6/20/09 - Avalon, Catalina - Freediver drowned...

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Don,

Clearly you are, the best judge of your own limitations ... so permit me to help you out:

During descent:

  • Lung volume decreases due to chest compression, resulting in increased lung total pressure, and of course increased PO2, PCO2 and PN2.
  • In the lung, after hyperventilation, there is a reduced PCO2. E. g., if lung volume is reduced to one-half by descent to 33 feet, lung PO2 is doubled, lung PCO2 increases initially, but is followed by lowered PCO2 due to the reversed gradient.
  • The blood reacts by developing a respiratory alkalosis (more CO2).
  • Carotid body chemoreceptors cause a slow-down of the heart and permit longer breath holding.
  • Despite rapid O2 usage, the arterial PCO2 drops and a strong desire to breathe is not stimulated until sufficient oxyen is used up that the PCO2 rises sufficiently.
  • While at depth, increased lung PO2 (due to increased ambient pressure) provides a favorable gradient for O2 transfer from the lung to blood, occurring more rapidly than if the diver were on the surface.
  • Alveolar PCO2 increases with compression, CO2 does not leave the blood to enter the lung and arterial CO2 rises rapidly (especially with exercise) initially, then the tissues store CO2.
On Ascent:
  • As the lung re-expands, the PCO2 becomes elevated as more diffuses into the lung, but due to the drop in ambient pressure there is a concomitant dramatic drop in the PO2.
  • In the blood the PCO2 goes up with 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.
  • When the need to breathe point is reached , the chemoreceptors are stimulated by CO2, and there is a strong dsesire to take a breath. Low O2 also can cause this.
  • In the brain: CO2 goes up and makes you want to breathe; Vasodilation increases O2 consumption;PO2 drops with the drop in ambient pressure and if PO2 drops enough, unconsciousness occurs.
  • On ascent the lungs re-expand; this decreases the diffusion gradient for oxygen. Shallower depths can cause this gradient to approach zero, and the diver goes out like a light due to extreme hypoxia, possibly before the diver reaches the surface.
 
Don,

Clearly you are, the best judge of your own limitations ... so permit me to help you out:

During descent:

  • Lung volume decreases due to chest compression, resulting in increased lung total pressure, and of course increased PO2, PCO2 and PN2.
  • In the lung, after hyperventilation, there is a reduced PCO2. E. g., if lung volume is reduced to one-half by descent to 33 feet, lung PO2 is doubled, lung PCO2 increases initially, but is followed by lowered PCO2 due to the reversed gradient.
  • The blood reacts by developing a respiratory alkalosis (more CO2).
  • Carotid body chemoreceptors cause a slow-down of the heart and permit longer breath holding.
  • Despite rapid O2 usage, the arterial PCO2 drops and a strong desire to breathe is not stimulated until sufficient oxyen is used up that the PCO2 rises sufficiently.
  • While at depth, increased lung PO2 (due to increased ambient pressure) provides a favorable gradient for O2 transfer from the lung to blood, occurring more rapidly than if the diver were on the surface.
  • Alveolar PCO2 increases with compression, CO2 does not leave the blood to enter the lung and arterial CO2 rises rapidly (especially with exercise) initially, then the tissues store CO2.
On Ascent:
  • As the lung re-expands, the PCO2 becomes elevated as more diffuses into the lung, but due to the drop in ambient pressure there is a concomitant dramatic drop in the PO2.
  • In the blood the PCO2 goes up with 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.
  • When the need to breathe point is reached , the chemoreceptors are stimulated by CO2, and there is a strong dsesire to take a breath. Low O2 also can cause this.
  • In the brain: CO2 goes up and makes you want to breathe; Vasodilation increases O2 consumption;PO2 drops with the drop in ambient pressure and if PO2 drops enough, unconsciousness occurs.
  • On ascent the lungs re-expand; this decreases the diffusion gradient for oxygen. Shallower depths can cause this gradient to approach zero, and the diver goes out like a light due to extreme hypoxia, possibly before the diver reaches the surface.

That was a bit more than I was expecting but certainly educational although I had to read it 3 times to begin to understand it:shakehead:

So basically it's low level carbon dioxide poisoning in the tissues that the body reacts to and puts you out in order to maintain brain function and use what little O2 is remaining to sustain life with exception to the fact that this environment is not condusive to this?
 
I wonder since this person had been scuba diving prior to the accident, if bubble pumping might have been in play here.

If the diver had sufficient N2 loading from the dive(s) prior, he could have compressed micro bubbles upon the freedive decent leading to a venous gas embolism when he rapidly surfaced.

Just a thought...

Sad story and I feel for his loved ones.
 
No. Basically you drop the CO2 and descend, oxygen P02 goes up with the ambient pressure rise. You stay there and raise CO2 as you use up oxygen. As you ascend the ambient pressure drops and as a result so does the PO2. If the PO2 was low enough at the start of your ascent it's drop resulting from the rop in ambient can leave you with too low a PO2 to remain conscious before you even ger to the surface.
I wonder since this person had been scuba diving prior to the accident, if bubble pumping might have been in play here.

If the diver had sufficient N2 loading from the dive(s) prior, he could have compressed micro bubbles upon the freedive ascent leading to a venous gas embolism when he rapidly surfaced.

Just a thought...

Sad story and I feel for his loved ones.
A good insight.
 
Thalassamania you sound like an MD/PhD in Pulmonology. Great description.
I am saddened to hear of these things. My condolenses to the family.
I often snorkel solo around palos verdes and laguna beach and this just makes me sad.
 
I just got word from his family that the autopsy concluded that cause of death was drowning due to shallow water blackout. No signs of embolism or any other common dive related injuries.

Thank you all for your thoughts. I will pass them on to his family. Tony will be missed.
 
I'd be interested in knowing how the coroner arrived at that finding. What sign is there at autopsy that indicates SWB?

While it is possible to suffer SWB in rather shallow dives, they have to be rather long; it is more frequently seen in free dives that are below 60 feet and outside of two minutes.
 
Maybe a combination of blood gas content and other indications of drowning.
 
Maybe - but no cigar.
 
I wonder since this person had been scuba diving prior to the accident, if bubble pumping might have been in play here.

If the diver had sufficient N2 loading from the dive(s) prior, he could have compressed micro bubbles upon the freedive decent leading to a venous gas embolism when he rapidly surfaced.

Just a thought...

Sad story and I feel for his loved ones.
I don't think we can know here, but it is too little known it seems that free diving after scuba is an increased risk to DCS. Seen some do it. I asked a DM working a liveaboard about it and he had to think about it - then agreed.
I just got word from his family that the autopsy concluded that cause of death was drowning due to shallow water blackout. No signs of embolism or any other common dive related injuries.

Thank you all for your thoughts. I will pass them on to his family. Tony will be missed.
Thank you very much. Please do accept that our discussions here are only intended to help protect others from similar problems, and condolences are not allowed in this forum according to rules so as to avoid undue confusions - but we all have them in our hearts, and some still offer them here even tho it's discouraged.
 
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