(Stroke. 1998;29:1069-1070.)
© 1998 American Heart Association, Inc.
Microembolic Signals Under Increased Ambient Pressure
H. Bot, PhD;
E.F. Bruggemans, MA;
B.J. Delemarre, MD, PhD;
G.L. van Rijk-Zwikker, MD, PhD
Department of Cardio-Thoracic Surgery,
Leiden University Medical Center,
Leiden, The Netherlands
A. van der Kleij, MD, PhD
Department of Hyperbaric Medicine,
Academic Medical Center,
Amsterdam, The Netherlands
To the Editor:
We read with interest the article by Kaps et al1
concerning the nature of Doppler-detected
microembolic signals (MES) in the cerebral arteries of
patients with an artificial prosthetic heart valve. Their
oxygen experiment provides strong evidence for the conclusion that
these MES are gas bubbles. They noted a strong reduction in the number
of MES when patients breathed 100% oxygen instead of air (21% oxygen)
at atmospheric pressure (ie, 100 kPa and not 1 kPa, as mentioned in the
article). The nitrogen present in air bubbles is replaced by
oxygen, and because oxygen bubbles have a shorter life span because of
higher solubility in blood, the number of MES reaching the brain is
reduced. Up to this point, we agree with the authors.
Kaps et al also performed a hyperbaric chamber experiment (n=1).
Compared with the baseline condition (air respiration at atmospheric
pressure), they noted a strong reduction in the number of MES when the
patient inhaled 100% oxygen at an increased ambient pressure of 175
kPa, an intermediate reduction in the number of MES under inhalation of
100% oxygen at 250 kPa, and no reduction under breathing air at 250
kPa. In the discussion, they stated that the (negligible) increase in
MES found in the latter condition agreed with the results observed for
one patient in Spencer's hyperbaric study,2 and could be
explained by the increase of cavitation under hyperbaric conditions. On
this point, we differ.
We twice performed a hyperbaric chamber experiment using the same sheep
with a prosthetic heart valve (Medtronic Parallel) implanted in
the mitral position. MES were measured for 30-minute periods in the
right carotid artery, because the sheep's thick temporal bone
precluded ultrasonic examination of the cerebral vessels. With the
sheep breathing air, we observed an increase in the number of MES
recorded at 300 kPa (mean, 4.9 MES/min) compared with the number of
MES recorded at 100 kPa (mean, 3.5 MES/min). Although this result
agrees with that of both Kaps et al and Spencer, no increase in MES
numbers was expected for the following reasons.
According to the oxygen saturation curve of hemoglobin, inhalation of
100% oxygen at increased ambient pressure will result in the
saturation of the hemoglobin and hence a reduced solubility and
increased life span of oxygen bubbles when compared with the situation
of 100% oxygen at atmospheric pressure. This would explain why Kaps et
al found an intermediate number of MES under inhalation of 100% oxygen
at 250 kPa. Switching to respiration of air at increased
ambient pressure results in the return of nitrogen in blood, and
nitrogen-containing bubbles will be formed. Since nitrogen is less
soluble than oxygen, this will result in the baseline number of MES,
although these MES might be smaller in diameter.3
In addition, we disagree with Kaps et al with respect to the postulated
increased effectivity of cavitation under hyperbaric conditions. It is
well established that cavitation induced by prosthetic heart
valves is a threshold phenomenon. When the pressure drop induced by
valve closure has a sufficiently large amplitude to decrease the
regional pressure to 0 kPa, valve closure will induce cavitation in
blood near the point of impact.4 From the studies with air
respiration at increased ambient pressure, we can deduce that the
change from 0 to 300 kPa is a minor change when compared with pressure
fluctuations induced by valve closure. We therefore anticipate that a
further increase in ambient pressure will suppress rather than amplify
cavitation.
References
1.
Kaps M, Hansen J, Weiher M, Tiffert K, Kayser I,
Droste DW. Clinically silent microemboli in patients with artificial
prosthetic aortic valves are predominantly gaseous not solid.
Stroke. 1997;28:322–325.[Abstract/Free Full Text]
2.
Spencer MP. Hyperbaric compression and
Doppler-detected microemboli in prosthetic valve patients.
Cerebrovasc Dis. 1996;6(suppl 3):69. Abstract.
3.
Tovar EA, Del Campo C, Borsari A, Webb RP, Dell JR,
Weinstein PB. Postoperative management of cerebral air embolism: gas
physiology for surgeons. Ann Thorac Surg. 1995;60:1138–1142.[Abstract/Free Full Text]
4.
Graf T, Reul H, Dietz W, Wilmes R, Rau G. Cavitation
of mechanical heart valves under physiologic conditions. J
Heart Valve Dis. 1992;1:131–141.[Medline]
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Response
Manfred Kaps, PhD;
Jochen Hansen, PhD;
Michael Weiher, PhD;
Karsten Tiffert, MD;
Dirk Droste, MD
Neurologische Klinik zu Lübeck,
University Zu Lübeck,
Lübeck, Germany
We would like to thank Dr Bot and his colleagues for their
letter, which has provided us with another opportunity to bring
microembolic signals rising from artificial heart
valves into focus. It is clear that we agree with the view that such
signals are primarily due to the effects of gas bubbles. However, we
could not quite comprehend the remaining statements that were made.
What needed to be known was the nature of the
microembolic signals which were being
measured.
In this regard, the saturation of hemoglobin could not be considered to
play any role at all. It was, in fact, the amount of physical dissolved
gas being released by cavitation that acted as the only decisive factor
in bringing about these effects.
Under normobaric conditions, when breathing air at standard room
temperature and pressure, the largest component of physically released
gas appearing in the blood is nitrogen. Under hyperbaric conditions,
the quantity of gas released will increase in line with the increased
partial pressures of the individual gases, as defined by the laws of
Henry and Dalton. The increased ambient pressure has absolutely no
effect on the magnitude of the cavitation, because liquids are
noncompressible. As such, we could not agree with the view that "a
further increase in ambient pressure will suppress rather than amplify
cavitation." The comments made concerning the unitary measure kPa are
justified, and all units that were given in kPa must be corrected by a
factor of 100.
Aside from that, it should be pointed out that the rate of
microembolic signals due to cavitation is dependent on
the design of the artificial valve; the position of the valve, of
course; and the site at which the microembolic signals
were recorded. In this respect, one can not make direct conclusions
on the rate of microembolic signals arising from the
aortic valve in experiments in which microembolic
signals from a mitral valve are being measured.
