Human ventilatory response to CO2 after 8 h of isocapnic or poikilocapnic hypoxia

1998 ◽  
Vol 85 (5) ◽  
pp. 1922-1928 ◽  
Author(s):  
Marzieh Fatemian ◽  
Peter A. Robbins
Keyword(s):  
Healthy Volunteers ◽  
Ventilatory Response ◽  
Analysis Of Covariance ◽  
Pairwise Comparisons ◽  
Air Breathing ◽  
Before And After ◽  
End Tidal ◽  
The Relationship ◽  
Ventilatory Response To Co2

During ventilatory acclimatization to hypoxia (VAH), the relationship between ventilation (V˙e) and end-tidal[Formula: see text]([Formula: see text]) changes. This study was designed to determine 1) whether these changes can be seen early in VAH and 2) if these changes are present, whether the responses differ between isocapnic and poikilocapnic exposures. Ten healthy volunteers were studied by using three 8-h exposures: 1) isocapnic hypoxia (IH), end-tidal [Formula: see text]([Formula: see text]) = 55 Torr and[Formula: see text] held at the subject’s normal prehypoxic value; 2) poikilocapnic hypoxia (PH),[Formula: see text] = 55 Torr; and 3) control (C), air breathing. TheV˙e-[Formula: see text]relationship was determined in hyperoxia ([Formula: see text] = 200 Torr) before and after the exposures. We found a significant increase in the slopes ofV˙e-[Formula: see text]relationship after both hypoxic exposures compared with control (IH vs. C, P < 0.01; PH vs. C, P < 0.001; analysis of covariance with pairwise comparisons). This increase was not significantly different between protocols IH and PH. No significant changes in the intercept were detected. We conclude that 8 h of hypoxia, whether isocapnic or poikilocapnic, increases the sensitivity of the hyperoxic chemoreflex 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.

Effect of posture on the ventilatory response to CO2

1982 ◽  
Vol 53 (3) ◽  
pp. 761-765 ◽  
Author(s):  
C. Weissman ◽  
B. Abraham ◽  
J. Askanazi ◽  
J. Milic-Emili ◽  
A. I. Hyman ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Sitting Position ◽  
Breathing Patterns ◽  
Arterial Pco2 ◽  
Air Breathing ◽  
Supine Posture ◽  
The Relationship ◽  
Ventilatory Response To Co2

The effect of sitting and supine posture on breathing patterns and gas exchange during room air breathing and administration of 2 and 4% CO2 was studied in nine normal subjects using a noninvasive canopy system. During air breathing minute ventilation (VE) was 21% (P less than 0.005) higher in the sitting position. Tidal volume (VT) and mean inspiratory flow (VT/TI) were also greater in the sitting position. With the administration of 4% CO2, VE was 13.9 and 20.0 1/min in the supine and seated position, respectively. The relationship between VE and VT was the same in both cases. For any given level of VE, VT/TI was higher in the seated position. No difference in response to CO2 as measured by delta VE/delta PaCO2 and (delta VT/TI)/delta PaCO2 was observed. However, arterial PCO2 was lower both in the resting and stimulated states when sitting.

Effects of CO2 breathing on ventilatory response to sustained hypoxia in normal adults

1989 ◽  
Vol 66 (3) ◽  
pp. 1071-1078 ◽  
Author(s):  
D. Georgopoulos ◽  
D. Berezanski ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Inhibitory Effect ◽  
Hypoxic Exposure ◽  
Initial Increase ◽  
Co2 Levels ◽  
End Tidal ◽  
The Relationship ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Co2

The relationship between CO2 and ventilatory response to sustained hypoxia was examined in nine normal young adults. At three different levels of end-tidal partial pressure of CO2 (PETCO2, approximately 35, 41.8, and 44.3 Torr), isocapnic hypoxia was induced for 25 min and after 7 min of breathing 21% O2, isocapnic hypoxia was reinduced for 5 min. Regardless of PETCO2 levels, the ventilatory response to sustained hypoxia was biphasic, characterized by an initial increase (acute hypoxic response, AHR), followed by a decline (hypoxic depression). The biphasic response pattern was due to alteration in tidal volume, which at all CO2 levels decreased significantly (P less than 0.05), without a significant change in breathing frequency. The magnitude of the hypoxic depression, independent of CO2, correlated significantly (r = 0.78, P less than 0.001) with the AHR, but not with the ventilatory response to CO2. The decline of minute ventilation was not significantly affected by PETCO2 [averaged 2.3 +/- 0.6, 3.8 +/- 1.3, and 4.5 +/- 2.2 (SE) 1/min for PETCO2 35, 41.8, and 44.3 Torr, respectively]. This decay was significant for PETCO2 35 and 41.8 Torr but not for 44.3 Torr. The second exposure to hypoxia failed to elicit the same AHR as the first exposure; at all CO2 levels the AHR was significantly greater (P less than 0.05) during the first hypoxic exposure than during the second. We conclude that hypoxia exhibits a long-lasting inhibitory effect on ventilation that is independent of CO2, at least in the range of PETCO2 studied, but is related to hypoxic ventilatory sensitivity.

Effect of sustained hypoxia on ventilatory response to CO2 in normal adults

1990 ◽  
Vol 68 (3) ◽  
pp. 891-896 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Initial Increase ◽  
Similar Amount ◽  
Base Line ◽  
Similar Time ◽  
Air Breathing ◽  
Before And After ◽  
Sustained Hypoxia ◽  
Normal Adults ◽  
Ventilatory Response To Co2

In adult humans the ventilatory response to sustained hypoxia is biphasic, characterized by an early increase followed by a decline to an intermediate plateau. Recently, we have shown that this decrease in hypoxic sensitivity is long lasting, because up to 1 h of room air breathing is required for complete recovery of the initial hypoxic response (J. Appl. Physiol. 64: 521-528, 1988). It is not known whether this posthypoxia decrease in ventilatory response is general or specific only to hypoxic stimuli. We therefore examined responses to CO2 before and after hypoxia. The ventilatory response to 5 min of normoxic CO2 breathing was evaluated in eight normal adults on 2 days: 5 min before and after 25 min of normocapnic hypoxia (arterial O2 saturation +/- 80%) and 5 min before and after 25 min of room air breathing (control day). During hypoxia, ventilation (VI), after an initial increase, declined significantly. At the end of hypoxia, abrupt exposure to room air transiently dropped VI to values that were significantly below base line. On each experimental day, the first and second exposure to CO2 increased ventilation by a similar amount, averaging, respectively, 8.46 +/- 0.9 and 8.84 +/- 0.92 (SE) l/min on the hypoxic day and 8.24 +/- 0.96 and 7.65 +/- 0.94 l/min on the control day. All the hypercapnic increases of VI were accomplished through similar changes of breathing pattern with similar time courses. We conclude that sustained hypoxia does not affect the ventilatory response to CO2, but it selectively depresses hypoxic sensitivity.

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.

Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

1988 ◽  
Vol 65 (3) ◽  
pp. 1383-1388 ◽  
Author(s):  
J. I. Schaeffer ◽  
G. G. Haddad
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
The Relationship ◽  
Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

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.

The Effect of Upper Abdominal Surgery on the Relationship of Airway Closing Point to End Tidal Position

1972 ◽  
Vol 43 (2) ◽  
pp. 137-141 ◽  
Author(s):  
J. I. Alexander ◽  
P. W. Horton ◽  
W. T. Millar ◽  
R. K. Parikh ◽  
A. A. Spence
Keyword(s):  
Abdominal Surgery ◽  
Significant Negative Correlation ◽  
Contributory Factor ◽  
Upper Abdominal Surgery ◽  
Before And After ◽  
End Tidal ◽  
Upper Abdominal ◽  
Relationship Of ◽  
The Relationship ◽  
Arterial Po2

1. The relationship between end tidal position (ETP) and the point of lung emptying at which there is significant airways closure (CP) has been investigated before and after upper abdominal surgery in thirty-one patients. 2. A significant negative correlation between the index (ETP-CP) and the alveolar-arterial Po2 difference (A-ado2) was found. 3. Nineteen of these patients had a vagotomy and drainage operation and, in this group, there was a greater fall in ETP than in CP in the first and second postoperative days. 4. It is suggested that airway closure is a contributory factor to the known hypoxaemia following abdominal surgery.

Increased chemoreceptor output and ventilatory response to sustained hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1157-1163 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Peripheral Chemoreceptor ◽  
Depressant Action ◽  
Before And After ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3–5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmentation of ventilatory response to asphyxia by prochlorperazine in humans

1982 ◽  
Vol 53 (3) ◽  
pp. 637-643 ◽  
Author(s):  
L. G. Olson ◽  
M. J. Hensley ◽  
N. A. Saunders
Keyword(s):  
Ventilatory Response ◽  
Blocking Agent ◽  
Control Value ◽  
Before And After ◽  
Venous Pco2 ◽  
Hypercapnic Hypoxia ◽  
Dopamine Hydrochloride ◽  
Response Line ◽  
Arterial O2 Saturation ◽  
Ventilatory Response To Co2

The effect of the dopamine-receptor blocking agent prochlorperazine on the ventilatory response to hypercapnic hypoxia was studied in six healthy adults. Repeated episodes of transient hypoxia were induced at the mixed venous PCO2 level by a nonrebreathing technique in five males and one female before and after an intravenous bolus injection of prochlorperazine mesylate (12.5 mg = 10 mg base). The ventilatory response to CO2 was also studied before and after drug administration. Prochlorperazine produced a modest (15%) increase in resting ventilation (P less than 0.05) but a marked increase in the ventilatory response to asphyxia such that the group mean response was double the control value [2.0 +/- 0.7 vs. 4.2 +/- 1.5 l . min-1 . % arterial O2 saturation (%SaO2); P less than 0.001]. Two-thirds of this change in ventilatory response was due to an increase in frequency response to hypoxia (0.34 +/- 0.20 vs. 0.81 +/- 0.52 breaths . min-1 . %SaO2; P less than 0.001). The position of the ventilatory response line, as judged by the computed ventilation at 95% SaO2, was increased by prochlorperazine (22.2 +/- 9.6 vs. 35.9 +/- 10.9 l . min-1; P less than 0.01) due to an increase in both tidal volume (P less than 0.05) and frequency of breathing (P less than 0.0125). The ventilatory response to CO2 was unchanged by drug injection. In separate experiments prochlorperazine was shown to 1) increase the ventilatory response to steady-state eucapnic hypoxia (P less than 0.01) demonstrating that the drug effect was not dependent on either the presence of hypercapnia or rapidly changing states of arterial oxygenation; and 2) reverse the depressant effect of intravenously infused dopamine hydrochloride (5 micrograms . kg-1 . min-1) on the ventilatory response to transient asphyxia (P less than 0.01). We conclude that prochlorperazine augments hypoxic responsiveness in humans. The mechanism may be blockade of dopaminergic receptors that modulate carotid body discharge.

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