scholarly journals Going to Extremes of Lung Physiology–Deep Breath-Hold Diving

2021 ◽  
Vol 12 ◽  
Author(s):  
Kay Tetzlaff ◽  
Frederic Lemaitre ◽  
Christof Burgstahler ◽  
Julian A. Luetkens ◽  
Lars Eichhorn
Keyword(s):  
Water Immersion ◽  
Respiratory Physiology ◽  
Neurological Injury ◽  
Breath Hold ◽  
Deep Breath ◽  
Pulmonary Physiology ◽  
Lung Physiology ◽  
Body Tissues ◽  
Increase Risk ◽  
Decompression Stress

Breath-hold diving involves environmental challenges, such as water immersion, hydrostatic pressure, and asphyxia, that put the respiratory system under stress. While training and inherent individual factors may increase tolerance to these challenges, the limits of human respiratory physiology will be reached quickly during deep breath-hold dives. Nonetheless, world records in deep breath-hold diving of more than 214 m of seawater have considerably exceeded predictions from human physiology. Investigations of elite breath-hold divers and their achievements revised our understanding of possible physiological adaptations in humans and revealed techniques such as glossopharyngeal breathing as being essential to achieve extremes in breath-hold diving performance. These techniques allow elite athletes to increase total lung capacity and minimize residual volume, thereby reducing thoracic squeeze. However, the inability of human lungs to collapse early during descent enables respiratory gas exchange to continue at greater depths, forcing nitrogen (N2) out of the alveolar space to dissolve in body tissues. This will increase risk of N2 narcosis and decompression stress. Clinical cases of stroke-like syndromes after single deep breath-hold dives point to possible mechanisms of decompression stress, caused by N2 entering the vasculature upon ascent from these deep dives. Mechanisms of neurological injury and inert gas narcosis during deep breath-hold dives are still incompletely understood. This review addresses possible hypotheses and elucidates factors that may contribute to pathophysiology of deep freediving accidents. Awareness of the unique challenges to pulmonary physiology at depth is paramount to assess medical risks of deep breath-hold diving.

Risk of Neurological Insult in Competitive Deep Breath-Hold Diving

2017 ◽  
Vol 12 (2) ◽  
pp. 268-271 ◽  
Author(s):  
Kay Tetzlaff ◽  
Holger Schöppenthau ◽  
Jochen D. Schipke
Keyword(s):  
Web Search ◽  
Breath Hold ◽  
Gas Embolism ◽  
Short Delay ◽  
Deep Breath ◽  
Single Breath ◽  
Single Breath Hold ◽  
Arterial Gas Embolism ◽  
Neurological Insult ◽  
Decompression Stress

Context:It has been widely believed that tissue nitrogen uptake from the lungs during breath-hold diving would be insufficient to cause decompression stress in humans. With competitive free diving, however, diving depths have been ever increasing over the past decades.Methods:A case is presented of a competitive free-diving athlete who suffered stroke-like symptoms after surfacing from his last dive of a series of 3 deep breath-hold dives. A literature and Web search was performed to screen for similar cases of subjects with serious neurological symptoms after deep breath-hold dives.Case Details:A previously healthy 31-y-old athlete experienced right-sided motor weakness and difficulty speaking immediately after surfacing from a breathhold dive to a depth of 100 m. He had performed 2 preceding breath-hold dives to that depth with surface intervals of only 15 min. The presentation of symptoms and neuroimaging findings supported a clinical diagnosis of stroke. Three more cases of neurological insults were retrieved by literature and Web search; in all cases the athletes presented with stroke-like symptoms after single breath-hold dives of depths exceeding 100 m. Two of these cases only had a short delay to recompression treatment and completely recovered from the insult.Conclusions:This report highlights the possibility of neurological insult, eg, stroke, due to cerebral arterial gas embolism as a consequence of decompression stress after deep breath-hold dives. Thus, stroke as a clinical presentation of cerebral arterial gas embolism should be considered another risk of extreme breath-hold diving.

scholarly journals Non‐Invasive Pulmonary Gas Exchange Measurements Following Deep Breath‐Hold Diving

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Alexander Patrician ◽  
Ivan Drvis ◽  
Tony Dawkins ◽  
Barak Otto ◽  
Geoff Coombs ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Gas Exchange ◽  
Breath Hold ◽  
Deep Breath ◽  
Non Invasive

scholarly journals Effect of Dietary Carotenoids on Reproducers of Amazon River Prawn Macrobrachium amazonicum. Part 2: External Coloration, Accumulation of Astaxanthin in Body Tissues and Pigment Stability in Feed

2021 ◽  
Vol 9 (2) ◽  
pp. 57
Author(s):  
Daniel Pereira da Costa ◽  
Claudiana De Lima Castilho ◽  
Uclédia Roberta Alberto dos Santos ◽  
Tainára Cunha Gemaque ◽  
Leandro Fernandes Damasceno ◽  
...  
Keyword(s):  
Water Immersion ◽  
The Body ◽  
Amazon River ◽  
Control Group ◽  
Body Tissues ◽  
Pigment Stability ◽  
Macrobrachium Amazonicum ◽  
Wild Group ◽  
Reflective Spectroscopy ◽  
Productive Development

The color is an important factor to distinguish the commercialized Amazon river prawns. The accumulation of pigments in the body can vary according to the prawn’s diet. In this work, ethanolic extracts of “buriti” and annatto rich in pigments were obtained and tested comparatively with synthetic astaxanthin in the feeding of adults of Macrobrachium amazonicum, together with a control group without pigments and a newly captured wild group. Levels of body pigments were measured using UV reflective spectroscopy and external staining by colorimetry. Differences were observed in the accumulation of astaxanthin in body tissues, differences in saturation between genders and that annatto extract has greater stability in the feed after water immersion (P˂0.05). Further studies are recommended to verify the ideal dosage of natural pigments in relation to synthetic astaxanthin that benefits the productive development of prawns.

Mechanical Ventilation: Respiratory Physiology and Conventional Ventilation

2018 ◽  
Author(s):  
Adrian A. Maung ◽  
Lewis J Kaplan
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Distress Syndrome ◽  
Functional Unit ◽  
Respiratory Physiology ◽  
Pulmonary Physiology ◽  
Functional Understanding ◽  
Ground Ambulance ◽  
Prerequisite Knowledge ◽  
Ventilation Modes

This three-part review is intended to enable the reader to manage the fundamentals of mechanical ventilation in both the urgent and the nonurgent setting. This first chapter provides a functional understanding of basic pulmonary physiology as a prerequisite knowledge base prior to reviewing the concepts central to basic, traditional, and cyclical ventilation that is regularly employed in the air or ground ambulance, emergency department, operating room, and intensive care unit. Subsequent chapters will review advanced ventilation modes, adjuncts, and special problems encountered in patients with respiratory failure requiring mechanical ventilation. Each segment is intended to build on the preceding one and therefore establishes a functional unit with regard to mechanical ventilation, whether it is provided in an invasive or a noninvasive fashion.   This review contains 5 Figures and 10 references Key Words: acute respiratory failure, acute respiratory distress syndrome, hypercapnia/therapy, hypoxia/therapy, mechanical ventilation, pulmonary gas exchange

Breath-Hold Time During Cold Water Immersion: Effects of Habituation with Psychological Training

2007 ◽  
Vol 78 (11) ◽  
pp. 1029-1034 ◽  
Author(s):  
Martin J. Barwood ◽  
Avijit K. Datta ◽  
Richard C. Thelwell ◽  
Michael J. Tipton
Keyword(s):  
Cold Water ◽  
Water Immersion ◽  
Hold Time ◽  
Cold Water Immersion ◽  
Breath Hold ◽  
Psychological Training

scholarly journals Standardised 3D-CT Lung Volumes for Patients with Idiopathic Pulmonary Fibrosis

2021 ◽  
Author(s):  
Yuko Tanaka ◽  
Yuzo Suzuki ◽  
Hirotsugu Hasegawa ◽  
Koshi Yokomura ◽  
Atsuki Fukada ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Function Tests ◽  
Three Dimensional ◽  
Ct Images ◽  
3D Ct ◽  
Pulmonary Physiology ◽  
Lung Physiology ◽  
Lower Lung

Abstract Background: The assessment of lung physiology via pulmonary function tests (PFTs) is essential for patients with idiopathic pulmonary fibrosis (IPF). However, PFTs require active participation, which can be challenging for patients with severe respiratory failure, such as during acute exacerbations (AE) of IPF. Recently advances enabled to re-construct of 3-dimensional computed-tomography (3D-CT) images. Methods: This is a retrospective multi-center cohort study. This study established a standardisation method and quantitative analysis of lung volume (LV) based on anthropometry using three-dimensional computed tomography (3D-CT) images. The standardised 3D-CT LV in patients with IPF at diagnosis (n=140) and during AE (cohort1; n=61 and cohort2; n=50) and those of controls (n=53) were measured. Results: The standardised 3D-CT LVs at IPF diagnosis were less than those of control patients, especially in the lower lung lobes. The standardised 3D-CT LVs were correlated with forced vital capacity (FVC) and validated using the modified Gender-Age-Physiology (GAP) index. The standardised 3D-CT LVs at IPF diagnosis were independently associated with prognosis. During AE, PFTs were difficult to perform, 3D-CT analyses revealed reduced lung capacity in both the upper and lower lobes compared to those obtained at diagnosis. Lower standardised 3D-CT LVs during AE were independently associated with worse outcomes in independent two cohorts. Particularly, volume loss in the upper lobe at AE had prognostic values.Conclusion: A novel image quantification method for assessing pulmonary physiology using standardised 3D-CT-derived LVs was developed. This method successfully predicts mortality in patients with IPF and AE of IPF, and may be a useful alternative to PFTs when PFTs cannot be performed.

Blood Gas Analyses in Hyperbaric and Underwater Environments: A Systematic Review

2021 ◽  
Author(s):  
Matteo Paganini ◽  
Richard E. Moon ◽  
Nicole Boccalon ◽  
Giorgio E.M. Melloni ◽  
Tommaso Antonio Giacon ◽  
...  
Keyword(s):  
Water Immersion ◽  
Correlation Coefficients ◽  
Blood Gases ◽  
Breath Hold ◽  
Blood Gas ◽  
Arterial Blood ◽  
Gas Measurement ◽  
Hyperbaric Environment ◽  
Blood Gas Analyses ◽  
Hyperbaric Conditions

Background: Pulmonary gas exchange during diving or in a dry hyperbaric environment is affected by increased breathing gas density and possibly water immersion. During free diving there is also the effect of apnea. Few studies have published blood gas data in underwater or hyperbaric environments: this review summarizes the available literature and was used to test the hypothesis that arterial PO2 under hyperbaric conditions can be predicted from blood gas measurement at 1 atmosphere assuming a constant arterial/alveolar PO2 ratio (a:A). Methods: A systematic search was performed on traditional sources including arterial blood gases obtained on humans in hyperbaric or underwater environments. The a:A was calculated at 1 atmosphere absolute (ATA). For each condition, predicted PaO2 at pressure was calculated using the 1 ATA a:A, and the measured PaO2 was plotted against the predicted value with Spearman correlation coefficients. Results: Of 3640 records reviewed, 30 studies were included: 25 were reports describing values obtained in hyperbaric chambers, and the remaining were collected while underwater. Increased inspired O2 at pressure resulted in increased PaO2, although underlying lung disease in patients treated with hyperbaric oxygen attenuated the rise. PaCO2 generally increased only slightly. In breath-hold divers, hyperoxemia generally occurred at maximum depth, with hypoxemia after surfacing. The a:A adequately predicted the PaO2 under various conditions: dry (r=0.993, p< 0.0001); rest vs. exercise (r=0.999, p< 0.0001); and breathing mixtures (r=0.995, p< 0.0001). Conclusion: Pulmonary oxygenation under hyperbaric conditions can be reliably and accurately predicted from 1 ATA a:A measurements.

scholarly journals Erythropoietic responses to a series of repeated maximal dynamic and static apnoeas in elite and non-breath-hold divers

2019 ◽  
Vol 119 (11-12) ◽  
pp. 2557-2565 ◽  
Author(s):  
Antonis Elia ◽  
Matthew J. Barlow ◽  
Kevin Deighton ◽  
Oliver J. Wilson ◽  
John P. O’Hara
Keyword(s):  
Water Immersion ◽  
Significant Negative Correlation ◽  
Group Differences ◽  
Breath Hold ◽  
The Novel ◽  
Peripheral Oxygen Saturation ◽  
Blood Samples ◽  
And Control ◽  
Maximal Effort ◽  
Serum Erythropoietin

Abstract Purpose Serum erythropoietin (EPO) concentration is increased following static apnoea-induced hypoxia. However, the acute erythropoietic responses to a series of dynamic apnoeas in non-divers (ND) or elite breath-hold divers (EBHD) are unknown. Methods Participants were stratified into EBHD (n = 8), ND (n = 10) and control (n = 8) groups. On two separate occasions, EBHD and ND performed a series of five maximal dynamic apnoeas (DYN) or two sets of five maximal static apnoeas (STA). Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on EPO. Peripheral oxygen saturation (SpO2) levels were monitored up to 30 s post each maximal effort. Blood samples were collected at 30, 90, and 180 min after each protocol for EPO, haemoglobin and haematocrit concentrations. Results No between group differences were observed at baseline (p > 0.05). For EBHD and ND, mean end-apnoea SpO2 was lower in DYN (EBHD, 62 ± 10%, p = 0.024; ND, 85 ± 6%; p = 0.020) than STA (EBHD, 76 ± 7%; ND, 96 ± 1%) and control (98 ± 1%) protocols. EBHD attained lower end-apnoeic SpO2 during DYN and STA than ND (p < 0.001). Serum EPO increased from baseline following the DYN protocol in EBHD only (EBHD, p < 0.001; ND, p = 0.622). EBHD EPO increased from baseline (6.85 ± 0.9mlU/mL) by 60% at 30 min (10.82 ± 2.5mlU/mL, p = 0.017) and 63% at 180 min (10.87 ± 2.1mlU/mL, p = 0.024). Serum EPO did not change after the STA (EBHD, p = 0.534; ND, p = 0.850) and STE (p = 0.056) protocols. There was a significant negative correlation (r = − 0.49, p = 0.003) between end-apnoeic SpO2 and peak post-apnoeic serum EPO concentrations. Conclusions The novel findings demonstrate that circulating EPO is only increased after DYN in EBHD. This may relate to the greater hypoxemia achieved by EBHD during the DYN.

scholarly journals Microparticles generated by decompression stress cause central nervous system injury manifested as neurohypophysial terminal action potential broadening

2013 ◽  
Vol 115 (10) ◽  
pp. 1481-1486 ◽  
Author(s):  
Ming Yang ◽  
Paul Kosterin ◽  
Brian M. Salzberg ◽  
Tatyana N. Milovanova ◽  
Veena M. Bhopale ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Action Potential ◽  
Central Nervous System Injury ◽  
Neurological Injury ◽  
Circulating Microparticles ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase ◽  
Decompression Stress ◽  
Nadph Oxidase Activation

The study goal was to use membrane voltage changes during neurohypophysial action potential (AP) propagation as an index of nerve function to evaluate the role that circulating microparticles (MPs) play in causing central nervous system injury in response to decompression stress in a murine model. Mice studied 1 h following decompression from 790 kPa air pressure for 2 h exhibit a 45% broadening of the neurohypophysial AP. Broadening did not occur if mice were injected with the MP lytic agent polyethylene glycol telomere B immediately after decompression, were rendered thrombocytopenic, or were treated with an inhibitor of nitric oxide synthase-2 (iNOS) prior to decompression, or in knockout (KO) mice lacking myeloperoxidase or iNOS. If MPs were harvested from control (no decompression) mice and injected into naive mice, no AP broadening occurred, but AP broadening was observed with injections of equal numbers of MPs from either wild-type or iNOS KO mice subjected to decompression stress. Although not required for AP broadening, MPs from decompressed mice, but not control mice, exhibit NADPH oxidase activation. We conclude that inherent differences in MPs from decompressed mice, rather than elevated MPs numbers, mediate neurological injury and that a component of the perivascular response to MPs involves iNOS. Additional study is needed to determine the mechanism of AP broadening and also mechanisms for MP generation associated with exposure to elevated gas pressure.

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