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Method Article

A Model to Simulate Clinically Relevant Hypoxia in Humans

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DOI:

10.3791/54933

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December 22nd, 2016

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In This Article

Summary

Hypoxia simulation in humans has usually been performed by inhaling hypoxic gas mixtures. For this study, apneic divers were used to simulate dynamic hypoxia in humans. Additionally, physiological changes in desaturation and re-saturation kinetics were evaluated with non-invasive tools such as Near-Infrared-Spectroscopy (NIRS) and peripheral oxygenation saturation (SpO2).

Abstract

In case of apnea, arterial partial pressure of oxygen (pO2) decreases, while partial pressure of carbon dioxide (pCO2) increases. To avoid damage to hypoxia sensitive organs such as the brain, compensatory circulatory mechanisms help to maintain an adequate oxygen supply. This is mainly achieved by increased cerebral blood flow. Intermittent hypoxia is a commonly seen phenomenon in patients with obstructive sleep apnea. Acute airway obstruction can also result in hypoxia and hypercapnia. Until now, no adequate model has been established to simulate these dynamics in humans. Previous investigations focusing on human hypoxia used inhaled hypoxic gas mixtures. However, the resulting hypoxia was combined with hyperventilation and is therefore more representative of high altitude environments than of apnea. Furthermore, the transferability of previously performed animal experiments to humans is limited and the pathophysiological background of apnea induced physiological changes is poorly understood. In this study, healthy human apneic divers were utilized to mimic clinically relevant hypoxia and hypercapnia during apnea. Additionally, pulse-oximetry and Near Infrared Spectroscopy (NIRS) were used to evaluate changes in cerebral and peripheral oxygen saturation before, during, and after apnea.

Introduction

Clinically relevant acute hypoxia and concomitant hypercapnia is mostly seen in patients with obstructive sleep apnea syndrome (OSAS), acute airway obstruction or during cardiopulmonary resuscitation. Major limitations in the field of OSAS and other hypoxemic conditions include the limited transferable knowledge about the pathophysiology derived from animal studies and that human models are non-existent 1. To mimic hypoxia in humans, hypoxic gas mixtures have so far been used 2-7. However, these conditions are more representative of high altitude surroundings than of clinical situations where hypoxia, in general, is accompan....

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Protocol

Ethics statement
All procedures performed in studies involving human participants were in accordance with the ethical standards of the 1964 Helsinki declaration and its later amendments. The design of this study was approved by the local ethics committee of the University Hospital of Bonn, Germany.

NOTE: Ensure that subjects are in good and healthy condition, free of any anti-hypertensive medicine and at least 24 hours free of catecholamine inducing agents like caffeine or equal substances.

1. Preparation of the Test Subject

  1. Clean the skin of the forehead with 70% alcohol to degrease the skin prior to NIRS electrode pos....

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Results

Figure 1 displays simultaneous recordings of SpO2 and NIRS values (NIRScerebral and NIRStissue) during apnea in one patient. Total apnea time was 363 sec. Following apnea NIRS and SpO2 values remained stable for approximately 140 sec. A decrease in SpO2 was detected after 204 sec by peripheral SpO2 whereas a decrease of NIRScerebral was detected after 238 sec. The lowest measured SpO2 .......

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Discussion

The total apnea time is mainly caused by lung size and oxygen consumption per minute and influenced by an individuals' ability to withstand the breathing reflex caused by increasing pCO2 or decreasing pO2. Apnea divers are trained to maximize their breath-hold duration and are used to doing so in maximal inspiration. Therefore, the time until hypoxia is detectable differs between individuals and depends on the subject's physical condition and training status and might even vary by their dail.......

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Disclosures

The authors have nothing to disclose.

Acknowledgements

Special thanks to all volunteers who participated in the original study. The work of L. Eichhorn was supported through a scholarship of the Else-Kröner-Fresenius Foundation. The authors would like to thank Springer, Part of Springer Science+Business Media, for copyright clearance (License Number 3894660871180) and the kind permission of reusing previously published data.

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Materials

List of materials used in this article
NameCompanyCatalog NumberComments
SpO2Dräger Medical AG&CO.KGSHP ACC MCABLE-Masimo Setperipheral SpO2-Monitoring
Non Invasive Blood Pressure (NIBP)Dräger Medical AG&CO.KGNIBP cuff M+,  MP00916 
Electrocardiographic (ECG)  Dräger Medical AG&CO.KGInfinity M540 MonitorECG monitoring
Docking stationDräger Medical AG&CO.KGM500 Docking Stationconnection of M540 to laptop
NIRSNONIN Medical’s EQUANOXModel 7600 Regional Oximeter Systemmeasuring of cerebral and  tissue oxygenation
NIRS diodesEQUANOX Advance SensorModel 8004CAsuited for measuring cerebral and somatic oxygen-saturation
Laptop 
DataGrabberDräger Medical AG&CO.KGDataGrabber v2005.10.16software to synchronize M540 with laptop
eVisionNonin Medical. Inc.Version 1.3.0.0software to synchronize NONIN with laptop

References

  1. Drager, L. F., Polotsky, V. Y., O'Donnell, C. P., Cravo, S. L., Lorenzi-Filho, G., Machado, B. H. Translational approaches to understanding metabolic dysfunction and cardiovascular consequences of obstructive sleep apnea. Am J Physiol Heart Circ Physiol. 309 (7), 1101-1111 (2015).
  2. Shah, N., Trivedi, N. K., Clack, S. L., Shah, M., Shah, P. P., Barker, S.

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