Microembolic Signals Under Increased Ambient Pressure
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.
- Copyright © 1998 by American Heart Association
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.
Spencer MP. Hyperbaric compression and Doppler-detected microemboli in prosthetic valve patients. Cerebrovasc Dis. 1996;6(suppl 3):69. Abstract.
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.