|
 
 |
| RESEARCH ARTICLE |
|
| Year : 2022 | Volume
: 12
| Issue : 4 | Page : 153-157 |
|
Hyperoxia and the cardiovascular system: experiences with hyperbaric oxygen therapy
Jochen D Schipke1, Thomas Muth2, Clark Pepper3, Johannes Schneppendahl4, Martin Hoffmanns4, Sven Dreyer4
1 Research Group Experimental Surgery, University Hospital Düsseldorf, Düsseldorf, Germany
2 Institute of Occupational, Social and Environmental Medicine, Heinrich-Heine-University, Medical Faculty, Düsseldorf, Germany
3 Department of Anesthesiology, Johanna Etienne Hospital, Neuss, Germany
4 Department of Trauma and Hand Surgery, University Hospital Düsseldorf, Düsseldorf, Germany
| Date of Submission | 12-Dec-2020 |
| Date of Decision | 20-Jan-2021 |
| Date of Acceptance | 15-Feb-2021 |
| Date of Web Publication | 17-Apr-2022 |
Correspondence Address:
Jochen D Schipke
Research Group Experimental Surgery, University Hospital Düsseldorf, Düsseldorf
Germany
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2045-9912.337997
Hyperoxia has been described to induce bradycardia by direct stimulation of the parasympathetic nervous system. Also, hyperoxia has been found to increase blood pressure by an elevation of vascular resistance. However, the latter effect itself would induce bradycardia by baroreceptor stimulation. This single-arm monocentric retrospective study aims to evaluate the correlation between these effects by investigating the relation between oxygen (O2) administration and heart rate over time. Data were collected from 23 patients without cardiovascular problems undergoing hyperbaric oxygen therapy (2.4 bar) retrospectively. During single oxygen bouts, transcutaneously measured partial pressure of O2 was increased. During this surge of oxygen pressure, the arterial blood pressure was increased while the heart rate was decreased. Respiration rate was maintained independently from breathing 100% O2 or air. During single oxygen bouts, the half-life of transcutaneously measured partial pressure of O2 was 5.4 ± 2.1 mmHg/s, and the half-life of heart rate was 0.45 ± 0.19 beats/min. It has been shown that hyperbaric oxygen therapy increases the transcutaneously measured partial pressure of O2. This increase was rather fast, followed by a rather slow decrease in HR. This finding does not support direct vagal activation. Heart rate is not decreased due to a direct vagal activation during hyperbaric oxygen therapy. Our single-arm, retrospective study has additionally confirmed that oxidative stress injures the endothelium, and the reduced endothelial-derived vasodilators cause vasoconstriction. As a consequence, blood pressure increases, and heart rate is then further decreased via the baroreceptor reflex.
Keywords: autonomic nervous system; blood pressure; endothelium; heart rate; hyperbaric oxygen therapy; oxidative stress; vascular resistance; wound healing
How to cite this article:
Schipke JD, Muth T, Pepper C, Schneppendahl J, Hoffmanns M, Dreyer S. Hyperoxia and the cardiovascular system: experiences with hyperbaric oxygen therapy. Med Gas Res 2022;12:153-7 |
How to cite this URL:
Schipke JD, Muth T, Pepper C, Schneppendahl J, Hoffmanns M, Dreyer S. Hyperoxia and the cardiovascular system: experiences with hyperbaric oxygen therapy. Med Gas Res [serial online] 2022 [cited 2022 Jul 4];12:153-7. Available from: https://www.medgasres.com/text.asp?2022/12/4/153/337997 |
| Introduction | |  |
Hyperoxia occurs when organs or cells are exposed to an excess supply of oxygen (O2) or higher than the normal partial pressure of oxygen. It is unlikely that hyperoxia had much impact during the evolution of vertebrates, and the effects of hyperoxia on the human body remain relatively unclear.[1]
Over the last 50 years or so, hyperoxia has been employed in a wide range of clinical interventions and pathologies.[2] In addition, hyperoxic conditions develop in the context of diving and hyperbaric oxygen (HBO) therapy.
Adverse effects of oxidative stress on the central nervous system and the lungs are well described. Also, adverse effects to the eyes,[3] to the DNA of isolated lymphocytes,[4] and to in vivo DNA of leucocytes[5] were described.
While the results of the studies mentioned above are consistently accepted, the effect of hyperoxia on the autonomous nervous system is discussed controversially. On the one hand, hyperoxia is described to induce bradycardia by direct stimulation of the parasympathetic nervous system.[6],[7] On the other hand, hyperoxia is described to increase vascular resistance,[8] thereby increasing blood pressure. With an intact baroreceptor reflex, bradycardia will be induced.[9],[10]
The purpose of this retrospective study was to help answer the question, whether hyperoxia affects the heart rate (HR) directly or indirectly. This was done by investigating the scheduled course between partial oxygen pressure (pO2), HR, and blood pressure.
| Subjects and Methods | | |
Patients
Data from 23 patients (13 females) were collected during HBO treatment. The age of the patients ranged from 22 to 79 years. Included in this study were routine patients that did not suffer from cardiovascular problems as hypertension but underwent HBO treatment for other reasons, predominantly for wound healing problems and tinnitus. Excluded from the study were patients having major problems with pressure equalization. The trial flow chart is shown in [Figure 1].
This single-arm, retrospective study was registered in the former study register of the University Hospital Düsseldorf (ID 2020-05-5532) and approved by the Ethical Committee of the Medical Faculty of the Heinrich-Heine-University Düsseldorf (Study No. 2020-998) on August 18, 2020.
HBO treatment scheme
In line with the diagnoses of our patient group, the problem wounds scheme was employed. Thus, all patients followed the protocol outlined in [Figure 2], i.e., they all spent 135 minutes in the HBO chamber. Using breathing masks, 100% oxygen was administered at a pressure of 2.4 bar (= 240 kPa) (three times 30 minutes with 10-minute air breakes). At that treatment pressure, pO2 within the chamber was 0.5 bar (= 50 kPa).
Transcutaneous pO2
The transcutaneous pO2 (tcpO2) was assessed continuously using oximetry (TCM4, Radiometer, Copenhagen, Germany).[11] The tcpO2 electrode was attached to the supraclavicular area. If needed, a second electrode was attached close to the healthy margin of a wound. The electrodes are sensitive to only oxygen that generates a current proportional to the pO2.[12] The electrodes were heated throughout to 44°C as hyperthermia creates underlying capillary vasodilatation allowing more oxygen diffusion.[13] TcpO2 measurement is widely applied for the evaluation of chronic limb-threatening ischemia[14] but also to predict responders to hyperoxia.[15] The minimum pO2 value at the onset of 100% O2 administration was subtracted from the maximum O2 value before an air break. The result was divided by two and that value was added to the value at the onset (= ΔpO2). The time between the onset of O2 administration and the time of ΔpO2 was termed Δt. The ratio between ΔpO2 and Δt represents the pO2 half-life. The half-life of the HR was determined analogously.
Electrocardiogram and arterial blood pressure
An electrocardiogram (Haux-Life-Support, Karlsbad, Germany) was assessed using three leads that were attached to the chest. The best signal was used to calculate HR. The tcpO2 and the HR are presented in the individual tracings, respectively [Figure 3] and [Figure 4], and the tcpO2 half-life and the HR were assessed from these tracings. Finally, the arterial blood pressure was measured in 5-minute intervals using an inflatable cuff connected to a blood pressure monitor (Haux-Life-Support) [Figure 5]. | Figure 3: Time course of the transcutaneous partial oxygen pressure (pO2).
Note: (A) Time course of the transcutaneous pO2 during an entire problem wound scheme session in one patient. (B) Determination of the slope of the pO2 signal by calculating the pO2 half-life. Horizontal arrows, Bottom: minimal pO2 at the onset of 100% O2-breathing. Middle: mean pO2 between maximal and minimal values. Top: Maximum pO2 before the first air break. Δt: Time from minimal pO2 at the onset of 100% O2 and mean increase. This variable rapidly increases after patients start breathing 100% oxygen via their masks.
Click here to view |
 | Figure 4: Original tracing of the time course of the heart rate (HR).
Note: (A) Time course of the HR during an entire problem wound scheme session in one patient. (B) Determination of the slope of the HR signal by calculating the HR half-life. This variable slowly decreases after patients start breathing 100% oxygen via their masks.
Click here to view |
 | Figure 5: Representative arterial blood pressure during the wound scheme protocol
Click here to view |
Respiration
To account for respiratory effects, the respiration rate during both air and O2 intervals was assessed in a blinded manner on three patients that kept their masks on during an air break.
Sample size
The sample size was calculated based on expected O2-induced changes in the HR. If the expected HR decreases were moderate (Cohen’s δ = 0.6), a power of 0.8, and a significance level of 0.05 were chosen, then the sample size of n = 19 resulted.[16]
Statistical analysis
MicroSoft Excel 2007 (MicroSoft, Redmond, WA, USA) was used for calculations and creating tables and graphs. HR between the onset and the end of the HBO treatment was compared using the one-side t-test for paired samples and continuous variables (SPSS Statistics 24, IBM, Armonk, NY, USA). Differences were considered significant at the P ≤ 0.05 level. Results are presented as mean ± standard deviation (SD). To assess the effect size, Cohen’s δ was calculated.
| Results | | |
Transcutaneous pO2
During single oxygen bouts, tcpO2 increased from 101 ± 46 to 1089 ± 178 mmHg, and ΔtcpO2 was equal to 5.4 ± 2.1 mmHg/s.
Heart rate
Within a single bout of oxygen, HR decreased from 71.7 ± 15.2 to 63.6 ± 13.5 beats/min (P < 0.05; Cohen’s d = 0.58), and ΔHR was equal to –0.45 ± 0.19 beat/min2, i.e., the decrease in HR was drastically slower than the increase in the tcpO2.
Blood pressure
Both systolic and diastolic arterial blood pressure increased from 115 ± 15 to 148 ± 21 mmHg (31%) and from 62 ± 8 to 81 ± 11 mmHg (31%), respectively during the entire HBO session. This entire pressure increase was not linear, but the pressure decreased shortly during both air breaks (n = 8).
| Discussion | | |
It is the main finding of this retrospective study that tcpO2 rapidly increases following exposure to HBO while the HR decreases rather slowly.
It is well established that respiration rate and HR are synchronized: cardiorespiratory synchronization.[17],[18] It is also established that breathing oxygen exerts bradycardia.[6],[19] To evaluate whether or not breathing oxygen would affect the respiration rate and thereby the HR in this study, the breathing gas (air/oxygen) was exchanged in a blinded manner in one of the 30-minute cycles. This maneuver was done in only three patients to not endanger the effects of HBO therapy. No obvious HR differences were found between the breathing of normal air compared to oxygen.
While the half-life of the increase in the tcpO2 was roughly 5 mmHg/s rather short, the half-life of the decrease in HR was roughly 0.5 beats/min rather long. This means that tcpO2 increased 600 times faster than HR decreased. Due to this huge difference, hyperoxia will not directly activate the parasympathetic system as previously reported.[19],[20] It could, however, well be that those findings came about, after steady state conditions had established, i.e., sometime had elapsed after the onset of oxygen breathing. In case the increased vagal activity had been determined via indices of the HR variability,[21] it is remembered that indices of vagal activity can increase while HR decreases.[22]
It is well known that hypoxia is associated with vascular dilatation to secure sufficient oxygen supply. In turn, hyperoxia is associated with systemic vasoconstriction.[23],[24] More precisely, arterioles in the peripheral microcirculation constrict with higher oxygen concentrations, e.g. during normobaric or hyperbaric oxygenation therapy.[25]
As a result, perfusion is reduced in most tissues.[26] This oxygen-induced vasoconstriction is thought to serve as a protective mechanism to reduce oxidative stress.[24],[27] Although that topic is beyond the aim of this study, a minor excursion may be permitted: The mechanisms underlying the effect of hyperoxia are not fully understood.[28] Yet, increases in the contracting potential, decreases in the dilatating potential, or both have been suggested. One study favors the hypothesis that hyperoxic vasoconstriction is mediated by inhibition of prostaglandin synthesis.[28] Others suggest that reactive oxidative species are generated in the vessel wall[29] and rapidly react with nitric oxide[30],[31] thereby reducing/inactivating the vasodilating potential.[32],[33]
The hypothesis that the vasodilating nitric oxide potential is reduced is supported by data derived from scuba diving. Here, the pO2 levels increase with the diving depth. As a result of the hyperoxic condition, the vasodilator capacity was reduced by about 95% after a dive.[34] For comparison: this value is comparable to patients having significant atherosclerosis.[35] Other studies,[36],[37] as well as this study describe a decrease in the flow-mediated dilatation as well,[38] and yet another study reports significantly impaired vasodilation after diving that does not recover until the next dive.[39] Likewise, single air dives were also shown to reduce arterial endothelial function.[34],[40] Seemingly, hyperoxia-associated formation of reactive oxygen species induces endothelial dysfunction[41] that can be attenuated using antioxidants.[42]
Although the hyperbaric chamber was used as an experimental model to investigate a physiological issue, the results might also have clinical importance. Since oxidative stress does contribute to the development of atherosclerosis,[43],[44] patients that suffer from atherosclerosis should be monitored carefully when undergoing HBO therapy. This is of particular importance since atherosclerosis is a common comorbidity in diabetes.[45] Diabetic patients frequently undergo HBO therapy for the treatment of diabetic foot syndrome. It is also conceivable that the fitness of professional divers could be screened in a hyperbaric chamber to assess responses of hyperoxia toward blood pressure and electrocardiograms, because these divers will be confronted with elevated pO2 levels both using open or closed-circuit breathing apparatuses.
Assessment of the blood pressure is not well tolerated by the patients inside the chamber. Thus, measurements were made only randomly in some patients. We are presenting pressure data from eight patients with typical reactions of the blood pressure towards hyperoxia. In line with the previous literature,[46],[47] systolic and diastolic pressures increased after the onset of O2 breathing
Assessment of the arterial blood pressure via the inflatable cuff provides a limited temporal resolution, as the pressure was measured at five-minute intervals. Still, as the curve shape was of no importance, blood pressure values at all permitted a sound analysis.
One might consider that our results originated from a synergistic effect of hyperbaric and hyperoxic conditions. However, we exclude effects owing to increased pressure as it does not affect arterial blood pressure.[48],[49],[50]
We conclude that after administration of HBO, increases in the vascular tone lead to increases in blood pressure. In our patient group, blood pressure increases stimulated the baroreceptor reflex thereby decreasing the HR. Thus, because of the large differences in the temporal course between tcpO2 and HR responses, hyperoxia will unlikely directly activate the parasympathetic system.
Acknowledgements
We greatly appreciate the comprehensive cooperation with our patients.
Author contributions
JDS and MH: developed the concept and design of this study; TM: performed the statistical analyses; CP: did multiple proofreading and correct usage of the English language; JS: covered the medical portion of the study: patient care, information on the current approach; MH: took care of providing the tools for measurements, collected the data; SD: secured the correct execution of the HBO treatment prerequisites.
Conflicts of interest
There is no conflict of interest to declare for any of the authors.
Open access statement
This is an open access journal, and articles are distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
| References | | |
| 1. | Winklewski PJ, Kot J, Frydrychowski AF, Nuckowska MK, Tkachenko Y. Effects of diving and oxygen on autonomic nervous system and cerebral blood flow. Diving Hyperb Med. 2013;43:148-156.  |
| 2. | Brugniaux JV, Coombs GB, Barak OF, Dujic Z, Sekhon MS, Ainslie PN. Highs and lows of hyperoxia: physiological, performance, and clinical aspects. Am J Physiol Regul Integr Comp Physiol. 2018;315:R1-r27. |
| 3. | Williams DL. Oxidative stress and the eye. Vet Clin North Am Small Anim Pract. 2008;38:179-192, vii. |
| 4. | Gröger M, Oter S, Simkova V, et al. DNA damage after long-term repetitive hyperbaric oxygen exposure. J Appl Physiol (1985). 2009;106:311-315. |
| 5. | Dennog C, Hartmann A, Frey G, Speit G. Detection of DNA damage after hyperbaric oxygen (HBO) therapy. Mutagenesis. 1996;11:605-609. |
| 6. | Lund V, Kentala E, Scheinin H, Klossner J, Sariola-Heinonen K, Jalonen J. Hyperbaric oxygen increases parasympathetic activity in professional divers. Acta Physiol Scand. 2000;170:39-44. |
| 7. | Shibata S, Iwasaki K, Ogawa Y, Kato J, Ogawa S. Cardiovascular neuroregulation during acute exposure to 40, 70, and 100% oxygen at sea level. Aviat Space Environ Med. 2005;76:1105-1110. |
| 8. | Stirban A, Lentrodt S, Nandrean S, Pop A, Tschoepe D, Scherbaum WA. Functional changes in microcirculation during hyperbaric and normobaric oxygen therapy. Undersea Hyperb Med. 2009;36:381-390. |
| 9. | Bak Z, Sjöberg F, Rousseau A, Steinvall I, Janerot-Sjoberg B. Human cardiovascular dose-response to supplemental oxygen. Acta Physiol (Oxf). 2007;191:15-24. |
| 10. | Smit B, Smulders YM, van der Wouden JC, Oudemans-van Straaten HM, Spoelstra-de Man AME. Hemodynamic effects of acute hyperoxia: systematic review and meta-analysis. Crit Care. 2018;22:45. |
| 11. | Heyboer M, Byrne J, Pons P, Wolner E, Seargent S, Wojcik SM. Use of in-chamber transcutaneous oxygen measurement to determine optimal treatment pressure in patients undergoing hyperbaric oxygen therapy. Undersea Hyperb Med. 2018;45:389-394. |
| 12. | Clark LC, Jr. Continuous measurement of circulating glucose using the transcutaneous PO 2 electrode. Birth Defects Orig Artic Ser. 1979;15:39-42. |
| 13. | Huch R, Huch A, Lübbers DW. Transcutaneous measurement of blood Po 2 (tcPo 2) -- Method and application in perinatal medicine. J Perinat Med. 1973;1:183-191. |
| 14. | Leenstra B, Wijnand J, Verhoeven B, et al. Applicability of Transcutaneous Oxygen Tension Measurement in the Assessment of Chronic Limb-Threatening Ischemia. Angiology. 2020;71:208-216. |
| 15. | Sheffield PJ. Measuring tissue oxygen tension: a review. Undersea Hyperb Med. 1998;25:179-188. |
| 16. | |
| 17. | Bainbridge FA. The relation between respiration and the pulse-rate. J Physiol. 1920;54:192-202. |
| 18. | Schäfer C, Rosenblum MG, Kurths J, Abel HH. Heartbeat synchronized with ventilation. Nature. 1998;392:239-240. |
| 19. | Daly WJ, Bondurant S. Effects of oxygen breathing on the heart rate, blood pressure, and cardiac index of normal men--resting, with reactive hyperemia, and after atropine. J Clin Invest. 1962;41:126-132. |
| 20. | Kot J, Sićko Z, Wozniak M. Oxidative stress during oxygen tolerance test. Int Marit Health. 2003;54:117-126. |
| 21. | Lund VE, Kentala E, Scheinin H, et al. Heart rate variability in healthy volunteers during normobaric and hyperbaric hyperoxia. Acta Physiol Scand. 1999;167:29-35. |
| 22. | Tsuji H, Venditti FJ, Jr., Manders ES, et al. Determinants of heart rate variability. J Am Coll Cardiol. 1996;28:1539-1546. |
| 23. | Gole Y, Gargne O, Coulange M, et al. Hyperoxia-induced alterations in cardiovascular function and autonomic control during return to normoxic breathing. Eur J Appl Physiol. 2011;111:937-946. |
| 24. | Jackson WF. Arteriolar oxygen reactivity: where is the sensor and what is the mechanism of action? J Physiol. 2016;594:5055-5077. |
| 25. | Kisilevsky M, Mardimae A, Slessarev M, Han J, Fisher J, Hudson C. Retinal arteriolar and middle cerebral artery responses to combined hypercarbic/hyperoxic stimuli. Invest Ophthalmol Vis Sci. 2008;49:5503-5509. |
| 26. | Koch AE, Kähler W, Wegner-Bröse H, et al. Monitoring of CBFV and time characteristics of oxygen-induced acute CNS toxicity in humans. Eur J Neurol. 2008;15:746-748. |
| 27. | Wu O, Lu J, Mandeville JB, et al. Dynamic functional cerebral blood volume responses to normobaric hyperoxia in acute ischemic stroke. J Cereb Blood Flow Metab. 2012;32:1800-1809. |
| 28. | Rousseau A, Tesselaar E, Henricson J, Sjöberg F. Prostaglandins and radical oxygen species are involved in microvascular effects of hyperoxia. J Vasc Res. 2010;47:441-450. |
| 29. | Lee PJ, Choi AM. Pathways of cell signaling in hyperoxia. Free Radic Biol Med. 2003;35:341-350. |
| 30. | Landmesser U, Spiekermann S, Dikalov S, et al. Vascular oxidative stress and endothelial dysfunction in patients with chronic heart failure: role of xanthine-oxidase and extracellular superoxide dismutase. Circulation. 2002;106:3073-3078. |
| 31. | Lavi S, Yang EH, Prasad A, et al. The interaction between coronary endothelial dysfunction, local oxidative stress, and endogenous nitric oxide in humans. Hypertension. 2008;51:127-133. |
| 32. | Radi R. Oxygen radicals, nitric oxide, and peroxynitrite: Redox pathways in molecular medicine. Proc Natl Acad Sci U S A. 2018;115:5839-5848. |
| 33. | Stamler JS, Jia L, Eu JP, et al. Blood flow regulation by S-nitrosohemoglobin in the physiological oxygen gradient. Science. 1997;276:2034-2037. |
| 34. | Brubakk AO, Duplancic D, Valic Z, et al. A single air dive reduces arterial endothelial function in man. J Physiol. 2005;566:901-906. |
| 35. | Kuvin JT, Patel AR, Sliney KA, et al. Assessment of peripheral vascular endothelial function with finger arterial pulse wave amplitude. Am Heart J. 2003;146:168-174. |
| 36. | Balestra C, Cimino F, Theunissen S, et al. A red orange extract modulates the vascular response to a recreational dive: a pilot study on the effect of anthocyanins on the physiological consequences of scuba diving. Nat Prod Res. 2016;30:2101-2106. |
| 37. | Theunissen S, Guerrero F, Sponsiello N, et al. Nitric oxide-related endothelial changes in breath-hold and scuba divers. Undersea Hyperb Med. 2013;40:135-144. |
| 38. | |
| 39. | Obad A, Marinovic J, Ljubkovic M, et al. Successive deep dives impair endothelial function and enhance oxidative stress in man. Clin Physiol Funct Imaging. 2010;30:432-438. |
| 40. | Madden LA, Chrismas BC, Mellor D, et al. Endothelial function and stress response after simulated dives to 18 msw breathing air or oxygen. Aviat Space Environ Med. 2010;81:41-45. |
| 41. | Wang Q, Mazur A, Guerrero F, et al. Antioxidants, endothelial dysfunction, and DCS: in vitro and in vivo study. J Appl Physiol (1985). 2015;119:1355-1362. |
| 42. | Theunissen S, Balestra C, Boutros A, De Bels D, Guerrero F, Germonpré P. The effect of pre-dive ingestion of dark chocolate on endothelial function after a scuba dive. Diving Hyperb Med. 2015;45:4-9. |
| 43. | Ho YS, Magnenat JL, Gargano M, Cao J. The nature of antioxidant defense mechanisms: a lesson from transgenic studies. Environ Health Perspect. 1998;106 Suppl 5:1219-1228. |
| 44. | Bauer V, Bauer F. Reactive oxygen species as mediators of tissue protection and injury. Gen Physiol Biophys. 1999;18 Spec No:7-14. |
| 45. | Yuan T, Yang T, Chen H, et al. New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis. Redox Biol. 2019;20:247-260. |
| 46. | Heyboer Rd M, Wojcik SM, Smith G, Santiago W. Effect of hyperbaric oxygen therapy on blood pressure in patients undergoing treatment. Undersea Hyperb Med. 2017;44:93-99. |
| 47. | Schiavo S, Djaiani C, DeBacker J, et al. Magnitude and clinical predictors of blood pressure changes in patients undergoing hyperbaric oxygen therapy: a retrospective study. Int J Environ Res Public Health. 2020;17:7586. |
| 48. | Sieber A, L’Abbate A, Passera M, Garbella E, Benassi A, Bedini R. Underwater study of arterial blood pressure in breath-hold divers. J Appl Physiol (1985). 2009;107:1526-1531. |
| 49. | Weaver LK, Howe S. Noninvasive Doppler blood pressure monitoring in the monoplace hyperbaric chamber. J Clin Monit. 1991;7:304-308. |
| 50. | Duvallet AL, Duvallet E, Lhuissier F, Constantin P, Beaudry M. Can hyperoxia and hyperbaric conditions induce a increase in systemic pressures (SBP, DBP, MAP) to the breathing of 100 percent oxygen at normal and hyperbaric barometric pressure? FASEB J. 2017;31:711-718. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
|
Search Pubmed for