Chest wall responses to rebreathing in halothane-anesthetized dogs

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background: The pattern of respiratory muscle use during halothane- induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. Methods: Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. Results: Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (V̇(E)) and PCO2 (0.34 ± 0;04 [M ± SE] and 0.28 ± 0.05 l · min-1 · mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated V̇(E) at a PCO2 of 60 mmHg (from 7.4 ± 1.2 to 4.0 ± 0.6 l · min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (ΔV(th)), with percentage of δV(th) attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 ± 6% to 48 ± 2% of ΔV(th)). Conclusions: Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.

Original languageEnglish (US)
Pages (from-to)835-843
Number of pages9
JournalAnesthesiology
Volume83
Issue number4
DOIs
StatePublished - 1995

Fingerprint

Thoracic Wall
Halothane
Dogs
Anesthesia
Muscles
Respiratory Muscles
Intercostal Muscles
Abdominal Muscles
Respiration
Ventilation
Anesthetics
Implanted Electrodes
Supine Position
Tidal Volume
Electromyography
Diaphragm
Leg
Thorax
Rib Cage

Keywords

  • Anesthetics, volatile: halothane
  • Lung: breathing pattern; blood volume; diaphragm; functional residual capacity; intrathoracic rib cage
  • Measurement technique: computed tomography; electromyography
  • Muscle: diaphragm; external oblique; parasternal intercostal; respiratory; transversus abdominis

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Chest wall responses to rebreathing in halothane-anesthetized dogs. / Warner, David Oman; Joyner, Michael Joseph; Ritman, E. L.

In: Anesthesiology, Vol. 83, No. 4, 1995, p. 835-843.

Research output: Contribution to journalArticle

@article{dbeb1f28d2e343af8cb08de1ec750478,
title = "Chest wall responses to rebreathing in halothane-anesthetized dogs",
abstract = "Background: The pattern of respiratory muscle use during halothane- induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. Methods: Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. Results: Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (V̇(E)) and PCO2 (0.34 ± 0;04 [M ± SE] and 0.28 ± 0.05 l · min-1 · mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated V̇(E) at a PCO2 of 60 mmHg (from 7.4 ± 1.2 to 4.0 ± 0.6 l · min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (ΔV(th)), with percentage of δV(th) attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 ± 6{\%} to 48 ± 2{\%} of ΔV(th)). Conclusions: Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.",
keywords = "Anesthetics, volatile: halothane, Lung: breathing pattern; blood volume; diaphragm; functional residual capacity; intrathoracic rib cage, Measurement technique: computed tomography; electromyography, Muscle: diaphragm; external oblique; parasternal intercostal; respiratory; transversus abdominis",
author = "Warner, {David Oman} and Joyner, {Michael Joseph} and Ritman, {E. L.}",
year = "1995",
doi = "10.1097/00000542-199510000-00024",
language = "English (US)",
volume = "83",
pages = "835--843",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Chest wall responses to rebreathing in halothane-anesthetized dogs

AU - Warner, David Oman

AU - Joyner, Michael Joseph

AU - Ritman, E. L.

PY - 1995

Y1 - 1995

N2 - Background: The pattern of respiratory muscle use during halothane- induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. Methods: Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. Results: Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (V̇(E)) and PCO2 (0.34 ± 0;04 [M ± SE] and 0.28 ± 0.05 l · min-1 · mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated V̇(E) at a PCO2 of 60 mmHg (from 7.4 ± 1.2 to 4.0 ± 0.6 l · min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (ΔV(th)), with percentage of δV(th) attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 ± 6% to 48 ± 2% of ΔV(th)). Conclusions: Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.

AB - Background: The pattern of respiratory muscle use during halothane- induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. Methods: Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. Results: Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (V̇(E)) and PCO2 (0.34 ± 0;04 [M ± SE] and 0.28 ± 0.05 l · min-1 · mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated V̇(E) at a PCO2 of 60 mmHg (from 7.4 ± 1.2 to 4.0 ± 0.6 l · min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (ΔV(th)), with percentage of δV(th) attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 ± 6% to 48 ± 2% of ΔV(th)). Conclusions: Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.

KW - Anesthetics, volatile: halothane

KW - Lung: breathing pattern; blood volume; diaphragm; functional residual capacity; intrathoracic rib cage

KW - Measurement technique: computed tomography; electromyography

KW - Muscle: diaphragm; external oblique; parasternal intercostal; respiratory; transversus abdominis

UR - http://www.scopus.com/inward/record.url?scp=0029132051&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029132051&partnerID=8YFLogxK

U2 - 10.1097/00000542-199510000-00024

DO - 10.1097/00000542-199510000-00024

M3 - Article

C2 - 7574064

AN - SCOPUS:0029132051

VL - 83

SP - 835

EP - 843

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 4

ER -