scholarly journals Ventilatory response to CO2 in patients with epilepsy

Epilepsia ◽  
2019 ◽  
Vol 60 (3) ◽  
pp. 508-517 ◽  
Author(s):  
Rup K. Sainju ◽  
Deidre N. Dragon ◽  
Harold B. Winnike ◽  
Marcus B. Nashelsky ◽  
Mark A. Granner ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Patients With Epilepsy ◽  
Ventilatory Response To Co2

Ventilatory Response to CO2 Following Intravenous and Epidural Lidocaine

1986 ◽  
Vol 6 (1) ◽  
pp. 188
Author(s):  
T. Labaille ◽  
F. Clergue ◽  
K. Samii ◽  
C. Ecoffey ◽  
A. Berdaux
Keyword(s):  
Ventilatory Response ◽  
Ventilatory Response To Co2

Nemaline Myopathy as a Cause of Sleep Hypoventilation

PEDIATRICS ◽  
1986 ◽  
Vol 77 (3) ◽  
pp. 390-395
Author(s):  
Ch. Maayan ◽  
C. Springer ◽  
Y. Armon ◽  
E. Bar-Yishay ◽  
V. Shapira ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Ventilatory Response ◽  
Nemaline Myopathy ◽  
Cor Pulmonale ◽  
Systemic Hypertension ◽  
Older Patient ◽  
And Function ◽  
Ventilatory Response To Co2

Two siblings, a 14.5-year-old boy and his 11.5-year-old sister, with congenital nemaline myopathy presented with severe respiratory failure and, in the case of the older patient, with cor pulmonale and systemic hypertension. The children were treated initially by continuous mechanical ventilation, but after a few weeks they only required ventilation at night. At the start of treatment, both were found to have a decreased ventilatory response to CO2 which apparently improved during 4 to 5 years of follow-up treatment. It has not been possible to wean them from nocturnal mechanical ventilation, but during the daytime they attend school and function almost normally. It is postulated that respiratory failure in nemaline myopathy may not be related to the severity of the muscle weakness but may result from a disturbance of the feedback required for normal control of breathing.

Ventilatory response to CO2 in panic disorder

1991 ◽  
Vol 39 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Jan Zandbergen ◽  
Henk Pols ◽  
Cathrien de Loof ◽  
Eric J.L. Griez
Keyword(s):  
Panic Disorder ◽  
Ventilatory Response ◽  
Ventilatory Response To Co2

scholarly journals Ventilatory response to CO2 rebreathing at rest in the ama.

1981 ◽  
Vol 31 (3) ◽  
pp. 423-426 ◽  
Author(s):  
Miharu MIYAMURA ◽  
Taizo TSUNODA ◽  
Noriaki FUJITSUKA ◽  
Yoshiyuki HONDA
Keyword(s):  
Ventilatory Response ◽  
Co2 Rebreathing ◽  
Ventilatory Response To Co2

CLONIDINE DOES NOT DEPRESS THE VENTILATORY RESPONSE TO CO2 IN MAN

1990 ◽  
Vol 70 (Supplement) ◽  
pp. S383 ◽  
Author(s):  
R. J. Sperry ◽  
P. L. Bailey ◽  
N. L. Pace ◽  
S. Eldredge ◽  
K. Johnson ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Ventilatory Response To Co2

The effect of Airway Anaesthesia on the Control of Breathing and the Sensation of Breathlessness in Man

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Cough Reflex ◽  
Before And After ◽  
Median Diameter ◽  
Receptor Block ◽  
Normal Man ◽  
End Tidal ◽  
Ventilatory Response To Co2

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.

Ventilatory response of intact cats to carbon monoxide hypoxia

1983 ◽  
Vol 55 (4) ◽  
pp. 1064-1071 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora
Keyword(s):  
Carbon Monoxide ◽  
Brain Stem ◽  
Ventilatory Response ◽  
Hypoxic Hypoxia ◽  
Small Decrease ◽  
Low Concentrations ◽  
Initial Decrease ◽  
Respiratory Centers ◽  
Ventilatory Response To Co2

Adult intact conscious or anesthetized cats have been exposed to either hypoxia or low concentrations of CO in air. In addition, the ventilatory response to CO2 was studied in air, hypoxic hypoxia, and CO hypoxia. The results show that 1) in conscious cats, low concentrations of CO (0.15%) induce a slight decrease in ventilation and higher concentrations of CO (0.20%) induce first a small decrease in ventilation and then a characteristic tachypnea similar to the hypoxic tachypnea described in carotid-denervated cats; 2) in anesthetized cats, CO hypoxia induces only mild changes in ventilation; and 3) the ventilatory response to CO2 is increased in CO hypoxia in both conscious and anesthetized animals but differs from the increase observed during hypoxia. It is concluded that the initial decrease in ventilation may be caused by some brain stem depression of the respiratory centers with CO hypoxia, whereas the tachypnea originates probably at some suprapontine level. Conversely, the possible central acidosis may account for the potentiation of the ventilatory response to CO2 observed in either conscious or anesthetized animals.

Respiratory stimulation by female hormones in awake male rats

1991 ◽  
Vol 71 (1) ◽  
pp. 37-42 ◽  
Author(s):  
K. Tatsumi ◽  
M. Mikami ◽  
T. Kuriyama ◽  
Y. Fukuda
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Blood Gases ◽  
Male Rats ◽  
Co2 Production ◽  
Male Rat ◽  
O2 Consumption ◽  
Estradiol Treatment ◽  
Respiratory Stimulation ◽  
Ventilatory Response To Co2

The respiratory effect of progestin differs among various animal species and humans. The rat does not hyperventilate in response to exogenous progestin. The present study was conducted to determine whether administration of combined progestin and estrogen prompts ventilatory stimulation in the male rat. Ventilation, blood gases, and metabolic rates (O2 consumption and CO2 production) were measured in the awake and unrestrained male Wistar rat. The combined administration of a synthetic potent progestin (TZP4238) and estradiol for 5 days significantly increased tidal volume and minute expiratory ventilation (VE), reduced arterial PCO2, and enhanced the ventilatory response to CO2 inhalation (delta VE/delta PCO2). On the other hand, respiratory frequency, O2 consumption, CO2 production, and body temperature were not affected. The arterial pH increased slightly, with a concomitant decrease in plasma [HCO3-]. Administration of either TZP4238 or estradiol alone or vehicle (Tween 80) had no effect on respiration, blood gases, and ventilatory response to CO2. The results indicated that respiratory stimulation following combined progestin plus estradiol treatment in the male rat involves activation of process(es) that regulate tidal volume and its augmentation during CO2 stimulus.

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