Is voluntary hyperventilation an effective method of generating subjective anxiety?

2009 ◽  
Author(s):  
Cristina Mae Wood ◽  
A. R. Cano-Vindel
NeuroImage ◽  
2004 ◽  
Vol 22 (1) ◽  
pp. 222-231 ◽  
Author(s):  
Minna J. Mäkiranta ◽  
Jyrki Ruohonen ◽  
Kalervo Suominen ◽  
Eila Sonkajärvi ◽  
Timo Salomäki ◽  
...  

2004 ◽  
Vol 41 (7) ◽  
pp. 745-749 ◽  
Author(s):  
Barry A. Spiering ◽  
Daniel A. Judelson ◽  
Kenneth W. Rundell

1987 ◽  
Vol 73 (3) ◽  
pp. 311-318 ◽  
Author(s):  
S. Freedman ◽  
R. Lane ◽  
A. Guz

1. Six patients with chronic airflow limitation rebreathed CO2. Subsequently they voluntarily copied their stimulated breathing pattern while normocapnia was maintained. On a separate occasion four of these patients performed progressively increasing exercise and later copied these breathing patterns. 2. During all experiments flow, ventilation and pleural pressures were recorded. In addition, breathlessness was measured on a visual analogue scale every 30 s. 3. In these patients voluntary copying of either form of stimulated breathing resulted in diminished breathlessness and in some cases in complete abolition of the sensation, despite similar levels and patterns of ventilation in the two situations. 4. No systematic or consistent differences in the mechanics of breathing between stimulated and voluntarily copied breathing were found. 5. There was no correlation found between breathlessness score and any mechanical variable measured. 6. These results show that despite similarity in mechanics between stimulated and voluntary hyperventilation, the sensation of breathlessness is much diminished during the latter in these patients. This suggests that the sensation of breathlessness is more dependent upon the awareness of central processing than upon input from peripheral mechanoreceptors.


1990 ◽  
Vol 68 (5) ◽  
pp. 2100-2106 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
J. Leitner ◽  
M. D. Altose ◽  
N. S. Cherniack

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)


CHEST Journal ◽  
1996 ◽  
Vol 109 (6) ◽  
pp. 1520-1524 ◽  
Author(s):  
Gregory J. Argyros ◽  
James M. Roach ◽  
Kenneth M. Hurwitz ◽  
Am H. Eliasson ◽  
Yancy Y. Phillips

1959 ◽  
Vol 14 (2) ◽  
pp. 187-190 ◽  
Author(s):  
John F. Murray

The oxygen cost of voluntary hyperventilation was measured using an open circuit technique with three variations, unaided hyperventilation of air, breathing through an increased dead space and adding carbon dioxide to the inspired air. After a given minute volume had been maintained for 10 minutes, the oxygen consumption was the same with the three methods, in spite of marked differences in the respiratory exchange ratio and volume of carbon dioxide produced. The mean oxygen cost for all three methods was 3.2 ml/l. of ventilation. The amount of nonmetabolic oxygen stored during the first minute of hyperventilation was estimated by finding the difference between the oxygen uptake during the 1st minute and the amount utilized when a steady state is reached. It is concluded that the effects of changing oxygen stores are minimal after 10 minutes of hyperventilation and probably after 5 minutes, at a constant minute volume. Note: (With the Technical Assistance of Liana Nebel) Submitted on June 27, 1958


1996 ◽  
Vol 81 (3) ◽  
pp. 1379-1387 ◽  
Author(s):  
K. Chin ◽  
M. Ohi ◽  
M. Fukui ◽  
H. Kita ◽  
T. Tsuboi ◽  
...  

We investigated the effects of an intellectual task on posthyperventilation (PHV) breathing by using a video game. Eight normal subjects were placed in a supine positions. The game task by itself led to increase ventilation compared with the control tasks via an increase in the average inspiratory flow rate (P < 0.01) and the respiratory frequency (P < 0.001). After hypocapnic voluntary hyperventilation (VHV), the task led to a decrease in the 1-min PHV breathing level compared with the control tasks after VHV [after VHV, first 60 s average minute ventilation while watching television and while playing a video game are 5.54 +/- 2.91 (SD) and 2.05 +/- 1.40 l/min, respectively; P < 0.01]. Only one subject showed PHV apnea for at least 10 s during the control protocol, whereas seven of the same eight subjects showed PHV apnea while performing the task. After isocapnic VHV, the task still led to a decrease in PHV breathing compared with the control tasks. However, this decrease was smaller than in the hypocapnic studies and was only significant during the first 15 s of recovery. These results suggest that increased activity in the higher centers of the central nervous system has an inhibitory effect on PHV breathing at a time when the effects of short-term potentiation after VHV, hypocapnia, and perhaps other mechanisms would be expected to be acting on breathing.


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