What is inspired oxygen tension

Before an arterial blood draw, the healthcare worker may check blood circulation to your arm or leg. Tell the healthcare worker if you use supplemental oxygen as this may affect the test results. An artery in the wrist is the most common site to draw arterial blood. However, an artery at the inside bend of the arm or groin may be used. The area will be swabbed clean with antiseptic. Anesthetic may be used to numb the skin over the area where the blood will be drawn.

A needle is used to puncture the skin. You will be asked to hold very still while your blood is collected. When enough blood is collected, the needle will be removed. Before having blood collected, tell the person drawing your blood if you are allergic to latex. Tell the healthcare worker if you have a medical condition or are using a medication or supplement that causes excessive bleeding.

Also tell the healthcare worker if you have felt nauseated, lightheaded, or have fainted while having blood drawn in the past. The amount of discomfort you feel will depend on many factors, including your sensitivity to pain. Communicate how you are feeling with the person doing the procedure.

Inform the person doing the procedure if you feel that you cannot continue with the procedure. If you receive anesthetic to numb the skin before an arterial blood draw, you may feel discomfort at the location where the anesthetic needle is inserted into the skin.

You may feel discomfort as the needle used to draw your blood is inserted into the skin, and you may have cramping at the site during the procedure.

Inform the person doing the test if you feel faint or nauseated or if the discomfort is severe. If blood is collected from an existing catheter inserted into an artery, you will feel little or no discomfort.

Laboratory test results may vary depending on your age, gender, health history, the method used for the test, and many other factors. If your results are different from the results suggested below, this may not mean that you have a disease. Contact your healthcare worker if you have any questions. The following are considered to be normal results for this test:. Arterial blood: During an arterial blood draw, a hematoma blood-filled bump under the skin or slight bleeding from the puncture site may occur.

After a blood draw, a bruise or infection may occur at the puncture site. The person doing this test may need to perform it more than once. If you have a medical condition, or are using a medication or supplement that causes excessive bleeding, you are at a higher risk of bleeding from the puncture site. Rarely, damage to the artery that affects blood flow to the arm or the leg may occur.

Talk to your healthcare worker if you have any concerns about the risks of this test. Ask your healthcare worker how you will be informed of the test results. You may be asked to call for results, schedule an appointment to discuss results, or notified of results by mail.

Follow up care varies depending on many factors related to your test. Sometimes there is no follow up after you have been notified of test results. At other times follow up may be suggested or necessary. Some examples of follow up care include changes to medication or treatment plans, referral to a specialist, more or less frequent monitoring, and additional tests or procedures. Talk with your healthcare worker about any concerns or questions you have regarding follow up care or instructions.

This test measures the difference between the amount of oxygen in the blood, and the amount of oxygen that is inhaled while breathing. This test measures the extent of decreased lung function[1]. Results increased in [2]: Oxygen enriched air Exercise Angiomas of the brain Results decreased in [2]: Advancing age High altitude eg, hypoxemia Decreased cardiac output Carbon monoxide poisoning Anesthesia Near drowning.

If blood was drawn from an artery in your arm or leg, cotton will be placed over the site and held firmly for at least five minutes to stop the bleeding. Bleeding may continue beyond five minutes if you are using medications or supplements that thin your blood or have a medical condition that causes excessive bleeding. When bleeding has stopped, a bandage will be placed firmly over the site and should be left on for 30 to 60 minutes.

You should rest for at least 15 minutes after the test. Avoid heavy use of the arm or leg from which the blood was drawn for 24 hours after the blood is collected. Representative continuous measurements of PaO 2 top, black , pulmonary artery pressure middle, light grey , and airway pressure bottom, dark grey are presented as a function of time. Lung volumes measured for each breath hold are reported for Ve end-expiratory breath hold with PEEP set at 3.

Ventilation was in volume control mode, inspired-to-expired ratio was , and respiratory rate was 12 breaths per minute. Associated CT images were captured at the beginning and end of the breath holding periods, and are presented in the supplementary information. The rates of PaO 2 decline ranged from 6.

Table 1 also shows whole lung atelectatic mass fraction measured with CT as soon as the breath hold manoeuvre began and just before breathing was restored. There was no significant difference in the whole lung atelectatic mass fraction at the beginning and at the end of the breath hold manoeuvres [C.

Similarly, Fig. Effects of volume and pressure control ventilation, and inspiration-to-expiration ratio on PaO 2 oscillations in the uninjured lung at a respiratory rate of 12 breaths per minute. Ventilation was managed in volume control VC, upper panels or pressure control PC, lower panels mode. Inspired-to-expired ratio ranged from to ; respiratory rate was 12 breaths per minute. Effects of volume and pressure control ventilation, and inspiration-to-expiration ratio on PaO 2 oscillations in the uninjured lung at a respiratory rate of 6 breaths per minute.

See Fig. Table 3 shows the similar exaggerated changes observed at RR6. Figure 5 shows the proportions of the lung slice mass associated with atelectasis, poor and normal aeration over the period of the respiratory cycle, for each ventilatory condition studied. The atelectatic mass was not different between inspiration and expiration in any of the conditions studied. In contrast, the fraction of normally aerated lung mass increased during inspiration, with a corresponding decrease in the fraction of poorly aerated lung mass.

The portion of overinflated lung slice never exceeded 0. Variation in mass of different density fractions of a single CT slice during tidal ventilation in uninjured animals in different ventilation modes. During inspiration, atelectatic lung dark grey decreased marginally with a greater decrease in poorly aerated mass light grey and a reciprocal increase in normally aerated lung white.

Overdistended lung represented less than 0. Error bars represent SD at each time point. Panel subtitles indicate ventilation mode and I:E ratio.

VC — volume control; PC — pressure control. Predicted rate of alveolar PO 2 decline versus measured rate of PaO 2 decline during breath hold manoeuvres. Results were obtained in eight animals. EELV was measured in four animals Figure 7 shows results from the simulations of PaO 2. These simulations showed changes in mean PaO 2 , and PaO 2 oscillation amplitudes that were similar to those observed in vivo under the various conditions imposed.

Simulations of PaO 2 oscillations in the uninjured, ventilated lung from single alveolar model compartment. Simulations of PaO 2 top, black and airway pressure bottom, dark grey are presented as a function of time. Simulated inspired-to-expired ratio ranged from to , and respiratory rate was 12 breaths per minute. In this experimental study in mechanically ventilated pigs with uninjured lungs, we showed that PaO 2 declined at different rates during breath hold manoeuvres depending on lung volume in vivo , that significant dynamic PaO 2 oscillations occur, and that these PaO 2 oscillations are determined by alveolar oxygen changes within the respiratory cycle.

In this sense, any shunt should be of the same magnitude throughout the respiratory cycle, unless blood flow is redistributed within the breath. The observed increase in PaO 2 during inspiration suggests that this redistribution of blood flow to non- or poorly ventilated regions did not occur, indicating that it was not a determinant of respiratory PaO 2 oscillations.

In agreement with the results obtained during breath holds, the weighted-average lung volume was a strong determinant of mean PaO 2 value, as observed by altering I:E ratios and ventilation control mode. In particular, mean PaO 2 was higher when inspiration lasted longer than expiration, which is when lung volume is greater across the respiratory cycle.

Moreover, the amplitude of the PaO 2 oscillations was smaller at greater mean lung volume, suggesting that there was a slower PaO 2 decline during the expiratory phase at I:E of and than when these I:E ratios were inverted.

Overall, these respiratory PaO 2 oscillations could be predicted from the oscillations in arterial partial pressure of carbon dioxide Respiratory PaO 2 oscillations have previously been interpreted primarily as being caused by cyclical atelectasis associated with tidal recruitment and derecruitment during ventilation in animal models of the acute respiratory distress syndrome ARDS 5 , 6 , 9 , Differences between our work and the published literature include animal species, smaller tidal volumes, greater RR, reduced airway pressures, physiological mean PaO 2 , and crucially that in our work we studied uninjured lung as opposed to animal models of lung injury.

It is possible that the use of much larger tidal volumes as it appears in the literature might have resulted in larger PaO 2 oscillations in our uninjured lung model; we did not investigate this possibility as tidal volumes greater than those studied in our experiments are neither physiological, nor of clinical interest In this respect, it is possible that the oscillations reported in the literature were caused in part by oxygen mass balance as described in equations 4 and 5 ventilatory delivery vs pulmonary uptake rather than cyclical recruitment and derecruitment.

To emphasize the observation that PaO 2 rate of decline was associated with lung volume, we performed a series of breath hold experiments at EELV with 5 cmH 2 O, end-inspiration and at the end of a large inspiration. We showed that PaO 2 declined more rapidly at smaller lung volumes than it did at larger lung volumes. This difference in the rate of PaO 2 decline could be partly explained by lung recruitment and derecruitment in anaesthetized animals.

Lung recruitment could be observed during end-inspiratory breath holds, especially during a breath hold performed after a large inspiration, and derecruitment could be observed during an end-expiratory breath hold.

Lung recruitment during an end-inspiratory breath hold could reduce the rate of PaO 2 decline, and vice versa during an end-expiratory breath hold. However, in this study, we were unable to detect atelectatic mass changes during breath holds using CT image analysis, which did not provide any evidence for recruitment or derecruitment during end-inspiratory or end-expiratory breath holds respectively.

Indeed, this result was partly expected given the short duration of the breath hold manoeuvres, the relatively low pressures used during the inspiratory breath holds, the application of 5 cmH 2 O PEEP during the end-expiratory breath holds, and the lack of known lung injury or gross regional ventilation-perfusion mismatch. Ventilation and perfusion changes during a breath hold could determine real time changes in PaO 2 ; in particular, elevated airway pressures applied to the lung during inspiration could cause a prevalence of zone 1 aeration 29 , 30 , where the non-dependent lung regions receive little or no perfusion also due to changes in lung blood volume This phenomenon per se would increase the rate of PaO 2 decline during an end-inspiratory breath hold, due to a reduced oxygen uptake in the zone 1 regions of the pulmonary circulation.

The highest airway pressure applied in our experiments was 24 cmH 2 O during breath holds at the end of a large inspiration, when the rate of PaO2 decline was slower than during end-inspiratory and end-expiratory breath holds. Importantly, the airway pressure did not exceed the pulmonary artery pressure at any time during breath holds, and overinflated lung mass was never greater than 0. Two main limitations of this technology are that it is unable to demonstrate whether a respiratory PaO 2 change is caused by alterations in either ventilation, or perfusion, or both, and that it does not provide evidence for their spatial distribution within the lung.

In our study, the dynamic CT image analysis partly compensated for this limitation by providing an index of lung aeration and atelectasis. Although this information was anatomically limited to a single slice during tidal breathing, the antero-posterior orientation of the slice could be representative for the effect of the gravitational gradient on pulmonary aeration Our study demonstrates that cyclical atelectasis is not necessary for respiratory PaO 2 oscillations to appear during mechanical ventilation.

We conclude that the mechanism determining these respiratory PaO 2 oscillations is the variation of alveolar oxygen tension within the breath, with oxygen entering the alveoli during each inspiration, and that these cyclic variations in alveolar oxygen tension are transmitted all the way to the systemic arteries.

Our results in an anaesthetized, ventilated pig model, in the absence of lung injury, may have implications for the interpretation of the results from conditions of lung disease 33 , in particular from patients with lung injury, and from animal models of ARDS.

Details regarding the anaesthesia, mechanical ventilation, instrumentation and measurements are reported in the supplementary information. The intravascular, fibre optic oxygen sensor was inserted in a carotid artery via a standard arterial catheter, and PaO 2 was recorded continuously, simultaneously with analogue signals for cardiovascular and respiratory parameters from patient monitors.

Breath hold manoeuvres associated with these three lung volumes were performed six times each, in a sequence that covered each possible sequential effect, for a total of 18 breath hold manoeuvres per animal.

The sequence in which breath hold manoeuvres were performed is presented in Table S1. PaO 2 decline was normalized to account for small differences in body weight between animals. We aimed to establish the effect of altering I:E ratios vs , and vs on mean PaO 2 and PaO 2 oscillation amplitudes, and the potential effect of cyclical atelectasis, if present, in determining PaO 2 during tidal breathing.

We studied the effects of ventilation in pressure control mode, and also explored the effect of delivering the same V T gradually in volume control mode, recording PaO 2 changes and determining oscillation amplitudes at the four I:E ratios. Airway pressure was monitored and controlled throughout the experiments. In total, we included 16 conditions four I:E ratios, each in two control modes, and at two respiratory rates.

PEEP of 5 cmH 2 O was used throughout the experiments in order to prevent, or at least reduce the likelihood of collapse of dependent regions at end expiration. We used computed tomography CT to measure lung volumes as well as to estimate pulmonary atelectasis and its changes during the breath hold manoeuvres and dynamically during tidal breathing in two animals. Details of the CT images acquisition, analysis procedure, calculation of air volume and tissue mass are presented in the supplementary information.

We hypothesised that the uninjured lung could be modelled as a single alveolar compartment with a constant oxygen uptake. The rate of change of oxygen in this compartment is equal to the difference in the rates of uptake by the pulmonary circulation and input via ventilation during inspiration, or elimination during expiration. Details of the mathematical modelling are presented in the supplementary information. Ventilation mode included two levels volume and pressure control mode , and I:E ratio consisted of two levels either and , or and Hall, J.

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