Respiratory heat exchange in normal subjects and in patients with pulmonary disease.

1969 ◽  
Vol 26 (1) ◽  
pp. 82-88 ◽  
Author(s):  
P R Caldwell ◽  
D M Gomez ◽  
H W Fritts
1979 ◽  
Vol 46 (3) ◽  
pp. 467-475 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
R. H. Strauss ◽  
J. J. Jaeger

We have hypothesized that it is the total heat flux in the tracheobronchial tree during exercise that determines the degree of postexertional obstruction in asthma, and have developed quanititative expressions that relate these two events. We tested this hypothesis by comparing the observed responses to exercise, while our subjects inhaled dry air at various temperatures ranging from subzero to 80 degrees C in a random fashion, to those that we predicted would occur based upon calculations of respiratory heat exchange. We further determined if heat could be transferred from the inspired air to the mucosa so as to offset evaporative losses from the airways. The observed responses fell as air temperature was increased from -11 to +37 degrees C and exactly matched theoretical predictions. Above 37 degrees C, the observed response exceeded predictions, indicating that it was not possible to provide sufficient heat per se in the air to offset the vaporization of water. However, when small amounts of water vapor were added to the inspirate at high temperatures, bronchospasm was virtually abolished and the response again closely matched theoretical expectations. We conclude that the magnitude of exercise-induced asthma is directly proportional to the thermal load placed on the airways and that this reaction is quantifiable in terms of respiratory heat exchange.


CHEST Journal ◽  
1984 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
W.C. Hodgson ◽  
D.J. Cotton ◽  
G.D. Werner ◽  
D.W. Cockcroft ◽  
J. A Dosman

1985 ◽  
Vol 58 (5) ◽  
pp. 1469-1476 ◽  
Author(s):  
D. Laporta ◽  
A. Grassino

Maximal force developed by the diaphragm at functional residual capacity is a useful index to establish muscle weakness; however, great disparity in its reproducibility can be observed among reports in the literature. We evaluated five maneuvers to measure maximal transdiaphragmatic pressure (Pdimax) in order to establish best reproducibility and value. Thirty-five naive subjects, including 10 normal subjects (group 1), 12 patients with chronic obstructive pulmonary disease (group 2), and 13 patients with restrictive pulmonary disease (group 3), were studied. Each subject performed five separate maneuvers in random order that were repeated until reproducible values were obtained. The maneuvers were Mueller with (A) and without mouthpiece (B), abdominal expulsive effort with open glottis (C), two-step (maneuver C combined with Mueller effort) (D), and feedback [two-step with visual feedback of pleural (Ppl) and abdominal (Pab) pressure] (E). The greatest reproducible Pdimax values were obtained with maneuver E (P less than 0.01) (group 1: 180 +/- 14 cmH2O). The second best maneuvers were A, B, and D (group 1: 154 +/- 25 cmH2O). Maneuver C produced the lowest values. For all maneuvers, group 1 produced higher values than groups 2 and 3 (P less than 0.001), which were similar. The Ppl to Pdi ratio was 0.6 in maneuvers A and B, 0.4 in D and E, and 0.2 in C. We conclude that visual feedback of Ppl and Pab helped the subjects to elicit maximal diaphragmatic effort in a reproducible fashion. It is likely that the great variability of values in Pdimax previously reported are the result of inadequate techniques.


1984 ◽  
Vol 57 (2) ◽  
pp. 608-609 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
J. J. Jaeger

1964 ◽  
Vol 19 (2) ◽  
pp. 233-235 ◽  
Author(s):  
M. Henry Williams ◽  
Cecile Kane

When normal subjects listened to simulated breath sounds while breathing at their natural respiratory frequency there was a significant decrease of alveolar Pco2. The alveolar Pco2 did not fall further when these subjects listened to the simulator and breathed slowly, but when they breathed with the simulator at a very rapid frequency there was further fall of the PaCOCO2. When patients with chronic obstructive pulmonary disease listened to simulated breath sounds while breathing at their natural respiratory frequency there was a decrease of arterial Pco2 which fell further when the subjects breathed with the simulator at a slow respiratory rate. breathing, effect of auditory stimuli on; breathing rate and pulmonary function on chronic obstructive pulmonary disease; alveolar ventilation and auditory respiratory stimuli; respiratory frequency and ventilation Submitted on July 12, 1963


Thorax ◽  
1996 ◽  
Vol 51 (5) ◽  
pp. 516-519 ◽  
Author(s):  
T. Q. Howes ◽  
S. E. Keilty ◽  
V. L. Maskrey ◽  
C. R. Deane ◽  
S. V. Baudouin ◽  
...  

1983 ◽  
Vol 55 (1) ◽  
pp. 8-15 ◽  
Author(s):  
F. Bellemare ◽  
A. Grassino

The fatigue threshold of the human diaphragm in normal subjects corresponds to a transdiaphragmatic pressure (Pdi)-inspiratory time integral (TTdi) of about 15% of Pdimax. The TTdi of resting ventilation was measured in 20 patients with chronic obstructive pulmonary disease (COPD) and ranged between 1 and 12% of Pdimax (mean 5%). TTdi was significantly related to total airway resistance (Raw) (r = 0.57; P less than 0.05). Five of these patients were asked to voluntarily modify their TI/TT (ratio of inspiratory time to total cycle duration; from 0.33 to 0.49) so as to increase their TTdi from a control value of 8% to an imposed value of 17% of Pdimax. The imposed pattern induced a progressive decline in the high-frequency (150-350 Hz)/low-frequency (20-40 Hz) power ratio (H/L) of the diaphragm electromyogram (fatigue pattern), quantitatively similar to that seen in normal subjects breathing with similar TTdi levels. The decay in H/L was followed by a progressive fall in mean Pdi meanly due to decrease in gastric pressure swings. It is concluded that 1) the force reserve of the diaphragm in COPD patients is decreased because of a decrease in Pdimax; 2) the remaining force reserve of the diaphragm can be exhausted by even minor modifications in the breathing pattern; and 3) at a TI/TT of 0.40 our COPD patients can increase their mean Pdi 3-fold before reaching a fatiguing pattern of breathing compared with 8-fold in normal subjects.


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