A Model to Simulate Clinically Relevant Hypoxia in Humans

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).

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The overall goal of this model is to simulate apnoea caused hypoxia and hypercapnia in a human model with a focus on intermittent apnoea, which occurs during sleep apnoea, and emergencies such as air way obstruction. This model may help to understand physiological mechanisms to avoid hypoxic damage to the brain despite prolonged apnoea. The main advantage of this dynamic model is that we could simulate clinically relevant hypoxia in humans.

Apnoea dependent hypoxia often decreases heart rate. Hypoxia caused by lowered oxygen and the inspired air increases heart rate. Thus, different models of hypoxia induce opposite effects in circulation.

Our reproducible model enables us to investigate different technical devices. This gives us an opportunity to focus on different physiological aspects of apnoea without changing the setup or model. Prior to attaching electrodes to a subject, clean the attachment points using 70%alcohol.

Now, place an NIRS electrode over the frontal polar two locus on the right side of the forehead above the eyebrow, and to the right of the midsagittal sulcus. Use a second electrode to measure the peripheral tissue oxygenation. Place it on the inside of the lower arm.

Avoid placing this electrode above a venous plexus or an artery. The saturation should be greater than 80%Before taking a cerebral tissue oxygenation value, wait for the NIRS signal to show a variation of 3%or less for at least five minutes. Similarly, wait for the peripheral oxygen level signal to stabilize.

Next, place the ECG electrodes on the chest where there is no hair. Place the R-lead on the sternocostal head of the pectoralis major right. Place the L-lead on the sternocostal head of pectoralis major left.

Place the C-Lead on the fifth intercostal space in the middle of the medial clavicular line. Place the F-lead on the left lower rib edge, and place the N-lead on the right lower rib edge. Now, measure peripheral pulse oximetry from a fingertip on the same extremity used to measure peripheral tissue oxygenation.

Next, measure non-invasive blood pressure using a blood pressure cuff on the contra-lateral extremity from the peripheral pulse oximetry measurement. In the programmable settings, choose a one-minute interval, and choose NIBP. At least 20 minutes before the apnoea, establish an intravenous line into the medial cubital vein on the right or left arm to draw blood samples during and after the apnoea.

Before beginning, synchronize the internal clocks of the monitoring devices, so the measurements are synchronized. Next, send a network cable from the computer to the monitor device. Attach it at the docking station.

Then, program in the correct network settings and the software will be able to control the device and save data. Also, position the monitor so the data is not visible to the subject. Check the signals from the NIRS electrodes.

If any one is too erratic, reposition the electrode. Be sure to avoid placing the electrode over the bigger venous plexus, or any arteries. The signal should then stabilize.

A highly variable cerebral NIRS signal may be due to hyperventilation. Instruct the subject to breathe more slowly with less tidal volume, and reevaluate the signal. Have the subjects rest for at least 15 minutes in a prone position, and instruct them to breathe normally using 15 or fewer breaths per minute.

Before taking a baseline, draw blood samples. Two things to remember, are to not use the first five milliliters of drawn blood, and always flush the catheter after each collection using sterile saline. Throughout the test timeline draw blood samples as needed.

Double check each device's functionality and signal quality before proceeding. Also, ensure that electrodes cannot be removed by involuntary movements of the test subject at the end of apnoea. In the last two minutes of preparation for the apnoea test, count down the time verbally.

Then, have the subject indicate their last three inhalations with their fingers. The end of the final breath marks the start of the apnoea. Record this time point on the NIRS device.

The apnoea should be performed as long as possible. During the second half, movements of the chest and stomach are common, and indicate the struggle phase. The end of apnoea is marked by the first inspiration.

Record this time point on the NIRS device. To process the data from the monitor device, open the saved file on the computer. First, click review to access the trend monitor and select tools, and then option in the menu submask.

If needed, the time interval can be changed via the trend interval. Now, select the mask trends and save the data. Use resultingtrends.

txtdata to open it in a spreadsheet program, where it can be analyzed. To process the data from the NIRS device, open the software on the computer and connect the NIRS device via WiFi. Then, transfer the data from the NIRS device and save it in CSV format to open as a spreadsheet.

In the analysis, do not include the final three inspirations pre-apnoea in the baseline values or the first 30 seconds after the maximal inspiration at the beginning of the apnoea. During a six minute apnoea of one subject, simultaneous recordings were made of peripheral oxygen saturation, and NIRS. Interestingly, after initiation of the apnoea, a decrease in oxygen saturation was detected earlier by peripheral oxygen saturation monitoring, compared to cerebral NIRS monitoring.

In a study of ten apneic divers, cerebral NIRS values decreased significantly later than saturation values measured by pulse oximetry. Even in comparison to pulse oximetry, peripheral NIRS showed the earliest desaturation. After re-start of respiration, re-saturation was detected significantly earlier by cerebral NIRS compared to peripheral O2 saturation measured by pulse oximetry.

There was no time delay notable between peripheral NIRS and pulse oximetry. From another point of view, de-saturation values and total apnoea time was normalized to 100%After watching this video, you should have a good understanding of how to measure O2 saturation in different parts of the body. Our investigation revealed physiological mechanisms to avoid hypoxic damage.

In case of apnoea, redistribution of blood flow helps to maintain an adequate oxygen supply to the brain while peripheral tissues are already desataurated.

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Journal (Medicine)

Journal (Medicine)

A Model to Simulate Clinically Relevant Hypoxia in Humans

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