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

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.

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.

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

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+].

Effect of aerosolized histamine on occlusion pressure and ventilation in humans

1982 ◽  
Vol 53 (3) ◽  
pp. 690-697 ◽  
Author(s):  
R. P. Millman ◽  
D. A. Silage ◽  
D. D. Peterson ◽  
A. I. Pack
Keyword(s):  
Smooth Muscle ◽  
Neural Activity ◽  
Occlusion Pressure ◽  
Bronchial Smooth Muscle ◽  
Co2 Partial Pressure ◽  
Residual Capacity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Airway Conductance ◽  
Stimulation Of

To define further the mechanism by which inspiratory neural activity is increased in asthma, we studied the effect of aerosolized histamine on occlusion pressure (P100) and ventilation in conscious humans while end-tidal CO2 partial pressure was maintained at a constant, slightly hypercapnic level. The dose of histamine we employed varied from subject to subject but was such that it produced a 70% reduction in specific airway conductance in each subject. In 9 of the 13 subjects tested, inhaled histamine significantly increased P100. This increase was not due to changes in functional residual capacity, which was not affected by aerosolized histamine. Inhalation of isoproterenol abolished the effects of histamine on specific airway conductance and P100. Anesthesia of the airways by lidocaine eliminated the effect of histamine on P100 but did not alter the magnitude of the change in specific airway conductance produced by histamine. We conclude that the increase in occlusion pressure seen after the inhalation of histamine in humans depends on both contraction of bronchial smooth muscle and stimulation of airway receptors.

Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise

1990 ◽  
Vol 68 (6) ◽  
pp. 2312-2321 ◽  
Author(s):  
D. R. Brown ◽  
H. V. Forster ◽  
L. G. Pan ◽  
A. G. Brice ◽  
C. L. Murphy ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Partial Pressure ◽  
Venous Return ◽  
Ventilatory Response ◽  
Co2 Partial Pressure ◽  
Human Spinal Cord ◽  
Co2 Output ◽  
Hamstring Muscles ◽  
Exercise Hyperpnea ◽  
End Tidal

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.

Blood osmolality during in vivo changes of CO2 pressure

1983 ◽  
Vol 54 (1) ◽  
pp. 123-129 ◽  
Author(s):  
D. Boning ◽  
U. Vaas ◽  
K. M. Braumann
Keyword(s):  
Venous Blood ◽  
Hysteresis Loops ◽  
Whole Body ◽  
Co2 Partial Pressure ◽  
Rapid Restoration ◽  
Body Compartments ◽  
End Tidal ◽  
Buffer Capacities ◽  
End Tidal Co2

In 16 experiments male subjects, age 22.4 +/- 0.5 (SE) yr, inspired CO2 for 15 min (8% end-tidal CO2) or hyperventilated for 30 min (2.5% end-tidal CO2). Osmolality (Osm) and acid-base status of arterialized venous blood were determined at short intervals until 30 min after hypo- and hypercapnia, respectively. During hypocapnia [CO2 partial pressure (PCO2) -2.31 +/- 0.32 kPa (-17.4 Torr), pH + 0.19 units], Osm decreased by 3.9 +/- 0.3 mosmol/kg H2O; during hypercapnia [PCO2 + 2.10 +/- 0.28 kPa (+15.8 Torr), pH -0.12 units], Osm increased by 5.8 +/- 0.7 mosmol/kg H2O. Presentation of the data in Osm-PCO2 or Osm-pH diagrams yields hysteresis loops probably caused by exchange between blood and tissues. The dependence of Osm on PCO2 must result mainly from CO2 buffering and therefore from the formation of bicarbonate. In spite of the different buffer capacities in various body compartments, water exchange allows rapid restoration of osmotic equilibrium throughout the organism. Thus delta Osm/delta pH during a PCO2 jump largely depends on the mean buffer capacity of the whole body. The high estimated buffer value during hypercapnia (38 mmol/kg H2O) compared with hypocapnia (19 mmol/kg H2O) seems to result from very strong muscle buffering during moderate acidosis.

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