Abstract: The purpose of the study was to analyze the ultrasound lung comets (ULCs) variation, which are a sign of extra-vascular lung water. Forty-two healthy individuals performed breath-hold diving in different conditions: dynamic surface apnea; deep variable-weight apnea and shallow, face immersed without effort (static maximal and non-maximal). The number of ULCs was evaluated by means of an ultrasound scan of the chest, before and after breath-hold diving sessions. The ULC score increased significantly from baseline after dynamic surface apnea (p = 0.0068), after deep breath-hold sessions (p = 0.0018), and after static maximal apnea (p = 0.031). There was no statistically significant difference between the average increase of ULC scores after dynamic surface apnea and deep breath-hold diving. We, therefore, postulate that extravascular lung water accumulation may be due to other factors than (deep) immersion alone, because it occurs during dynamic surface apnea as well. Three mechanisms may be responsible for this. First, the immersion-induced hydrostatic pressure gradient applied on the body causes a shift of peripheral venous blood towards the thorax. Second, the blood pooling effect found during the diving response Redistributes blood to the pulmonary vascular bed. Third, it is possible that the intense involuntary diaphragmatic contractions occurring during the "struggle phase" of the breath-hold can also produce a blood shift from the pulmonary capillaries to the pulmonary alveoli. A combination of these factors may explain the observed increase in ULC scores in deep, shallow maximal and shallow dynamic apneas, whereas shallow non-maximal apneas seem to be not "ULC provoking".
Abstract: To evaluate the separate cardiovascular response to body immersion and increased environmental pressure during diving, 12 healthy male subjects (mean age 35.2 +/- 6.5 yr) underwent two-dimensional Doppler echocardiography in five different conditions: out of water (basal); head-out immersion while breathing (condition A); fully immersed at the surface while breathing (condition B) and breath holding (condition C); and breath-hold diving at 5-m depth (condition D). Heart rate, left ventricular volumes, stroke volume, and cardiac output were obtained by underwater echocardiography. Early (E) and late (A) transmitral flow velocities, their ratio (E/A), and deceleration time of E (DTE) were also obtained from pulsed-wave Doppler, as left ventricular diastolic function indexes. The experimental protocol induced significant reductions in left ventricular volumes, left ventricular stroke volume (P < 0.05), cardiac output (P < 0.001), and heart rate (P < 0.05). A significant increase in E peak (P < 0.01) and E/A (P < 0.01) and a significant reduction of DTE (P < 0.01) were also observed. Changes occurring during diving (condition D) accounted for most of the changes observed in the experimental series. In particular, cardiac output at condition D was significantly lower compared with each of the other experimental conditions, E/A was significantly higher during condition D than in conditions A and C. Finally, DTE was significantly shorter at condition D than in basal and condition C. This study confirms a reduction of cardiac output in diving humans. Since most of the changes were observed during diving, the increased environmental pressure seems responsible for this hemodynamic rearrangement. Left ventricular diastolic function changes suggest a constrictive effect on the heart, possibly accounting for cardiac output reduction.
Abstract: Cardiac response to breath-hold diving in human beings is primarily characterized by the reduction of both heart rate and stroke volume. By underwater Doppler-echocardiography we observed a "restrictive/constrictive" left ventricular filling pattern compatible with the idea of chest squeeze and heart compression during diving. We hypothesized that underwater re-expansion of the chest would release heart constriction and normalize cardiac function. To this aim, 10 healthy male subjects (age 34.2 +/- 10.4) were evaluated by Doppler-echocardiography during breath-hold immersion at a depth of 10 m, before and after a single maximal inspiration from a SCUBA device. During the same session, all subjects were also studied at surface (full-body immersion) and at 5-m depth in order to better characterize the relationship of echo-Doppler pattern with depth. In comparison to surface immersion, 5-m deep diving was sufficient to reduce cardiac output (P = 0.042) and increase transmitral E-peak velocity (P < 0.001). These changes remained unaltered at a 10-m depth. Chest expansion at 10 m decreased left ventricular end-systolic volume (P = 0.024) and increased left ventricular stroke volume (P = 0.024). In addition, it decreased transmitral E-peak velocity (P = 0.012) and increased deceleration time of E-peak (P = 0.021). In conclusion the diving response, already evident during shallow diving (5 m) did not progress during deeper dives (10 m). The rapid improvement in systolic and diastolic function observed after lung volume expansion is congruous with the idea of a constrictive effect on the heart exerted by chest squeeze.
Abstract: Breath-hold divers may experience haemoptysis during diving. Central pooling of blood as well as compression of pulmonary gas content can damage the integrity of the blood-gas barrier, resulting in alveolar hemorrhage. The single-breath carbon monoxide test (DL,CO) was used to investigate the blood-gas barrier following diving. The study population consisted of 30 divers recruited from a training course. DL,CO levels were measured before diving and at 2, 10 and 25 min after the last of a series of four dives to depths of 10, 15, 20 and 30 m. When compared to pre-diving values, DL,CO values increased significantly at 2 min following diving in all subjects except one. Thereafter values progressively decreased toward baseline at 10 and 25 min in all subjects but one, while in four divers DL,CO values decreased below baseline. The early but transient increase in DL,CO levels shortly after diving supports the persistence of capillary pooling of red blood cells following emersion. Persistence at 25 min of high DL,CO values in one subject could be attributed by lung CT to extravasation of blood into the alveoli. Early or late DL,CO values >10% below baseline values suggest the presence of pulmonary edema. The relatively high prevalence of DL,CO alterations found suggests caution on the safety of breath-hold diving activities.
Abstract: During maximal breath-holding six healthy elite breath-hold divers, after an initial "easy-going" phase in which cardiovascular changes resembled the so-called "diving response", exhibited a sudden and severe rise in blood pressure during the "struggle" phase of the maneuver. These changes may represent the first tangible expression of a defense reaction, which overrides the classic diving reflex, aiming to reduce the hypoxic damage and to break the apnea before the loss of consciousness.
Abstract: Ultrasound lung comets (ULCs) detected by chest sonography are a simple, noninvasive, semiquantitative sign of increased extravascular lung water. Pulmonary edema may occur in elite apnea divers, possibly triggered by centralization of blood flow from the periphery to pulmonary vessels. We assessed the prevalence of ULCs in top-level breath-hold divers after immersion.
Abstract: Breath-hold diving induces, in marine mammals, a reduction of cardiac output due to a decrease of both heart rate and stroke volume. Cardiovascular changes in humans during breath-hold diving are only partially known due to the technical difficulty of studying fully immersed subjects. Recently, a submersible echocardiograph has been developed, allowing a feasible assessment of cardiac anatomy and function of subjects during diving. Aim of the study was to evaluate, by Doppler-echocardiography, the cardiovascular changes inducedby breath-hold diving in humans. Ten male subjects were studied by Doppler echocardiography in dry conditions and during breath-hold diving at 3 m depth. In addition 14 male subjects were studied, using the same protocol, before and during breath-hold diving at 10 m depth. At 3 m depth significant reductions in heart rate (-17%), stroke volume (-17%), cardiac output (-29%), left atrial dimensions, and deceleration time of early diastolic transmitral flow (DTE) were observed. At 10 m depth similar but more pronounced changes occurred. In particular, increase in early transmitral flow velocity became significant (+33%), while DTE decreased by 34%. At both depths dimensions of right cardiac chambers remained unchanged. Breath-hold diving at shallow depth induced, in humans, cardiovascular changes qualitatively similar to those observed in natural divers such as seals. The reduced dimensions of left atrium associated to a left ventricular diastolic pattern resembling that of restrictive/constrictive heart disease, suggest that the hemodynamic effects of diving could be explained, at least in part, by a constriction exerted on the heart by the reduced chest volume and the increased blood content of the lungs. Finally, the absence of dimensional changes in the right chambers suggests that most of the pulmonary blood shift occurred before cardiac imaging.
