Ventilatory responses to dead space and CO2 breathing under inspiratory resistive load

1995 ◽  
Vol 78 (2) ◽  
pp. 555-561 ◽  
Author(s):  
D. A. Sidney ◽  
C. S. Poon
Keyword(s):  
Breathing Pattern ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Resistive Load ◽  
Healthy Human ◽  
Ventilatory Responses ◽  
Ventilatory Pattern ◽  
Volume Relationship ◽  
The Mean ◽  
End Tidal

To investigate how breathing is controlled during CO2 stimulation, steady-state ventilatory responses to rebreathing through a tube (DS) and inspiring a fixed PCO2 (INH) were compared in healthy human subjects. Tests were performed in hyperoxia with (IRL) and without (NL) an inspiratory resistive load (15 cmH2O.l–1.s at 1 l/s). The mean slope of the minute ventilation (VE)-end-tidal PCO2 relationship was significantly higher in DS-IRL than in INH-IRL [1.86 +/- 0.67 (SD) vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.01], and it was significantly different between INH-NL and INH-IRL (1.64 +/- 0.41 vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.05) but not between DS-NL and DS-IRL (1.85 +/- 0.72 vs. 1.86 +/- 0.67 l.min-1.Torr-1). The slope of the VE-tidal volume relationship was significantly lower in DS-NL than in INH-NL (19.6 +/- 3.8 vs. 21.2 +/- 5.1 min-1, P < 0.05), but other comparisons in breathing pattern between NL and IRL and between DS and INH failed to reach significance. We concluded that 1) alterations in alveolar PCO2 temporal profile by DS could induce changes in VE-end-tidal PCO2 sensitivity and ventilatory pattern, 2) these changes may be modified by increased mechanical impairment resulting from IRL, and 3) carotid chemoreceptor mediation is not necessary for the observed effects of DS.

Time course of ozone-induced changes in breathing pattern in healthy exercising humans

2007 ◽  
Vol 102 (2) ◽  
pp. 688-697 ◽  
Author(s):  
Edward S. Schelegle ◽  
William F. Walby ◽  
William C. Adams
Keyword(s):  
Time Course ◽  
Breathing Pattern ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Cumulative Exposure ◽  
Healthy Human ◽  
Percent Change ◽  
Atropine Treatment ◽  
Induced Changes ◽  
Time To Onset

We examined the time course of O3-induced changes in breathing pattern in 97 healthy human subjects (70 men and 27 women). One- to five-minute averages of breathing frequency (fB) and minute ventilation (V̇e) were used to generate plots of cumulative breaths and cumulative exposure volume vs. time and cumulative exposure volume vs. cumulative breaths. Analysis revealed a three-phase response; delay, no response detected; onset, fB began to increase; response, fB stabilized. Regression analysis was used to identify four parameters: time to onset, number of breaths at onset, cumulative inhaled dose of ozone at onset of O3-induced tachypnea, and the percent change in fB. The effect of altering O3 concentration, V̇e, atropine treatment, and indomethacin treatment were examined. We found that the lower the O3 concentration, the greater the number of breaths at onset of tachypnea at a fixed ventilation, whereas number of breaths at onset of tachypnea remains unchanged when V̇e is altered and O3 concentration is fixed. The cumulative inhaled dose of O3 at onset of tachypnea remained constant and showed no relationship with the magnitude of percent change in fB. Atropine did not affect any of the derived parameters, whereas indomethacin did not affect time to onset, number of breaths at onset, or cumulative inhaled dose of O3 at onset of tachypnea but did attenuate percent change in fB. The results are discussed in the context of dose response and intrinsic mechanisms of action.

Breathing pattern in humans: elevated CO2 or low O2 on positive airway pressure

1984 ◽  
Vol 56 (3) ◽  
pp. 777-784 ◽  
Author(s):  
J. A. Hirsch ◽  
B. Bishop
Keyword(s):  
Elevated Co2 ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Sensory Information ◽  
Positive Pressure ◽  
Ventilatory Responses ◽  
Chemical Stimuli ◽  
The Individual ◽  
End Tidal ◽  
End Tidal Co2

The purpose of this study was to determine effects on breathing pattern of pressure breathing alone and in combination with chemical stimulation. We analyzed ventilatory responses to elevated airway pressures (positive-pressure breathing, PPB) in subjects breathing air, 12% O2, or elevated CO2. Each subject sat in a body box and breathed via mouth-piece from a bag-in-box. Responses to PPB on air were increased minute ventilation (VI), tidal volume (VT), frequency (f), mean inspiratory (VT/TI) and expiratory (VT/TE) flows, decreased expiratory duration (TE) and end-tidal CO2. If end-tidal CO2 were held constant, VI, VT, and VT/TI increased less. Responses greater than predicted from summing responses to either stimulus alone were observed for VT, f, VT/TI, and VT/TE during 3 and 5% CO2 and for VT, f, and VT/TE during isocapnic hypoxia. Responses to other combined stimuli were sums of responses to the individual stimuli. Thus ventilatory responses to combined PPB and chemical stimuli cannot be predicted simply from summating responses to each independently imposed stimulus, suggesting that sensory information arises from and is integrated at multiple sites.

Effects of expiratory resistive load on respiratory motor output in conscious humans

1987 ◽  
Vol 63 (5) ◽  
pp. 1837-1845 ◽  
Author(s):  
C. S. Poon ◽  
M. Younes ◽  
C. G. Gallagher
Keyword(s):  
Tidal Volume ◽  
Time Course ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Resistive Load ◽  
Quiet Breathing ◽  
Relative Time ◽  
Ventilatory Pattern ◽  
Resistive Loading ◽  
Residual Capacity

We examined, in five conscious human subjects, the steady-state effects of expiratory resistive loading (ERL; R = 8 cmH2O.l–1.s) on the time course of inspiratory and postinspiratory muscle activities (IA and PIA, respectively) and ventilatory pattern during quiet breathing. Driving pressure (DP) was calculated by means of a respiratory neuromechanical model (J. Appl. Physiol. 51: 963–989, 1981) that permitted the derivation, from tidal volume and flow, of the occlusion pressure equivalent (at functional residual capacity) of respiratory neural output throughout the breath. ERL caused a prolongation of both neural inspiratory duration (12.2 +/- 6.9% SD) and expiratory duration (25.0 +/- 10.1%) and an increase in the amplitude of DP (16.5 +/- 10.2%) without any changes in the waveshape of IA and in end-expiratory level. The relative time course of PIA was not altered by ERL. Minute ventilation was depressed (-6.75 +/- 2.88%) during ERL with little change in alveolar PCO2. The results indicate that pulmonary gas exchange may be improved during ERL through increased tidal volume as well as delayed expiratory lung emptying secondary to sustained PIA.

Detection of Soluble Fibrin Monomer Complexes in Blood by Means of Protamine Sulphate Test

1968 ◽  
Vol 20 (01/02) ◽  
pp. 044-049 ◽  
Author(s):  
B Lipiński ◽  
K Worowski
Keyword(s):  
Human Subjects ◽  
Coronary Thrombosis ◽  
Mean Value ◽  
Healthy Human ◽  
Protamine Sulphate ◽  
Soluble Fibrin ◽  
Fibrin Monomer ◽  
Dog Plasma ◽  
The Mean ◽  
Precipitable Protein

SummaryIn the present paper described is a simple test for detecting soluble fibrin monomer complexes (SFMC) in blood. The test consists in mixing 1% protamine sulphate with diluted oxalated plasma or serum and reading the optical density at 6190 Å. In experiments with dog plasma, enriched with soluble fibrin complexes, it was shown that OD read in PS test is proportional to the amount of fibrin recovered from the precipitate. It was found that SFMC level in plasma increases in rabbits infused intravenously with thrombin and decreases after injection of plasmin with streptokinase. In both cases PS precipitable protein in serum is elevated indicating enhanced fibrinolysis. In healthy human subjects the mean value of OD readings in plasma and sera were found to be 0.30 and 0.11, while in patients with coronary thrombosis they are 0.64 and 0.05 respectively. The origin of SFMC in circulation under physiological and pathological conditions is discussed.

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.

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work

1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Work Load ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Phase Lag ◽  
Ventilatory Responses ◽  
Load Tests ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.

An assessment of nasal functions in control of breathing

1988 ◽  
Vol 65 (4) ◽  
pp. 1520-1524 ◽  
Author(s):  
Y. Tanaka ◽  
T. Morikawa ◽  
Y. Honda
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Control Of Breathing ◽  
Mouth Breathing ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults. In addition, the effect of warming and humidification of the inspired air on the ventilatory response was observed during breathing through a mouthpiece. We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. 2) The slope of CO2 ventilatory responses did not differ appreciably during the two types of breathing, but CO2 occlusion pressure response was significantly enhanced during nose breathing. 3) Inhalation of warm and humid air through a mouthpiece significantly depressed CO2 ventilation and occlusion pressure responses. These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep.

Ventilatory adjustments during sustained mechanical loading in conscious humans

1983 ◽  
Vol 55 (4) ◽  
pp. 1211-1218 ◽  
Author(s):  
K. Axen ◽  
S. S. Haas ◽  
F. Haas ◽  
D. Gaudino ◽  
A. Haas
Keyword(s):  
Mechanical Loading ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Ventilatory Responses ◽  
Frequency Responses ◽  
Group Response ◽  
Resistive Loading ◽  
Elastic Loading ◽  
Resistive Loads ◽  
Load Size

Ventilatory responses to inspiratory elastic and resistive loads of 67 men were analyzed. During the 1st, 5th, and 10th consecutively loaded breaths 1) individual responses ranged from a rapid-shallow to a slow-deep breathing pattern; 2) strong tidal volume (VT) defenders employed longer inspirations than did weak VT defenders; and 3) individual frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively similar on the 1st, 5th, and 10th loaded breaths. Quantitatively, however, the group's mean minute ventilation increased throughout each episode owing to progressively larger tidal volumes coupled with equal breathing frequencies. During elastic loading this amplified VT defense was achieved by stronger inspirations with no systematic changes in timing, whereas during resistive loading it was achieved both by stronger and longer inspirations. Inspiring 5% CO2 induced a degree of hypercapnia exceeding that accompanying mechanical loading and yet elicited a comparatively modest enhancement of respiratory output. These findings suggest that in conscious humans 1) repeated mechanical loading activates neural load-compensating mechanisms; 2) the range of these neural adjustments varies with both load size and type; and 3) the stimulus to initiate this behavior is largely nonchemical.

Breuer-Hering inflation reflex and breathing pattern in anesthetized humans and cats

1981 ◽  
Vol 51 (5) ◽  
pp. 1162-1168 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora ◽  
J. H. Gaudy
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Respiratory Activity ◽  
Human Subjects ◽  
Threshold Curve ◽  
Ventilatory Pattern ◽  
Tracheal Pressure ◽  
Switch Mechanism

In nine cats and nine human subjects anesthetized with alfaxalone, respiratory activity and tracheal pressure were recorded prior to and during occlusion of the airway at end inspiration or end expiration. Lung inflations at the end of expiration were also performed. In addition, the ventilatory pattern was analyzed during hypercapnia. The results show that occlusions at the end of inspiration or inflations provoked an apnea in both cats and humans. However, concomitant with increases in tidal volume during hypercapnia, inspiratory duration decreased in cats and did not change in human subjects. These results indicate that the Breuer-Hering reflex, which delays the onset of inspiration during inflation was equally operative in cats and humans. In contrast, the “Breuer-Hering threshold curve,” which accounts for the off-switch“ of inspiration was different in cats and humans. Thus, in summary, the Breuer-Hering inflation reflex is operative in human subjects, but it does not seem to be involved in the control of the inspiratory off-switch mechanism during increases respiratory activity resulting from hypercapnia.

Role of Vagal Airway Reflexes in Control of Ventilation in Pulmonary Fibrosis

1981 ◽  
Vol 61 (6) ◽  
pp. 781-784 ◽  
Author(s):  
J. Savoy ◽  
S. Dhingra ◽  
N. R. Anthonisen
Keyword(s):  
Pulmonary Fibrosis ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Arterial Oxygen ◽  
Control Subjects ◽  
Cough Response ◽  
Before And After ◽  
The Mean ◽  
Breath Cycle

1. in 10 patients with pulmonary fibrosis and in seven control subjects, we measured the pressure at the mouth 0.1 s after onset of an inspiration against occluded airway (P0.1), minute ventilation (VI), breathing frequency (fr), tidal volume (VT), inspiratory duration (Tl) and calculated the mean inspiratory flow (VT/Tl) and the fraction of the breath cycle devoted to inspiration (Tl/Ttot.). in the patients measurements were made at normal arterial oxygen saturations (Sao2), before and after lignocaine airway anaesthesia. 2. Efficacy of airway anaesthesia was tested by the cough response to citric acid inhalation. 3. in pulmonary fibrosis P0.1, f1 and VT/Tl were greater than in the control subjects, VT and Tl, were smaller and Tl/Ttot. and VI were not different. 4. Effective airway anaesthesia did not modify P0.1 and breathing pattern parameters observed in pulmonary fibrosis. 5. These results suggest that airway receptors do not contribute to a major extent to the control of breathing in pulmonary fibrosis.

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