Effect of quiet sleep on resting and CO2-stimulated breathing in humans

1981 ◽  
Vol 50 (4) ◽  
pp. 724-730 ◽  
Author(s):  
B. Gothe ◽  
M. D. Altose ◽  
M. D. Goldman ◽  
N. S. Cherniack
Keyword(s):  
Partial Pressure ◽  
Tidal Volume ◽  
Quiet Sleep ◽  
Rib Cage ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Quantitative Measurements ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Different Levels

We examined the effects of different levels of inspired CO2 on ventilation and the pattern of breathing in healthy adults during the awake and the stage II quiet-sleep states. During both states, subjects were studied supine with their heads enclosed in a canopy. Tidal volume (VT) was determined from quantitative measurements of abdominal and rib cage excursions with magnetometers. Inspired CO2 was raised by blending CO2-enriched gas into the airflow, which continuously flushed the canopy. During sleep, while room air was breathed, VT decreased significantly from 410 to 360 ml, and respiratory rate also fell from 17 to 16 breaths/min. As a consequence, ventilation was significantly reduced from 6.5 to 5.8 l/min, and end-tidal CO2 partial pressure (PCO2) rose from 39.1 to 42.5 Torr. Ventilatory responses to CO2 were reduced, on the average, during sleep to 79% of waking levels. The change in average inspiratory flow produced by CO2 was also less during sleep. Waking and sleeping ventilatory responses to CO2 correlated inversely with the rise in end-tidal PCO2 when room air was breathed during sleep. At all levels of VT, the rib cage contribution to VT was greater during quiet sleep than during wakefulness. These findings suggest that quiet sleep, in addition to depressing ventilation and the response to CO2 alters the manner in which VT is attained by rib cage and abdominal displacements.

Diaphragm electrical activity during negative lower torso pressure in quadriplegic men

1981 ◽  
Vol 51 (3) ◽  
pp. 654-659 ◽  
Author(s):  
R. B. Banzett ◽  
G. F. Inbar ◽  
R. Brown ◽  
M. Goldman ◽  
A. Rossier ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Tidal Volume ◽  
Respiratory System ◽  
Afferent Pathways ◽  
Co2 Partial Pressure ◽  
Inspiratory Muscles ◽  
Spinal Lesions ◽  
Diaphragm Electrical Activity ◽  
End Tidal ◽  
End Tidal Co2

We recorded the diaphragm electromyogram (EMG) of quadriplegic men before and during exposure of the lower torso to continuous negative pressure, which caused shortening of the inspiratory muscles by expanding the respiratory system by one tidal volume. The moving-time-averaged diaphragm EMG was larger during expansion of the respiratory system. When we repeated the experiment with subjects who breathed through a mouthpiece, we found qualitatively similar EMG changes and little or no change in tidal volume or end-tidal CO2 partial pressure. When the pressure was applied or removed rapidly, changes in EMG occurred within one or two breaths. Because end-tidal CO2 partial pressure did not increase, and because the response was rapid, we suggest that the response results from proprioceptive, rather than chemoreceptive, reflexes. As most of these men had complete spinal lesions at C6 or C7 the afferent pathways are likely to be vagal or phrenic.

METABOREFLEX CHANGES RELATIONSHIP BETWEEN END-TIDAL CO2 PARTIAL PRESSURE AND VENTILATION

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S229
Author(s):  
N Hayashi ◽  
T Miyamoto ◽  
Y Fukuba ◽  
T Yoshida
Keyword(s):  
Partial Pressure ◽  
Co2 Partial Pressure ◽  
End Tidal ◽  
End Tidal Co2

Recovery from central apnea: effect of stimulus duration and end-tidal CO2 partial pressure

1982 ◽  
Vol 53 (1) ◽  
pp. 105-109 ◽  
Author(s):  
E. E. Lawson
Keyword(s):  
Partial Pressure ◽  
Stimulus Duration ◽  
Respiratory Activity ◽  
Control Level ◽  
Superior Laryngeal Nerve ◽  
Regression Function ◽  
Co2 Partial Pressure ◽  
Natural Logarithm ◽  
End Tidal ◽  
End Tidal Co2

The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (PCO2). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal PCO2. After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal PCO2 following long (30 s) stimuli, was independent of the end-tidal PCO2 level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.

Initial end-tidal CO2 partial pressure predicts outcomes of in-hospital cardiac arrest

2016 ◽  
Vol 34 (12) ◽  
pp. 2367-2371 ◽  
Author(s):  
An-Yi Wang ◽  
Chien-Hua Huang ◽  
Wei-Tien Chang ◽  
Min-Shan Tsai ◽  
Chih-Hung Wang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Partial Pressure ◽  
Co2 Partial Pressure ◽  
End Tidal ◽  
Hospital Cardiac Arrest ◽  
End Tidal Co2

Decreased Carbon Dioxide Sensitivity in Infants of Substance-Abusing Mothers

PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Demographic Data ◽  
Substance Abusing ◽  
Quiet Sleep ◽  
Co2 Level ◽  
The Difference ◽  
End Tidal ◽  
Drug Free

Objective. To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. Methods. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. Results. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 ± 7.14 (mean ± SE), whereas that of ISAMs was 16.28 ± 3.14. Conclusions. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.

Mechanics of the rib cage and diaphragm during sleep

1977 ◽  
Vol 43 (4) ◽  
pp. 600-602 ◽  
Author(s):  
K. Tusiewicz ◽  
H. Moldofsky ◽  
A. C. Bryan ◽  
M. H. Bryan
Keyword(s):  
Tidal Volume ◽  
Supine Position ◽  
Marked Reduction ◽  
Normal Subjects ◽  
Upright Position ◽  
Rapid Eye Movement Sleep ◽  
Sleep State ◽  
Quiet Sleep ◽  
Rib Cage ◽  
The Subject

The pattern of motion of the rib cage and abdomen/diaphragm was studied in three normal subjects during sleep. Sleep state was monitored by electroencephalograph and electrocculograph. Intercostal electromyographs (EMG's) were recorded from the second interspace parasternally. Abdominothoracic motion was monitored with magnetometers and these signals calibrated by isovolume lines either immediately before going to sleep, or if there was movement, on awakening. Respiration was recorded using a jerkin plethysmograph. In the awake subject in the supine position, the rib cage contributed 44% to the tidal volume and had essentially the same contribution in quiet sleep. However, in active or rapid eye movement sleep the rib cage contribution fell to 19% of the tidal volume. This was accompanied by a marked reduction in the intercostal EMG. With the subject in the upright position the rib cage appears to be passively driven by the diaphragm. However, the present data suggest that active contraction of the intercostal muscles is required for normal rib cage expansion in the supine position.

Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation

1983 ◽  
Vol 55 (3) ◽  
pp. 813-822 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Positive Pressure ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Apnea Duration ◽  
O2 Concentration ◽  
End Tidal ◽  
End Tidal Co2

The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].

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.

The Ventilatory Effects of Doxapram in Normal Man

1983 ◽  
Vol 65 (1) ◽  
pp. 65-69 ◽  
Author(s):  
P. M. A. Calverley ◽  
R. H. Robson ◽  
P. K. Wraith ◽  
L. F. Prescott ◽  
D. C. Flenley
Keyword(s):  
Oxygen Uptake ◽  
Ventilatory Response ◽  
Co2 Production ◽  
Central Action ◽  
Ventilatory Responses ◽  
Ventilatory Effects ◽  
Normal Man ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from − 0.8 ± 0.4 litre min−1 (%Sao2)−1 to −1.63 ± 0.9 litres min−1 (%Sao2)−1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 ± 5.3 litres min−1 kPa−1 to 20,4 ± 9.8 litres min−1 kPa−1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

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