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.

The Ventilatory Response to CO2 after Administration of Frusemide in Normal Man

1972 ◽  
Vol 43 (1) ◽  
pp. 47-54 ◽  
Author(s):  
H. W. Iff ◽  
D. C. Flenley
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Oxygen Balance ◽  
Co2 Response ◽  
Small Shift ◽  
Normal Man ◽  
Slight Rise ◽  
End Tidal ◽  
The Right ◽  
Ventilatory Response To Co2

1. We have determined the ventilatory response to CO2 inhaled in 30% oxygen (balance nitrogen) in eight normal subjects (1) before and during 4 days of 80 mg of oral frusemide daily and (2) within 55–75 min of 80 mg of frusemide orally. 2. Over 4 days the drug decreased serum potassium concentrations, but increased end tidal (and arterial) Pco2 and serum bicarbonate, thus inducing a mild metabolic alkalosis with an appropriate but small shift in CO2 response to the right without a significant change in the slope of the response. The CO2 response was unaltered by oral frusemide 55–75 min earlier. 3. This slight rise in Pco2 during 4 days of frusemide therapy contrasts with the absence of rise in Pco2 after treatment with thiazide diuretics, as reported by others. 4. We discuss possible implications of these results for the selection of an appropriate diuretic in patients with CO2 retention at various phases of their illness.

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 Bendrofluazide and Frusemide on the Ventilatory Response to Carbon Dioxide and Hypoxia in Normal Man

1974 ◽  
Vol 47 (4) ◽  
pp. 377-385 ◽  
Author(s):  
A. G. Leitch ◽  
L. Clancy ◽  
D. C. Flenley
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Co2 Response ◽  
Acute Exacerbations ◽  
Before And After ◽  
Ventilatory Failure ◽  
End Tidal ◽  
Response Line ◽  
The Right ◽  
End Tidal Co2

1. We have determined the ventilatory response to CO2 at two levels of end-tidal O2 tension in eight normal subjects before and after (1) 4 days of 0.242 mmol (80 mg) oral frusemide daily and (2) 4 days of 0.024 mmol (10 mg) bendrofluazide daily. 2. Frusemide produced no significant alkalosis, change in end-tidal CO2 tension or alteration in the CO2 response line. However, we did demonstrate a linear relationship between the change in plasma total CO2 content and the change in intercept of the CO2 response line in hyperoxia after frusemide. 3. Bendrofluazide produced a metabolic alkalosis with no significant change in end-tidal CO2 tension. The CO2 response line after the drug showed a decrease in slope in hyperoxia and a shift to the right of the intercept in hypoxia. There was no relationship between change in plasma total CO2 content and change in the intercept of the CO2 response line in hyperoxia. 4. If these results obtained on normal subjects are applicable to patients with chronic bronchitis and emphysema, frusemide might be the diuretic of choice for use with controlled oxygen therapy in the management of acute exacerbations of this disease when it is complicated by ventilatory failure.

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.

Pattern of breathing and ventilatory response to CO2 in subjects practicing hatha-yoga

1981 ◽  
Vol 51 (6) ◽  
pp. 1625-1629 ◽  
Author(s):  
D. C. Stanescu ◽  
B. Nemery ◽  
C. Veriter ◽  
C. Marechal
Keyword(s):  
Tidal Volume ◽  
Vital Capacity ◽  
Matched Control ◽  
Ventilatory Response ◽  
Hatha Yoga ◽  
Control Group ◽  
Control Subjects ◽  
Yoga Group ◽  
End Tidal ◽  
Ventilatory Response To Co2

WE studied eight Belgian subjects well advanced in the practice of hatha-yoga and compared them with eight sex-, age-, and height-matched control subjects. Practice of yoga (range 4–12 yr) involves control of posture and manipulation of breathing, including slow near-vital capacity maneuvers accompanied by apnea at end inspiration and end expiration. Average values for the yoga and the control group (in parentheses) are as follows: ventilation (VE) 5.53 1 X min-1 (7.07); tidal volume (VT), 1.03 liters (0.56); rate of breathing, 5.5 min-1 (13.4); end-tidal PCO2, 39.0 Torr (35.3). All differences are significant (P less than 0.05). Ventilatory response to CO2 (rebreathing technique) was significantly lower in the yoga group (P less than 0.01). The regression relating VE to VT during rebreathing of CO2 was VE = 8.1 (VT - 0.23) for the yoga group and VE = 15.8 (VT - 0.16) for the control group (P less than 0.005). We attribute these changes to chronic manipulation of respiration.

Adenosine infusion and periodic breathing during sleep

1992 ◽  
Vol 72 (3) ◽  
pp. 1004-1009 ◽  
Author(s):  
K. Gleeson ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Correlation Coefficients ◽  
Periodic Breathing ◽  
Normal Subjects ◽  
Adenosine Infusion ◽  
Amplitude Maximum ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

Intravenously administered adenosine may increase ventilation (VI) and the ventilatory response to CO2 (HCVR). Inasmuch as we have previously hypothesized that those with higher HCVR may be more prone to periodic breathing during sleep, we measured VI and HCVR and monitored ventilatory pattern in seven healthy subjects before and during an infusion of adenosine (80 micrograms.kg-1.min-1) during uninterrupted sleep. Adenosine increased the mean sleeping VI (7.6 +/- 0.4 vs. 6.5 +/- 0.4 l/min, P less than 0.05) and decreased mean end-tidal CO2 values (42.4 +/- 1.2 vs. 43.7 +/- 1.0 Torr, P = 0.06, paired t test) during stable breathing. In six of seven subjects, periodic breathing occurred during this infusion. The amplitude (maximum VI--mean VI) and period length of this periodic breathing was variable among subjects and not predicted by baseline HCVR [correlation coefficients (r) = 0.64, P = 0.17 and r = -0.1, P = 0.9, respectively]. Attempts to measure HCVR during adenosine infusion were unsuccessful because of frequent arousals and continued periodic breathing despite hyperoxic hypercapnia. We conclude that adenosine infusion increases VI and produces periodic breathing during sleep in most normal subjects studied.

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.

scholarly journals Lung elastic recoil during breathing at increased lung volume

1999 ◽  
Vol 87 (4) ◽  
pp. 1491-1495 ◽  
Author(s):  
Joseph R. Rodarte ◽  
Gassan Noredin ◽  
Charles Miller ◽  
Vito Brusasco ◽  
Riccardo Pellegrino ◽  
...  
Keyword(s):  
Stress Relaxation ◽  
Tidal Volume ◽  
Lung Volume ◽  
Normal Subjects ◽  
Dynamic Hyperinflation ◽  
Airway Closure ◽  
Elastic Recoil ◽  
Volume Increase ◽  
Before And After ◽  
Residual Capacity

During dynamic hyperinflation with induced bronchoconstriction, there is a reduction in lung elastic recoil at constant lung volume (R. Pellegrino, O. Wilson, G. Jenouri, and J. R. Rodarte. J. Appl. Physiol. 81: 964–975, 1996). In the present study, lung elastic recoil at control end inspiration was measured in normal subjects in a volume displacement plethysmograph before and after voluntary increases in mean lung volume, which were achieved by one tidal volume increase in functional residual capacity (FRC) with constant tidal volume and by doubling tidal volume with constant FRC. Lung elastic recoil at control end inspiration was significantly decreased by ∼10% within four breaths of increasing FRC. When tidal volume was doubled, the decrease in computed lung recoil at control end inspiration was not significant. Because voluntary increases of lung volume should not produce airway closure, we conclude that stress relaxation was responsible for the decrease in lung recoil.

Control of breathing at the start of exercise as influenced by posture

1983 ◽  
Vol 55 (5) ◽  
pp. 1460-1466 ◽  
Author(s):  
D. Weiler-Ravell ◽  
D. M. Cooper ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Stroke Volume ◽  
Phase I ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Co2 Output ◽  
End Tidal ◽  
Response To Exercise ◽  
Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effort sensation, chemoresponsiveness, and breathing pattern during inspiratory resistive loading

1992 ◽  
Vol 73 (2) ◽  
pp. 440-445 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. Calverley
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Sustained Load ◽  
Resistive Loading ◽  
End Tidal ◽  
Few Data ◽  
Normal Men

Although inspiratory resistive loading (IRL) reduces the ventilatory response to CO2 (VE/PCO2) and increases the sensation of inspiratory effort (IES), there are few data about the converse situation: whether CO2 responsiveness influences sustained load compensation and whether awareness of respiratory effort modifies this behavior. We studied 12 normal men during CO2 rebreathing while free breathing and with a 10-cmH2O.l-1.s IRL and compared these data with 5 min of resting breathing with and without the IRL. Breathing pattern, end-tidal PCO2, IES, and mouth occlusion pressure (P0.1) were recorded. Free-breathing VE/PCO2 was inversely related to an index of effort perception (IES/VE; r = -0.63, P less than 0.05), and the reduction in VE/PCO2 produced by IRL was related to the initial free-breathing VE/PCO2 (r = 0.87, P less than 0.01). IRL produced variable increases in inspiratory duration (TI), IES, and P0.1 at rest, and the change in tidal volume correlated with both VE/PCO2 (r = 0.63, P less than 0.05) and IES/VE (r = -0.69, P less than 0.05), this latter index also predicting the changes in TI with loading (r = -0.83, P less than 0.01). These data suggest that in normal subjects perception of inspiratory effort can modify free-breathing CO2 responsiveness and is as important as CO2 sensitivity in determining the response to short-term resistive loading. Individuals with good perception choose a small-tidal volume and short-TI breathing pattern during loading, possibly to minimize the discomfort of breathing.

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