scholarly journals End-tidal arterial CO2 partial pressure gradient in patients with severe hypercapnia undergoing noninvasive ventilation

2013 ◽  
pp. 1
Author(s):  
D'Antini ◽  
Defilippis ◽  
Gilda Cinnella ◽  
Dambrosio ◽  
Schiraldi ◽  
...  
1981 ◽  
Vol 51 (3) ◽  
pp. 654-659 ◽  
Author(s):  
R. B. Banzett ◽  
G. F. Inbar ◽  
R. Brown ◽  
M. Goldman ◽  
A. Rossier ◽  
...  

We recorded the diaphragm electromyogram (EMG) of quadriplegic men before and during exposure of the lower torso to continuous negative pressure, which caused shortening of the inspiratory muscles by expanding the respiratory system by one tidal volume. The moving-time-averaged diaphragm EMG was larger during expansion of the respiratory system. When we repeated the experiment with subjects who breathed through a mouthpiece, we found qualitatively similar EMG changes and little or no change in tidal volume or end-tidal CO2 partial pressure. When the pressure was applied or removed rapidly, changes in EMG occurred within one or two breaths. Because end-tidal CO2 partial pressure did not increase, and because the response was rapid, we suggest that the response results from proprioceptive, rather than chemoreceptive, reflexes. As most of these men had complete spinal lesions at C6 or C7 the afferent pathways are likely to be vagal or phrenic.


2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S229
Author(s):  
N Hayashi ◽  
T Miyamoto ◽  
Y Fukuba ◽  
T Yoshida

1990 ◽  
Vol 68 (6) ◽  
pp. 2312-2321 ◽  
Author(s):  
D. R. Brown ◽  
H. V. Forster ◽  
L. G. Pan ◽  
A. G. Brice ◽  
C. L. Murphy ◽  
...  

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.


1981 ◽  
Vol 50 (4) ◽  
pp. 724-730 ◽  
Author(s):  
B. Gothe ◽  
M. D. Altose ◽  
M. D. Goldman ◽  
N. S. Cherniack

We examined the effects of different levels of inspired CO2 on ventilation and the pattern of breathing in healthy adults during the awake and the stage II quiet-sleep states. During both states, subjects were studied supine with their heads enclosed in a canopy. Tidal volume (VT) was determined from quantitative measurements of abdominal and rib cage excursions with magnetometers. Inspired CO2 was raised by blending CO2-enriched gas into the airflow, which continuously flushed the canopy. During sleep, while room air was breathed, VT decreased significantly from 410 to 360 ml, and respiratory rate also fell from 17 to 16 breaths/min. As a consequence, ventilation was significantly reduced from 6.5 to 5.8 l/min, and end-tidal CO2 partial pressure (PCO2) rose from 39.1 to 42.5 Torr. Ventilatory responses to CO2 were reduced, on the average, during sleep to 79% of waking levels. The change in average inspiratory flow produced by CO2 was also less during sleep. Waking and sleeping ventilatory responses to CO2 correlated inversely with the rise in end-tidal PCO2 when room air was breathed during sleep. At all levels of VT, the rib cage contribution to VT was greater during quiet sleep than during wakefulness. These findings suggest that quiet sleep, in addition to depressing ventilation and the response to CO2 alters the manner in which VT is attained by rib cage and abdominal displacements.


2015 ◽  
Vol 2015 ◽  
pp. 1-5
Author(s):  
Kenichi Satoh ◽  
Ayako Ohashi ◽  
Miho Kumagai ◽  
Masahito Sato ◽  
Akiyoshi Kuji ◽  
...  

Objective. The aim of this study was to evaluate the arterial to end-tidal partial pressure gradient of carbon dioxide according to age in the supine position during general anesthesia. Methods. From January 2001 to December 2013, we evaluated 596 patients aged ≥16 years who underwent general anesthesia in the supine position. The anesthetic charts of these 596 patients, all classified as American Society of Anesthesiologists physical status I or II, were retrospectively reviewed to investigate the accuracy of PaCO2 and ETCO2. Results. The a-ETCO2 was 3.0 ± 2.1 mmHg for patients aged 16 to <65 years and 4.1±3.1 mmHg for patients ≥65 years. The a-ETCO2 was 2.4±3.1 mmHg for patients aged 16 to 25 years, 3.1±2.2 mmHg for patients aged 26 to 35 years, 3.0±2.2 mmHg for patients aged 36 to 45 years, 3.4±2.0 mmHg for patients aged 46 to 55 years, 3.2±2.0 mmHg for patients aged 56 to 64 years, 4.3±3.2 mmHg for patients aged 65 to 74 years, and 3.7±2.8 mmHg for patients aged 75 to 84 years. Conclusion. The arterial to end-tidal partial pressure gradient of carbon dioxide tended to increase with increasing age.


1983 ◽  
Vol 55 (3) ◽  
pp. 736-741 ◽  
Author(s):  
R. A. Steinbrook ◽  
V. Fencl ◽  
R. A. Gabel ◽  
D. E. Leith ◽  
S. E. Weinberger

Whether CO2 partial pressure (PCO2) in expired gas may exceed that in arterial blood has been controversial. We measured arterial PCO2 (Paco2) and end-tidal PCO2 (PETco2) in four awake goats during air breathing and during hyperoxic CO2 rebreathing in various conditions of acid-base balance. During air breathing, Paco2 was slightly higher than PETco2; i.e., the mean (+/- SE) difference, Paco2 - PETco2, was positive by + 2.36 +/- 0.53 Torr (P less than 0.001). In contrast, during CO2 rebreathing with the same techniques of measurement, this difference was always negative (mean +/- SE = -11.63 +/- 0.22 Torr, P less than 0.001), and it widened as Paco2 increased with rebreathing. Magnitude of the negative difference during rebreathing was too great to be accounted for by incorrect assumptions or measurement error, even if reasonable contributions from all known sources of error were concurrently invoked. We conclude that during hyperoxic CO2 rebreathing in goats, PETco2 exceeds Paco2.


1982 ◽  
Vol 53 (1) ◽  
pp. 105-109 ◽  
Author(s):  
E. E. Lawson

The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (PCO2). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal PCO2. After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal PCO2 following long (30 s) stimuli, was independent of the end-tidal PCO2 level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.


1985 ◽  
Vol 59 (6) ◽  
pp. 1747-1751 ◽  
Author(s):  
R. J. Castele ◽  
A. F. Connors ◽  
M. D. Altose

The purpose of this study was to determine whether a change in respiratory sensation accompanies an increase in CO2 partial pressure (PCO2) in the absence of any changes in the level and pattern of thoracic displacement and respiratory muscle force. Eleven normal subjects were artificially hyperventilated with a positive-pressure mechanical respirator. In separate trials the tidal volume (VT) was set at 10 and 18 ml/kg and the frequency of ventilation (f) was adjusted to maintain the base-line end-tidal PCO2 at approximately 30 Torr. Thereafter, at a constant controlled VT and f, the PCO2 was progressively increased by raising the inspired CO2 concentration. There were no changes in respiratory motor activity as determined from the peak inspiratory airway pressure (Paw) until the PCO2 reached 40.8 +/- 1.0 and 40.1 +/- 1.0 (SE) Torr in the large and small VT trials, respectively. Initially there was no conscious awareness of the change in respiratory activity. Subjects first signaled that ventilatory needs were not being satisfied only after a further increase in PCO2 to 44.7 +/- 1.3 and 42.3 +/- 1.0 (SE) Torr in the large and small VT trials and after the Paw had fallen to 55–60% of the base-line value. The results suggest that changes in respiratory sensation produced by increasing chemical drive are a consequence of increases in respiratory efferent activity, but a direct effect of changes in PCO2 on respiratory sensation cannot be excluded.


2016 ◽  
Vol 34 (12) ◽  
pp. 2367-2371 ◽  
Author(s):  
An-Yi Wang ◽  
Chien-Hua Huang ◽  
Wei-Tien Chang ◽  
Min-Shan Tsai ◽  
Chih-Hung Wang ◽  
...  

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