PO2 Difference Research Articles

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale.

What is the central question of this study? Do individuals with a patent foramen ovale (PFO+ ) have a larger alveolar-to-arterial difference in ( ) than those without (PFO- ) and/or an exaggerated increase in pulmonary artery systolic pressure (PASP) in response to hypoxia? What is the main finding and its importance? PFO+ had a greater while breathing air, 16% and 14% O2 , but not 12% or 10% O2 . PASP increased equally in hypoxia between PFO+ and PFO- . These data suggest that PFO+ may not have an exaggerated acute increase in PASP in response to hypoxia. Patent foramen ovale (PFO) is present in 30-40% of the population and is a potential source of right-to-left shunt. Accordingly, those with a PFO (PFO+ ) may have a larger alveolar-to-arterial difference in ( ) than those without (PFO- ) in normoxia and with mild hypoxia. Likewise, PFO is associated with high-altitude pulmonary oedema, a condition known to have an exaggerated pulmonary pressure response to hypoxia. Thus, PFO+ may also have exaggerated pulmonary pressure increases in response to hypoxia. Therefore, the purposes of the present study were to systematically determine whether or not: (1) the was greater in PFO+ than in PFO- in normoxia and mild to severe hypoxia and (2) the increase in pulmonary artery systolic pressure (PASP) in response to hypoxia was greater in PFO+ than in PFO- . We measured arterial blood gases and PASP via ultrasound in healthy PFO+ (n=15) and PFO- (n=15) humans breathing air and 30min after breathing four levels of hypoxia (16%, 14%, 12%, 10% O2 , randomized and balanced order) at rest. The was significantly greater in PFO+ compared to PFO- while breathing air (2.1±0.7vs. 0.4±0.3Torr), 16% O2 (1.8±1.2vs. 0.7±0.8Torr) and 14% O2 (2.3±1.2vs. 0.7±0.6Torr), but not 12% or 10% O2 . We found no effect of PFO on PASP at any level of hypoxia. We conclude that PFO influences pulmonary gas exchange efficiency with mild hypoxia, but not the acute increase in PASP in response to hypoxia.

Measuring the efficiency of pulmonary gas exchange using expired gas instead of arterial blood: comparing the "ideal" Po2 of Riley with end-tidal Po2.

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.

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

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.

Validation of a Noninvasive Assessment of Pulmonary Gas Exchange During Exercise in Hypoxia

Pulmonary gas exchange efficiency, determined by the alveolar-to-arterial Po2 difference (A-aDo2), progressively worsens during exercise at sea-level; this response is further elevated during exercise in hypoxia. Traditionally, pulmonary gas exchange efficiency is assessed through measurements of ventilation and end-tidal gases paired with direct arterial blood gas (ABG) sampling. Because these measures have a number of caveats, particularly invasive blood sampling, the development of new approaches for the noninvasive assessment of pulmonary gas exchange is needed. Is a noninvasive method of assessing pulmonary gas exchange valid during rest and exercise in acute hypoxia? Twenty-five healthy participants (10 female) completed a staged maximal exercise test on a cycle ergometer in a hypoxic chamber (Fio2= 0.11). Simultaneous ABGs via a radial arterial catheter and noninvasive gas-exchange measurements (AGM100) were obtained in 2-minute intervals. Noninvasive gas exchange, termed the O2 deficit, was calculated from the difference between the end-tidal and the calculated Pao2 (via pulse oximetry and corrected for the Bohr effect by using the end-tidal Pco2). Noninvasive O2 deficit was compared with the traditional alveolar to arterial oxygen difference (A-aDo2), using the traditional Riley analysis. Under conditions of rest at room air, hypoxic rest, and hypoxic exercise, strong correlations between the calculated gPao2 and directly measured Pao2 (R2= 0.97; P< .001; mean bias= 1.70mmHg) were observed. At hypoxic rest and exercise, strong relationships between the estimated and directly measured Pao2 (R2= 0.68; P< .001; mean bias= 1.01mmHg) and O2 deficit with the traditional A-aDo2 (R2= 0.70; P< .001; mean bias= 5.24mmHg) remained. Our findings support the use of a noninvasive measure of gas exchange during acute hypoxic exercise in heathy humans. Further studies are required to determine whether this approach can be used clinically as a tool during normoxic exercise in patients with preexisting impairments in gas exchange efficiency.

Oxygen Deficit Is a Sensitive Measure of Mild Gas Exchange Impairment at Inspired O2 between 12.5%–21%

The oxygen deficit (OD) is the difference between the end‐tidal alveolar PO2 and the estimated PO2 of arterial blood derived from the SpO2 that has the potential to be used clinically as a proxy for the alveolar‐arterial PO2 difference. Previous work has shown that a recently developed technology, the Alveolar Gas Meter, is accurate in measuring the efficiency of pulmonary gas exchange, via the OD, in patients with a history of lung disease as well as in normal subjects breathing a hypoxic mixture of 12.5% O2. This study sought to determine how the OD varied as the percent of inspired O2 changed from 21% to 12.5% in 36 healthy subjects split by age (young 22–31, n=23; old 42–90, n=13) to assess the possibility of use in a clinical setting. The PO2 and PCO2 were continually measured as the subject breathed through a mouthpiece using rapidly responding electrochemical cells, and the end‐tidal PO2 and PCO2 were calculated and averaged over 5 steady‐state breaths, while a fingertip pulse oximeter measured the SpO2. After correcting for any change in P50 resulting from the PCO2 differing from 40 mmHg, the arterial PO2 was calculated from the SpO2 by inverting the Hill‐equation. Subjects breathed 12.5, 15, 17.5 and 21% oxygen mixtures (balanced order) and their OD was measured in triplicate. Across all inspired O2 levels, the OD was higher in the older cohort than the young (p &lt;0.0001, repeated measures ANOVA, Table 1). The older cohort had a larger OD at all four oxygen levels (all p&lt;0.0001), with that difference and its variance being greater at higher inspired O2 values (age × O2 interaction p=0.002). The OD at an inspired O2 of 12.5% was significantly less than at 21% for both age cohorts. This is consistent with the known increase in ventilation‐perfusion mismatching that occurs in healthy aging. The decrease in OD magnitude as the inspired oxygen was reduced in both cohorts is consistent with the increased accuracy of the estimated arterial PO2 when based on saturation values on the steep part of the O2‐Hb dissociation curve. Further, as arterial saturation decreases there is an expected decrease in the alveolar‐arterial PO2 difference. The persisting higher OD seen in older subjects, irrespective of inspired O2, suggests that the measurement of oxygen deficit remains sensitive to mild gas exchange impairment, even when breathing air (21% O2).Support or Funding InformationFinancial support from UCSD Measured Oxygen Deficit by Age Young Old p‐value All Inspired O2 (mean±SE) −0.4±0.6 10.6±1.0 &lt;0.0001 Inspired O2 by Age Interaction 0.002 12.5% −1.4±0.7 5.7±0.6 ‐ 15% −2.7±1.0 5.2±1.8 15% vs 12.5%: NS 17.5% −2.7±1.0 9.4±1.8 17.5% vs 12.5%: NS 21% 5.1±1.3 21.9±2.1 21% vs 12.5%: &lt;0.0001

37: Duration of maternal oxygen exposure and umbilical cord oxygen content

Maternal oxygen (O2) administration is a commonly performed intrauterine resuscitation technique. O2 is frequently administered for several minutes, sometimes hours, in order to maximize fetal oxygenation. We tested the hypothesis that a longer duration of O2 exposure is associated with higher umbilical cord pO2. This is a planned secondary analysis of a randomized noninferiority trial comparing O2 to room air (RA) in laboring patients. Patients were randomized to 10 L/min O2 or RA at any point in active labor when they developed Category II EFM. Interventions were generally continued until delivery. The primary outcome for this analysis was umbilical vein (UV) pO2. A secondary outcome was umbilical artery (UA) pO2. These were compared between patients with short and long durations of O2 exposure, defined as < 75th and ≥75th percentile of the duration of exposure in O2 arm, respectively. Outcomes were also compared between RA, short O2, and long O2 groups. Of the 114 randomized patients, 99 patients (48 O2 and 51 RA) had paired cord gases and were included in this analysis. Among O2 patients, the median duration of exposure was 96 minutes (IQR 47, 176). The 75th percentile for duration of exposure was 176 minutes. UV pO2 was lower in patients who received long durations (≥176 minutes) of O2 compared to those who received shorter durations (< 176 minutes) (median [IQR] 25.5 [21.5,33] vs 32.5 [26.5, 37.5] mm Hg, p=0.03) (Figure 1). There was no difference in UA pO2 between short and long duration O2 groups (Figure 2). There was no difference in UA or UV pO2 between RA, short duration O2, and long duration O2 groups (Table 1). Long durations of O2 exposure are not associated with higher cord pO2. In fact, patients with longer O2 exposure had lower UV pO2, suggesting impaired placental O2 transfer, possibly mediated by hyperoxia-induced placental vasoconstriction.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

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

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 , 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 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.

In Which the Gain is more from Pulmonary Rehabilitation? Asthma or COPD?

Pulmonary rehabilitation (PR) is useful for patients with chronic obstructive pulmonary disease (COPD) but not clear for patients with asthma. The aim of the present study was to evaluate the effectiveness of PR in patients with asthma by comparing patients with COPD. The study was designed as a retrospective case series. We recruited patients with COPD and asthma. Demographics, respiratory symptoms, medications, smoking history, comorbidities, exercise capacity, respiratory function tests, and quality of life (QOL) were recorded. Exercise capacity was evaluated by the 6-minute walk test (6MWT), QOL with St. George's Respiratory Questionnaire (SGRQ), 36-item Short Form Health Survey (SF-36) Quality of Life Questionnaire, and Hospital Anxiety and Depression (HAD) Scale. Forty-two patients with asthma and 25 COPD who completed PR were included in the study. There was no difference in terms of age and sex between the groups (p=0.100 and p=0.365, respectively); however, body mass index was higher in the asthmatic group (p=0.007). Partial oxygen pressure (pO2) difference and arterial oxygen saturation (SpO2) difference were significantly higher in the COPD group than in the asthma group after PR (p<0.05). When the patients were compared before and after PR in both groups, a significant increase was detected in exercise capacity and QOL (6MWT, HADa, SGRQ, and SF-36 in all domains) (p<0.05). When two groups are contrasted according to the difference between pre- and post-PR of variables, there was no significant difference except pO2, SpO2, and Medical Research Council (p>0.05). Physicians refer patients with COPD to PR; however, patients with asthma are not generally referred to the same frequency. We would like to emphasize that PR may be as effective as COPD in asthma.

EFFECTS OF OXYGEN AND ISOFLURANE ANESTHESIA ON HEMOLYMPH GAS ANALYSIS AND RIGHTING REFLEX OF ASIAN FOREST (HETEROMETRUS LONGIMANUS) AND DICTATOR SCORPIONS (PANDINUS DICTATOR).

Large arachnids are commonly managed under professional care, and anesthesia is occasionally required for physical examination and diagnostic and therapeutic procedures. Anesthetic responses and hemolymph gas analysis have been studied previously in spiders, but scorpions have yet to be investigated. This study measured hemolymph gas values with an i-STAT point of care blood gas analyzer in healthy adult Asian forest scorpions (Heterometrus longimanus = HL, n = 8) and dictator scorpions (Pandinus dictator = PD, n = 12) breathing: 1) room air (RA), 2) 100% oxygen for 10 min in a chamber (OX), and 3) 5% isoflurane and oxygen (ISO) in a chamber until induction or loss of righting reflex. All scorpions recovered without complications, and there were no cartridge failures. Analysis of hemolymph gas values revealed that pH was lower in OX compared with RA and ISO and was lower in PD compared with HL scorpions. The partial pressure of carbon dioxide did not differ between inhaled gases but was higher in PD compared with HL. The partial pressure of oxygen (pO2) was higher in ISO compared with OX, and both were higher than when breathing RA. Despite a lack of species difference in pO2, PD had a more dramatic increase in pO2 in ISO compared with HL (significant species and inhalant interaction). PD had a significantly shorter induction time than HL, but recovery time (return of righting reflex) did not differ between species. Subjectively, HL exhibited rough inductions compared with PD, characterized by violent whole-body and tail movements. The unexpected increase in pO2 in ISO compared with OX, along with the species-specific differences and anesthetic effects, emphasizes the unique respiratory physiology of scorpions and demonstrates that further species-specific studies of anesthetics are warranted.

Impact of shifting epithelial Na+ transport on renal medullary oxygen tension: Modeling and analysis

The mammalian kidney is particularly vulnerable to hypoperfusion, because O2 supply to the renal medulla barely exceeds its O2 requirements. Renal O2 consumption is mainly driven by the metabolic work of tubular Na+ reabsorption. In this study, we examined the impact of shifting the Na+ transport site on medullary oxygen tension (PO2) of the rat kidney. To accomplish that goal, we extended our published model of renal epithelial transport to include renal vasculature and to simulate the crosstalk among nephron segments and vasculature. The model represents the complex structural organization of the medulla, which is believed to have a significant impact on medullary O2 distribution. The transport of red blood cells, hemoglobin, and O2 was explicitly represented. We considered basal cellular O2 consumption and O2 consumption for Na+/K+‐ATPase‐mediated transport. Our model predicts that the structural organization of the outer medulla results in significant Po2 gradients in the axial and radial directions. The segregation of descending vasa recta, the main supply of O2, at the center and immediate periphery of the vascular bundles gives rise to large radial differences in Po2, limits O2 reabsorption from long descending vasa recta, and helps preserve O2 delivery to the inner medulla. When Na+ delivery to the S3 and thick ascending limb segments is elevated (e.g., by pharmacological manipulation), local interstitial PO2 may decrease significantly, a result that indicates elevated risk of hypoxia.Support or Funding InformationThis research was supported by the Canada 150 Research Chair program and by the National Institutes of Health: National Institute of Diabetes and Digestive and Kidney Diseases, grant R01DK106102.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Anatomical backgrounds on gas exchange parameters in the lung

Many problems regarding structure-function relationships have remained unsolved in the field of respiratory physiology. In the present review, we highlighted these uncertain issues from a variety of anatomical and physiological viewpoints. Model A of Weibel in which dichotomously branching airways are incorporated should be used for analyzing gas mixing in conducting and acinar airways. Acinus of Loeschcke is taken as an anatomical gas-exchange unit. Although it is difficult to define functional gas-exchange unit in a way entirely consistent with anatomical structures, acinus of Aschoff may serve as a functional gas-exchange unit in a first approximation. Based on anatomical and physiological perspectives, the multiple inert-gas elimination technique is thought to be highly effective for predicting ventilation-perfusion heterogeneity between acini of Aschoff under steady-state condition. Changes in effective alveolar PO2, the most important parameter in classical gas-exchange theory, are coherent with those in mixed alveolar PO2 decided from the multiple inert-gas elimination technique. Therefore, effective alveolar-arterial PO2 difference is considered useful for assessing gas-exchange abnormalities in lung periphery. However, one should be aware that although alveolar-arterial PO2 difference sensitively detects moderately low ventilation-perfusion regions causing hypoxemia, it is insensitive to abnormal gas exchange evoked by very low and high ventilation-perfusion regions. Pulmonary diffusing capacity for CO (DLCO) and the value corrected for alveolar volume (VAV), i.e. DLCO/VAV (KCO), are thought to be crucial for diagnosing alveolar-wall damages. DLCO-related parameters have higher sensitivity to detecting abnormalities in pulmonary microcirculation than those in the alveolocapillary membrane. We would like to recommend four categories derived from combining behaviors of DLCO with those of KCO for differential diagnosis on anatomically morbid states in alveolar walls: type-1 abnormality defined by decrease in both DLCO and KCO; type-2 abnormality by decrease in DLCO but increase in KCO; type-3 abnormality by decrease in DLCO but restricted rise in KCO; and type-4 abnormality by increase in both DLCO and KCO.

Three classical papers in respiratory physiology by Christian Bohr (1855-1911) whose work is frequently cited but seldom read.

History has been kind to Christian Bohr (1855-1911). His name is attached eponymously to three different areas of respiratory physiology. The first is the Bohr dead space, which refers to the portion of the tidal volume that does not undergo gas exchange. The second is the increase in oxygen affinity of hemoglobin caused by the addition of carbon dioxide to the blood. This is known as the Bohr effect and is a very important feature of gas exchange, both in the lung and in peripheral tissues. Both of these contributions by Bohr are familiar to most students. Bohr's third contribution refers to the calculation of the changes in the Po2 of blood as oxygen is loaded in the pulmonary capillary, the so-called Bohr integration. This contribution is less well known now, partly because of the advent of digital computing, but it was important in its day. The analysis is challenging because the very nonlinear shape of the oxygen dissociation curve means that the Po2 difference between the alveolar gas and the capillary blood, which is the driving pressure for diffusion, changes in a complicated way. All three papers are in German, and two of them are long and tedious to read. English translations are available, but few people read the papers, despite the fact that the first two articles are very frequently cited. In the present article, Bohr's contributions are reviewed, and some parts of the articles that are particularly difficult to understand are clarified.

A clinical study of lung function protection in patients with robot assisted laparoscopic radical prostatectomy

Objective To evaluate the effect of manipulative pulmonary protective strategy on the pulmonary function of the patients undergoing robotic assisted laparoscopic radical prostatectomy under multiple-mode monitoring. Methods One hundred and twenty patients who underwent robot-assisted laparoscopic radical prostatectomy were divided into 4 groups (30 cases in each group) according to ASA Ⅰ-Ⅲ. Multimodal monitoring + manual relaxation group (group Mm), multimodal monitoring group (group M), conventional anesthesia + manual relaxation group (group m) and conventional anesthesia group (group C). In group Mm and group M, propofol was infused to achieve the BIS value of 45-55, then we monitored the muscle relaxation to conduct closed-loop infusion of cisatracurium. We also monitored and managed liquid input by vigileo. Group M and group C maintained peak airway pressure (≤30 cmH2O) (1 cmH2O=0.098 kPa) and PETCO2 35-40 mmHg (1 mmHg=0.133 kPa). Group Mm and group m received manual lung recruitment maneuver one times every 30 min after establishment of pneumoperitoneum until the end of operation. Blood gas analysis was performed before anesthesia induction (T1), 15 min after intubation (T2), 10 min after pneumoperitoneum (T3), 30 min after pneumoperitoneum (T4), 60 min after Trendelenburg (T5), 10 min after pneumoperitoneum cessation (T6), 5 min after extubation (T7). Airway peak pressure (Ppeak) and airway plateau pressure (Pplat) were recorded. The value of dynamic lung compliance (Cdyn), spiro-index (RI), dying cavity rate (VD/VT), oxygenation index (PaO2/FiO2) and alveolar arterial PO2 difference (A-aDO2) were calculated at different time points. Results Ppeak of group Mm and group m were more stable than Ppeak of group M and group C at T3 and T4 (P<0.05). Pplat of group Mm and group m were more stable than Pplat of group M and group C at T3 and T5 (P<0.05). Oxygenation indexes of group Mm and group m were higher than indexes of group M and group C at T5-T7 (P<0.05). A-aDO2 and RI were lower than group M and group C at T4, T5, T7 (P<0.05). At T4-T6, Cdyn was higher than Cdyn in group M and group C (P<0.05). Conclusions Manipulative pulmonary protective ventilation can improve the pulmonary function in patients undergoing robotic assisted laparoscopic radical prostatectomy under multimode monitoring. Key words: Robot; Therapeutic laparoscopy; Protective lung ventilation; Multi-mode monitoring; Prostate cancer

Abstract 191: Effects of Anesthetic Agents on Blood Parameters in Rats With Acute Hemorrhagic Shock

Background: Recent studies in our laboratory indicate that isoflurane (ISO) has protective properties including improved survival in rats with hemorrhagic shock compared to ketamine and xylazine (K/X) anesthesia. The effects of these two anesthetic agents upon blood counts, gases and chemistries in the setting of hemorrhagic shock is unknown. The purpose of the present study was to examine the effects of these two commonly used anesthetic regimens on blood parameters in rats with acute hemorrhagic shock. Methods and Results: Sprague Dawley rats (both genders) were anesthetized with either intraperitoneal K/X (90mg/kg and 10mg/kg; n=12) or with isoflurane (5% isoflurane induction and 2% maintenance in room air; n=12). Rats were intubated and ventilated with room air. After heparinization, hemorrhagic shock was induced by withdrawing blood to a fixed mean blood pressure of 30 mmHg for one hour and then shed blood was reinfused. Arterial blood samples were collected at 1 hour after resuscitation with shed blood. We found that K/X was associated with lower PH and lower level of standard bicarbonate concentration (SBC) and oxygen saturation (SO 2 %) and more negative base excess; and had a significantly elevated anion gap, potassium, sodium and chloride levels compared to isoflurane (Table). Platelet counts were preserved and there was less elevation of white blood cell (WBC) in ISO (Table). There were no significant differences in PO 2 , PCO 2 , hematocrit, hemoglobin, glucose and lactate levels between the two types of anesthesia. Conclusions: The anesthesia influenced the levels of blood counts, gases and chemistries in rats with acute hemorrhagic shock, favoring ISO over K/X. Blood parameters remained essentially normal in ISO group, which may help explain the protective role of ISO in hemorrhagic shock.

Arterial pH and Blood Gas Values in Rats Under Three Types of General Anesthesia: a Chronobiological Study

The aim of study was to review the status of arterial pH, pO(2) and pCO(2) under general anesthesias in dependence on the light-dark (LD) cycle in spontaneously breathing rats. The experiments were performed using three- to four-month-old pentobarbital(P)-, ketamine/xylazine(K/X)- and zoletil(Z)-anesthetized female Wistar rats after a four-week adaptation to an LD cycle (12 h light:12 h dark). The animals were divided into three experimental groups according to the anesthetic agent used: P (light n=11; dark n=8); K/X (light n=13; dark n=11); and Z (light n=18; dark n=26). pH and blood gases from arterial blood were analyzed. In P anesthesia, LD differences in pH, pO(2), and pCO(2) were eliminated. In K/X anesthesia, parameters showed significant LD differences. In Z anesthesia, LD differences were detected for pH and pO(2) only. Acidosis, hypoxia, and hypercapnia have been reported for all types of anesthesia during the light period. In the dark period, except for P anesthesia, the environment was more stable and values fluctuated within normal ranges. From a chronobiological perspective, P anesthesia was not the most appropriate type of anesthesia in these rat experiments. It eliminated LD differences, and also produced a more acidic environment and more pronounced hypercapnia than K/X and Z anesthesias.

Intraoperative partial pressure of oxygen measurement to predict flap survival.

Introduction:Flap monitoring using partial pressure of oxygen (pO2) is a proven modality. Instruments needed are expensive and are not readily available to a clinician. Here, pO2 of flap has been determined using readily available and cheap methods, and a cut-off value is calculated which helps in predicting flap outcome.Methods and Results:Total 235 points on 84 skin flaps were studied. Capillary blood was collected from flap and fingertip using 1-ml syringes after at least 30 min of flap inset, and pO2 analysed using blood gas analyser. Fall/change of pO2 (difference of mean of pO2 [diff-pO2]) was also calculated by subtracting the flap pO2 from the finger pO2. Flap was monitored clinically in post-operative period and divided into two groups depending on its survival with Group 1 – dead points and Group 2 – alive points. pO2 and diff-pO2 amongst both the groups were compared and found to be statistically different (P = 0.0001). Cut-off value calculated for pO2 was found to be <86.3 mmHg with a sensitivity of 100% and specificity of 89.05%. The difference of >68.503 mmHg of flap pO2 compared from finger pO2 was calculated as a cut-off with sensitivity of 94.12 and specificity of 79.60%.Conclusions:Flap areas having intra-operative pO2 value <86.3 mmHG have higher chances (60.71%) of getting necrosis later. Similarly, if diff-pO2 compared to fingertip is >68.5 mmHg, chances of those points getting necrosed in post-operative period are high.

A New, Noninvasive Method of Measuring Pulmonary Gas Exchange: Results in Normal Subjects and Patients with Lung Disease

MethodsThe person breathes through a device that continually measures and displays the inspired and expired PO2 and PCO2. An oximeter is worn, and the arterial PO2 is calculated from the SpO2 and the oxygen dissociation curve, using the end–tidal PCO2 to account for the effect of PCO2 on the oxygen affinity of hemoglobin. The PO2 difference between the end‐tidal gas and the calculated arterial value is called the Oxygen Deficit. Since the calculation is only accurate when the arterial oxygen saturations are 94% or less, the normal subjects breathed 12.5% oxygen.ResultsStudies were made on 17 patients with a variety of pulmonary diseases who were attending an outpatient clinic. The mean oxygen deficit was 48.7 mm Hg, SE 3.1. This can be contrasted with a mean oxygen deficit of 4.0 mm Hg, SE 0.91 in a group of 30 normal subjects who were previously studied. The p value for the difference between the two groups was &lt; 0.0001. Within the normal subjects, the mean oxygen deficit for the 19 younger participants (ages 22–31) was 2.02 mm Hg, SE 0.84 while that in the 11 older participants (ages 47–88) was 7.53 mm Hg, SE 1.55. The p value for the difference between the young and old groups was 0.0015. The mean oxygen deficit in younger normal subjects is remarkably small. This implies that there is very little difference between the calculated arterial PO2 and the alveolar PO2, consistent with little impairment of gas exchange. However, the mean oxygen deficit in older normal subjects is significantly higher consistent with the increased Alveolar‐arterial (A‐a) PO2 gradient with age, which has been well documented in the literature. Analysis of the factors determining the magnitude of the oxygen deficit showed that the end–tidal PO2 was the most important factor, followed by the end–tidal PCO2, and the calculated arterial PO2. Interestingly the SpO2 had a minor influence in spite of the fact that the oximeter reading is frequently used to guide therapy. The analysis emphasizes the value of measuring the composition of alveolar gas in determining ventilation‐perfusion ratio inequality. Remarkably, this factor is largely ignored in the classical index of impaired pulmonary gas exchange using the ideal alveolar PO2 to calculate the A‐a O2 gradient. We argue that ignoring the actual alveolar value gives an incomplete picture of gas exchange in the lungs because the traditional index is heavily biased by lung units with low ventilation‐perfusion ratios. Therefore, by using the new index of oxygen deficit, we derive a more comprehensive measurement of gas exchange in the lungs.Support or Funding InformationSupported by MediPines IncThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A New, Noninvasive Method of Measuring Impaired Pulmonary Gas Exchange in Lung Disease: An Outpatient Study

It would be valuable to have a noninvasive method of measuring impaired pulmonary gas exchange in patients with lung disease and thus reduce the need for repeated arterial punctures. This study reports the results of using a new test in a group of outpatients attending a pulmonary clinic. Inspired and expired partial pressure of oxygen (PO2) and Pco2 are continually measured by small, rapidly responding analyzers. The arterial PO2 is calculated from the oximeter blood oxygen saturation level and the oxygen dissociation curve. The PO2 difference between the end-tidal gas and the calculated arterial value is called the oxygen deficit. Studies on 17 patients with a variety of pulmonary diseases are reported. The mean ± SE oxygen deficit was 48.7 ± 3.1mmHg. This finding can be contrasted with a mean oxygen deficit of 4.0 ± 0.88mmHg in a group of 31 normal subjects who were previously studied (P< .0001). The analysis emphasizes the value of measuring the composition of alveolar gas in determining ventilation-perfusion ratio inequality. This factor is largely ignored in the classic index of impaired pulmonary gas exchange using the ideal alveolar PO2 to calculate the alveolar-arterial oxygen gradient. The results previously reported in normal subjects and the present studies suggest that this new noninvasive test will be valuable in assessing abnormal gas exchange in the clinical setting.

Short-term outcomes of minimally invasive mitral valve repair: a propensity-matched comparison.

We aimed to investigate the effect of minimally invasive mitral valve repair on early pulmonary function and haemodynamics, as well as its short-term efficacy. From March 2012 to July 2015, 78 cases of minimally invasive mitral valve repair and 89 cases of conventional mitral valve repair were included in this study, with 67 well-matched pairs of patients identified by a propensity score matching, who were divided into the conventional sternotomy group and the right minithoracotomy group (the RT group). The in-hospital mortality was similar between the 2 groups (3.0% vs 1.5%, P = 1.000). Both cross-clamp time and bypass time were higher in the RT group (P < 0.001), whereas drainage amount, blood transfusion and length of intensive care unit stay were higher in the conventional sternotomy group (P < 0.001). There was not much discrepancy in pulmonary function between the 2 groups, except that partial pressure of O2 in arterial blood (PaO2)/fraction of inspired oxygen (FiO2) in the RT group was significantly lower than that in the conventional sternotomy group 0, 4 and 8 h after surgery (P < 0.05), whereas the extravascular lung water index (ELWI), pulmonary vascular permeability index (PVPI) and alveolar-arterial PO2 difference (PA-aO2) of the RT group was higher (P < 0.05). We found no disparity in haemodynamics (P > 0.05), incidence of complications (P > 0.05) and short-term recurrence between the 2 groups (P = 0.7697). When compared with the median sternotomy approach, the RT approach shows comparable results in short-term efficacy and safety. On relatively increasing cardiopulmonary bypass time and operation time, the RT approach shortens the patient's intensive care unit stay and reduces the need for blood transfusion. Pulmonary function may be affected shortly post-surgery in the RT approach, with insignificant difference in haemodynamics.

Inhaled Budesonide Does Not Affect Hypoxic Pulmonary Vasoconstriction at 4559 Meters of Altitude.

Berger, Marc Moritz, Franziska Macholz, Peter Schmidt, Sebastian Fried, Tabea Perz, Daniel Dankl, Josef Niebauer, Peter Bärtsch, Heimo Mairbäurl, and Mahdi Sareban. Inhaled budesonide does not affect hypoxic pulmonary vasoconstriction at 4559 meters of altitude. High Alt Med Biol 19:52-59, 2018.-Oral intake of the corticosteroid dexamethasone has been shown to lower pulmonary artery pressure (PAP) and to prevent high-altitude pulmonary edema. This study tested whether inhalation of the corticosteroid budesonide attenuates PAP and right ventricular (RV) function after rapid ascent to 4559 m. In this prospective, randomized, double-blind, and placebo-controlled trial, 50 subjects were randomized into three groups to receive budesonide at 200 or 800 μg twice/day (n = 16 and 17, respectively) or placebo (n = 17). Inhalation was started 1 day before ascending from 1130 to 4559 m within 20 hours. Systolic PAP (SPAP) and RV function were assessed by transthoracic echocardiography at low altitude (423 m) and after 7, 20, 32, and 44 hours at 4559 m. Ascent to high altitude increased SPAP about 1.7-fold (p < 0.001), whereas RV function was preserved. There was no difference in SPAP and RV function between groups at low and high altitude (all p values >0.10). Capillary partial pressure of oxygen (PO2) and carbon dioxide as well as the alveolar to arterial PO2 difference were decreased at high altitude but not affected by budesonide. Prophylactic inhalation of budesonide does not attenuate high-altitude-induced pulmonary vasoconstriction and RV function after rapid ascent to 4559 m.