scholarly journals Comparing the novel microstream and the traditional mainstream method of end-tidal CO2 monitoring with respect to PaCO2 as gold standard in intubated critically ill children

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Muhterem Duyu ◽  
Anıl Dogan Bektas ◽  
Zeynep Karakaya ◽  
Meral Bahar ◽  
Aybuke Gunalp ◽  
...  

AbstractThe objective of this study was to evaluate a novel microstream method by comparison with PaCO2 and the more standard mainstream capnometer in intubated pediatric patients. We hypothesized that the novel microstream method would superior compared to the traditional mainstream method in predicting PaCO2. This was a prospective single-center comparative study. The study was carried out on 174 subjects with a total of 1338 values for each method. Data were collected prospectively from mainstream and microstream capnometer simultaneously and compared with PaCO2 results. Although both mainstream PetCO2 (mainPetCO2) and microstream PetCO2 (microPetCO2) were moderately correlated (r = 0.63 and r = 0.68, respectively) with PaCO2 values, mainPetCO2 was in better agreement with PaCO2 in all subjects (bias ± precision values of 3.8 ± 8.9 and 7.3 ± 8.2 mmHg, respectively). In those with severe pulmonary disease, the mainPetCO2 and microPetCO2 methods were highly correlated with PaCO2 (r = 0.80 and r = 0.81, respectively); however, the biases of both methods increased (14.8 ± 9.1 mmHg and 16.2 ± 9.0 mmHg, respectively). In cases with increased physiologic dead space ventilation, the agreement levels of mainPetCO2 and microPetCO2 methods became distorted (bias ± precision values of 20.9 ± 11.2 and 25.0 ± 11.8 mm Hg, respectively) even though mainPetCO2 and microPetCO2 were highly correlated (r = 0.78 and r = 0.78, respectively). It was found that the novel microstream capnometer method for PetCO2 measurements provided no superiority to the traditional mainstream method. Both capnometer methods may be useful in predicting the trend of PaCO2 due to significant correlations with the gold standard measurement in cases with severe pulmonary disease or increased physiological dead space –despite reduced accuracy.

1983 ◽  
Vol 54 (6) ◽  
pp. 1745-1753 ◽  
Author(s):  
A. Zwart ◽  
S. C. Luijendijk ◽  
W. R. de Vries

Inert tracer gas exchange across the human respiratory system is simulated in an asymmetric lung model for different oscillatory breathing patterns. The momentary volume-averaged alveolar partial pressure (PA), the expiratory partial pressure (PE), the mixed expiratory partial pressure (PE), the end-tidal partial pressure (PET), and the mean arterial partial pressure (Pa), are calculated as functions of the blood-gas partition coefficient (lambda) and the diffusion coefficient (D) of the tracer gas. The lambda values vary from 0.01 to 330.0 inclusive, and four values of D are used (0.5, 0.22, 0.1, and 0.01). Three ventilation-perfusion conditions corresponding to rest and mild and moderate exercise are simulated. Under simulated exercise conditions, we compute a reversed difference between PET and Pa compared with the rest condition. This reversal is directly reflected in the relation between the physiological dead space fraction (1--PE/Pa) and the Bohr dead space fraction (1--PE/PET). It is argued that the difference (PET--Pa) depends on the lambda of the tracer gas, the buffering capacity of lung tissue, and the stratification caused by diffusion-limited gas transport in the gas phase. Finally some determinants for the reversed difference (PET--Pa) and the significance for conventional gas analysis are discussed.


2000 ◽  
Vol 29 (2) ◽  
pp. 200-205 ◽  
Author(s):  
Francisco J. Teixeira Neto ◽  
Stelio P.L. Luna ◽  
Flavio Massone ◽  
Armen Thomassian ◽  
Jose L.R. Vargas ◽  
...  

1996 ◽  
Vol 6 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Luc Mertens ◽  
Ralph Rogers ◽  
Tony Reybrouck ◽  
Monique Dumoulin ◽  
Luc Vanhees ◽  
...  

AbstractThe purpose of this study was to assess cardiorespiratory responses to submaximal exercise in patients with univentricular atrioventricular connection after the Fontan operation, and to evaluate whether changes occur during medium-term follow-up. Eighteen patients (age 12.1±5.5 years) underwent graded exercise test on a treadmill 2.3±1.4 year after the Fontan repair. Ventilatory gases were measured using breath-by-breath analysis. Results were compared to gender/age-matched controls. Twelve patients (age 14.2±5.4 years) were reevaluated 2.4±2.1 years after the first test. Aerobic exercise performance was subnormal in all patients during the first test. At the lowest level of exercise, the ventilatory threshold was already surpassed in 6/18 patients, while it was reduced in all other patients (p<0.001). All patients were in stable sinus rhythm throughout the test. Heart rate at all exercise levels was ±10% below normal (p<0.05). The respiratory frequency was increased at all exercise levels (p<0.001). The ventilatory equivalent for oxygen was increased (p<0.001), and the end-tidal tension of carbon dioxide was decreased (p<0.001). The ratio of physiological dead space/tidal volume was increased in all patients (p<0.001), while the normal decrease of this ratio during exercise was not observed. Upon reevaluation heart rate, respiratory rate, oxygen uptake, venti latory equivalent for oxygen, end-tidal carbon dioxide tension and physiological dead space did not change signifi cantly. Only a slight further decrease in ventilatory threshold was observed. Aerobic performance after the Fontan procedure ranges widely from just above resting metabolic rate to the lower limit of normal. Dyspnea during exercise is exacerbated by a decreased ventilatory threshold, increased physiological dead space, and decreased respir-atory efficiency. Cardiorespiratory response to exercise, nonetheless, remains relatively stable during medium-term follow-up.


1995 ◽  
Vol 79 (4) ◽  
pp. 1290-1298 ◽  
Author(s):  
G. K. Prisk ◽  
A. R. Elliott ◽  
H. J. Guy ◽  
J. M. Kosonen ◽  
J. B. West

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.


1995 ◽  
Vol 79 (4) ◽  
pp. 1299-1309 ◽  
Author(s):  
H. S. Sekhon ◽  
W. M. Thurlbeck

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.


1960 ◽  
Vol 15 (3) ◽  
pp. 383-389 ◽  
Author(s):  
J. F. Nunn ◽  
D. W. Hill

Observations were made during both spontaneous and artificial respiration on 12 fit patients anesthetized for routine surgical procedures. Above a tidal volume of 350 ml (BTPS), the anatomical dead space was close to the predicted normal value for the subject. Below 350 ml, it was reduced in proportion to the tidal volume. The physiological dead space (below the carina) approximated to 0.3 times the tidal volume for tidal volumes between 163 and 652 ml (BTPS). Throughout the range the physiological dead space was considerably in excess of the anatomical dead space measured simultaneously. The difference (alveolar dead space) varied from 15 to 231 ml, being roughly proportional to the tidal volume. The mean arterial to end-tidal CO2 tension difference was 4.6 (S.D. ±2.5) mm Hg and not related to tidal volume or arterial CO2 tension. None of the findings appeared to depend on whether the respiration was spontaneous or artificial. Submitted on September 25, 1959


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Matteo Bonifazi ◽  
Federica Romitti ◽  
Mattia Busana ◽  
Maria Michela Palumbo ◽  
Irene Steinberg ◽  
...  

Abstract Background The physiological dead space is a strong indicator of severity and outcome of acute respiratory distress syndrome (ARDS). The “ideal” alveolar PCO2, in equilibrium with pulmonary capillary PCO2, is a central concept in the physiological dead space measurement. As it cannot be measured, it is surrogated by arterial PCO2 which, unfortunately, may be far higher than ideal alveolar PCO2, when the right-to-left venous admixture is present. The “ideal” alveolar PCO2 equals the end-tidal PCO2 (PETCO2) only in absence of alveolar dead space. Therefore, in the perfect gas exchanger (alveolar dead space = 0, venous admixture = 0), the PETCO2/PaCO2 is 1, as PETCO2, PACO2 and PaCO2 are equal. Our aim is to investigate if and at which extent the PETCO2/PaCO2, a comprehensive meter of the “gas exchanger” performance, is related to the anatomo physiological characteristics in ARDS. Results We retrospectively studied 200 patients with ARDS. The source was a database in which we collected since 2003 all the patients enrolled in different CT scan studies. The PETCO2/PaCO2, measured at 5 cmH2O airway pressure, significantly decreased from mild to mild–moderate moderate–severe and severe ARDS. The overall populations was divided into four groups (~ 50 patients each) according to the quartiles of the PETCO2/PaCO2 (lowest ratio, the worst = group 1, highest ratio, the best = group 4). The progressive increase PETCO2/PaCO2 from quartile 1 to 4 (i.e., the progressive approach to the “perfect” gas exchanger value of 1.0) was associated with a significant decrease of non-aerated tissue, inohomogeneity index and increase of well-aerated tissue. The respiratory system elastance significantly improved from quartile 1 to 4, as well as the PaO2/FiO2 and PaCO2. The improvement of PETCO2/PaCO2 was also associated with a significant decrease of physiological dead space and venous admixture. When PEEP was increased from 5 to 15 cmH2O, the greatest improvement of non-aerated tissue, PaO2 and venous admixture were observed in quartile 1 of PETCO2/PaCO2 and the worst deterioration of dead space in quartile 4. Conclusion The ratio PETCO2/PaCO2 is highly correlated with CT scan, physiological and clinical variables. It appears as an excellent measure of the overall “gas exchanger” status.


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