Question...

[The Iceni]

Rick Murchison once bubbled...
Blood leaving them will have offgassed to, essentially, ambient partial pressures; the gradient for bubble formation and growth just isn't there.
Rick

I can understand that but let me have a think about it!

 

[The Iceni]

Rick Murchison once bubbled...
Don't think so, Doc.

At risk of spending too much time on an academic exercise, as there is very little that can done for any diver who makes a rapid ascent following an extended period at depth, I have looked again at this scenario.

Yes, Rick, you are right. When the lungs are functioning properly the pulmonary arterial blood will be in equilibrium with ambient pressure and there will be no pressure gradient encouraging the generation of new bubble nuclei within the pulmonary veins. But there will have been a number of pathological events taking place in the period leading up to the time when the right ventricle contains so much gas that it cannot function as a pump, if that is indeed the terminal event.

I found the following reference after a rapid search of the net.

http://blue.vm.temple.edu/~pathphys/pulmonary/pulmonary_vascular_disease.html

If I can summarise;

General Concepts of the pulmonary circulation

1) Positioned between the right and left hearts

2) Accommodates the entire cardiac output

3) Capable of accommodating a large variability in blood flow between rest and exercise

4) "Passive" vascular bed

5) At sea level, pulmonary blood flow is accompanied by an average mean pressure drop between the pulmonary artery (PA) and left atrium (LA) of 5-10 mm Hg

6) Pulmonary circulation is a high capacity, low resistance circuit. In health, pulmonary systolic arterial pressure seldom exceeds 35 mmHg.

The last consideration is the important one, confirming that the right ventricle needs only to raise its internal pressure by 35 mmHg above ambient pressure during systole for normal pulmonary circulation to take place and this is during strenuous exercise. As central venous pressure is about 4 mmHg above ambient pressure it is about 764 mmHg. This represents a compression of only 795/764 or under 4%. Therefore any inert gas bubble within the right ventricle with be compressed to 1/1.04 or 96% of its former size within the great veins. I therefore find it hard to believe that a vapour lock within the right ventricle alone can explain cardiac arrest in such extreme cases of DCI.

If, as is likely, the venous return in the initial stages of this scenario consists of blood teeming with millions of small bubbles and micronuclei these will simply pass through the right heart into the pulmonary arteries and thence to the lungs. I believe this is where the primary pathological events must take place when these numerous bubbles embolise in the pulmonary vascular bed. As most divers know the lungs filter out these small bubbles. Under normal circumstances this has very little effect on lung function but I believe such a large number of bubbles blocking such a large number of pulmonary capillaries will disturb the ventilation/perfusion ratio of the lungs and greatly reduce the efficiency of lung function in gaseous exchange and the ability of the lungs to off-gas.

There are four two possible sequelae to this.

1) The first is that pulmonary venous return to the heart retains a high nitrogen load because of the abnormal V/Q ratio, which may (only may) be sufficient to facilitate new bubble growth.

2) The second is that pulmonary capillary resistance increases leading to a rise in pulmonary arterial pressure and consequential right ventricular strain, highly dangerous in itself.

3) The third is that this pulmonary hypertension will be increase the shunting of pulmonary arterial blood to the pulmonary veins, via those pulmonary vessels that remain patent and increasingly dilated;- a right to left shunt further disturbing the V/Q ratio.

4) These dilated shunt vessels will allow the passage of both micronuclei and small bubbles directly into the pulmonary veins and thence to the left side of the heart

Thus, long before the efficiency of the right ventricle can be compromised by any vapour lock, the pulmonary veins will contain an increasing number of micronuclei and nascent bubbles. These find their way to the aorta to cause overwhelming type II DCI and some of these bubbles with inevitably find their way into the coronary circulation to cause an ischaemic event.

Right ventricular strain by itself (secondary to acute pulmonary hypertension) could cause cardiac arrest but suspect that the sequence of pathological events is a little more complicated than a vapour lock in the right ventricle alone.

Divers can recover from most injuries, including pulmonary barotrauma and the associated disfiguring surgical emphysema, but if myocardial infarction is a part of this pathological process it explains why it is so difficult to resucitate such casulaties, since even if all the bubbles are compressed by the hyperbaric treatment, sadly (as with any heart attack) if the coronary circulation is not rapidly restored heart muscle dies and the dead heart tissue never functions properly again.

As ever, it is not as simple as it first appears.

:doctor:

 

[Rick Murchison]

Dr Paul Thomas once bubbled...
As ever, it is not as simple as it first appears.

Indeed...
I recommend tight control on ascent rates for all...
Rick

 

[The Iceni]

Rick Murchison once bubbled...

Indeed...
I recommend tight control on ascent rates for all...
Rick

And most divers have enough trouble understanding the concept of a "vapour lock". So why complicate it, heh?

Kind regards,

 

[Dr Deco]

Dear Paul:

Bubbles in the Pulmonary veins

In actuality, the partial pressure of gas in the pulmonary vein is equal to ambient since there is a rapid equilibration with the respired gas. The gas bubbles in the peripheral veins, in contrast, arise in the capillaries and the dissolved inert gas is supplied by the tissues . Additionally, in the capillaries are found the all-important micronuclei , probably arising from viscous (Stefan) adhesion when muscles contract and endothelial cells make contact. This was first mentioned in Fulton’s book in 1952 (but I do not recall by whom). Even in the presence of horrific decompressions, both visual (in animals) and Doppler studies (also in animals) have demonstrated that the pulmonary veins and the systemic arterial system are devoid of gas bubbles until they appear first in the systemic veins.

Bubbles can enter the pulmonary veins (and systemic circulation) through pulmonary shunts or the PFO. I have personally noted many times in animals that arterial bubbles are not present until venous side bubbles appear from capillary drainage.
The following abstract also illustrates this.
- - - -
Lee YC, Wu YC, Gerth WA, Vann RD. Absence of intravascular bubble nucleation in dead rats. Undersea Hyperb Med 1993 ;20(4):289-96

{Abridged abstract} Bubble formation in the inferior vena cavae (IVC) of dead rats was investigated after 6-15-h exposures to air at 123 atm abs (12.5 MPa) and decompression to 1 atm abs at 13.6 atm/min (1.4 MPa/min). The maximum estimated air-supersaturation attained in the IVCs after decompression was 6.1-18.3 atm (0.6-1.8 MPa). Bubbles were detected by light microscopy, buoyancy, and underwater dissection. No bubbles formed in 42 blood-filled IVCs that were isolated from the circulation by ligatures, but bubbles were always observed in unisolated IVCs. Results indicate that at the air supersaturations attained in the isolated IVCs blood is resistant to de novo bubble formation.

- - - - -

We have also examined the question of reduced inert gas exchange during decompression and found that this doen NOT occur, even with Grade IV bubbles on the Spencer/Johanson scale..

Vapor lock

I believe that some of the earliest studies were performed by Durant (Durant, T. M.; J. Long and M. J. Oppenheimer (1947).) Pulmonary (venous) air embolism. Am. Heart J., 33, 269.) They were the originators of the vapor lock hypothesis with infused air. If bubbles only arise in the tissue capillaries (experimental observation), the two mechanisms would be similar. This was also my original concept of what I called “decompression death” in small animals to differentiate it from true joint pain DCS (the bends). {Powell MR. Gas phase separation following decompression in asymptomatic rats: visual and ultrasound monitoring. Aerosp Med 1972 Nov; 43(11): 1240-4; Powell MR. Leg pain and gas bubbles in the rat following decompression from pressure: monitoring by ultrasound. Aerosp Med 1972 Feb; 43(2): 168-72}

Coronary artery embolism

This certainly occurs, and I have observed it numerous times (in animals) as a change in the ECG and a reduction in cardiac output. It is always observed to be preceded by a large venous gas bubble load , however. Without question, you can find bubbles in coronary vessels and these will be eliminated upon repressurization. Many will pass though the coronary circulation unhindered without repressurization. The major problem is a drop in cardiac output, because the right ventricle is contracting against compressible gas. The flow of blood is reduced because the RV is not exerting the force it should and is also pumping gas bubbles. The Durant position (or sometimes the Trendelenburg) position has been suggested as a way to modify the effect of bubbles. Intracranial pressure increases, however, and this has its own problems.

It is true that in cases where a diver as expired at depth, the post mortem examination will often show gas bubbles in many vessels, and confound the cause of death.

Dr Deco :doctor:

 

[The Iceni]

Dr Deco once bubbled...
Dear Paul:

Bubbles in the Pulmonary veins

I have personally noted many times in animals that arterial bubbles are not present until venous side bubbles appear from capillary drainage.

We have also examined the question of reduced inert gas exchange during decompression and found that this doen NOT occur, even with Grade IV bubbles on the Spencer/Johanson scale..

Dear Dr Deco,

I was considering the events immediately before bubbles are found in the right ventricle during the final phase of a rapid ascent sufficient to cause the described vapour lock and why the prognosis is so dire. (Is that what you mean by grade IV Dr D?) I have no doubt, whatsoever, that this can only occur when bubbles are already present in the venous system. I think we all accept that this is a universal finding during any form of DCI.

Is there any evidence that a masive bubble load causes, or does not cause, acute obstructive pulpmonary hypertension, right ventricular strain and pulmonary shunts as I have suggested that it must?

Coronary artery embolism

This certainly occurs, and I have observed it numerous times (in animals) as a change in the ECG and a reduction in cardiac output. It is always observed to be preceded by a large venous gas bubble load , however. Without question, you can find bubbles in coronary vessels and these will be eliminated upon repressurization. . .

It is true that in cases where a diver as expired at depth, the post mortem examination will often show gas bubbles in many vessels, and confound the cause of death.

Dr Deco :doctor:

A question Dr D.

You say

Without question, you can find bubbles in coronary vessels and these will be eliminated upon repressurization

This begs the question. Is it not true that -

the embolisation of a thrombus or a bubble in a coronary artery can cause myocardial ischaemia and irreversible infarction, which can both lead to fatal arrythmias?

that the myocardium is irreversibly damaged if revacularisation in acute myocardial infarction is delayed?

that early thromolysis or angioplasty in acute MI provides considerbly improved outcomes because of early revacularisation of the myocardium?

that, in the case of coronary AGE in a recreational diver, that revascularisation by the means of recompression is likely to delayed beyond the point when the myocardium will have suffered irreversible infarction as a consequence such gaseous embolus?

that asystole (or at least complete heart block) is the inevitable sequel if the AV node has been infarcted?

that the prognosis for prolonged asystole following infarction in acute MI is very poor indeed?

that when myocardial infarction is not present, such as is the case for prolonged cold immersion injury, the outcome is much more optimistic?

I pose these questions because I feel that many apparenty fatal examples of DCI could quite possibly be treatable if

1) effective BLS has been provided continuously to prevent cerebral ischaemia

2) there is effective ventilation during all phases of the rescue (eg. no untreated pulmonary barotrauma)

3) there is little or no myocardial infarction.

I do not expect definitive answers as this post more properly belongs on the diving medicine forum (and is somewhat esoteric to say the least!). It is just that I feel the role of coronary artery AGE in diver fatalities is much more important than is generally accepted.

I write from the perspective of a doctor who has used domiciliary thrombolysis in acute MI successfully for many years. I suppose rapid recompression is an equivalent treatment in DCI.

 

[Rick Murchison]

For the Docs...
I want y'all to know that I find your discussion extremely informative, thought provoking and valuable. It's the kind of discourse that gets the old brain cells goin'.
Thanks,
Rick

 

[mddolson]

This is an report on what did happen, not what might!
I believe this to be true and factual.
It was reported to me by the patient.
It is obvious that there were a number of mistakes were made by both divers. I am offering no comment on their actions.
I am reporting this because of the ascent and results.
(names are being omitted in respect of confidence)
Time frame : Late 1980's
Location: St Lawrence River. ship wreck Henry C Daryaw
Conditions: swift current
Two divers started as a buddy team as usual.
Divers were using single 80 aluminum tanks.
They descended together on down line.
About 15 minutes into the dive they become separated.
Diver A looks around , can't find Diver B and heads back to the acsent line. Max depth 75 feet, time 25 minutes. (confirmed by bottom timer, and max needle on depth guage)
Diver A discovers he's out of air. he's at 60 feet.
Remebering his training, he keeps the regulator in his mouth and makes an emergency swimming ascent, during the ascent he got two partial breaths from the regulator.
Diver B surfaces 5 minutes later.
There was a heated verbal exchange.
Both A&B divers discontinue diving the rest of the day.
Diver B who had a 30 minute bottom time and a normal ascent,
had no ill effects.
Diver A, developed decompression sickness (Pain in right shoulder, and general flue like symptoms, including nausea and sweating.) 6 hours after the dive.
He was diagnosed at Brockville General Hopital received 50% oxygen, and was transported to Toronto General Hospital (3 hrs by Ambulance) the nearest hyperbaric chamber.
He was treated at Toronto General with higher concentrations of oxygen, but did not actually enter the chamber.
He was discharged next morning at about 9:00 am

Mike D

 

[Rick Murchison]

mddolson once bubbled...
This is an report on what did happen, not what might!
I believe this to be true and factual.
It was reported to me by the patient.
It is obvious that there were a number of mistakes were made by both divers. I am offering no comment on their actions.
I am reporting this because of the ascent and results.
(names are being omitted in respect of confidence)
Time frame : Late 1980's
Location: St Lawrence River. ship wreck Henry C Daryaw
Conditions: swift current
Two divers started as a buddy team as usual.
Divers were using single 80 aluminum tanks.
They descended together on down line.
About 15 minutes into the dive they become separated.
Diver A looks around , can't find Diver B and heads back to the acsent line. Max depth 75 feet, time 25 minutes. (confirmed by bottom timer, and max needle on depth guage)
Diver A discovers he's out of air. he's at 60 feet.
Remebering his training, he keeps the regulator in his mouth and makes an emergency swimming ascent, during the ascent he got two partial breaths from the regulator.
Diver B surfaces 5 minutes later.
There was a heated verbal exchange.
Both A&B divers discontinue diving the rest of the day.
Diver B who had a 30 minute bottom time and a normal ascent,
had no ill effects.
Diver A, developed decompression sickness (Pain in right shoulder, and general flue like symptoms, including nausea and sweating.) 6 hours after the dive.
He was diagnosed at Brockville General Hopital received 50% oxygen, and was transported to Toronto General Hospital (3 hrs by Ambulance) the nearest hyperbaric chamber.
He was treated at Toronto General with higher concentrations of oxygen, but did not actually enter the chamber.
He was discharged next morning at about 9:00 am

Mike D

This incident is entirely consistent with what we might expect given the dive profiles - Diver "A," with a fairly significant nitrogen load, violated the normal ascent rate from 60 feet with a CESA (there was no option) and ended up with a mild case of DCS - but not with any overpressure injury from the rapid ascent because he did it properly. Had he had enough gas, and taken a full minute to ascend from 60' he'd likely not have had the DCS - but there's no way to know.
Rick

 

[Dr Deco]

Dear Dr Thomas:

Pulmonary artery hypertension and gas bubbles

The aspect of right ventricular systolic pressure with infusion of gas bubbles is addressed in the reports list below.
- - - -
Spencer MP, Oyama Y. Pulmonary capacity for dissipation of venous gas emboli. Aerosp Med 1971 Aug; 42(8): 822-7; Powell, Spencer and von Ramm, “Ultrasonic Surveillance of Decompression in “ Physiology and Medicine of Diving ”, 3rd Edition (1982); Vik A, Jenssen BM, Eftedal O, Brubakk AO. Relationship between venous bubbles and hemodynamic responses after decompression in pigs. Undersea Hyperb Med 1993 Sep; 20(3): 233-48; Vik A, Jenssen BM, Brubakk AO. Comparison of haemodynamic effects during venous air infusion and after decompression in pigs. Eur J Appl Physiol Occup Physiol 1994; 68(2): 127-33; Juvik E, et al. Arterial air embolism after venous air infusion in newborn piglets. Acta Paediatr 2001 Jul; 30(7): 786-92
- - - -

It is surprising that the increase of RVSP is relatively small for the gas bubble loads found in actual decompression (compared to what is obtained by big loads during infusion). See ATTACHMENT adapted from Powell, Spencer and von Ramm [vide supra] and Diesel DA, et al. Non-invasive measurement of pulmonary artery pressure in humans with simulated altitude-induced venous gas emboli. Aviat Space Environ Med 2002 Feb; 73(2): 128-33. I suspect that the very small decompression-generated bubbles pass through pulmonary shunts with small RVSP elevations.

Diver rescue and MI

Not being a clinician, I cannot say what would happen in humans, but I can say that in animals, recompression will often be effective if there is some vestige of cardiac activity. This involves placing the animals back into a pressure chamber in short interval of time. In the case of humans, electric shock would probably be of benefit, but it is possible that this would need to be performed in the chamber with the gas bubbles reduced in size. I am not aware of any electro conversion devices in chamber (because the chambers are metal). My experience with animals, however, is that it would be of value.

The bottom line to the several questions is that a diver could be saved if s/he could be repressurized and given electro shock. I believe that under current conditions, this is difficult outside of a laboratory setting.

Dr Deco :doctor: