Detection of Hypercapnia by Normal Subjects

1987 ◽  
Vol 73 (3) ◽  
pp. 333-335 ◽  
Author(s):  
R. M. Schwartzstein ◽  
K. La Hive ◽  
A. Pope ◽  
R. A. Steinbrook ◽  
D. E. Leith ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Pulmonary Ventilation ◽  
Control Period ◽  
Feedback System ◽  
Normal Subjects ◽  
Test Period ◽  
Absolute Level ◽  
End Tidal ◽  
Induced Changes ◽  
Different Levels

1. To investigate whether changes in Paco2 can be detected independently of the CO2-induced changes in pulmonary ventilation, we tested five normal subjects for the ability to distinguish different levels of end-tidal Pco2 (PETco2) while holding minute ventilation constant. 2. Helped by a visual feedback system, the subjects maintained a constant ventilation targeted at a level that was higher than that dictated by the chemical drive at PETco2 = 50 mmHg (6.7 kPa). End-tidal Pco2 was held at 40 mmHg (5.3 kPa) during the first 2 min of each test trial ('control period'); then, for 4 min ('test period'), PETco2 was either elevated to 50 mmHg or kept at 40 mmHg. Twelve runs were performed by each subject. 3. In 24 out of the total 30 trials (80%) in which PETco2 was raised during the test period to 50 mmHg, the subjects detected the changes. There was one false positive result (3%), when PETco2 kept at 40 mmHg during the test period was reported as different from control. In four out of the five subjects the ability to detect the change in PETco2 from 40 to 50 mmHg was statistically significant. 4. We conclude that increases in PETco2 can be detected independently of changes in the absolute level of ventilation.

Effect of different levels of hyperoxia on breathing in healthy subjects

1996 ◽  
Vol 81 (4) ◽  
pp. 1683-1690 ◽  
Author(s):  
Heinrich F. Becker ◽  
Olli Polo ◽  
Stephen G. McNamara ◽  
Michael Berthon-Jones ◽  
Colin E. Sullivan
Keyword(s):  
Healthy Subjects ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Normal Subjects ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
End Tidal ◽  
Dose Dependent ◽  
Different Levels

Becker, Heinrich F., Olli Polo, Stephen G. McNamara, Michael Berthon-Jones, and Colin E. Sullivan. Effect of different levels of hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683–1690, 1996.—We have recently shown that breathing 50% O2 markedly stimulates ventilation in healthy subjects if end-tidal [Formula: see text]([Formula: see text]) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O2 for 30 min, with[Formula: see text] being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O2 experiment was repeated without controlling[Formula: see text] in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (V˙i) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O2 without any control on[Formula: see text] led to a 16% increase inV˙i, but[Formula: see text] decreased by 3.6 Torr (9%). There was a linear correlation ( r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, withV˙i more than doubling after 30 min of 75% O2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial[Formula: see text]. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.

Ventilatory and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.

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.

Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

2013 ◽  
Vol 125 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hidehiro Nakahara ◽  
Kazunobu Okazaki ◽  
Damian M. Bailey ◽  
Tadayoshi Miyamoto
Keyword(s):  
Lower Body Negative Pressure ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Respiratory Chemoreflex ◽  
Underlying Mechanisms ◽  
End Tidal ◽  
Induced Changes ◽  
The Relationship

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA Vmean (middle cerebral artery mean blood velocity) and V̇E (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO2 levels (0, 3.5 and 5% CO2). The regression line of the linear relationship between V̇E and PETCO2 (end-tidal CO2) shifted leftwards during orthostatic stress without any change in sensitivity (1.36±0.27 l/min per mmHg at supine to 1.06±0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA Vmean and PETCO2 was not shifted by LBNP-induced changes in PETCO2. However, changes in V̇E from rest to LBNP were more related to changes in MCA Vmean than changes in PETCO2. These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO2 from the brain causing hyperpnoea following activation of the central chemoreflex.

Ozone-induced changes in pulmonary function and bronchial responsiveness in asthmatics

1989 ◽  
Vol 66 (1) ◽  
pp. 217-222 ◽  
Author(s):  
J. W. Kreit ◽  
K. B. Gross ◽  
T. B. Moore ◽  
T. J. Lorenzen ◽  
J. D'Arcy ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Ozone Exposure ◽  
Bronchial Responsiveness ◽  
Before And After ◽  
Effective Doses ◽  
Induced Changes ◽  
Percent Decrease

To compare the responses of asthmatic and normal subjects to high effective doses of ozone, nine asthmatic and nine normal subjects underwent two randomly assigned 2-h exposures to filtered, purified air and 0.4 ppm ozone with alternating 15-min periods of rest and exercise on a cycle ergometer (minute ventilation = 30 l.min-1.m-2). Before and after each exposure, pulmonary function and bronchial responsiveness to methacholine were measured and symptoms were recorded. Ozone exposure was associated with a statistically significant decrease in forced vital capacity (FVC), forced expired volume in 1 s (FEV1), percent FEV1 (FEV1%), and forced expired flow at 25–75% FVC (FEF25–75) in both normal and asthmatic subjects. However, comparing the response of asthmatic and normal subjects to ozone revealed a significantly greater percent decrease in FEV1, FEV1%, and FEF25–75 in the asthmatic subjects. The effect of ozone on FVC and symptom scores did not differ between the two groups. In both normal and asthmatic subjects, exposure to ozone was accompanied by a significant increase in bronchial responsiveness. We conclude that exposure to a high effective ozone dose produces 1) increased bronchial responsiveness in both normal and asthmatic subjects, 2) greater airways obstruction in asthmatic than in normal subjects, and 3) similar symptoms and changes in lung volumes in the two groups.

Effect of episodic hypoxia on upper airway mechanics in humans during NREM sleep

2002 ◽  
Vol 92 (6) ◽  
pp. 2565-2570 ◽  
Author(s):  
Mahdi Shkoukani ◽  
Mark A. Babcock ◽  
M. Safwan Badr
Keyword(s):  
Minute Ventilation ◽  
Recovery Period ◽  
Control Period ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Hypoxic Exposure ◽  
Airway Mechanics ◽  
Episodic Hypoxia ◽  
Long Term Facilitation

We hypothesized that long-term facilitation (LTF) is due to decreased upper airway resistance (Rua). We studied 11 normal subjects during stable non-rapid eye movement sleep. We induced brief isocapnic hypoxia (inspired O2fraction = 8%) (3 min) followed by 5 min of room air. This sequence was repeated 10 times. Measurements were obtained during control, hypoxia, and at 20 min of recovery (R20) for ventilation, timing, and Rua. In addition, nine subjects were studied in a sham study with no hypoxic exposure. During the episodic hypoxia study, inspiratory minute ventilation (V˙i) increased from 7.1 ± 1.8 l/min during the control period to 8.3 ± 1.8 l/min at R20 (117% of control; P < 0.05). Conversely, there was no change in diaphragmatic electromyogram (EMGdia) between control (16.1 ± 6.9 arbitrary units) and R20 (15.3 ± 4.9 arbitrary units) (95% of control; P > 0.05). In contrast, increasedV˙i was associated with decreased Rua from 10.7 ± 7.5 cmH2O · l−1 · s during control to 8.2 ± 4.4 cmH2O · l−1 · s at R20 (77% of control; P < 0.05). No change was noted in V˙i, Rua, or EMGdia during the recovery period relative to control during the sham study. We conclude the following: 1) increased V˙i in the recovery period is indicative of LTF, 2) the lack of increased EMGdia suggests lack of LTF to the diaphragm, 3) reduced Rua suggests LTF of upper airway dilators, and 4) increased V˙i in the recovery period is due to “unloading” of the upper airway by LTF of upper airway dilators.

Relation between work output of respiratory muscles and end-tidal CO2 tension

1963 ◽  
Vol 18 (3) ◽  
pp. 497-504 ◽  
Author(s):  
J. Milic-Emili ◽  
J. M. Tyler
Keyword(s):  
Carbon Dioxide ◽  
Pulmonary Ventilation ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Work Output ◽  
Inspiratory Muscles ◽  
Expiratory Muscles ◽  
End Tidal ◽  
End Tidal Co2

End-tidal CO2 tension, pulmonary ventilation, and work output of respiratory muscles were determined in six normal subjects breathing various mixtures of carbon dioxide in air, with three graded resistances added to both inspiration and expiration. In two individuals, the resistances were also added separately to inspiration or expiration. A linear relationship was found between work output of inspiratory muscles and end-tidal CO2 tension; this relationship was uninfluenced by added resistance. No consistent relationship was observed between either ventilation or work output of expiratory muscles and end-tidal CO2 tension. These results suggest that carbon dioxide controls directly the activity of inspiratory muscles alone and that the activity of expiratory muscles is only coincidentally involved. The possible role of intrinsic properties of respiratory muscles and of nervous mediation in the control of breathing is discussed. Submitted on October 22, 1962

scholarly journals Control of breathing during sleep assessed by proportional assist ventilation

1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes
Keyword(s):  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Control Of Breathing ◽  
Respiratory Drive ◽  
Proportional Assist Ventilation ◽  
End Tidal

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.

Coupling of ventilation to pulmonary gas exchange during nonsteady-state work in men

1983 ◽  
Vol 54 (2) ◽  
pp. 587-593 ◽  
Author(s):  
D. H. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Load Cycle ◽  
Constant Load ◽  
Response Dynamics ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Nonsteady State ◽  
End Tidal

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.

No effect of naloxone on hypoxia-induced ventilatory depression in adults

1982 ◽  
Vol 52 (4) ◽  
pp. 1030-1034 ◽  
Author(s):  
S. Kagawa ◽  
M. J. Stafford ◽  
T. B. Waggener ◽  
J. W. Severinghaus
Keyword(s):  
Opioid Peptides ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Control Period ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Steady Level ◽  
Ventilatory Depression ◽  
End Tidal

The ventilatory response to acute isocapnic hypoxia is prompt but is not maintained at its peak. Within 10 min, it begins to fall, and by 30 min has reached an approximately steady level, usually still above control. We used naloxone to test in four men the hypothesis that this fade is hypoxic depression mediated by endogenous opioid peptides, e.g, endorphins. Breath by breath minute ventilation was recorded during a hyperoxic control period (FIO2 = 0.3) to establish control alveolar PCO2. After 15 min. of isocapnic hypoxia (end-tidal PO2 = 45 Torr), naloxone injection (1.2 or 10 mg, iv) failed to alter the slow decrement of ventilation. Hypoxic ventilatory depression appears not to be mediated by endorphins in adults.

Sign in / Sign up

Export Citation Format

Share Document