EFFECTS OF BREATHING ROUTE, TEMPERATURE AND VOLUME OF INSPIRED GAS, AND AIRWAY ANESTHESIA ON THE RESPONSE OF RESPIRATORY OUTPUT TO VARYING INSPIRATORY FLOW

Citation
D. Georgopoulos et al., EFFECTS OF BREATHING ROUTE, TEMPERATURE AND VOLUME OF INSPIRED GAS, AND AIRWAY ANESTHESIA ON THE RESPONSE OF RESPIRATORY OUTPUT TO VARYING INSPIRATORY FLOW, American journal of respiratory and critical care medicine, 153(1), 1996, pp. 168-175
Citations number
34
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
153
Issue
1
Year of publication
1996
Pages
168 - 175
Database
ISI
SICI code
1073-449X(1996)153:1<168:EOBRTA>2.0.ZU;2-V
Abstract
The determinants of the response of the respiratory output to inspirat ory flow rates (Vover dotI) were examined in awake normal subjects. Su bjects were connected to a volume-cycle ventilator in the assist/contr ol mode, and Vover dotI was increased in steps from 30 to 90 L/min and then back to 30 L/min. Vover dotI pattern was square, and all breaths were subject-triggered. In six subjects the effects of breathing rout e (nasal or mouth) and temperature and volume of inspired gas (Protoco l A) and in 8 subjects the effects of airway anesthesia (upper and low er airways; Protocol B) on the response of respiratory output to varyi ng Vover dotI were studied. In Protocol B, in order to calculate muscl e pressure during inspiration (Pmus), respiratory system mechanics wer e measured using the interrupter method at end-inspiration. Independen t of conditions studied, breathing frequency increased significantly a nd end-tidal concentration of CO2 decreased as Vover dotI increased. T he response was graded and reversible and not affected by breathing ro ute, temperature and volume of inspired gas, and airway anesthesia. Wi th and without airway anesthesia (Protocol B), neural inspiratory and expiratory time and neural duty cycle, estimated from Pmus waveform, d ecreased significantly as Vover dotI increased. At all conditions stud ied, the rate of change in airway pressure prior to triggering the ven tilator tended to increase as Vover dotI increased. The changes in tim ing and drive were nearly complete within the first two breaths after transition, with no evidence of adaptation during a given Vover dotI p eriod. We conclude that Vover dotI exerts an excitatory effect on resp iratory output which is independent of breathing route, temperature an d volume of inspirate, and airway anesthesia. The response most likely is neural in origin, mediated through receptors not accessible to ane sthesia, such as those located in the chest wall or below the airway m ucosa.