scholarly journals Non-invasive Measurement of Pulmonary Gas Exchange Efficiency: The Oxygen Deficit

2021 ◽  
Vol 12 ◽  
Author(s):  
G. Kim Prisk ◽  
John B. West
Keyword(s):  
Gas Exchange ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Arterial Oxygen ◽  
Non Invasive ◽  
Arterial Blood ◽  
Age Related ◽  
End Tidal ◽  
Serial Measurements

The efficiency of pulmonary gas exchange has long been assessed using the alveolar-arterial difference in PO2, the A-aDO2, a construct developed by Richard Riley ~70years ago. However, this measurement is invasive (requiring an arterial blood sample), time consuming, expensive, uncomfortable for the patients, and as such not ideal for serial measurements. Recent advances in the technology now provide for portable and rapidly responding measurement of the PO2 and PCO2 in expired gas, which combined with the well-established measurement of arterial oxygen saturation via pulse oximetry (SpO2) make practical a non-invasive surrogate measurement of the A-aDO2, the oxygen deficit. The oxygen deficit is the difference between the end-tidal PO2 and the calculated arterial PO2 derived from the SpO2 and taking into account the PCO2, also measured from end-tidal gas. The oxygen deficit shares the underlying basis of the measurement of gas exchange efficiency that the A-aDO2 uses, and thus the two measurements are well-correlated (r2~0.72). Studies have shown that the new approach is sensitive and can detect the age-related decline in gas exchange efficiency associated with healthy aging. In patients with lung disease the oxygen deficit is greatly elevated compared to normal subjects. The portable and non-invasive nature of the approach suggests potential uses in first responders, in military applications, and in underserved areas. Further, the completely non-invasive and rapid nature of the measurement makes it ideally suited to serial measurements of acutely ill patients including those with COVID-19, allowing patients to be closely monitored if required.

scholarly journals Measurements of pulmonary gas exchange efficiency using expired gas and oximetry: results in normal subjects

2018 ◽  
Vol 314 (4) ◽  
pp. L686-L689 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk
Keyword(s):  
Gas Exchange ◽  
Lung Disease ◽  
Normal Subjects ◽  
Mean Value ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Arterial Blood ◽  
Age Related ◽  
Expired Gas ◽  
End Tidal

We are developing a novel, noninvasive method for measuring the efficiency of pulmonary gas exchange in patients with lung disease. The patient wears an oximeter, and we measure the partial pressures of oxygen and carbon dioxide in inspired and expired gas using miniature analyzers. The arterial Po2 is then calculated from the oximeter reading and the oxygen dissociation curve, using the end-tidal Pco2 to allow for the Bohr effect. This calculation is only accurate when the oxygen saturation is <94%, and therefore, these normal subjects breathed 12.5% oxygen. When the procedure is used in patients with hypoxemia, they breathe air. The Po2 difference between the end-tidal and arterial values is called the “oxygen deficit.” Preliminary data show that this index increases substantially in patients with lung disease. Here we report measurements of the oxygen deficit in 20 young normal subjects (age 19 to 31 yr) and 11 older normal subjects (47 to 88 yr). The mean value of the oxygen deficit in the young subjects was 2.02 ± 3.56 mmHg (means ± SD). This mean is remarkably small. The corresponding value in the older group was 7.53 ± 5.16 mmHg (means ± SD). The results are consistent with the age-related trend of the traditional alveolar-arterial difference, which is calculated from the calculated ideal alveolar Po2 minus the measured arterial Po2. That measurement requires an arterial blood sample. The present study suggests that this noninvasive procedure will be valuable in assessing the degree of impaired gas exchange in patients with lung disease.

scholarly journals Measuring the efficiency of pulmonary gas exchange using expired gas instead of arterial blood: comparing the “ideal” Po2 of Riley with end-tidal Po2

2020 ◽  
Vol 319 (2) ◽  
pp. L289-L293
Author(s):  
John B. West ◽  
Matthew A. Liu ◽  
Phoebe C. Stark ◽  
G. Kim Prisk
Keyword(s):  
Gas Exchange ◽  
Present Report ◽  
Oxygen Affinity ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Arterial Blood ◽  
The Difference ◽  
End Tidal ◽  
The Ideal

When using a new noninvasive method for measuring the efficiency of pulmonary gas exchange, a key measurement is the oxygen deficit, defined as the difference between the end-tidal alveolar Po2 and the calculated arterial Po2. The end-tidal Po2 is measured using a rapid gas analyzer, and the arterial Po2 is derived from pulse oximetry after allowing for the effect of the Pco2 on the oxygen affinity of hemoglobin. In the present report we show that the values of end-tidal Po2 and Pco2 are highly reproducible, providing a solid foundation for the measurement of the oxygen deficit. We compare the oxygen deficit with the classical ideal alveolar-arterial Po2 difference (A-aDO2) as originally proposed by Riley, and now extensively used in clinical practice. This assumes Riley’s criteria for ideal alveolar gas, namely no ventilation-perfusion inequality, the same Pco2 as arterial blood, and the same respiratory exchange ratio as the whole lung. It transpires that, in normal subjects, the end-tidal Po2 is essentially the same as the ideal value. This conclusion is consistent with the very small oxygen deficit that we have reported in young normal subjects, the significantly higher values seen in older normal subjects, and the much larger values in patients with lung disease. We conclude that this noninvasive measurement of the efficiency of pulmonary exchange is identical in many respects to that based on the ideal alveolar Po2, but that it is easier to obtain.

scholarly journals Noninvasive measurement of pulmonary gas exchange: comparison with data from arterial blood gases

2019 ◽  
Vol 316 (1) ◽  
pp. L114-L118 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk ◽  
Janelle M. Fine ◽  
Amy Bellinghausen ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Noninvasive Method ◽  
Arterial Blood Gases ◽  
Noninvasive Technique ◽  
Arterial Blood ◽  
End Tidal

A new noninvasive method was used to measure the impairment of pulmonary gas exchange in 34 patients with lung disease, and the results were compared with the traditional ideal alveolar-arterial Po2 difference (AaDO2) calculated from arterial blood gases. The end-tidal Po2 was measured from the expired gas during steady-state breathing, the arterial Po2 was derived from a pulse oximeter if the [Formula: see text] was 95% or less, which was the case for 23 patients. The difference between the end-tidal and the calculated Po2 was defined as the oxygen deficit. Oxygen deficit was 42.7 mmHg (SE 4.0) in this group of patients, much higher than the means previously found in 20 young normal subjects measured under hypoxic conditions (2.0 mmHg, SE 0.8) and 11 older normal subjects (7.5 mmHg, SE 1.6) and emphasizes the sensitivity of the new method for detecting the presence of abnormal gas exchange. The oxygen deficit was correlated with AaDO2 ( R2 0.72). The arterial Po2 that was calculated from the noninvasive technique was correlated with the results from the arterial blood gases ( R2 0.76) and with a mean bias of +2.7 mmHg. The Pco2 was correlated with the results from the arterial blood gases (R2 0.67) with a mean bias of −3.6 mmHg. We conclude that the oxygen deficit as obtained from the noninvasive method is a very sensitive indicator of impaired pulmonary gas exchange. It has the advantage that it can be obtained within a few minutes by having the patient simply breathe through a tube.

scholarly journals Effect of a patent foramen ovale on pulmonary gas exchange efficiency at rest and during exercise

2011 ◽  
Vol 110 (5) ◽  
pp. 1354-1361 ◽  
Author(s):  
Andrew T. Lovering ◽  
Michael K. Stickland ◽  
Markus Amann ◽  
Matthew J. O'Brien ◽  
John S. Hokanson ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Patent Foramen Ovale ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Foramen Ovale ◽  
Healthy Humans ◽  
Significant Difference ◽  
Ergometer Exercise ◽  
Exchange Inefficiency

The prevalence of a patent foramen ovale (PFO) is ∼30%, and this source of right-to-left shunt could result in greater pulmonary gas exchange impairment at rest and during exercise. The aim of this work was to determine if individuals with an asymptomatic PFO (PFO+) have greater pulmonary gas exchange inefficiency at rest and during exercise than subjects without a PFO (PFO−). Separated by 1 h of rest, 8 PFO+ and 8 PFO− subjects performed two incremental cycle ergometer exercise tests to voluntary exhaustion while breathing either room air or hypoxic gas [fraction of inspired O2 (FiO2) = 0.12]. Using echocardiography, we detected small, intermittent boluses of saline contrast bubbles entering directly into the left atrium within 3 heart beats at rest and during both exercise conditions in PFO+. These findings suggest a qualitatively small intracardiac shunt at rest and during exercise in PFO+. The alveolar-to-arterial oxygen difference (AaDo2) was significantly ( P < 0.05) different between PFO+ and PFO− in normoxia (5.9 ± 5.1 vs. 0.5 ± 3.5 mmHg) and hypoxia (10.1 ± 5.9 vs. 4.1 ± 3.1 mmHg) at rest, but not during exercise. However, arterial oxygen saturation was significantly different between PFO+ and PFO− at peak exercise in normoxia (94.3 ± 0.9 vs. 95.8 ± 1.0%) as a result of a significant difference in esophageal temperature (38.4 ± 0.3 vs. 38.0 ± 0.3°C). An asymptomatic PFO contributes to pulmonary gas exchange inefficiency at rest but not during exercise in healthy humans and therefore does not explain intersubject variability in the AaDo2 at maximal exercise.

Oxygen deficit is a sensitive measure of mild gas exchange impairment at inspired O2 between 12.5% and 21%

2020 ◽  
Vol 319 (1) ◽  
pp. L91-L94 ◽  
Author(s):  
Matthew A. Liu ◽  
Phoebe C. Stark ◽  
G. Kim Prisk ◽  
John B. West
Keyword(s):  
Gas Exchange ◽  
Repeated Measures ◽  
Age Groups ◽  
Normal Subjects ◽  
Oxygen Deficit ◽  
Arterial Blood ◽  
History Of ◽  
Older Subjects ◽  
The Difference ◽  
End Tidal

The oxygen deficit (OD) is the difference between the end-tidal alveolar Po2 and the calculated Po2 of arterial blood based on measured oxygen saturation that acts as a proxy for the alveolar-arterial Po2 difference. Previous work has shown that the alveolar gas meter (AGM100) can measure pulmonary gas exchange, via the OD, in patients with a history of lung disease and in normal subjects breathing 12.5% O2. The present study measured how the OD varied at different values of inspired O2. Healthy subjects were split by age (young 22–31; n = 23; older 42–90; n = 13). Across all inspired O2 levels (12.5, 15, 17.5, and 21%), the OD was higher in the older cohort 10.6 ± 1.0 mmHg compared with the young −0.4 ± 0.6 mmHg ( P < 0.0001, using repeated measures ANOVA), the difference being significant at all O2 levels (all P < 0.0001). The OD difference between age groups and its variance was greater at higher O2 values (age × O2 interaction; P = 0.002). The decrease in OD with lower values of inspired O2 in both cohorts is consistent with the increased accuracy of the calculated arterial Po2 based on the O2-Hb dissociation curve and with the expected decrease in the alveolar-arterial Po2 difference due to a lower arterial saturation. The persisting higher OD seen in older subjects, irrespective of the inspired O2, shows that the measurement of OD remains sensitive to mild gas exchange impairment, even when breathing 21% O2.

Hypoxemia and pulmonary gas exchange during hemodialysis

1981 ◽  
Vol 50 (2) ◽  
pp. 259-264 ◽  
Author(s):  
R. W. Patterson ◽  
A. R. Nissenson ◽  
J. Miller ◽  
R. T. Smith ◽  
R. G. Narins ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Oxygen Tension ◽  
Minute Ventilation ◽  
Arterial Oxygen Tension ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Exchange Relationships ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Alveolar Oxygen

With measured values of arterial blood gas tensions, of expired respiratory gas fractions, and volume of the expired ventilation, the determinants of alveolar oxygen tension (PAO2) were used to evaluate their influence on the development of the arterial hypoxemia that occurs in spontaneously breathing patients undergoing hemodialysis using an acetate dialysate. Dialysis produced no significant changes in the alveolar-arterial O2 tension gradient (AaDO2). The extracorporeal dialyzer removed an average of 30 ml.m-2.min-1 of CO2. Accordingly the pulmonary gas exchange ratio (R) dropped from a mean predialysis value of 0.81 to 0.62 (P less than 0.001). The arterial CO2 tension remained constant throughout, whereas the minute ventilation, both total (P less than 0.01) and alveolar (P less than 0.01), decreased during dialysis. This decrease in ventilation accounts for more than 80% of the fall in PAO2. During dialysis there was a decrease (P less than 0.001) in arterial oxygen tension (PaO2), which varied among the individuals from 9 to 23% of control. During the postdialysis hour PaO2 returns to control values concomitant with increase in ventilation. The quantitative gas exchange relationships among R, alveolar ventilation, and AaDO2 predict the PaO2 values actually measured.

Atelectasis affects the rate of arterial desaturation during obstructive apnea

1990 ◽  
Vol 69 (5) ◽  
pp. 1863-1868 ◽  
Author(s):  
E. C. Fletcher ◽  
S. Goodnight ◽  
T. Miller ◽  
R. A. Luckett ◽  
J. Rosborough ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Gas Exchange ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Apnea Duration ◽  
Obstructive Sleep ◽  
Spontaneously Breathing ◽  
Arterial Po2

Chronic hemodynamic disturbances are more profound in patients with obstructive sleep apnea when underlying lung disease with abnormal gas exchange (low arterial PO2) is present. Previous studies suggest that pulmonary gas exchange could influence the rate of fall of arterial oxygen saturation (dSaO2/dt) in obstructive sleep apnea. We postulated that abnormal gas exchange in the form of atelectasis would steepen dSaO2/dt and thereby lower nadir arterial oxyhemoglobin saturation (SaO2) for the same duration of apnea. Apneas were created by clamping an indwelling cuffed endotracheal tube at end expiration in eight spontaneously breathing adult baboons. Apneas of the same duration were then repeated during temporary endobronchial occlusion of one lobe of the lung. SaO2 and mixed venous O2 saturation were continuously monitored, and cardiac output was calculated. Worsening of pulmonary gas exchange during atelectasis was documented by an increase in calculated venous admixture from 10.5 +/- 0.8 to 25.0 +/- 0.7% (P less than 0.001). The dSaO2/dt was independent of apnea duration at 30, 45, and 60 s. During endobronchial occlusion, apnea dSaO2/dt increased 20%, and nadir SaO2 was significantly lower. Possible mechanisms for steepening of dSaO2/dt during atelectasis are discussed.

Cardiopulmonary and acid–Base effects of desflurane and sevoflurane in spontaneously breathing cats

2005 ◽  
Vol 7 (2) ◽  
pp. 95-100 ◽  
Author(s):  
Almir Pereira Souza ◽  
Piedad Natalia Henao Guerrero ◽  
Celina Tie Nishimori ◽  
Danielli Parrilha Paula ◽  
Paulo Sergio Patto Santos ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Arterial Oxygen Saturation ◽  
Respiratory Acidosis ◽  
Ion Concentration ◽  
Arterial Oxygen ◽  
Normal Limits ◽  
Arterial Blood ◽  
Short Period ◽  
End Tidal

The cardiopulmonary effects of desflurane and sevoflurane anesthesia were compared in cats breathing spontaneously. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressures; partial pressure of end tidal carbon dioxide (PETCO2), arterial blood pH (pH), arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. Anesthesia was induced with propofol (8±2.3 mg/kg IV) and maintained with desflurane (GD) or sevoflurane (GS), both at 1.3 MAC. Data were analyzed by analysis of variance (ANOVA), followed by the Tukey test ( P<0.05). Both anesthetics showed similar effects. HR and RR decreased when compared to the basal values, but remained constant during inhalant anesthesia and PETCO2 increased with time. Both anesthetics caused acidemia and hypercapnia, but BD stayed within normal limits. Therefore, despite reducing HR and SAP (GD) when compared to the basal values, desflurane and sevoflurane provide good stability of the cardiovascular parameters during a short period of inhalant anesthesia (T20–T60). However, both volatile anesthetics cause acute respiratory acidosis in cats breathing spontaneously.

scholarly journals Deriving the arterial Po2 and oxygen deficit from expired gas and pulse oximetry

2019 ◽  
Vol 127 (4) ◽  
pp. 1067-1074 ◽  
Author(s):  
G. Kim Prisk ◽  
John B. West
Keyword(s):  
Gas Exchange ◽  
Pulse Oximetry ◽  
Base Excess ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Dissociation Curve ◽  
Quiet Breathing ◽  
Arterial Blood ◽  
Expired Gas ◽  
The Ideal

The efficiency of pulmonary gas exchange is often assessed by the ideal alveolar-arterial partial pressure difference (A-aDO2). Through a combination of pulse oximetry and rapidly responding gas analyzers to measure the partial pressures of O2 and CO2 in expired gas, one can measure the oxygen deficit. Defined as the difference between the measured alveolar Po2 and the arterial Po2 calculated from [Formula: see text], the oxygen deficit is a substitute for the alveolar-arterial Po2 difference. The oxygen deficit is physiologically reasonable in that it increases with age in healthy subjects and is well correlated with the A-aDO2. To calculate arterial Po2 from saturation, the saturation should be below the very flat upper part of the O2-Hb dissociation curve; good estimates can be made provided the arterial O2 saturation is below ~95%. Since saturations at or above 95% imply reasonably well-maintained gas exchange efficiency, this limitation is of only minor concern. Calculations show that it is necessary to take into account the change in Po2 at a saturation of 50% of the O2-Hb dissociation curve based on the measured alveolar Pco2. As the measurement is designed to be noninvasive, determination of any base excess is not practical, but calculations show that the effect of assuming a zero base excess is modest, with a similar small effect from an abnormal body temperature. Taken together, these results show that a noninvasive assessment of pulmonary gas exchange efficiency can be obtained from subjects with below-normal arterial O2 saturations through a combination of expired O2 and CO2 measurements and [Formula: see text] made during quiet breathing. NEW & NOTEWORTHY The details and limitations of a noninvasive measurement of pulmonary gas exchange efficiency, the oxygen deficit, are described. The oxygen deficit, calculated from expired gas measurements made during quiet breathing coupled with pulse oximetry, is a good surrogate measurement of the ideal alveolar-arterial Po2 difference and does not require arterial blood gas sampling.

Normal pulmonary gas exchange efficiency and absence of exercise-induced arterial hypoxemia in adults with bronchopulmonary dysplasia

2013 ◽  
Vol 115 (7) ◽  
pp. 1050-1056 ◽  
Author(s):  
Andrew T. Lovering ◽  
Steven S. Laurie ◽  
Jonathan E. Elliott ◽  
Kara M. Beasley ◽  
Ximeng Yang ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Function ◽  
Bronchopulmonary Dysplasia ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Peak Power Output ◽  
Arterial Hypoxemia ◽  
Very Preterm ◽  
Arterial Blood ◽  
Exercise Induced

Cardiopulmonary function is reduced in adults born very preterm, but it is unknown if this results in reduced pulmonary gas exchange efficiency during exercise and, consequently, leads to reduced aerobic capacity in subjects with and without bronchopulmonary dysplasia (BPD). We hypothesized that an excessively large alveolar to arterial oxygen difference (AaDO2) and resulting exercise-induced arterial hypoxemia (EIAH) would contribute to reduced aerobic fitness in adults born very preterm with and without BPD. Measurements of pulmonary function, lung volumes and diffusion capacity for carbon monoxide (DLco) were made at rest. Measurements of maximal oxygen consumption, peak workload, temperature- and tonometry-corrected arterial blood gases, and direct measure of hemoglobin saturation with oxygen (SaO2) were made preexercise and during cycle ergometer exercise in ex-preterm subjects ≤32-wk gestational age, with BPD ( n = 12), without BPD (PRE; n = 12), and full term controls (CONT; n = 12) breathing room air. Both BPD and PRE had reduced pulmonary function and reduced DLco compared with CONT. The AaDO2 was not significantly different between groups, and there was no evidence of EIAH (SaO2 < 95% and/or AaDO2 ≥ 40 Torr) in any subject group preexercise or at any workload. Arterial O2 content was not significantly different between the groups preexercise or during exercise. However, peak power output was decreased in BPD and PRE subjects compared with CONT. We conclude that EIAH in adult subjects born very preterm with and without BPD does not likely contribute to the reduction in aerobic exercise capacity observed in these subjects.

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