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

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.

2020 ◽  
Vol 319 (2) ◽  
pp. L289-L293
Author(s):  
John B. West ◽  
Matthew A. Liu ◽  
Phoebe C. Stark ◽  
G. Kim Prisk

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.


2019 ◽  
Vol 316 (1) ◽  
pp. L114-L118 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk ◽  
Janelle M. Fine ◽  
Amy Bellinghausen ◽  
...  

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.


2018 ◽  
Vol 314 (4) ◽  
pp. L686-L689 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
G. Kim Prisk ◽  
John B. West

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.


1990 ◽  
Vol 68 (5) ◽  
pp. 2100-2106 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
J. Leitner ◽  
M. D. Altose ◽  
N. S. Cherniack

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)


2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Michihiro Sakai ◽  
Noriko Murakami ◽  
Yuji Kitamura ◽  
Shin Sato ◽  
Hiroshi Iwama ◽  
...  

Malignant hyperthermia (MH) is a rare but potentially fatal complication that may develop under general anesthesia (GA) and is rarely reported in elderly patients. We encountered a case of mild-onset MH in a 70-year-old patient who was receiving an elective thoracoscopic pulmorrhaphy and had a history of several GA procedures. Anesthesia was induced with propofol, fentanyl, and rocuronium and maintained with sevoflurane and remifentanil. His body temperature (BT) was 37.9°C after induction. During the procedure, the end-tidal CO2(ETCO2) increased steadily to 47–50 mmHg, presumably in response to the single lung ventilation. At the end, BT was 38.1°C and ETCO2was 47 mmHg under spontaneous breathing. After extubation, the patient wheezed on inspiration and expiration, and his trachea was reintubated. Sixty minutes after surgery, BT increased to 40.5°C and the arterial blood gas analysis showed severe metabolic acidosis. Based on these findings, MH was suspected and a bolus dose of dantrolene was administered. He responded to the dantrolene, and no complications or recurrence of MH was observed postoperatively. In this patient, the initial signs of MH were so subtle that making the diagnosis of MH was difficult. A high degree of suspicion is necessary to prevent a fulminant MH crisis.


1985 ◽  
Vol 58 (6) ◽  
pp. 1975-1981 ◽  
Author(s):  
G. L. Hirsch ◽  
D. Y. Sue ◽  
K. Wasserman ◽  
T. E. Robinson ◽  
J. E. Hansen

To determine the acute action of cigarette smoking on cardiorespiratory function under stress, the immediate effects of cigarette smoking on the ventilatory, gas exchange, and cardiovascular responses to exercise were studied in nine healthy male subjects. Each subject performed an incremental exercise test to exhaustion on two separate days, one without smoking (control) and one after smoking 3 cigarettes/h for 5 h. The order of the two tests was randomized. Arterial blood gases and pH were measured during rest and all levels of exercise; CO blood levels confirmed the absorption of cigarette smoke. In addition, minute ventilation (VE), end-tidal PCO2 and PO2, O2 uptake (VO2), CO2 production, directly measured blood pressure, electrocardiogram, and heart rate (HR) were recorded every 30 s. The dead space-to-tidal volume ratio (VD/VT), maximal aerobic capacity (VO2max), and anaerobic threshold (AT) were determined from the gas exchange data. Cigarette smoking resulted in a significantly lower VO2max, AT, and VO2/HR (O2 pulse) and a significantly higher HR, pulse-pressure product, and pulse pressure (P less than 0.05) compared with the control. Additionally, a trend toward a higher VD/VT and arterial-end-tidal PCO2 difference was found during exercise after smoking. We conclude that cigarette smoking causes immediate detrimental effects on cardiovascular function during exercise, including tachycardia, increased pulse-pressure product, and impaired O2 delivery. The acute effects on respiratory function were less striking and primarily limited to abnormalities reflecting ventilation-perfusion mismatching.


1982 ◽  
Vol 52 (6) ◽  
pp. 1453-1457 ◽  
Author(s):  
S. C. Morrison ◽  
D. G. Stubbing ◽  
P. V. Zimmerman ◽  
E. J. Campbell

The effect of a voluntary reduction in lung volume on arterial O2 saturation (SaO2) was studied in 10 normal subjects aged 19–63 yr. SaO2 was measured by ear oximetry first during tidal breathing at functional residual capacity, and then during tidal breathing at 380 ml above residual volume. Tidal volume and breathing frequency were kept constant, and end-tidal CO2 partial pressure remained stable or fell in 9 out of 10 subjects. When lung volume was reduced, SaO2 fell by a mean of 1.5% (range 0–3%). Closing volume (CV) was measured by the N2-washout method (mean 0.89 liter, range 0.41–1.44). There was a close correlation between CV and the fall in SaO2 (r = 0.867, P = 0.001). Arterial and mixed venous CO2 were measured in one subject; the results indicated some fall in cardiac output following the lung volume change, but this accounted for less than half of the fall in SaO2. The relationship between CV and the lung volume at which tidal breathing occurs is an important determinant of pulmonary gas exchange through its effect on the matching of ventilation to perfusion.


PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249945
Author(s):  
Lisika Gawas ◽  
Aparna Rao

Purpose To evaluate changes in central corneal thickness (CCT) following vitrectomy. Methods All consecutive old and new patients referred to glaucoma services for possible secondary glaucoma after vitrectomy and who had undergone corneal pachymetry between July 2013 to June 2020, were included. The eye that developed elevated intraocular pressure (IOP) and was diagnosed clinically as glaucoma after vitrectomy, was labelled as the “affected” eye. The contralateral eye of the patient with normal IOP and no history of vitrectomy was labelled as the “control” eye. The difference in CCT in the affected eye and the contralateral control eye (ΔCCT) and CCT were compared between different age groups. Correlation of CCT in the affected eye with age, diagnosis, type of surgery done, lens status and pre-existing glaucoma was done using multivariate regression analysis. Results Of 127 eyes of 120 patients (M:F = 85:35), the average CCT in the affected eye was significantly higher than the unaffected contralateral control eye (p<0.0001). The ΔCCT in eyes presenting at an age <25 years was higher (median 582, 497–840) than those that presented later (median 518, 384–755), p <0.0001, with maximum ΔCCT seen in eyes that had undergone vitrectomy at age<12 years. The CCT in the affected eye was significantly higher in aphakic eyes (588±81.6 microns) than in pseudophakic eyes (552±79.03 microns), p = 0.03. On multivariate analysis, age<25 years remained as a significant influencer of CCT in the affected eye (β = -1.7, p<0.001, R2 = 28.3%). Conclusions Young age group<25 years are more prone to corneal remodelling and CCT changes after vitrectomy.


2021 ◽  
Vol 23 (4) ◽  
pp. 347-357
Author(s):  
Fatima Kh. Dzgoeva ◽  
◽  
Evgenia V. Ekusheva ◽  
Evgenia V. Ekusheva ◽  
Diana S. Rafikova ◽  
...  

Stroke in young adults is a serious medical and socio-economic problem. The relevance and complexity of the problem of ischemic stroke (IS) in young patients is due to insufficient knowledge of this issue, the complexity of medical and diagnostic aspects, as well as the difference in the causes of strokes from those in older age groups. Due to the variety of clinical manifestations, IS is of big interest for cardiologists, neurologists, obstetriciansgynecologists, hematologists, rheumatologists and is also relevant for endocrinologists and nutritionists. This article examines a clinical case of a patient with IS at a young age and a history of obesity and confirmed hemophilia.


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