Response to external inspiratory resistive loading and bronchospasm in anesthetized dogs

1982 ◽  
Vol 53 (2) ◽  
pp. 355-360 ◽  
Author(s):  
J. Savoy ◽  
M. E. Arnup ◽  
N. R. Anthonisen
Keyword(s):  
Breathing Pattern ◽  
External Loading ◽  
Vagal Activity ◽  
Occlusion Pressure ◽  
Ventilatory Drive ◽  
Resistive Loading ◽  
Lung Resistance ◽  
Anesthetized Dogs ◽  
Mouth Occlusion Pressure ◽  
Pentobarbital Sodium Anesthesia

Mouth occlusion pressure (P0.1) and breathing-pattern responses to external inspiratory resistive loading and methacholine chloride-induced bronchospasm were assessed in six dogs under pentobarbital sodium anesthesia. There was no change in P0.1 with external loading, but, in response to bronchospasm, we observed a P0.1 increase proportional to the change in lung resistance. These results indicate that, unlike external loading, the ventilatory-drive adaptation to bronchospasm does not require consciousness of the animal. The breathing-pattern response to bronchospasm consisted of tachypnea associated with decreased tidal volume (VT), decreased inspiratory duration (TI), and unchanged mean inspiratory flow (VT/TI). In response to resistive loading there was no tachypnea, VT decreased, TI was unchanged, and VT/TI decreased. We suggest that in response to resistive loading there was no modification of vagal activity, whereas in bronchospasm there was an increase of vagal activity, which was responsible for the changes in breathing pattern and, at least in part, for the changes in P0.1.

Relationship between inspiratory drive and perceived inspiratory effort in normal man

1990 ◽  
Vol 78 (5) ◽  
pp. 493-496 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Ventilatory Response ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Resistive Loading ◽  
Mouth Occlusion Pressure ◽  
The Individual ◽  
Induced Changes

1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.

Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern

1984 ◽  
Vol 56 (4) ◽  
pp. 1027-1031 ◽  
Author(s):  
N. K. Burki
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Progressive Increase ◽  
Acute Exposure ◽  
Respiratory Pattern ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Ventilatory Pattern ◽  
Ventilatory Drive ◽  
Mouth Occlusion Pressure

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.

Ventilatory Pattern and Drive after Acute Myocardial Infarction

1980 ◽  
Vol 59 (2) ◽  
pp. 115-121 ◽  
Author(s):  
H. Clarke ◽  
S. Dhingra ◽  
N. R. Anthonisen
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Occlusion Pressure ◽  
Breathing Cycle ◽  
Left Heart Failure ◽  
Ventilatory Drive

1. In 18 patients with acute myocardial infarction, we measured ventilation, frequency, inspiratory duration and the pressure at the mouth 0.1 s after the onset of inspiration against an occluded airway; mean inspiratory flow and the fraction of the breathing cycle devoted to inspiration were calculated. Measurements were made on 2–3 consecutive days soon after admission and repeated 4–10 days after admission. 2. Eight patients showed no clinical evidence of left heart failure at any time; in these patients no changes in breathing pattern, ventilation or occlusion pressure were observed. 3. Ten patients were in heart failure, as judged by the presence of râles and/or hypoxaemia on day 1 of the study, and all had recovered on the last day. When in failure these patients demonstrated increased minute ventilation, occlusion pressure was increased more than was mean inspiratory flow and their breathing pattern was altered. Tidal volume was similar to that in patients without failure and did not change with time, but frequency was initially high and fell as recovery from failure occurred. The duration of inspiration was decreased during failure, so mean inspiratory flow was increased. The fraction of the breathing cycle devoted to inspiration was constant and similar to that in patients without failure. 4. While in failure no patients were acidotic and not all patients were hypoxaemic; administration of oxygen did not influence results in two patients during failure. 5. These results indicate that clinically detectable pulmonary oedema is associated with increased ventilatory drive, which cannot be explained on the basis of hypoxaemia or hypercapnia. The observed changes in breathing pattern were probably due at least in part to vagal reflexes, and these may have contributed to the increase in drive.

scholarly journals Effect of expiratory resistive loading on the noninvasive tension-time index in COPD

2000 ◽  
Vol 89 (5) ◽  
pp. 2007-2014 ◽  
Author(s):  
William H. Thompson ◽  
Paula Carvalho ◽  
James P. Souza ◽  
Nirmal B. Charan
Keyword(s):  
Normal Subjects ◽  
Respiratory Cycle ◽  
Inspiratory Pressure ◽  
Occlusion Pressure ◽  
Time Index ◽  
Inspiratory Muscles ◽  
Copd Patients ◽  
Resistive Loading ◽  
Tension Time ◽  
Mouth Occlusion Pressure

Expiratory resistive loading (ERL) is used by chronic obstructive pulmonary disease (COPD) patients to improve respiratory function. We, therefore, used a noninvasive tension-time index of the inspiratory muscles (TTmus =P̄i/Pi max × Ti/Tt, where P̄i is mean inspiratory pressure estimated from the mouth occlusion pressure, Pi max is maximal inspiratory pressure, Ti is inspiratory time, and Tt is total respiratory cycle time) to better define the effect of ERL on COPD patients. To accomplish this, we measured airway pressures, mouth occlusion pressure, respiratory cycle flow rates, and functional residual capacity (FRC) in 14 COPD patients and 10 normal subjects with and without the application of ERL. TTmus was then calculated and found to drop in both COPD and normal subjects ( P < 0.05). The decline in TTmus in both groups resulted solely from a prolongation of expiratory time with ERL ( P < 0.001 for COPD, P < 0.05 for normal subjects). In contrast to the COPD patients, normal subjects had an elevation in P̄i and FRC, thus minimizing the decline in TTmus. In conclusion, ERL reduces the potential for inspiratory muscle fatigue in COPD by reducing Ti/Tt without affecting FRC andP̄i.

Effects of bronchoconstriction and external resistive loading on the sensation of dyspnea

1991 ◽  
Vol 71 (6) ◽  
pp. 2183-2190 ◽  
Author(s):  
O. Taguchi ◽  
Y. Kikuchi ◽  
W. Hida ◽  
N. Iwase ◽  
M. Satoh ◽  
...  
Keyword(s):  
Normal Subjects ◽  
Vagal Afferents ◽  
Vagal Activity ◽  
Resistive Load ◽  
Occlusion Pressure ◽  
Analog Scale ◽  
External Resistance ◽  
Resistive Loading ◽  
Afferent Vagal

To determine whether the intensity of dyspnea at a given level of respiratory motor output differs between bronchoconstriction and the presence of an external resistance, we compared the sensation of difficulty in breathing during isocapnic voluntary hyperventilation in six normal subjects. An external resistance of 1.9 cmH2O.1–1.s was applied during both inspiration and expiration. To induce bronchoconstriction, histamine aerosol (5 mg/ml) was inhaled until airway resistance (Raw) increased to a level approximately equal to the subject's control Raw plus the added external resistance. To clarify the role of vagal afferents on the genesis of dyspnea during both forms of obstruction to airflow, the effect of airway anesthesia by lidocaine aerosol inhalation was also examined after histamine and during external resistive loading. The sensation of difficulty in breathing was rated at 30-s intervals on a visual analog scale during isocapnic voluntary hyperpnea, in which the subjects were asked to copy an oscilloscope volume trace obtained previously during progressive hypercapnia. Histamine inhalation significantly increased the intensity of the dyspneic sensation over the equivalent external resistive load at the same levels of ventilation and occlusion pressure during voluntary hyperpnea. Inhaled lidocaine decreased the sensation of dyspnea during bronchoconstriction with no change in Raw, but it did not significantly change the sensation during external resistive loading. These results suggest that afferent vagal activity plays a role in the genesis of dyspnea during bronchoconstriction.

Microcomputer-assisted on-line measurement of breathing pattern and occlusion pressure

1984 ◽  
Vol 56 (1) ◽  
pp. 235-239 ◽  
Author(s):  
F. G. Lind ◽  
A. B. Truve ◽  
B. P. Lindborg
Keyword(s):  
Breathing Pattern ◽  
Low Cost ◽  
Occlusion Pressure ◽  
Flexible System ◽  
Analog Signals ◽  
Occlusion Device ◽  
Mouth Pressure ◽  
Line Measurement ◽  
On Line ◽  
Mouth Occlusion Pressure

A flexible system has been developed for on-line breath-by-breath measurements of variables commonly included in studies of breathing pattern and mouth occlusion pressure (P0.1). The system, utilizing analog signals for mouth pressure and inspiratory flow as inputs, includes a breathing pattern monitor and a pneumatically driven occlusion device designed to be compatible with a low-cost microcomputer and analog and/or digital readout instruments. The design of the system permits accurate breathing pattern and P0.1 measurements even at the highest flow and breathing frequency encountered in muscular exercise studies.

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