permit longer breath holding.
  • There is vasodilatation of the brain vessels with hypoxia (low oxygen). There is rapid O2 usage, the arterial PCO2 is lowered so that respiration is not stimulated until )2 drops s low that the breath hold breakpoint is reached. The breakpoint (PCO2/PO2) in a trained person is less sensitive to increased PCO2 or lowered O2. The act of consuming oxygen rapidly (as in chasing a large fish), delays the breakpoint because of the higher PCO2 and the exercise per se. The diver becomes lightheaded, dizzy, has tingling, air hunger, muscle rigidity and unconsciousness.
  • While at depth, increased lung PO2 provides a favorable gradient for O2 transfer from the lung to blood, occurring more rapidly than if the diver were on the surface.
  • Because alveolar PCO2 increases with compression, CO2 does not leave the blood to enter the lung. Arterial CO2 rises rapidly (especially with exercise) initially, then the tissues store CO2. Trained divers use a timed bottom time ( 1.5 minute maximum) to avoid unconsciousness on return to the surface.
On Ascent to the Surface:
  • The lung re-expands to normal, the PCO2 becomes elevated as more diffuses into the lung and the PO2 drops dramatically.
  • In the blood the PCO2 elevates depending on the depth of the dive and the amount of exercise. Deep dives drive more CO2 from the lungs into the tissues and increases the problem. There is a right shift of the HgbO2 curve.
  • When the break point is reached , the chemoreceptors are stimulated by CO2, thus stimulation of respiration. Low O2 also stimulates respiration.
  • In the brain:
    • CO2 stimulates respirations
    • Vasodilation encourages O2 consumption
    • Latent hypoxia occurs
    • Unconsciousness ensues
  • On ascent the lungs re-expand reducing the favorable diffusion gradient for oxygen. Shallower depths cause this gradient to approach zero, the diver reaching a critical state of hypoxia.
  • Hypoxia causes unconsciousness, possibly before the diver reaches the surface.
  • Signs and symptoms of latent hypoxia (Shallow water blackout)
    • Extreme weakness, trembling, unconsciousness in the water, amnesia of the event, drowning. 

THE PHYSIOLOGY OF SHALLOW-WATER BLACKOUT
In addition to the changes due to the Physics of Dalton's Law, there are other physiological changes that take effect during shallow water blackout and free diving.
Diving Reflex
The human body is capable of remarkable adaptations to the underwater environment. Even untrained divers will show a dramatic slowing of the heart when immersed. This is commonly referred to as the diving reflex. Immersion of the face in cold water causes the heart to slow automatically. Chest compression can also slow the heart. Untrained divers can experience up to a 40 percent drop in heart rate. Trained divers can produce an even lower heart rate some can slow to an incredible 20 beats per minute.
Spleen Effects
Trained free divers develop several other physiological adaptations that lead to deeper and longer dives. The spleen, acting as a blood reservoir, assists trained divers in increasing their performance. Apparently their spleen shrinks while diving, causing a release of extra blood cells.
According to William E. Hurford M.D., and co-authors writing in The Journal of Applied Physiology, the spleens of the Japanese Ama divers (professional women shellfish free divers) they studied decreased in size by 20 percent when they dove. At the same time their hemoglobin concentration increased by 10 percent (Volume 69, pages 932-936, 1990).
This adaptation, similar to one observed in marine mammals (the Weddell seals' blood cell concentration increases by up to 65 percent), could increase the divers ability to take up oxygen at the surface. It could also increase oxygen delivery to critical tissues during the dive.
Interestingly, the spleens contraction and the resultant release of red cells is not immediate- it starts taking effect after a quarter-hour of sustained diving. This spleen adaptation, as well as other physiologic changes, probably take a half-hour for full effect. This might account for the increased performance trained free divers notice after their first half-hour of diving, and also may be one of the causes of unexplained heart failure in the diver with a border line heart condition.
Other adaptations
There are other known adaptations: blood vessels in the skin contract under conditions of low oxygen in order to leave more blood available for important organs, namely the heart, brain and muscles. Changes in blood chemistry allow the body to carry and use oxygen more efficiently. These changes, in effect, squeeze the last molecule of available oxygen from nonessential organs. Most importantly, the diver's mind adapts to longer periods of apnea (no breathing). He can ignore, for longer periods of time, his internal voice that requires him to breathe.