The Difference between End-tidal and Arterial PCO2 in Anesthetized Patients

1988 ◽  
Vol 21 (1) ◽  
pp. 205
Author(s):  
Byung Moon Ham
Keyword(s):  
Arterial Pco2 ◽  
The Difference ◽  
End Tidal

Mass spectrometry for monitoring respiratory and anesthetic gas waveforms in rats

1988 ◽  
Vol 65 (2) ◽  
pp. 955-963 ◽  
Author(s):  
D. R. Larach ◽  
H. G. Schuler ◽  
T. M. Skeehan ◽  
J. A. Derr
Keyword(s):  
Mass Spectrometric ◽  
Laboratory Animals ◽  
Sprague Dawley ◽  
Arterial Pco2 ◽  
Sprague Dawley Rats ◽  
Reflex Movement ◽  
The Difference ◽  
End Tidal ◽  
Respiratory Gases ◽  
End Tidal Co2

A method is presented for real-time monitoring of airway gas concentration waveforms in rats and other small animals. Gas is drawn from the tracheal tube, analyzed by a mass spectrometer, and presented as concentration vs. time waveforms simultaneously for CO2, halothane, and other respiratory gases and anesthetics. By use of a respiratory simulation device, the accuracy of mass spectrometric end-tidal CO2 analysis was compared with both the actual gas composition and infrared spectrophotometry. The effects of various ventilator rates and inspiration-to-expiration ratios on sampling accuracy were also examined. The technique was validated in male Sprague-Dawley rats being ventilated mechanically. The difference between the arterial PCO2 (PaCO2) and the end-tidal PCO2 (PETCO2) was not significantly different from zero, and the correlation between PETCO2 and PaCO2 was strong (r = 0.97, P less than 0.0001). Continuous gas sampling for periods up to 5 min did not affect PaCO2, PETCO2, or airway pressures. By use of this new method for measuring end-tidal halothane concentrations in rats approximately 6.5 mo of age, the minimum alveolar concentration of halothane that prevented reflex movement in response to tail clamping was 0.97 +/- 0.04% atmospheric (n = 14). This mass spectrometric technique can be used in small laboratory animals, such as rats, weighing as little as 250 g. Gas monitoring did not distort either PETCO2 or PaCO2. Under the defined conditions of this study, accurate and simultaneous measurements of phasic respiratory concentrations of anesthetic and respiratory gases can be achieved.

Decreased Carbon Dioxide Sensitivity in Infants of Substance-Abusing Mothers

PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Demographic Data ◽  
Substance Abusing ◽  
Quiet Sleep ◽  
Co2 Level ◽  
The Difference ◽  
End Tidal ◽  
Drug Free

Objective. To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. Methods. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. Results. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 ± 7.14 (mean ± SE), whereas that of ISAMs was 16.28 ± 3.14. Conclusions. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.

Gas exchange in dogs in the prone and supine positions

1992 ◽  
Vol 72 (6) ◽  
pp. 2292-2297 ◽  
Author(s):  
K. C. Beck ◽  
J. Vettermann ◽  
K. Rehder
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Prone Position ◽  
Pulmonary Blood Flow ◽  
Random Order ◽  
Arterial Pco2 ◽  
Supine Posture ◽  
Pulmonary Shunting ◽  
The Difference ◽  
Arterial Po2

To determine the cause of the difference in gas exchange between the prone and supine postures in dogs, gas exchange was assessed by the multiple inert gas elimination technique (MIGET) and distribution of pulmonary blood flow was determined using radioactively labeled microspheres in seven anesthetized paralyzed dogs. Each animal was studied in the prone and supine positions in random order while tidal volume and respiratory frequency were kept constant with mechanical ventilation. Mean arterial PO2 was significantly lower (P less than 0.01) in the supine [96 +/- 10 (SD) Torr] than in the prone (107 +/- 6 Torr) position, whereas arterial PCO2 was constant (38 Torr). The distribution of blood flow (Q) vs. ventilation-to-perfusion ratio obtained from MIGET was significantly wider (P less than 0.01) in the supine [ln SD(Q) = 0.75 +/- 0.26] than in the prone position [ln SD (Q) = 0.34 +/- 0.05]. Right-to-left pulmonary shunting was not significantly altered. The distribution of microspheres was more heterogeneous in the supine than in the prone position. The larger heterogeneity was due in part to dorsal-to-ventral gradients in Q in the supine position that were not present in the prone position (P less than 0.01). The decreased efficiency of oxygenation in the supine posture is caused by an increased ventilation-to-perfusion mismatch that accompanies an increase in the heterogeneity of Q distribution.

Sensation of dyspnea during hypercapnia, exercise, and voluntary hyperventilation

1990 ◽  
Vol 68 (5) ◽  
pp. 2100-2106 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
J. Leitner ◽  
M. D. Altose ◽  
N. S. Cherniack
Keyword(s):  
Visual Analog Scale ◽  
Line Intensity ◽  
Time Course ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Base Line ◽  
Analog Scale ◽  
Voluntary Hyperventilation ◽  
The Difference ◽  
End Tidal

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)

Ventilatory control during experimental maldistribution of VA/Q in the dog

1982 ◽  
Vol 52 (1) ◽  
pp. 245-253 ◽  
Author(s):  
C. E. Juratsch ◽  
B. J. Whipp ◽  
D. J. Huntsman ◽  
M. M. Laks ◽  
K. Wasserman
Keyword(s):  
Steady State ◽  
Early Phase ◽  
Main Pulmonary Artery ◽  
State Regulation ◽  
Balloon Inflation ◽  
Peripheral Chemoreceptors ◽  
Arterial Pco2 ◽  
Bilateral Carotid ◽  
End Tidal ◽  
Transient Elevation

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5–2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5–2.0 min) of acute maldistribution of VA/Q.

Infrared end-tidal CO2 measurement does not accurately predict arterial CO2 values or end-tidal to arterial PCO2, gradients in rabbits with lung injury

1994 ◽  
Vol 17 (3) ◽  
pp. 189-196 ◽  
Author(s):  
Andrew O. Hopper ◽  
Gerald A. Nystrom ◽  
Douglas D. Deming ◽  
Wesley R. Brown ◽  
Joyce L. Peabody
Keyword(s):  
Lung Injury ◽  
Arterial Pco2 ◽  
End Tidal ◽  
End Tidal Co2

scholarly journals Bedside estimates of dead space using end-tidal CO2 are independently associated with mortality in ARDS

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Paola Lecompte-Osorio ◽  
Steven D. Pearson ◽  
Cole H. Pieroni ◽  
Matthew R. Stutz ◽  
Anne S. Pohlman ◽  
...  
Keyword(s):  
Dead Space ◽  
Validation Cohort ◽  
Univariate Analysis ◽  
Multivariable Analysis ◽  
Separate Analysis ◽  
University Of Chicago ◽  
Derivation Cohort ◽  
Ventilator Mode ◽  
The Difference ◽  
End Tidal

Abstract Purpose In acute respiratory distress syndrome (ARDS), dead space fraction has been independently associated with mortality. We hypothesized that early measurement of the difference between arterial and end-tidal CO2 (arterial-ET difference), a surrogate for dead space fraction, would predict mortality in mechanically ventilated patients with ARDS. Methods We performed two separate exploratory analyses. We first used publicly available databases from the ALTA, EDEN, and OMEGA ARDS Network trials (N = 124) as a derivation cohort to test our hypothesis. We then performed a separate retrospective analysis of patients with ARDS using University of Chicago patients (N = 302) as a validation cohort. Results The ARDS Network derivation cohort demonstrated arterial-ET difference, vasopressor requirement, age, and APACHE III to be associated with mortality by univariable analysis. By multivariable analysis, only the arterial-ET difference remained significant (P = 0.047). In a separate analysis, the modified Enghoff equation ((PaCO2–PETCO2)/PaCO2) was used in place of the arterial-ET difference and did not alter the results. The University of Chicago cohort found arterial-ET difference, age, ventilator mode, vasopressor requirement, and APACHE II to be associated with mortality in a univariate analysis. By multivariable analysis, the arterial-ET difference continued to be predictive of mortality (P = 0.031). In the validation cohort, substitution of the arterial-ET difference for the modified Enghoff equation showed similar results. Conclusion Arterial to end-tidal CO2 (ETCO2) difference is an independent predictor of mortality in patients with ARDS.

Expiratory and arterial partial pressure relations under different ventilation-perfusion conditions

1983 ◽  
Vol 54 (6) ◽  
pp. 1745-1753 ◽  
Author(s):  
A. Zwart ◽  
S. C. Luijendijk ◽  
W. R. de Vries
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Gas Analysis ◽  
Lung Model ◽  
Breathing Patterns ◽  
Tracer Gas ◽  
Physiological Dead Space ◽  
Arterial Partial Pressure ◽  
The Difference ◽  
End Tidal

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.

Maturation of steady-state CO2 sensitivity in vagotomized anesthetized lambs

1992 ◽  
Vol 72 (4) ◽  
pp. 1255-1260 ◽  
Author(s):  
A. H. Jansen ◽  
S. Ioffe ◽  
V. Chernick
Keyword(s):  
Steady State ◽  
Test Procedure ◽  
Nerve Section ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Co2 Sensitivity ◽  
Carotid Bodies ◽  
Before And After ◽  
End Tidal ◽  
Respiratory Sensitivity

The maturation of the respiratory sensitivity to CO2 was studied in three groups of anesthetized (ketamine, acepromazine) lambs 2–3, 14–16, and 21–22 days old. The lambs were tracheostomized, vagotomized, paralyzed, and ventilated with 100% O2. Phrenic nerve activity served as the measure of respiration. The lambs were hyperventilated to apneic threshold, and end-tidal PCO2 was raised in 0.5% steps for 5–7 min each to a maximum 7–8% and then decreased in similar steps to apneic threshold. The sinus nerves were cut, and the CO2 test procedure was repeated. Phrenic activity during the last 2 min of every step change was analyzed. The CO2 sensitivity before and after sinus nerve section was determined as change in percent minute phrenic output per Torr change in arterial PCO2 from apneic threshold. Mean apneic thresholds (arterial PCO2) were not significantly different among the groups: 34.8 +/- 2.08, 32.7 +/- 2.08, and 34.7 +/- 2.25 (SE) Torr for 2- to 3-, 14- to 16-, and 21- to 22-day-old lambs, respectively. After sinus denervation, apneic thresholds were raised in all groups [39.9 +/- 2.08, 40.9 +/- 2.08, and 45.3 +/- 2.25 (SE) Torr, respectively] but were not different from each other. CO2 response slopes did not change with age before or after sinus nerve section. We conclude that carotid bodies contribute to the CO2 response during hyperoxia by affecting the apneic threshold but do not affect the steady-state CO2 sensitivity and the central chemoreceptors are functionally mature shortly after birth.

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