Case studies in Physiology: Breath-hold diving beyond 100 meters - cardiopulmonary responses in world champion divers

2021 ◽  
Author(s):  
Alexander Patrician ◽  
Christopher Gasho ◽  
Boris Spajić ◽  
Hannah G. Caldwell ◽  
Darija Bakovic-Kramaric ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Airway Resistance ◽  
Physiological Stress ◽  
Structural Characteristics ◽  
Compressive Strain ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Breath Hold ◽  
Valuable Insight ◽  
World Champion

In this case study, we evaluate the unique physiological profiles of two world-champion breath-hold divers. At close-to current world record depths, the extreme physiological responses to both exercise and asphyxia during progressive elevations in hydrostatic pressure are profound. As such, these professional athletes must be highly capable of managing such stress, to maintain performing at the forefront human capacity. In both divers, pulmonary function before and after deep dives to 102 and 117 meters in the open sea were assessed using non-invasive pulmonary gas exchange (indexed via the O2 deficit, which is analogous to the traditional alveolar to arterial oxygen difference), ultrasound B-line scores, airway resistance and airway reactance. Hydrostatic-induced lung compression was also quantified via spirometry. Both divers successfully performed their dives. Pulmonary gas exchange efficiency was impaired in both divers at 10 min, but had mostly restored within a few hours. Mild hemoptysis was transiently evident immediately following the 117m dive, whereas both divers experienced nitrogen narcosis. Although B-lines were only elevated in one diver post-dive, reductions in airway resistance and reactance occurred in both divers, suggesting the compressive strain on the structural characteristics of the airways can persist for up to 3.5hrs. Marked echocardiographic dyssynchrony was evident in one diver after 10m of descent, which persisted until resolving at ~77m during ascent. In summary, despite the enormous hydrostatic and physiological stress to diving beyond 100m on a single breath, these data provide valuable insight into the extraordinary capacity of those at the pinnacle of apneic performance.

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

Single breath‐hold measurement of pulmonary gas exchange and diffusion in humans with hyperpolarized 129 Xe MR

2019 ◽  
Vol 32 (5) ◽  
pp. e4068 ◽  
Author(s):  
Junshuai Xie ◽  
Haidong Li ◽  
Huiting Zhang ◽  
Xiuchao Zhao ◽  
Lei Shi ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Gas Exchange ◽  
Breath Hold ◽  
Single Breath ◽  
Single Breath Hold ◽  
And Diffusion

scholarly journals Effect of a patent foramen ovale on pulmonary gas exchange efficiency at rest and during exercise

2011 ◽  
Vol 110 (5) ◽  
pp. 1354-1361 ◽  
Author(s):  
Andrew T. Lovering ◽  
Michael K. Stickland ◽  
Markus Amann ◽  
Matthew J. O'Brien ◽  
John S. Hokanson ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Patent Foramen Ovale ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Foramen Ovale ◽  
Healthy Humans ◽  
Significant Difference ◽  
Ergometer Exercise ◽  
Exchange Inefficiency

The prevalence of a patent foramen ovale (PFO) is ∼30%, and this source of right-to-left shunt could result in greater pulmonary gas exchange impairment at rest and during exercise. The aim of this work was to determine if individuals with an asymptomatic PFO (PFO+) have greater pulmonary gas exchange inefficiency at rest and during exercise than subjects without a PFO (PFO−). Separated by 1 h of rest, 8 PFO+ and 8 PFO− subjects performed two incremental cycle ergometer exercise tests to voluntary exhaustion while breathing either room air or hypoxic gas [fraction of inspired O2 (FiO2) = 0.12]. Using echocardiography, we detected small, intermittent boluses of saline contrast bubbles entering directly into the left atrium within 3 heart beats at rest and during both exercise conditions in PFO+. These findings suggest a qualitatively small intracardiac shunt at rest and during exercise in PFO+. The alveolar-to-arterial oxygen difference (AaDo2) was significantly ( P < 0.05) different between PFO+ and PFO− in normoxia (5.9 ± 5.1 vs. 0.5 ± 3.5 mmHg) and hypoxia (10.1 ± 5.9 vs. 4.1 ± 3.1 mmHg) at rest, but not during exercise. However, arterial oxygen saturation was significantly different between PFO+ and PFO− at peak exercise in normoxia (94.3 ± 0.9 vs. 95.8 ± 1.0%) as a result of a significant difference in esophageal temperature (38.4 ± 0.3 vs. 38.0 ± 0.3°C). An asymptomatic PFO contributes to pulmonary gas exchange inefficiency at rest but not during exercise in healthy humans and therefore does not explain intersubject variability in the AaDo2 at maximal exercise.

Effect of increased gas density on pulmonary gas exchange in man

1976 ◽  
Vol 41 (2) ◽  
pp. 206-210 ◽  
Author(s):  
L. D. Wood ◽  
A. C. Bryan ◽  
S. K. Bau ◽  
T. R. Weng ◽  
H. Levison
Keyword(s):  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Minute Ventilation ◽  
Volume Ratio ◽  
Carbon Dioxide Tension ◽  
Mean Value ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Dense Gas ◽  
The One

Pulmonary gas exchange was measured in seven resting supine subjects breathing air or a dense gas mixture containing 21% O2 in sulfur hexafluoride (SF6). The mean value of the alveolar-arterial oxygen difference (AaDO2) decreased from 12.4 on air to 7.0 on SF6 (P less than 0.01), and increased again to 13.4 when air breathing resumed (P less than 0.01). No differences occurred between gas mixtures for O2 consumption, respiratory quotient, minute ventilation, breathing frequency, heart rate, or blood pressure, and theimproved oxygen transfer could not be attributed to changes in cardiac output or mixed venous oxygen content in the one subject in which they were measured. These results are best explained by an altered distribution of ventilation during dense gas breathing, so that the ventilation-perfusion ratio(VA/Q) variance was reduced. Of several considered mechanisms, we favor onein which SF6 promotes cardiogenic gas mixing between peripheral parallel units having different alveolar gas concentrations. This mechanism allows forobserved increases in arterial carbon dioxide tension and dead space-to-tidal volume ratio during dense gas breathing, and suggests that intraregionalVA/Q variance accounts for at least one-half of the resting AaDO2 in healthysupine young men.

Hypoxemia and pulmonary gas exchange during hemodialysis

1981 ◽  
Vol 50 (2) ◽  
pp. 259-264 ◽  
Author(s):  
R. W. Patterson ◽  
A. R. Nissenson ◽  
J. Miller ◽  
R. T. Smith ◽  
R. G. Narins ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Oxygen Tension ◽  
Minute Ventilation ◽  
Arterial Oxygen Tension ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Exchange Relationships ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Alveolar Oxygen

With measured values of arterial blood gas tensions, of expired respiratory gas fractions, and volume of the expired ventilation, the determinants of alveolar oxygen tension (PAO2) were used to evaluate their influence on the development of the arterial hypoxemia that occurs in spontaneously breathing patients undergoing hemodialysis using an acetate dialysate. Dialysis produced no significant changes in the alveolar-arterial O2 tension gradient (AaDO2). The extracorporeal dialyzer removed an average of 30 ml.m-2.min-1 of CO2. Accordingly the pulmonary gas exchange ratio (R) dropped from a mean predialysis value of 0.81 to 0.62 (P less than 0.001). The arterial CO2 tension remained constant throughout, whereas the minute ventilation, both total (P less than 0.01) and alveolar (P less than 0.01), decreased during dialysis. This decrease in ventilation accounts for more than 80% of the fall in PAO2. During dialysis there was a decrease (P less than 0.001) in arterial oxygen tension (PaO2), which varied among the individuals from 9 to 23% of control. During the postdialysis hour PaO2 returns to control values concomitant with increase in ventilation. The quantitative gas exchange relationships among R, alveolar ventilation, and AaDO2 predict the PaO2 values actually measured.

Atelectasis affects the rate of arterial desaturation during obstructive apnea

1990 ◽  
Vol 69 (5) ◽  
pp. 1863-1868 ◽  
Author(s):  
E. C. Fletcher ◽  
S. Goodnight ◽  
T. Miller ◽  
R. A. Luckett ◽  
J. Rosborough ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Gas Exchange ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Apnea Duration ◽  
Obstructive Sleep ◽  
Spontaneously Breathing ◽  
Arterial Po2

Chronic hemodynamic disturbances are more profound in patients with obstructive sleep apnea when underlying lung disease with abnormal gas exchange (low arterial PO2) is present. Previous studies suggest that pulmonary gas exchange could influence the rate of fall of arterial oxygen saturation (dSaO2/dt) in obstructive sleep apnea. We postulated that abnormal gas exchange in the form of atelectasis would steepen dSaO2/dt and thereby lower nadir arterial oxyhemoglobin saturation (SaO2) for the same duration of apnea. Apneas were created by clamping an indwelling cuffed endotracheal tube at end expiration in eight spontaneously breathing adult baboons. Apneas of the same duration were then repeated during temporary endobronchial occlusion of one lobe of the lung. SaO2 and mixed venous O2 saturation were continuously monitored, and cardiac output was calculated. Worsening of pulmonary gas exchange during atelectasis was documented by an increase in calculated venous admixture from 10.5 +/- 0.8 to 25.0 +/- 0.7% (P less than 0.001). The dSaO2/dt was independent of apnea duration at 30, 45, and 60 s. During endobronchial occlusion, apnea dSaO2/dt increased 20%, and nadir SaO2 was significantly lower. Possible mechanisms for steepening of dSaO2/dt during atelectasis are discussed.

Temporal changes in pulmonary gas exchange efficiency when breath‐hold diving below residual volume

2021 ◽  
Vol 106 (4) ◽  
pp. 1120-1133
Author(s):  
Alexander Patrician ◽  
Boris Spajić ◽  
Christopher Gasho ◽  
Hannah G. Caldwell ◽  
Tony Dawkins ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Temporal Changes ◽  
Pulmonary Gas Exchange ◽  
Breath Hold ◽  
Residual Volume

scholarly journals Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: a systematic review

2017 ◽  
Vol 123 (6) ◽  
pp. 1657-1670 ◽  
Author(s):  
Silvia Ulrich ◽  
Simon R. Schneider ◽  
Konrad E. Bloch
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Sea Level ◽  
Exercise Performance ◽  
Oxygen Delivery ◽  
Cerebral Oxygenation ◽  
Respiratory Control ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Healthy Individuals

Exercise performance is determined by oxygen supply to working muscles and vital organs. In healthy individuals, exercise performance is limited in the hypoxic environment at altitude, when oxygen delivery is diminished due to the reduced alveolar and arterial oxygen partial pressures. In patients with pulmonary hypertension (PH), exercise performance is already reduced near sea level due to impairments of the pulmonary circulation and gas exchange, and, presumably, these limitations are more pronounced at altitude. In studies performed near sea level in healthy subjects, as well as in patients with PH, maximal performance during progressive ramp exercise and endurance of submaximal constant-load exercise were substantially enhanced by breathing oxygen-enriched air. Both in healthy individuals and in PH patients, these improvements were mediated by a better arterial, muscular, and cerebral oxygenation, along with a reduced sympathetic excitation, as suggested by the reduced heart rate and alveolar ventilation at submaximal isoloads, and an improved pulmonary gas exchange efficiency, especially in patients with PH. In summary, in healthy individuals and in patients with PH, alterations in the inspiratory Po2 by exposure to hypobaric hypoxia or normobaric hyperoxia reduce or enhance exercise performance, respectively, by modifying oxygen delivery to the muscles and the brain, by effects on cardiovascular and respiratory control, and by alterations in pulmonary gas exchange. The understanding of these physiological mechanisms helps in counselling individuals planning altitude or air travel and prescribing oxygen therapy to patients with PH.

Effect of Inhaled Prostacyclin in Combination with Almitrine on Ventilation–Perfusion Distributions in Experimental Lung Injury

2001 ◽  
Vol 94 (3) ◽  
pp. 461-467 ◽  
Author(s):  
Rolf Dembinski ◽  
Martin Max ◽  
Frank López ◽  
Ralf Kuhlen ◽  
Roland Kurth ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Lung Injury ◽  
Analysis Of Variance ◽  
Pulmonary Ventilation ◽  
Specific Treatment ◽  
Lung Lavage ◽  
Pulmonary Gas Exchange ◽  
Repeated Measurements ◽  
Arterial Oxygen ◽  
Inhaled Prostacyclin

Background Inhaled prostacyclin and intravenous almitrine have both been shown to improve pulmonary gas exchange in acute lung injury (ALI). This study was performed to investigate a possible additive effect of prostacyclin and almitrine on pulmonary ventilation-perfusion (VA/Q) ratio in ALI compared with inhaled prostacyclin or intravenous almitrine alone. Methods Experimental ALI was established in 24 pigs by repeated lung lavage. Animals were randomly assigned to receive either 25 ng.kg(-1).min(-1) inhaled prostacyclin alone, 1 microg.kg(-1).min(-1) almitrine alone, 25 ng.kg(-1).min(-1) inhaled prostacyclin in combination with 1 microg.kg(-1).min(-1) almitrine, or no specific treatment (controls) for 30 min. For each intervention, pulmonary gas exchange and hemodynamics were analyzed and VA/Q distributions were calculated using the multiple inert gas elimination technique. The data was analyzed within and between the groups by analysis of variance for repeated measurements, followed by the Student-Newman-Keuls test for multiple comparison when analysis of variance revealed significant differences. Results All values are expressed as mean +/- SD. In controls, pulmonary gas exchange, hemodynamics, and VA/Q distribution remained unchanged. With prostacyclin alone and almitrine alone, arterial oxygen partial pressure (PaO2) increased, whereas intrapulmonary shunt (QS/QT) decreased (P &lt; 0.05). Combined prostacyclin and almitrine also increased PaO2 and decreased QS/QT (P &lt; 0.05). When compared with either prostacyclin or almitrine alone, the combined application of both drugs revealed no additional effect in gas exchange or VA/Q distribution. Conclusions The authors conclude that, in this experimental model of ALI, the combination of 25 ng.kg(-1).min(-1) prostacyclin and 1 microg.kg(-1).min(-1) almitrine does not result in an additive improvement of pulmonary gas exchange or VA/Q distribution when compared with prostacyclin or almitrine alone.

scholarly journals Non-invasive Measurement of Pulmonary Gas Exchange Efficiency: The Oxygen Deficit

2021 ◽  
Vol 12 ◽  
Author(s):  
G. Kim Prisk ◽  
John B. West
Keyword(s):  
Gas Exchange ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Arterial Oxygen ◽  
Non Invasive ◽  
Arterial Blood ◽  
Age Related ◽  
End Tidal ◽  
Serial Measurements

The efficiency of pulmonary gas exchange has long been assessed using the alveolar-arterial difference in PO2, the A-aDO2, a construct developed by Richard Riley ~70years ago. However, this measurement is invasive (requiring an arterial blood sample), time consuming, expensive, uncomfortable for the patients, and as such not ideal for serial measurements. Recent advances in the technology now provide for portable and rapidly responding measurement of the PO2 and PCO2 in expired gas, which combined with the well-established measurement of arterial oxygen saturation via pulse oximetry (SpO2) make practical a non-invasive surrogate measurement of the A-aDO2, the oxygen deficit. The oxygen deficit is the difference between the end-tidal PO2 and the calculated arterial PO2 derived from the SpO2 and taking into account the PCO2, also measured from end-tidal gas. The oxygen deficit shares the underlying basis of the measurement of gas exchange efficiency that the A-aDO2 uses, and thus the two measurements are well-correlated (r2~0.72). Studies have shown that the new approach is sensitive and can detect the age-related decline in gas exchange efficiency associated with healthy aging. In patients with lung disease the oxygen deficit is greatly elevated compared to normal subjects. The portable and non-invasive nature of the approach suggests potential uses in first responders, in military applications, and in underserved areas. Further, the completely non-invasive and rapid nature of the measurement makes it ideally suited to serial measurements of acutely ill patients including those with COVID-19, allowing patients to be closely monitored if required.

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