Effect of diaphragmatic fatigue on control of respiratory muscles and ventilation during CO2 rebreathing

1993 ◽  
Vol 75 (3) ◽  
pp. 1364-1370 ◽  
Author(s):  
S. Yan ◽  
I. Lichros ◽  
S. Zakynthinos ◽  
P. T. Macklem
Keyword(s):  
Minute Ventilation ◽  
Respiratory Muscles ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Transdiaphragmatic Pressure ◽  
Gastric Pressure ◽  
Diaphragmatic Fatigue ◽  
Before And After ◽  
Inspiratory Resistance ◽  
End Tidal

We studied the influence of diaphragmatic fatigue on the control of ventilation and respiratory muscle contribution to pressure swings in six normal seated subjects. CO2 was rebreathed before and after diaphragmatic fatigue induced by breathing against an inspiratory resistance requiring 60% maximal transdiaphragmatic pressure with each breath until exhaustion. After diaphragmatic fatigue for a given level of end-tidal PCO2, we found that tidal volume, breathing frequency, minute ventilation, duty cycle, and mean inspiratory flow did not change; esophageal pressure swings were the same, but gastric and transdiaphragmatic pressure swings were decreased; and the slope of the transpulmonary pressure-gastric pressure relationship determined at zero flow points at end expiration and end inspiration was increased. End-expiratory transpulmonary pressure progressively decreased and end-expiratory gastric pressure progressively increased with increasing end-tidal PCO2 by the same magnitude before and after diaphragmatic fatigue. We conclude that diaphragmatic fatigue induces proportionately greater contributions of inspiratory rib cage muscles than of the diaphragm, which results in the preservation of ventilatory response to CO2 despite impaired diaphragmatic contractility.

Sonomicrometric regional diaphragmatic shortening in awake sheep after thoracic surgery

1989 ◽  
Vol 67 (6) ◽  
pp. 2357-2368 ◽  
Author(s):  
A. Torres ◽  
W. R. Kimball ◽  
J. Qvist ◽  
K. Stanek ◽  
R. M. Kacmarek ◽  
...  
Keyword(s):  
Thoracic Surgery ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Breathing ◽  
Transdiaphragmatic Pressure ◽  
Right Thoracotomy ◽  
Before And After ◽  
End Tidal ◽  
End Tidal Co2

Through a right thoracotomy in seven sheep we chronically implanted sonomicrometry crystals and electromyographic electrodes in the costal and crural diaphragmatic regions. Awake sheep were studied during recovery for 4-6 wk, both during quiet breathing (QB) and during CO2 rebreathing. Tidal volume, respiratory frequency, and esophageal and gastric pressures were studied before and after surgery. Normalized resting length (LFRC) was significantly decreased for the costal segment on postoperative day 1 compared with postoperative day 28. Fractional costal shortening both during QB and at 10% end-tidal CO2 (ETCO2) increased significantly from postoperative days 1 to 28, whereas crural shortening did not change during QB but progressively increased at 10% ETCO2. Maximal costal shortening during electrophrenic stimulation was constant at 40% LFRC during recovery, although maximal crural shortening increased from 23 to 32% LFRC. Minute ventilation, tidal volume, and transdiaphragmatic pressure at 10% ETCO2 increased progressively after thoracotomy until postoperative day 28. Our results suggest there is profound diaphragmatic inhibition after thoracotomy and crystal implantation in sheep that requires at least 3-4 wk for stable recovery.

Diaphragmatic fatigue in normoxia and hyperoxia

1985 ◽  
Vol 58 (3) ◽  
pp. 738-742 ◽  
Author(s):  
R. L. Pardy ◽  
P. T. Bye
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Random Order ◽  
Similar Degree ◽  
Endurance Time ◽  
Transdiaphragmatic Pressure ◽  
Perceived Effort ◽  
Diaphragmatic Fatigue ◽  
End Tidal ◽  
Arterial O2 Saturation

Diaphragmatic fatigue was induced in six normal young men inspiring against a variable alinear resistance. Breathing pattern was rigidly controlled (tidal volume 0.75 liter, 12 breaths . min-1). Fatigue was defined as an inability to continue to generate a target transdiaphragmatic pressure (Pdi = 0.65 - 0.84 Pdimax). Diaphragmatic electromyogram (EMG, esophageal electrode) and perceived effort (PE, open-ended scale) were recorded. Subjects were tested on an identical resistance inspiring air or 100% O2 in random order on different days. They were unaware of the gas mixture inspired. Mean endurance time (tlim) +/- SE for air was 4.1 +/- 1.4 min and for O2 was 8.6 +/- 2.7 min (P less than 0.005). The increased tlim in O2 was associated with a delay in onset of EMG changes heralding diaphragmatic fatigue and a decrease in PE at any time during the study compared with the level of PE in air. Arterial O2 saturation (ear oximeter) remained at the resting level of 99.0 +/- 0.2% in O2 and decreased from the resting level of 97.2 +/- 0.2% by 2.8 +/- 0.7% (P less than 0.01) in air. The end-tidal CO2 fraction increased to a similar degree in air and O2 studies. We conclude that when breathing pattern, minute ventilation, and Pdi are held constant during inspiratory resistive loading, breathing O2 delays the onset of diaphragm fatigue and decreases PE.

Mechanics of the respiratory system and breathing pattern during sleep in normal humans

1984 ◽  
Vol 56 (1) ◽  
pp. 133-137 ◽  
Author(s):  
D. W. Hudgel ◽  
R. J. Martin ◽  
B. Johnson ◽  
P. Hill
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Transpulmonary Pressure ◽  
Dynamic Compliance ◽  
Face Mask ◽  
Esophageal Pressure ◽  
Rapid Eye Movement ◽  
Airflow Resistance

The purposes of this investigation were to describe the changes in 1) dynamic compliance of the lungs, 2) airflow resistance, and 3) breathing pattern that occur during sleep in normal adult humans. Six subjects wore a tightly fitting face mask. Flow and volume were obtained from a pneumotachograph attached to the face mask. Transpulmonary pressure was calculated as the difference between esophageal pressure obtained with a balloon and mask pressure. At least 20 consecutive breaths were analyzed for dynamic compliance, airflow resistance, and breathing pattern during wakefulness, non-rapid-eye-movement stage 2 and rapid-eye-movement (REM) sleep. Dynamic compliance did not change significantly. Airflow resistance increased during sleep; resistance was 3.93 +/- 0.56 cmH2O X 1–1 X s during wakefulness, 7.96 +/- 0.95 in stage 2 sleep, and 8.66 +/- 1.43 in REM sleep (P less than 0.02). By placing a catheter in the retroepiglottic space and thus dividing the airway into upper and lower zones, we found the increase in resistance occurred almost entirely above the larynx. Decreases in tidal volume, minute ventilation, and mean inspiratory flow observed during sleep were not statistically significant.

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading

1996 ◽  
Vol 81 (4) ◽  
pp. 1562-1571 ◽  
Author(s):  
D. M. Fothergill ◽  
N. A. Carlson
Keyword(s):  
Heart Rate ◽  
Steady State ◽  
Minute Ventilation ◽  
Esophageal Pressure ◽  
Incremental Exercise ◽  
Time To Exhaustion ◽  
Gas Mixture ◽  
Resistive Loading ◽  
Inspiratory Resistance ◽  
Sufficient Magnitude

Fothergill, D. M., and N. A. Carlson. Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading. J. Appl. Physiol. 81(4): 1562–1571, 1996.—The influence of nitrous oxide (N2O) narcosis on the responses to exercise and inspiratory resistive loading was studied in thirteen male US Navy divers. Each diver performed an incremental bicycle exercise test at 1 ATA to volitional exhaustion while breathing a 23% N2O gas mixture and a nonnarcotic gas of the same [Formula: see text], density, and viscosity. The same gas mixtures were used during four subsequent 30-min steady-state submaximal exercise trials in which the subjects breathed the mixtures both with and without an inspiratory resistance (5.5 vs. 1.1 cmH2O ⋅ s ⋅ l−1at 1 l/s). Throughout each test, subjective ratings of respiratory effort (RE), leg exertion, and narcosis were obtained with a category-ratio scale. The level of narcosis was rated between slight and moderate for the N2O mixture but showed great individual variation. Perceived leg exertion and the time to exhaustion were not significantly different with the two breathing mixtures. Heart rate was unaffected by the gas mixture and inspiratory resistance at rest and during steady-state exercise but was significantly lower with the N2O mixture during incremental exercise ( P< 0.05). Despite significant increases in inspiratory occlusion pressure (13%; P < 0.05), esophageal pressure (12%; P < 0.001), expired minute ventilation (4%; P < 0.01), and the work rate of breathing (15%; P < 0.001) when the subjects breathed the N2O mixture, RE during both steady-state and incremental exercise was 25% lower with the narcotic gas than with the nonnarcotic mixture ( P < 0.05). We conclude that the narcotic-mediated changes in ventilation, heart rate, and RE induced by 23% N2O are not of sufficient magnitude to influence exercise tolerance at surface pressure. Furthermore, the load-compensating respiratory reflexes responsible for maintaining ventilation during resistive breathing are not depressed by N2O narcosis.

Diaphragm function and respiratory response after upper abdominal surgery in dogs

1984 ◽  
Vol 57 (2) ◽  
pp. 576-582 ◽  
Author(s):  
J. D. Road ◽  
K. R. Burgess ◽  
W. A. Whitelaw ◽  
G. T. Ford
Keyword(s):  
Abdominal Surgery ◽  
General Anesthesia ◽  
Minute Ventilation ◽  
Esophageal Pressure ◽  
Transdiaphragmatic Pressure ◽  
Diaphragm Function ◽  
Upper Abdominal Surgery ◽  
Postoperative Changes ◽  
Upper Abdominal ◽  
Diaphragm Activity

Decreased diaphragm activity has been demonstrated after cholecystectomy in humans (Am. Rev. Respir. Dis. 127: 431–436, 1983). To investigate the mechanism(s) of postoperative diaphragm dysfunction we have established a dog model. Three groups of mongrel dogs were studied under general anesthesia: six dogs received no surgery (control); nine dogs underwent upper abdominal surgery (cholecystectomy); and six dogs underwent lower abdominal surgery (pseudoappendectomy). Diaphragm function was assessed by changes in transdiaphragmatic pressure swings, the ratio of changes in gastric to esophageal pressure swings, and the ratio of changes in abdominal to rib cage diameters during quiet tidal breathing. In the upper abdominal surgery group there were significant postoperative decreases in all parameters of diaphragm function and an increase in minute ventilation and respiratory frequency. However, there were no significant postoperative changes in the parameters of diaphragm function in the control or lower abdominal surgery groups. These studies establish that general anesthesia is not responsible for the reduced diaphragm activity seen postoperatively and that diaphragm function is not affected by lower abdominal surgery in dogs.

Diaphragmatic fatigue in man

1977 ◽  
Vol 43 (2) ◽  
pp. 189-197 ◽  
Author(s):  
C. S. Roussos ◽  
P. T. Macklem
Keyword(s):  
Energy Consumption ◽  
Lung Diseases ◽  
Respiratory Muscles ◽  
Transdiaphragmatic Pressure ◽  
Diaphragmatic Fatigue ◽  
Residual Capacity ◽  
The Subject ◽  
Time Required ◽  
The Relationship ◽  
Experimental Runs

The time required (tlim) to produce fatigue of the diaphragm was determined in three normal seated subjects, breathing through a variety of high alinear, inspiratory resistances. During each breath in all experimental runs the subject generated a transdiaphragmatic pressure (Pdi) which was a predetermined fraction of his maximum inspiratory Pdi (Pdimax) at functional residual capacity. The breathing test was performed until the subject was unable to generate this Pdi. The relationship between Pdi/Pdimax and tlim was curvilinear so that when Pdi/Pdimax was small tlim increased markedly for little changes in Pdi/Pdimax. The value of Pdi/Pdimax that could be generated indefinitely (Pdicrit) was around 0.4. Hypoxia appeared to have no influence on Pdicrit, but probably led to a reduction in tlim at Pdi greater than Pdicrit for equal rates of energy consumption. Insofar as the behavior of the diaphragm reflects that of other respiratory muscles it appears that quite high inspiratory loads can be tolerated indefinitely. However, when the energy consumption of the respiratory muscles exceeds a critical level, fatigue should develop. This may be a mechanism of respiratory failure in a variety in a variety of lung diseases.

Aminophylline and human diaphragm strength in vivo

1990 ◽  
Vol 68 (6) ◽  
pp. 2591-2596 ◽  
Author(s):  
R. D. Levy ◽  
S. Nava ◽  
L. Gibbons ◽  
F. Bellemare
Keyword(s):  
Motor Units ◽  
Normal Subjects ◽  
Acute Administration ◽  
Transdiaphragmatic Pressure ◽  
Gastric Pressure ◽  
Significant Difference ◽  
Before And After ◽  
Normal Human ◽  
Twitch Characteristics

The transdiaphragmatic pressure (Pdi) twitch response to single shocks from supramaximal bilateral phrenic nerve stimulation was studied before and after acute intravenous infusions of aminophylline [14.9 +/- 3.1 (SD) micrograms/ml] in nine normal subjects. Stimulation was performed with subjects in the sitting position against an occluded airway from end expiration. Baseline gastric pressure and abdominal and rib cage configuration were kept constant. There was no significant difference in peak twitch Pdi from the relaxed diaphragm between control (38.8 +/- 3.3 cmH2O) and aminophylline (40.2 +/- 5.2 cmH2O) experiments. Other twitch characteristics including contraction time, half-relaxation time, and maximum relaxation rate were also unchanged. The Pdi-twitch amplitude at different levels of voluntary Pdi was measured with the twitch occlusion technique, and this relationship was found to be similar under control conditions and after aminophylline. With this technique, maximum Pdi (Pdimax) was calculated as the Pdi at which stimulation would result in no Pdi twitch because all motor units are already maximally activated. No significant change was found in mean calculated Pdimax between control (146.9 +/- 27.0 cmH2O) and aminophylline (149.2 +/- 26.0 cmH2O) experiments. We conclude from this study that the acute administration of aminophylline at therapeutic concentrations does not significantly affect contractility or maximum strength of the normal human diaphragm in vivo.

Passive mechanics of upright human chest wall during immersion from hips to neck

1986 ◽  
Vol 60 (5) ◽  
pp. 1561-1570 ◽  
Author(s):  
M. B. Reid ◽  
S. H. Loring ◽  
R. B. Banzett ◽  
J. Mead
Keyword(s):  
Chest Wall ◽  
Esophageal Pressure ◽  
Vertical Surface ◽  
Repeated Measurements ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Gastric Pressure ◽  
Length Changes ◽  
Accessory Muscles

We have determined the mechanical effects of immersion to the neck on the passive chest wall of seated upright humans. Repeated measurements were made at relaxed end expiration on four subjects. Changes in relaxed chest wall configuration were measured using magnetometers. Gastric and esophageal pressures were measured with balloon-tipped catheters in three subjects; from these, transdiaphragmatic pressure was calculated. Transabdominal pressure was estimated using a fluid-filled, open-tipped catheter referenced to the abdomen's exterior vertical surface. We found that immersion progressively reduced mean transabdominal pressure to near zero and that the relaxed abdominal wall was moved inward 3–4 cm. The viscera were displaced upward into the thorax, gastric pressure increased by 20 cmH2O, and transdiaphragmatic pressure decreased by 10–15 cmH2O. This lengthened the diaphragm, elevating the diaphragmatic dome 3–4 cm. Esophageal pressure became progressively more positive throughout immersion, increasing by 8 cmH2O. The relaxed rib cage was elevated and expanded by raising water from hips to lower sternum; this passively shortened the inspiratory intercostals and the accessory muscles of inspiration. Deeper immersion distorted the thorax markedly: the upper rib cage was forced inward while lower rib cage shape was not systematically altered and the rib cage remained elevated. Such distortion may have passively lengthened or shortened the inspiratory muscles of the rib cage, depending on their location. We conclude that the nonuniform forcing produced by immersion provides unique insights into the mechanical characteristics of the abdomen and rib cage, that immersion-induced length changes differ among the inspiratory muscles according to their locations and the depth of immersion, and that such length changes may have implications for patients with inspiratory muscle deficits.

Increased chemoreceptor output and ventilatory response to sustained hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1157-1163 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Peripheral Chemoreceptor ◽  
Depressant Action ◽  
Before And After ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3–5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

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