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INTRATHORACIC PRESSURE CHANGES AFTER Balestra C.*, Germonpre P.** and Marroni A.*** * Laboratory of Biology, ULB, Brussels Introduction SCUBA divers with a patent Foramen Ovale (PFO) may be at risk for paradoxical (right-to-left) nitrogen gas embolisation when performing manoeuvres that cause a rebound blood loading to the right atrium (1). This can cause nitrogen bubbles in the venous blood flow to be shifted into the left heart and subsequently into the arterial blood flow without transit into the pulmonary circulation where bubble capture could occur. The best known example of these manoeuvres is the Valsalva manoeuvre (Antonio-Maria Valsalva 1666-1723), that is commonly used to augment the sensitivity of contrast trans-esophageal echocardiography (TEE). The release of the Valsalva manoeuvre results in a decrease of the airway and intrathoracic pressure (ITP). This will be followed by a sudden increase in systemic blood return to the right atrium and by an increase of the venous filling of the lungs, with a resultant decrease in flow into the left heart (2,3). The blood shift resulting from the release of ITP causes a rise in the right atrial pressure (RAP) that is easily seen during TEE as a leftwards bulging of the interatrial septum, and marked opening of a PFO, if present (4,5). By injecting agitated saline during the strain phase of this Valsalva manoeuvre, and releasing the strain when the first saline microbubbles are seen arriving in the right atrium, these bubbles may be swept through a PFO and thus reveal its presence. Because of intra-atrial blood flow patterns, these bubbles - injected in an antebrachial vein - may not come sufficiently close to the interatrial septum to transgress through an, even large, PFO (6). It has been suggested that the manoeuvres used by divers during their descent to equalize the pressure in the middle ear (tympanic) cavity with the ambient hydrostatic pressure, can likewise cause such an increase in right atrial pressure and lead to permeabilisation (opening) of a PFO if present. . Many different manoeuvres are available to perform such an equalization of pressure of the ear cavities; the most commonly used is a short and gentle “Valsalva manoeuvre” which is performed pinching nostrils with one hand and gently blowing through the blocked nose in order to increase the middle ear pressure by air insufflation through the Eustachian tube. The present work was undertaken to investigate if this “Diver's Valsalva manoeuvre” was somehow similar to the Valsalva technique that is being used to augment the sensitivity of contrast echocardiography , especially with regard to the intrathoracic pressure rise and fall. We further wanted to compare this “Diver's Valsalva manoeuvre” to other common events likely to increase the ITP, again with regard to the levels of ITP reached during the event and to the characteristics of ITP during the release phase of the manoeuvre or event. Methods Sixteen experienced divers (4 female and 12 male) participated in the study. Age range was from 22 to 39 years. All subjects were fully informed regarding the nature of the investigation and the experimental methods. All gave their informed consent prior to participation. We measured the rise and fall in intrathoracic pressure (ITP) during various manoeuvres by means of an 1,5 ml esophageal balloon catheter (filled with saline solution), positioned in the lower third of the esophagus (approximately 45 cm from the nostrils in a non-reflexogenic zone), connected to a Marquette TRAM 500 monitoring system (Marquette Electronics, Jupiter, FL 33468, USA) via an Abbott Invasive Blood Pressure Kit (Abbott Laboratories Ltd, Sligo, Rep. of Ireland) . The system was calibrated (“zero-ed”) at the level of the xyphoid process. The pressure values obtained were considered to be “relative” pressures, permitting a comparison between values from different manoeuvres. The curves were recorded onto thermal paper. The tested manoeuvres were :
The ITP value of the initial isometric muscle exercise was taken as 100 %, and the level of ITP reached by the others manoeuvres was related to this standard isometric effort. Next, the slope of the ITP fall was analyzed to find out if there was a difference for the tested manoeuvres and if there was a correlation with the ITP peak reached. The experimental results were statistically investigated with a standard procedure including mean, standard deviation, median and the analysis of variance ANOVA for repeated measures to test within and between groups effect. The regression lines were computed using the least squares procedure and the slopes were compared; regressions were calculated using the peak pressure point reached per each manoeuver and at least three points of the descending part of the curve for each subject (exempted "gentle valsalva" and the knee bend manoevers since the measurement of the releasing part of curve was inaccurate). Results
Discussion The Valsalva manoeuvre consists of a manual blockage of the nostrils, followed by a forced expiration against closed mouth and nose, to provoke an augmentation of the pressure in the nasopharyngeal cavity. Inevitably, this manoeuvre provokes a rise in intrathoracic pressure. There are 6 major sequences to be considered during the Valsalva manoeuvre (7): the initial inhaling phase, exhaling phase, strain phase, releasing phase and finally a second inhaling and exhaling phase (8). Each phase is accompanied by changes in airway and intrathoracic pressure. Those pressure changes will interfere with the right and left atrial pressure curves. During the profound inhalation, initiating the cycle, there is a right atrium pressure predominance due to a decrease in intrathoracic pressure and an increased gradient between the extrathoracic veins and the right atrium. An increased inflow from the (superior and) inferior caval vein to the right atrium, an increased filling capacity of the expanded lungs, as well as ventricular interdependence cause a successive decrease in left atrial return and pressure. During the exhaling phase against resistance, the airway and intrathoracic pressure increases with a resultant left atrial pressure predominance. The increased intrathoracic pressure diminishes the systemic venous return to the heart. The peripheral venous flow will first fill up the available venous capacity. This occurs at the expense of flow through the central veins, explaining the drop in right ventricular stroke volume already reported (3). During the first few heartbeats following the release of the Valsalva manoeuvre, Lee and co-workers (9) observed an increased right atrial pressure above the pulmonary wedge pressure and therefore, presumably above the left atrial pressure. Other manoeuvres can likewise induce a rise in ITP. From our investigations, we showed that the usual manoeuvres, used by divers to equalize the pressure in their middle ear cavities, only induces a very slight rise in ITP. Moreover, it is usually of short duration. Therefore, the release of this kind of manoeuvre is not likely to induce major blood shifts through an eventual PFO. However, this is drastically different if a “forced” Valsalva manoeuvre is considered (p<0.001 vs. “divers’ Valsalva” - fig.2 ), where the rise of ITP is even greater than that obtained by maximal isometric effort. Literature has reported embolisation during Valsalva manoeuvre in patients with PFO; our results permit to more precisely define this observation, in that the Valsalva manoeuvre performed was certainly a “forced” one (10). Certain morphological characteristics of the interatrial septum might not permit a right-to-left shunt in normal circumstances but allow a massive shunt if the “driving pressure” is sufficiently high (Balestra et al., unpublished data).
Based on this and other PFO studies (11,1), a common advice, given to divers with PFO, is not to perform any Valsalva manoeuvres causing a real rise of intrathoracic pressure immediately after ascent from their dive (e.g. to relieve residual pressure differences in the middle ears), because silent bubbles can be present in the central venous blood for 2 hours after a deep dive (12). On the basis of our findings, they should, to our view, also be advised not to perform sustained isometric exercise or abdominal strains (such as e.g. defecation, lifting of dive tanks, orally inflating buoyancy control device at the surface). Another important implication for diving instruction should be that divers should be taught not to perform forceful Valsalva manoeuvres to equalize middle ear pressures, i.e. using their abdominal muscles (intra-abdominal pressure can interfere with ITP (13)). Only jaw and throat muscles should be used and special attention should be placed on this during training (14). The anatomical characteristics of a patent Foramen Ovale are well known (2). The repeated rebound blood shift and subsequent rise in right atrial pressure may constitute a mechanical trigger for permeabilization of a previously closed (but only lightly fused) Foramen Ovale; a minimally patent Foramen Ovale may become largely patent in the course of (probably) years. This hypothesis , although as yet unproved, is firmly backed up by two findings. First, anatomopathological studies have shown that in an older age group, the incidence of PFO may be a little lower, but the diameter of the interatrial channel is always larger (15). Secondly, from our own experience, several older and experienced divers have been struck by repeated episodes of “unexplained decompression illness” (i.e. without having violated currently accepted diving technical rules, considered as “safe”) after having performed sometimes more than 1000 dives without any problem. In all of these divers, on TEE, a large PFO was detected. Conclusions We conclude that manoeuvres other than the usual “Divers' Valsalva manoeuvre” are more likely to cause post-release central blood shift, both by the higher levels of ITP reached and by the time during which these ITP's are sustained, thus causing "pooling" of blood beneath the diaphragm and subsequent release when the ITP falls. Although the mechanisms of rise and fall of ITP may be different in these different manoeuvres , the ITP release curves are identical since the slopes of the regression lines are not different. Any manoeuvre or exercise that is likely to cause such a ITP rise for a “prolonged” period, should be discouraged in divers with PFO, for a sufficiently long period after their dive. These divers (and maybe also those without PFO) should also be advised to refrain from strenuous leg or arm exercise (such as air tank handling and dive boat boarding with full equipment) after decompression dives. Nevertheless, it is important to remember that nitrogen bubbles embolizing through the Foramen Ovale is the cause of decompression sickness, not the patency of the foramen. In order to minimize the load of nitrogen bubbles after a dive, several techniques can be used. Diving no deeper 30m, making a slow ascent (not faster than 10m/minute) and performing a decompression stop of 5 minutes between 3 and 6 meters even if the dive tables do not impose one (the so-called “safety stop”) have all been shown to substantially reduce venous nitrogen bubble load after a dive (12). This work was supported by grants from the Divers Alert Network Europe.
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