Apnea after normocapnic mechanical ventilation during NREM sleep

1994 ◽  
Vol 77 (5) ◽  
pp. 2079-2085 ◽  
Author(s):  
A. M. Leevers ◽  
P. M. Simon ◽  
J. A. Dempsey
Keyword(s):  
Mechanical Ventilation ◽  
Nrem Sleep ◽  
Inspiratory Effort ◽  
Control Mechanical Ventilation ◽  
Inhibitory Effects ◽  
Inspiratory Motor ◽  
Ventilator Mode ◽  
Controlled Mechanical Ventilation ◽  
The Subject ◽  
End Tidal

We determined whether normocapnic mechanical ventilation at high tidal volume (VT) and breathing frequency (f) during non-rapid-eye-movement (NREM) sleep would cause apnea. Seven normal sleeping subjects were placed on assist-control mechanical ventilation (i.e., subject initiates inspiration) and VT was gradually increased to 2.1 times eupneic VT (1.17 +/- 0.04 liters). This high VT was maintained for 5 min, the ventilator mode was switched to controlled mechanical ventilation, and f was increased gradually from 9.5 +/- 1.0 (during assist-control mechanical ventilation) to 14.0 +/- 0.7 breaths/min. Normocapnia (end-tidal PCO2 = 44 +/- 1.2 Torr) was maintained throughout the trials. Inspiratory effort was completely inhibited during the period of sustained high VT and f, and apnea occurred immediately after cessation of the passive mechanical ventilation. The duration of the apnea preceding the first inspiratory effort was 20.3 +/- 2.3 s or 7.1 times the eupneic expiratory duration and 5 times the expiratory duration chosen by the subject during assist-control mechanical ventilation. We conclude that inhibition of inspiratory motor output occurs during and after normocapnic mechanical ventilation at high VT and f during NREM sleep. These neuromechanical inhibitory effects may serve to initiate and prolong apnea.

Respiratory control during volume-cycled ventilation in normal humans

1996 ◽  
Vol 80 (5) ◽  
pp. 1749-1758 ◽  
Author(s):  
A. Puddy ◽  
W. Patrick ◽  
K. Webster ◽  
M. Younes
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Rhythm ◽  
Respiratory Control ◽  
Control Mode ◽  
The Face ◽  
Controlled Mechanical Ventilation ◽  
Normal Humans ◽  
The Subject ◽  
End Tidal ◽  
Modest Reduction

The purpose of this study was to evaluate the extent of inhibition to respiratory rhythm associated with high volumes of ventilation during volume-cycled mechanical ventilation (neuromechanical inhibition). Two approaches were used. 1) In 18 normal awake subjects, ventilator tidal volume (VT) in the assist/control mode (A/C) was increased in steps from the minimum tolerable level up to 80% of the subject's inspiratory capacity or ventilator's maximum VT. We looked for appearance of intermittent apnea or a reduction in spontaneous rate (f). 2) Another 18 normal awake subjects were placed on controlled mechanical ventilation (CMV). When apnea was established, we abruptly terminated CMV and measured the time before the appearance of the next spontaneous effort. In the assist mode (protocol 1), we did not observe intermittent apnea because VT was increased from [from 944 +/- 198 to 1,867 +/- 277 (SD) ml], and there was only a modest reduction in f (14.1 +/- 3.9 to 12.4 +/- 4.0 breaths/min). End-tidal PCO2 (PETCO2) decreased precipitously as VT was increased. In protocol 2, we did not observe apnea after discontinuation of CMV in any subject. Total breath duration of the first breath after discontinuation did not differ significantly from total breath duration during A/C in the same subjects (4.84 +/- 2.2 vs. 5.2 +/- 2.0 s). This similarly applied regardless of route of breathing (nose vs. mouth) or PETCO2 level at time of discontinuation. We conclude that neuromechanical inhibition is quite weak and provides very little negative feedback that may help control PCO2 in the face of excessive VT and f demands of the subject.

Determinants of poststimulus potentiation in humans during NREM sleep

1992 ◽  
Vol 73 (5) ◽  
pp. 1958-1971 ◽  
Author(s):  
M. S. Badr ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Control Period ◽  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Central Apnea ◽  
Inhibitory Effects ◽  
Arterial Pco2 ◽  
End Tidal ◽  
Sustained Hypoxia

To test whether active hyperventilation activates the “afterdischarge” mechanism during non-rapid-eye-movement (NREM) sleep, we investigated the effect of abrupt termination of active hypoxia-induced hyperventilation in normal subjects during NREM sleep. Hypoxia was induced for 15 s, 30 s, 1 min, and 5 min. The last two durations were studied under both isocapnic and hypocapnic conditions. Hypoxia was abruptly terminated with 100% inspiratory O2 fraction. Several room air-to-hyperoxia transitions were performed to establish a control period for hyperoxia after hypoxia transitions. Transient hyperoxia alone was associated with decreased expired ventilation (VE) to 90 +/- 7% of room air. Hyperoxic termination of 1 min of isocapnic hypoxia [end-tidal PO2 (PETO2) 63 +/- 3 Torr] was associated with VE persistently above the hyperoxic control for four to six breaths. In contrast, termination of 30 s or 1 min of hypocapnic hypoxia [PETO2 49 +/- 3 and 48 +/- 2 Torr, respectively; end-tidal PCO2 (PETCO2) decreased by 2.5 or 3.8 Torr, respectively] resulted in hypoventilation for 45 s and prolongation of expiratory duration (TE) for 18 s. Termination of 5 min of isocapnic hypoxia (PETO2 63 +/- 3 Torr) was associated with central apnea (longest TE 200% of room air); VE remained below the hyperoxic control for 49 s. Termination of 5 min of hypocapnic hypoxia (PETO2 64 +/- 4 Torr, PETCO2 decreased by 2.6 Torr) was also associated with central apnea (longest TE 500% of room air). VE remained below the hyperoxic control for 88 s. We conclude that 1) poststimulus hyperpnea occurs in NREM sleep as long as hypoxia is brief and arterial PCO2 is maintained, suggesting the activation of the afterdischarge mechanism; 2) transient hypocapnia overrides the potentiating effects of afterdischarge, resulting in hypoventilation; and 3) sustained hypoxia abolishes the potentiating effects of after-discharge, resulting in central apnea. These data suggest that the inhibitory effects of sustained hypoxia and hypocapnia may interact to cause periodic breathing.

A volume-dependent apneic threshold during NREM sleep in the dog

1994 ◽  
Vol 76 (6) ◽  
pp. 2315-2325 ◽  
Author(s):  
C. M. Chow ◽  
L. Xi ◽  
C. A. Smith ◽  
K. W. Saupe ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Nrem Sleep ◽  
Inspiratory Effort ◽  
Central Apnea ◽  
Arterial Pco2 ◽  
Airway Occlusion ◽  
Vagal Blockade ◽  
Minor Contribution ◽  
Per Se ◽  
End Tidal

We determined the causes of central apnea that commonly follow the hyperpnea resulting from brief airway occlusion during non-rapid-eye-movement (NREM) sleep. Ventilation and end-tidal gases were measured before, during, and after 214 trials of 15–20 s of tracheal occlusion in three dogs during NREM sleep. Airway occlusion was accompanied by progressive increases in inspiratory effort and was followed by transient one- to four-breath hyperapneas, with subsequent central apnea [3–15 times eupneic control expiratory duration (TE)] in 62% of occlusion trials. Significant TE prolongation after hyperventilation did not occur until tidal volume (VT) was three times greater than control; i.e., there was a volume-dependent apneic threshold. Transient electroencephalogram arousal at the end of the occlusion often augmented VT, thereby contributing to the subsequent central apnea; however, arousal was not required for the apnea to occur. Significant transient hypocapnia (up to -12 Torr arterial PCO2) commonly occurred after release of airway occlusion but was not closely correlated with the length of central apnea. During vagal blockade, after release of airway occlusion, significant transient hyperventilation occurred but at VT < 40% greater than control, and TE prolongation was markedly reduced. In summary, after release of airway occlusion in NREM sleep, 1) VT greater than three times eupnea was necessary to cause central apnea, 2) transient arousal at the termination of airway occlusion caused longer apneas by augmenting VT, and 3) transient hypocapnia per se made a significant but minor contribution to the postocclusion central apnea.

scholarly journals Sustained hyperoxia stabilizes breathing in healthy individuals during NREM sleep

2010 ◽  
Vol 109 (5) ◽  
pp. 1378-1383 ◽  
Author(s):  
Susmita Chowdhuri ◽  
Prabhat Sinha ◽  
Sukanya Pranathiageswaran ◽  
M. Safwan Badr
Keyword(s):  
Mechanical Ventilation ◽  
Ventilatory Response ◽  
Random Order ◽  
Nrem Sleep ◽  
Minimal Change ◽  
Central Apnea ◽  
Noninvasive Mechanical Ventilation ◽  
Healthy Individuals ◽  
Air Exposure ◽  
End Tidal

The present study was designed to determine whether hyperoxia would lower the hypocapnic apneic threshold (AT) during non-rapid eye movement (NREM) sleep. Nasal noninvasive mechanical ventilation was used to induce hypocapnia and subsequent central apnea in healthy subjects during stable NREM sleep. Mechanical ventilation trials were conducted under normoxic (room air) and hyperoxic conditions (inspired Po2 > 250 Torr) in a random order. The CO2 reserve was defined as the minimal change in end-tidal Pco2 (PetCO2) between eupnea and hypocapnic central apnea. The PetCO2 of the apnea closest to eupnea was designated as the AT. The hypocapnic ventilatory response was calculated as the change in ventilation below eupnea for a given change in PetCO2. In nine participants, compared with room air, exposure to hyperoxia was associated with a significant decrease in eupneic PetCO2 (37.5 ± 0.6 vs. 41.1 ± 0.6 Torr, P = 0.001), widening of the CO2 reserve (−3.8 ± 0.8 vs. −2.0 ± 0.3 Torr, P = 0.03), and a subsequent decline in AT (33.3 ± 1.2 vs. 39.0 ± 0.7 Torr; P = 001). The hypocapnic ventilatory response was also decreased with hyperoxia. In conclusion, 1) hyperoxia was associated with a decreased AT and an increase in the magnitude of hypocapnia required for the development of central apnea. 2) Thus hyperoxia may mitigate the effects of hypocapnia on ventilatory motor output by lowering the hypocapnic ventilatory response and lowering the resting eupneic PetCO2, thereby decreasing plant gain.

Accuracy of End-Tidal Co2 Capnometers in Post-Cardiac Surgery Patients During Controlled Mechanical Ventilation

2013 ◽  
Vol 45 (1) ◽  
pp. 130-135 ◽  
Author(s):  
Serge J.H. Heines ◽  
Ulrich Strauch ◽  
Paul M.H. J. Roekaerts ◽  
Bjorn Winkens ◽  
Dennis C.J. J. Bergmans
Keyword(s):  
Mechanical Ventilation ◽  
Cardiac Surgery ◽  
Controlled Mechanical Ventilation ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Post Cardiac Surgery

Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep

2000 ◽  
Vol 89 (1) ◽  
pp. 192-199 ◽  
Author(s):  
X. S. Zhou ◽  
S. Shahabuddin ◽  
B. R. Zahn ◽  
M. A. Babcock ◽  
M. S. Badr
Keyword(s):  
Mechanical Ventilation ◽  
Sleep Apnea ◽  
Gender Difference ◽  
Minute Ventilation ◽  
Regression Line ◽  
Recovery Period ◽  
Premenopausal Women ◽  
Nrem Sleep ◽  
Central Apnea ◽  
End Tidal

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25–35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21–43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (Vt) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal Pco 2(Pet CO2 ) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in Vt to 155 ± 29% (mean ± SD) and a reduction of Pet CO2 by −4.72 ± 0.57 Torr. In men, induction of a central apnea required an increase in Vt to 142 ± 13% and a reduction of Pet CO2 by −3.54 ± 0.31 Torr ( P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.

scholarly journals Ionic and non-ionic intravenous X-ray contrast media: antibacterial agents?

2021 ◽  
pp. 028418512110198
Author(s):  
Frank Mosler ◽  
Johannes K Richter ◽  
Marc Schindewolf ◽  
Nando Mertineit ◽  
Hendrik von Tengg-Kobligk ◽  
...  
Keyword(s):  
Contrast Media ◽  
Bactericidal Effect ◽  
Future Research ◽  
Inhibitory Effects ◽  
X Ray ◽  
Percutaneous Abscess Drainage ◽  
Ionic Contrast ◽  
Bactericidal Effects ◽  
Free Iodine ◽  
The Subject

X-ray contrast media have been reported to have inhibitory effects on bacterial growth. Despite its potentially beneficial effect on patients, these features of contrast media have received relatively little attention in the medical literature in the past decades. The aim of this review is to evaluate the literature concerning the bactericidal and bacteriostatic effects of X-ray contrast media, specifically if there is a known difference concerning these effects between ionic and non-ionic contrast media. Systematic literature review was performed for the years of publication between 1911 and 2019. Since the publication of Grossich in 1911, the effect of iodine on the treatment of superficial infections in surgical procedures has been established clinical knowledge. Bacteriostatic and bactericidal effects of ionic X-ray contrast media are well established. However, non-ionic contrast agents have been the subject of little research in this respect. In past decades, the hypothesis emerged in the literature that mainly the concentration of free iodine might be responsible for any bacteriostatic or bactericidal effect of ionic X-ray contrast media. Nowadays, however, only non-ionic contrast media are used. The question regarding the mechanism and magnitude of bacteriostatic or bactericidal effects of these, non-ionic contrast media, could not be answered conclusively from this review. Non-ionic contrast media could be used intentionally when a local antibacterial effect is intended (e.g. in percutaneous abscess drainage), as well as to reduce the overall dose of antibiotics administered to a patient. Thus, this question remains relevant and might constitute the area of future research.

scholarly journals Transcriptome profiling of the diaphragm in a controlled mechanical ventilation model reveals key genes involved in ventilator-induced diaphragmatic dysfunction

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ruining Liu ◽  
Gang Li ◽  
Haoli Ma ◽  
Xianlong Zhou ◽  
Pengcheng Wang ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Signaling Pathway ◽  
Wistar Rats ◽  
Cholesterol Metabolism ◽  
Expression Profiles ◽  
Receptor Interaction ◽  
Pathophysiological Mechanism ◽  
Rna Seq ◽  
Diaphragmatic Dysfunction ◽  
Controlled Mechanical Ventilation

Abstract Background Ventilator-induced diaphragmatic dysfunction (VIDD) is associated with weaning difficulties, intensive care unit hospitalization (ICU), infant mortality, and poor long-term clinical outcomes. The expression patterns of long noncoding RNAs (lncRNAs) and mRNAs in the diaphragm in a rat controlled mechanical ventilation (CMV) model, however, remain to be investigated. Results The diaphragms of five male Wistar rats in a CMV group and five control Wistar rats were used to explore lncRNA and mRNA expression profiles by RNA-sequencing (RNA-seq). Muscle force measurements and immunofluorescence (IF) staining were used to verify the successful establishment of the CMV model. A total of 906 differentially expressed (DE) lncRNAs and 2,139 DE mRNAs were found in the CMV group. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the biological functions or pathways of these DE mRNAs. Our results revealed that these DE mRNAs were related mainly related to complement and coagulation cascades, the PPAR signaling pathway, cholesterol metabolism, cytokine-cytokine receptor interaction, and the AMPK signaling pathway. Some DE lncRNAs and DE mRNAs determined by RNA-seq were validated by quantitative real-time polymerase chain reaction (qRT-PCR), which exhibited trends similar to those observed by RNA-sEq. Co-expression network analysis indicated that three selected muscle atrophy-related mRNAs (Myog, Trim63, and Fbxo32) were coexpressed with relatively newly discovered DE lncRNAs. Conclusions This study provides a novel perspective on the molecular mechanism of DE lncRNAs and mRNAs in a CMV model, and indicates that the inflammatory signaling pathway and lipid metabolism may play important roles in the pathophysiological mechanism and progression of VIDD.

Upper airway muscle responsiveness to rising Pco 2 during NREM sleep

2000 ◽  
Vol 89 (4) ◽  
pp. 1275-1282 ◽  
Author(s):  
Giora Pillar ◽  
Atul Malhotra ◽  
Robert B. Fogel ◽  
Josee Beauregard ◽  
David I. Slamowitz ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Dilator Muscle ◽  
Pharyngeal Muscles ◽  
Stage 2 Sleep ◽  
Significant Change ◽  
End Tidal

Although pharyngeal muscles respond robustly to increasing Pco 2 during wakefulness, the effect of hypercapnia on upper airway muscle activation during sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO2-driven muscle activation may importantly stabilize the upper airway during stages 3 and 4 sleep. To test this hypothesis, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal Pco 2(Pet CO2 ) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO2(Pet CO2 = 6 Torr above the eupneic level) were also assessed during SWS ( n = 9) or stage 2 sleep ( n = 7). Pet CO2 increased spontaneously by 0.8 ± 0.1 Torr from stage 2 to SWS (from 43.3 ± 0.6 to 44.1 ± 0.5 Torr, P < 0.05), with no significant change in GG or TP EMG. Despite a significant increase in minute ventilation with induced hypercapnia (from 8.3 ± 0.1 to 11.9 ± 0.3 l/min in stage 2 and 8.6 ± 0.4 to 12.7 ± 0.4 l/min in SWS, P < 0.05 for both), there was no significant change in the GG or TP EMG. These data indicate that supraphysiological levels of Pet CO2 (50.4 ± 1.6 Torr in stage 2, and 50.4 ± 0.9 Torr in SWS) are not a major independent stimulus to pharyngeal dilator muscle activation during either SWS or stage 2 sleep. Thus hypercapnia-induced pharyngeal dilator muscle activation alone is unlikely to explain the paucity of sleep-disordered breathing events during SWS.

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