Repetitive Breath-hold Dives Research Articles

Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

Central Nervous System Involvement in Breath-Hold Diving

Diving accident in breath-hold (BH) divers (Ama) is a stroke-like neurological condition involving the brain. Ama divers are at a risk of ischemic brain injuries which are situated in watershed or terminal zones of cerebral arteries, and/or corticomedullary junctional area of cerebral arteries. The underlying mechanisms of brain damage in BH diving remains to be elucidated. After repetitive BH dives, nitrogen (N2) bubbles may be formed in the venous side of tissues and flow into the right atrium. N2 bubbles passing through the heart or the lungs is the most likely contributing factor. The pathophysiology of diving accident in BH diving is unclear, and more studies for stroke are needed to further elucidate its nature. (Received 29 July, 2019; Accepted 10 January, 2020; Published 1 May, 2020).

Vascular dysfunction following breath-hold diving.

The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 × 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41- and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% ± 56.6% (p = 0.050) and 60.0% ± 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS.

The association of kidney function with repetitive breath-hold diving activities of female divers from Korea, Haenyeo

BackgroundVoluntary apnea during breath-hold diving (BHD) induces cardiovascular changes including bradycardia, reduced cardiac output, and arterial hypertension. Although the impacts of repetitive BHD on cardiovascular health have been studied previously, the long-term risk for kidney dysfunction has never been investigated.MethodsA cross-sectional propensity score-matched study was performed to evaluate the influence of repetitive long-lasting BHD on kidney function. Using matching propensity scores (PS), 715 breath-hold female divers (Haenyeo) and non-divers were selected for analysis from 1,938 female divers and 3,415 non-divers, respectively. The prevalence of chronic kidney disease (CKD) defined as an estimated glomerular filtration rate (eGFR) calculated to be less than 60 ml/min/1.73 m2 was investigated in both diver and non-diver groups.ResultsThe prevalence of CKD was significantly higher in breath-hold divers compared with non-divers after PS matching (12.6% vs. 8.0%, P = 0.004). In multivariate analysis, BHD activity was significantly associated with the risk of CKD in an unmatched cohort (OR, 1.976; 95% CI, 1.465–2.664). In the PS-matched cohort, BHD remained the independent risk factor for CKD even after adjusting for multiple covariates (OR 1.967; 95% CI, 1.341–2.886).ConclusionShallow but repetitive intermittent apnea by BHD, sustained for a long period of time, may potentially cause a deterioration in kidney function, as a long-term consequence.

Doppler Detection in Ama Divers of Japan

Symptoms consistent with neurological decompression sickness (DCS) in commercial breath-hold (Ama) divers has been reported from a few districts of Japan. The aim of this study was to detect circulating intravascular bubbles after repetitive breath-hold diving in a local area where DCS has been reported in Ama divers. The participants were 12 partially assisted (descent using weights) male Ama divers. The equipment (AQUALAB system) consisted of continuous-wave Doppler with a 5-MHz frequency, and the Doppler probe was placed in the precordial site with the ultrasonic wave directed into the pulmonary infundibulum. We carried out continuous monitoring for 10 minutes at the end of the series of repetitive dives, and the recordings were made on numerical tracks and graded in a blind manner by 2 experienced investigators, according to the Spencer Doppler code. Depths and number of dives were 8 to 20 m and 75 to 131 times. Mean diving duration and surface interval were 64 ± 12 seconds and 48 ± 8 seconds, respectively (mean ± SD). We detected the lowest grade of intravascular bubbles (Spencer's grade I) in an Ama diver whose mean surface interval was only 35.2 ± 6.2 seconds. His mean descending, bottom, and ascending times were 10.4 ± 1.6 seconds, 39.2 ± 8 seconds, and 18.2 ± 3.0 seconds, respectively, over the course of 99 dives. Intravascular bubbles may be formed after repetitive breath-hold dives with short surface intervals or after a long breath-holding session in Ama divers. Symptoms consistent with neurological accidents in repetitive breath-hold diving may be caused in part by the intravascular presence of bubbles, indicating the need for safety procedures.

Investigation of the potential for vascular bubble formation in a repetitively diving dolphin

The production of venous gas emboli (VGE) resulting from altered dive behavior is postulated as contributing to the stranding of beaked whales exposed to mid-frequency active sonar. To test whether nitrogen gas uptake during repetitive breath-hold diving is sufficient for asymptomatic VGE formation in odontocetes, a bottlenose dolphin (Tursiops truncatus Montagu) was trained to perform 10-12 serial dives with 60 s surface intervals to depths of 30, 50, 70 or 100 m. The dolphin remained at the bottom depth for 90 s on each dive. Doppler and/or two-dimensional imaging ultrasound did not detect VGE in the portal and brachiocephalic veins following a dive series. Van Slyke analyses of serial, post-dive blood samples drawn from the fluke yielded blood nitrogen partial pressure (P(N(2))) values that were negligibly different from control samples. Mean heart rate (HR; +/-1 s.d.) recorded during diving was 50+/-3 beats min(-1) and was not significantly different between the 50, 70 and 100 m dive sessions. The absence of VGE and elevated blood P(N(2)) during post-dive periods do not support the hypothesis that N(2) supersaturation during repetitive dives contributes to VGE formation in the dolphin. The diving HR pattern and the presumed rapid N(2) washout during the surface-interval tachycardia probably minimized N(2) accumulation in the blood during dive sessions.

HEMATOLOGIC AND SERUM BIOCHEMICAL PROFILE OF THE NORTHERN ELEPHANT SEAL (MIROUNGA ANGUSTIROSTRIS): VARIATION WITH AGE, SEX, AND SEASON

The foraging success, and thus the survival and reproductive success, of deep-diving pinnipeds such as the northern elephant seal, Mirounga angustirostris, depends on the ability to withstand repetitive breath-hold dives. Health parameters can be incorporated as potential explanatory variables for differences observed in diving and migratory performance of individual seals. Furthermore, biomedical samples from apparently healthy individuals can provide valuable baseline data for evaluating effects of natural or anthropogenic threats to individuals and populations. We evaluated 42 blood parameters in 134 northern elephant seals during the breeding and molting seasons (1992-1999) to test for age, sex, and seasonal differences and to develop reference ranges. Adult males sampled during the breeding season differed from all other adult groups for a suite of parameters often associated with inflammation, infection, or other stressors: lower hematocrit, higher white blood cell count, higher band neutrophils, higher neutrophil count, lower albumin, and lower serum iron. Adult females during the breeding season differed from all other adult categories for two parameters (lower platelet counts, lower alanine aminotransferase activity). Molting males had higher blood urea nitrogen than all other classes; creatinine did not differ between breeding and molting adult males, but was higher in males than in females in both seasons. We found significant differences among age classes for 24 of 42 parameters measured, including higher levels of triglycerides, total protein, calcium, and iron in pups than we found in juveniles or adults. Unlike other mammals which undergo substantial decreases in energy expenditure during prolonged fasting (e.g., hibernation), northern elephant seals defend territories, give birth and suckle large offspring, mate, and molt during their bi-annual fasts. Nonetheless, many studies have described physiologic homeostasis during fasting in elephant seals. The genus Mirounga is superbly adapted to going without feeding for extended periods, and this is reflected in our hematologic and serum biochemical profiles.

Decompression Sickness Following Breath-hold Diving

Despite convincing evidence of a relationship between breath-hold diving and decompression sickness (DCS), the causal connection is only slowly being accepted. Only the more recent textbooks have acknowledged the risks of repetitive breath-hold diving. We compare four groups of breath-hold divers: (1) Japanese and Korean amas and other divers from the Pacific area, (2) instructors at naval training facilities, (3) spear fishers, and (4) free-dive athletes. While the number of amas is likely decreasing, and Scandinavian Navy training facilities recorded only a few accidents, the number of spear fishers suffering accidents is on the rise, in particular during championships or using scooters. Finally, national and international associations (e.g., International Association of Free Drives [IAFD] or Association Internationale pour Le Developpment De L'Apnee [AIDA]) promote free-diving championships including deep diving categories such as constant weight, variable weight, and no limit. A number of free-diving athletes, training for or participating in competitions, are increasingly accident prone as the world record is presently set at a depth of 171 m. This review presents data found after searching Medline and ISI Web of Science and using appropriate Internet search engines (e.g., Google). We report some 90 cases in which DCS occurred after repetitive breath-hold dives. Even today, the risk of suffering from DCS after repetitive breath-hold diving is often not acknowledged. We strongly suggest that breath-hold divers and their advisors and physicians be made aware of the possibility of DCS and of the appropriate therapeutic measures to be taken when DCS is suspected. Because the risk of suffering from DCS increases depending on depth, bottom time, rate of ascent, and duration of surface intervals, some approaches to assess the risks are presented. Regrettably, none of these approaches is widely accepted. We propose therefore the development of easily manageable algorithms for the prevention of those avoidable accidents.

Neurological accidents caused by repetitive breath-hold dives: two case reports

We report two Japanese male professional breath-hold divers (33 and 39 years of age) who experienced neurological disorders during repetitive dives to over 20 m of seawater. One patient had right homonymous hemianopsia, and the other presented with right hemiparesis with facial involvement and sensory deficit. In addition, they each had a history of neurological problems following such dives. Magnetic resonance images of their brains disclosed multiple T2-weighted hyperintensities corresponding to their neurological symptoms. Their brain lesions suggest a multiple cerebral infarction caused by occlusion of the cerebral arteries. We conclude that the repetitive deep breath-hold dives induced the brain involvement.

Nitrogen tensions in brachial vein blood of Korean ama divers.

Intravascular bubble formation and symptoms of decompression sickness have been reported during repetitive deep breath-hold diving. Therefore we examined the pattern of blood N2 kinetics during and after repetitive breath-hold diving. To study muscle N2 uptake and release, we measured brachial venous N2 partial pressure (PN2) in nine professional Korean breath-hold divers (ama) during a 3-h diving shift at approximately 4 m seawater depth and up to 4 h after diving. PN2 was determined with the manometric Van Slyke method. Diving time and depth were recorded using a backpack computer-assisted dive longer that allowed calculating the surface-to-depth time ratio to derive the effective depth. With the assumption that forearm muscle N2 kinetics follow the general Haldanian principles of compression and decompression, i.e., forearm muscle is a single compartment with a uniform tissue PN2 equal to venous PN2, PN2 data were fitted to monoexponential functions of time. In the early phase of the diving shift, PN2 rapidly increased to 640 Torr (half time = 6 min) and then slowly declined to baseline levels (half time = 36 min) after the work shift. Peak PN2 levels approximated the alveolar PN2 derived from the effective depth. We conclude that forearm muscle N2 kinetics are well described by a Haldanian single-compartment model. Decompression sickness is theoretically possible in the ama; it did not occur because the absolute PN2 remained low due to the shallow working depth of the ama we studied.

Splenic contraction during breath-hold diving in the Korean ama

Major increases of hemoglobin concentration and hematocrit, possibly secondary to splenic contraction, have been noted during diving in the Weddell seal. We sought to learn whether this component of the diving response could be present in professional human breath-hold divers. Splenic size was measured ultrasonically before and after repetitive breath-hold dives to approximately 6-m depth in ten Korean ama (diving women) and in three Japanese male divers who did not routinely practice breath-hold diving. Venous hemoglobin concentration and hematocrit were measured in nine of the ama and all Japanese divers. In the ama, splenic length and width were reduced after diving (P = 0.0007 and 0.0005, respectively) and calculated splenic volume decreased 19.5 +/- 8.7% (mean +/- SD, P = 0.0002). Hemoglobin concentration and hematocrit increased 9.5 +/- 5.9% (P = 0.0009) and 10.5 +/- 4% (P = 0.0001), respectively. In Japanese male divers, splenic size and hematocrit were unaffected by repetitive breath-hold diving and hemoglobin concentration increased only slightly over baseline (3.0 +/- 0.6%, P = 0.0198). Splenic contraction and increased hematocrit occur during breath-hold diving in the Korean ama.