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I strongly disagree that a "patent PFO" is an absolute contra-indication to
diving. The reasoning is not complex but lets start by defining our terms.
Just what is a PFO?
As early as 1930 Thompson and Evans suggested that gas emboli could pass
into the arterial circulation via a patent foramen ovale [Thompson & Evans
1930] which is one of several types of atrial septal defect. These defects
can be classified as either valvular competent (patent foramen ovale), an
atrial septal defect or as a large communication between the coronary sinus
and the left atrium (not a true atrial septal defect) [Edwards 1960]. In 20
to 25% of normal human hearts it is possible to pass a probe from the right
to the left atrium [Patten 1938; Scammon & Norris 1918; Wright et al 1948]
even though no functional inter-atrial communication can be demonstrated
under normal conditions.
A foramen ovale that is functionally closed by a competent valve which
prevents blood flowing from the left to the right atrium has been called a
"probe patent foramen ovale" [Patten 1931] or a "valvular-competent, patent
foramen ovale" [Kirklin et al 1955; Weidman et al 1957]. This condition
should be considered a VARIANT OF THE NORMAL because of its frequency and
because the vestigial channel remains closed except when there is a left to
right atrial pressure gradient [Edwards 1960].
Right to left shunting may occur during pulmonary hypertension (secondary,
for example, to venous gas embolism [Butler & Hills 1985]). Transient
reversal of the left to right atrial pressure gradient during a portion of
each cardiac cycle can be demonstrated in pigs [Black et al 1989].
Now, Eckenhoff et al dived subjects to 8 metres for 48 hours (a
comparatively shallow depth, but extended period) and produced no symptoms
of decompression disease, but was able to detect venous gas bubbles with an
ultrasonic Doppler device [Eckenhoff et al 1986] suggesting that
asymptomatic bubbles may occur more often than is commonly believed
(anectodatal evidence suggest ALL dysbaric episodes are associated with
venous bubbles).
The conventional view is that these "silent bubbles" trap in the pulmonary
capillaries [Butler & Hills 1979; Butler & Hills 1985]. But the bubbles may
proceed to the arterial circulation from the right heart to the left heart
when the right to left pressure gradient is high enough to open a patent
foramen ovale or other septal defect [Butler & Hills 1985; Butler & Katz
1988; Moon et al 1989].
But wait. If you expect 1 in 5 divers (20% of the population) to have a PFO
and arterialisation of bubbles via this PFO is expected to cause DCI why
isn't the incidence of DCI closer to 20% for new divers? What about people
with a pulmonary insufficiency which doesn't trap as much gas or trap gas a
efficiently? Should the efficiency of the pulmonary filter also be tested?
But there's more! Moon et al reported that 37% [11 of 30] divers with a
history of decompression sickness exhibited right-to-left shunting through a
patent foramen ovale. Of those with serious symptoms and signs 61% [11 of
18] exhibited shunting whereas only 5% [9 of 176] of the healthy volunteer
control group showed any sign of shunting during normal breathing. Whether
or not these data are statistically significant is not clear since the
expected count in one or more cells is less than 5 for this data set.
However, these authors report a p < 0.01, Chi2 = 49.5 Chi2. Ten subjects
exhibited right-to-left shunting during a Valsalva manoeuvre (during which
the right-left pressure gradient favours shunting of gas through the foramen
ovale) [Moon et al 1989]. Another study later in the same year by
Wilmshurst et al [1989] repeated the work of Moon et al [1989] but used
unaffected divers as a control group (rather than volunteers) reporting that
only 17% [4 of 24] of divers who developed symptoms more than 30 minutes
after surfacing had inter-atrial shunts [Wilmshurst et al
1989].
But wait! Cross et al [1992] recently published a study in which SCUBA
divers who had NEVER exhibited symptoms of decompression sickness were
examined by contrast echocardiography. They found that 30% [24 of 78] of
these divers had patent foramen ovale. BUT THEY DIDN'T GET DCI!
Are there not other risk factors?
The consequences of complement activation and the symptoms of decompression
sickness are similar. In rabbits, complement protein activity is essential
for the development of neurological dysfunction after a hyperbaric exposure.
In animal experiments the sensitivity and degree of activation of complement
proteins correlates well with the risk of disease during and after
decompression [Ward et al 1986; Ward et al 1990]. Anaphylatoxins C3a and
C5a are produced in plasma by the presence of air bubbles but anaphylatoxin
C4a is not, suggesting that air bubbles activate the complement system by
the alternate pathway. One group of subjects produced 3.3 times more C3a
and 5 times more C5a than expected. After being subjected to decompression
profiles severe enough to produce air bubbles in their circulation (verified
by ultrasonic Doppler monitoring) this group was found to be more
susceptible to DCI [Ward et al 1987].
I think you are all missing the point about this PFO thing. Divers who
undertake 'provocative' dives may simply be insensitive to the biochemical
effects initiated by the presence of the intravascular bubbles produced
during those dives.
The explanation for an episode of DCI after years of trouble free diving is
the normal variation in the normal biochemistry of the body, particularly
the biochemistry of the circulation.
The limitation with conventional techniques for preventing DCI is that they
are largely based on modelling physical processes. Not a big leap since
Haldane. Treating the body as a bunch of pipes and reservoirs for nitrogen
or other gases is only part of the problem.
/rat
ps;
Decompression DURING flying. Commercial aeroplanes are pressurised to
(approx) 2000 metres; cabin pressure (approx) 0.648 Bar. I would expect
intravenous bubble formation. Is jet lag DCI? [devil's advocate on this
one]. Should people who fly in aeroplanes be tested for PFO before buying
tickets?
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shelps@ac*.ma*.ad*.ed*.au*|Stephen Helps PhD Ack! ___/|
FAX (08)232-3283 |Anaesthesia & Intensive Care \O.o|
Voice (08)224-5495 |University of Adelaide =(___)=
|ADELAIDE, 5005, South Australia U
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"I believe OS/2 is destined to be the most important operating system, and
possibly program, of all time" Bill Gates, CEO, Microsoft Corporation
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