scholarly journals Extreme Hypoxia Causing Brady-Arrythmias During Apnea in Elite Breath-Hold Divers

2021 ◽  
Vol 12 ◽  
Author(s):  
Thomas Kjeld ◽  
Anders Brenøe Isbrand ◽  
Katrine Linnet ◽  
Bo Zerahn ◽  
Jens Højberg ◽  
...  

Introduction: The cardiac electrical conduction system is very sensitive to hypoglycemia and hypoxia, and the consequence may be brady-arrythmias. Weddell seals endure brady-arrythmias during their dives when desaturating to 3.2 kPa and elite breath-hold-divers (BHD), who share metabolic and cardiovascular adaptions including bradycardia with diving mammals, endure similar desaturation during maximum apnea. We hypothesized that hypoxia causes brady-arrythmias during maximum apnea in elite BHD. Hence, this study aimed to define the arterial blood glucose (Glu), peripheral saturation (SAT), heart rhythm (HR), and mean arterial blood pressure (MAP) of elite BHD during maximum apneas.Methods: HR was monitored with Direct-Current-Pads/ECG-lead-II and MAP and Glu from a radial arterial-catheter in nine BHD performing an immersed and head-down maximal static pool apnea after three warm-up apneas. SAT was monitored with a sensor on the neck of the subjects. On a separate day, a 12-lead-ECG-monitored maximum static apnea was repeated dry (n = 6).Results: During pool apnea of maximum duration (385 ± 70 s), SAT decreased from 99.6 ± 0.5 to 58.5 ± 5.5% (∼PaO2 4.8 ± 1.5 kPa, P < 0.001), while Glu increased from 5.8 ± 0.2 to 6.2 ± 0.2 mmol/l (P = 0.009). MAP increased from 103 ± 4 to 155 ± 6 mm Hg (P < 0.005). HR decreased to 46 ± 10 from 86 ± 14 beats/minute (P < 0.001). HR and MAP were unchanged after 3–4 min of apnea. During dry apnea (378 ± 31 s), HR decreased from 55 ± 4 to 40 ± 3 beats/minute (P = 0.031). Atrioventricular dissociation and junctional rhythm were observed both during pool and dry apneas.Conclusion: Our findings contrast with previous studies concluding that Glu decreases during apnea diving. We conclude during maximum apnea in elite BHD that (1) the diving reflex is maximized after 3–4 min, (2) increasing Glu may indicate lactate metabolism in accordance with our previous results, and (3) extreme hypoxia rather than hypoglycemia causes brady-arrythmias in elite BHD similar to diving mammals.

2009 ◽  
Vol 107 (5) ◽  
pp. 1526-1531 ◽  
Author(s):  
Arne Sieber ◽  
Antonio L'Abbate ◽  
Mirko Passera ◽  
Erika Garbella ◽  
Antonio Benassi ◽  
...  

Knowledge regarding arterial blood pressure (ABP) values during breath-hold diving is scanty. It derives from a few reports of measurements performed at the water's surface, showing slight or no increase in ABP, and from a single study of two simulated deep breath-hold dives in a hyperbaric chamber. Simulated dives showed an increase in ABP to values considered life threatening by standard clinical criteria. For the first time, using a novel noninvasive subaquatic sphygmomanometer, we successfully measured ABP in 10 healthy elite breath-hold divers at a depth of 10 m of freshwater (mfw). ABP was measured in dry conditions, at the surface (head-out immersion), and twice at a depth of 10 mfw. Underwater measurements of ABP were obtained in all subjects. Each measurement lasted 50–60 s and was accomplished without any complications or diver discomfort. In the 10 subjects as a whole, mean ABP values were 124/93 mmHg at the surface and 123/94 mmHg at a depth of 10 mfw. No significant statistical differences were found when blood pressure measurements at the water surface were compared with breath-hold diving conditions at a depth of 10 mfw. No systolic blood pressure values >140 mmHg or diastolic blood pressure values >115 mmHg were recorded. In conclusion, direct measurements of ABP during apnea diving showed no or only mild increases in ABP. However, our results cannot be extended over environmental conditions different from those of the present study.


Author(s):  
Tom Scott ◽  
Hanna van Waart ◽  
Xavier CE Vrijdag ◽  
David Mullins ◽  
Peter Mesley ◽  
...  

Arterial blood gas (ABG) measurements at both maximum depth and at re-surfacing prior to breathing have not previously been measured during freedives conducted to extreme depth in cold open-water conditions. An elite freediver was instrumented with a left radial arterial cannula connected to two sampling syringes through a low-volume splitting device. He performed two open-water dives to 60 metres depth (197', 7 atmospheres absolute pressure) in the constant weight with fins competition format. ABG samples were drawn at 60 metres (by a mixed-gas scuba diver), and again on re-surfacing before breathing. An immersed surface static apnea, of identical length to the dives and with ABG sampling at identical times, was also performed. Both dives lasted approximately two minutes. PaO2 increased during descent from an indicative baseline of 15.8 kPa (after hyperventilation and glossopharyngeal insufflation) to 42.8 and 33.3 kPa (dives one and two), and decreased precipitously (to 8.2 and 8.6 kPa) during ascent. PaCO2 also increased from a low indicative baseline of 2.8 kPa to 6.3 and 5.1 kPa on dives one and two; an increase not explained by metabolic production of CO2 alone since PaCO2 actually decreased during ascent (to 5.2 and 4.5 kPa). Surface static apnea caused a steady decrease in PaO2 and increase in PaCO2 without the inflections provoked by depth changes. Lung compression and expansion provoke significant changes in both PaO2 and PaCO2 during rapid descent and ascent on a deep freedive. These changes generally support predictive hypotheses and previous findings in less extreme settings.


2000 ◽  
Vol 279 (6) ◽  
pp. E1271-E1277 ◽  
Author(s):  
Mary Courtney Moore ◽  
Po-Shiuan Hsieh ◽  
Doss W. Neal ◽  
Alan D. Cherrington

The glycemic and hormonal responses and net hepatic and nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infusion of glucose at 10 mg · kg−1 · min−1 via a peripheral (Pe10, n = 5) or the portal (Po10, n = 6) vein. Arterial plasma insulin concentrations were not different during the glucose infusion in Pe10 and Po10 (37 ± 6 and 43 ± 12 μU/ml, respectively), and glucagon concentrations declined similarly throughout the two studies. Arterial blood glucose concentrations during glucose infusion were not different between groups (125 ± 13 and 120 ± 6 mg/dl in Pe10 and Po10, respectively). Portal glucose delivery made the hepatic glucose load significantly greater (36 ± 3 vs. 46 ± 5 mg · kg−1 · min−1 in Pe10 vs. Po10, respectively, P < 0.05). Net hepatic glucose uptake (NHGU; 1.1 ± 0.4 vs. 3.1 ± 0.4 mg · kg−1 · min−1) and fractional extraction (0.03 ± 0.01 vs. 0.07 ± 0.01) were smaller ( P < 0.05) in Pe10 than in Po10. Nonhepatic (primarily muscle) glucose uptake was correspondingly increased in Pe10 compared with Po10 (8.9 ± 0.4 vs. 6.9 ± 0.4 mg · kg−1 · min−1, P < 0.05). Approximately one-half of the difference in NHGU between groups could be accounted for by the difference in hepatic glucose load, with the remainder attributable to the effect of the portal signal itself. Even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to alter partitioning of a glucose load among the tissues, stimulating NHGU and reducing peripheral glucose uptake.


1977 ◽  
Vol 43 (2) ◽  
pp. 204-210 ◽  
Author(s):  
A. Capderou ◽  
J. Polianski ◽  
J. Mensch-Dechene ◽  
L. Drouet ◽  
G. Antezana ◽  
...  

An impairment of gluconeogenesis has been proposed to explain the low arterial blood glucose of highlanders. Therefore, we studied splanchnic blood flow, splanchnic uptake of oxygen and lactate, and output of glucose in nine normal and six anemic highlanders at an altitude of 3,750 m. Splanchnic blood flow, arteriovenous difference for oxygen, and oxygen consumption were comparable at rest in both groups and in lowlanders from the literature, whereas splanchnic output of glucose, and uptake of lactate were approximately twice those in lowlanders. After 10 min of mild exercise in 12 subjects (7 normals, 5 anemic), no significant changes in splanchnic hemodynamics and metabolism were found. During 29% oxygen breathing in 8 subjects (5 normals, 3 anemics), arterial lactate, splanchnic uptake of lactate and output of glucose fell to normal sea-level values. We concluded that splanchnic hemodynamics are similar in adapted highlanders and in lowlanders, and that there is no evidence of an impaired gluconeogenesis at the altitude of the present study.


2020 ◽  
Vol 24 (5) ◽  
pp. 317-322
Author(s):  
Olga G. Chekhova ◽  
V. A. Ostanina ◽  
A. H. Shmakov

Introduction. Arterial tourniquets are widely used to improve visualization of the surgical field and to reduce blood loss . However, the resulting ischemia and subsequent reperfusion make doctors seek for better options to reduce these complications. Objective. To find out how the regional nerve blockade impacts the reperfusion of ischemized limb when arterial tourniquets are removed during orthopedic surgeries in children. Material and methods. In 16 patients, who were operated on at the department of trauma and orthopedics of the Novosibirsk Children ‘s Clinical Hospital of Emergency Medical Care (CCHEMC) , surgical intervention required the application of an arterial tourniquet. These patients became participants in an observational pilot study. Patients with tourniquets were divided into two groups: Group I - had the regional nerve blockade ( 9 patients) and Group II - had no regional nerve blockade (7 patients). Parameters of acid-base homeostasis, lactate and arterial blood glucose were assessed in all patients at all stages: before surgery (stage 1), main stage (stage 2), 5 minutes after the tourniquet removal (stage 3). The following parameters were compared in this work: mean arterial pressure (MAP), mm Hg; heart rate (min-1); concentration of lactate in the arterial blood (mmol/l), glycemia (mmol/l). The obtained findings are presented as median (Me) of lower and upper quartiles [Q25; Q75]. Results. The found dynamics of lactate concentration in participants’ blood was the most significant result of the study. In Group I, where regional anesthesia was used, lactate level decreased at the stage 2 and returned to its baseline at the stage 3. In Group II (without regional anesthesia, but with a powerful central analgesic preparation) , lactate level did not change at stage 2, but significantly increased at stage 3. Conclusion. Topical anesthetic (Ropivakaine), used in the regional nerve blockade during orthopedic surgeries in children when arterial tourniquets are put, has less harmful effects in surgical aggression.


2002 ◽  
Vol 282 (2) ◽  
pp. E402-E411 ◽  
Author(s):  
Chang An Chu ◽  
Stephanie M. Sherck ◽  
Kayano Igawa ◽  
Dana K. Sindelar ◽  
Doss W. Neal ◽  
...  

The aim of this study was to determine the effect of high levels of free fatty acids (FFA) and/or hyperglycemia on hepatic glycogenolysis and gluconeogenesis. Intralipid was infused peripherally in 18-h-fasted conscious dogs maintained on a pancreatic clamp in the presence (FFA + HG) or absence (FFA + EuG) of hyperglycemia. In the control studies, Intralipid was not infused, and euglycemia (EuG) or hyperglycemia (HG) was maintained. Insulin and glucagon were clamped at basal levels in all four groups. The arterial blood glucose level increased by 50% in the HG and FFA + HG groups. It did not change in the EuG and FFA + EuG groups. Arterial plasma FFA increased by ∼140% in the FFA + EuG and FFA + HG groups but did not change significantly either in the EuG or HG groups. Arterial glycerol levels increased by ∼150% in both groups. Overall (3-h) net hepatic glycogenolysis was 196 ± 26 mg/kg in the EuG group. It decreased by 96 ± 20, 82 ± 16, and 177 ± 22 mg/kg in the HG, FFA + EuG, and FFA + HG groups, respectively. Overall (3-h) hepatic gluconeogenic flux was 128 ± 22 mg/kg in the EuG group, but it was suppressed by 30 ± 9 mg/kg in response to hyperglycemia. It was increased by 59 ± 12 and 56 ± 10 mg/kg in the FFA + EuG and FFA + HG groups, respectively. In conclusion, an increase in plasma FFA and glycerol significantly inhibited hepatic glycogenolysis and markedly stimulated hepatic gluconeogenesis.


1993 ◽  
Vol 75 (1) ◽  
pp. 285-293 ◽  
Author(s):  
J. Qvist ◽  
W. E. Hurford ◽  
Y. S. Park ◽  
P. Radermacher ◽  
K. J. Falke ◽  
...  

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3–7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4–5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32–95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15–20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.


2004 ◽  
Vol 286 (2) ◽  
pp. E226-E233 ◽  
Author(s):  
Mary Courtney Moore ◽  
Sylvain Cardin ◽  
Dale S. Edgerton ◽  
Ben Farmer ◽  
Doss W. Neal ◽  
...  

Portal infusion of glucose in the mouse at a rate equivalent to basal endogenous glucose production causes hypoglycemia, whereas peripheral infusion at the same rate causes significant hyperglycemia. We used tracer and arteriovenous difference techniques in conscious 42-h-fasted dogs to determine their response to the same treatments. The studies consisted of three periods: equilibration (100 min), basal (40 min), and experimental (180 min), during which glucose was infused at 13.7 μmol· kg–1·min–1 into a peripheral vein (PE, n = 5) or the hepatic portal (PO, n = 5) vein. Arterial blood glucose increased ∼0.8 mmol/l in both groups. Arterial and hepatic sinusoidal insulin concentrations were not significantly different between groups. PE exhibited an increase in nonhepatic glucose uptake (non-HGU; Δ8.6 ± 1.2 μmol·kg–1·min–1) within 30 min, whereas PO showed a slight suppression (Δ–3.7 ± 3.1 μmol·kg–1·min–1). PO shifted from net hepatic glucose output (NHGO) to uptake (NHGU; 2.5 ± 2.8 μmol·kg–1·min–1) within 30 min, but PE still exhibited NHGO (6.0 ± 1.9 μmol·kg–1·min–1) at that time and did not initiate NHGU until after 90 min. Glucose rates of appearance and disappearance did not differ between groups. The response to the two infusion routes was markedly different. Peripheral infusion caused a rapid enhancement of non-HGU, whereas portal delivery quickly activated NHGU. As a result, both groups maintained near-euglycemia. The dog glucoregulates more rigorously than the mouse in response to both portal and peripheral glucose delivery.


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