Document Detail

Central contribution to hypoventilation during severe inspiratory resistive loads.
MedLine Citation:
PMID:  8252898     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Recent observations suggest that central hypoventilation with slowing of respiratory frequency contributes to hypoventilation during severe inspiratory resistive loads. We carried out a study to further characterize this bradypneic response. DESIGN: Prospective, controlled laboratory study. SETTING: Basic science laboratory of a university hospital. SUBJECTS: Anesthetized adult cats (loading experiment n = 7, nonloaded hypercapnic controls n = 11). INTERVENTIONS: Experimental inspiratory loads increased transdiaphragmatic pressure to 75% of the maximum for each animal. Respiratory responses were observed at midrun or moderate conditions of respiratory insufficiency (defined as PaCO2 > or = 60 torr [> or = 8.0 kPa]) and failure (PaCO2 > or = 80 torr [> or = 10.6 kPa]). Nonloaded hypercapnic controls were studied with similar durations of exposure to CO2 in the same CO2 range. MEASUREMENTS: Inspiratory airflow, tidal volume, respiratory frequency, airway pressure, transdiaphragmatic pressure, transdiaphragmatic pressure response to phrenic nerve electrical stimulation, blood gas analysis. Severe inspiratory loads were applied to anesthetized adult cats to determine whether bradypnea could be observed in an anesthesized model that eliminated conscious responses. Experiments were performed in hyperoxic conditions to determine whether bradypnea develops in the absence of hypoxia. An additional control group was studied under hypercapnic conditions without loading to determine whether comparable hypercapnia is a sufficient stimulus to elicit bradypnea. RESULTS: From midrun until failure, minute ventilation decreased by 16% in loaded animals. Hypoventilation was associated with a decrease in respiratory frequency from 40.1 to 29.9 breaths/min, whereas tidal volume, spontaneous transdiaphragmatic pressure, and transdiaphragmatic pressure response to phrenic nerve electrical stimulation remained unchanged. Control animals had no significant reduction in ventilation or respiratory frequency over similar levels and durations of hypercapnia. CONCLUSIONS: Centrally mediated bradypnea contributed to hypoventilation in respiratory failure associated with inspiratory loading. Bradypnea preceded evidence of muscle fatigue. This change in respiratory cycle timing occurred under anesthesia, and thus, did not depend on conscious perception of dyspnea. Bradypnea does not depend on either hypercapnia or hypoxia.
R K Kanter; W E Fordyce
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Critical care medicine     Volume:  21     ISSN:  0090-3493     ISO Abbreviation:  Crit. Care Med.     Publication Date:  1993 Dec 
Date Detail:
Created Date:  1994-01-07     Completed Date:  1994-01-07     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1915-22     Citation Subset:  AIM; IM    
Department of Pediatrics, State University of New York Health Science Center, Syracuse 13210.
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MeSH Terms
Airway Resistance*
Anoxia / blood,  complications*,  physiopathology
Blood Gas Analysis
Carbon Dioxide / blood
Disease Models, Animal
Electric Stimulation
Hypercapnia / blood,  complications*,  physiopathology
Hypoventilation / blood,  etiology*,  physiopathology
Phrenic Nerve
Respiratory Insufficiency / blood,  etiology*,  physiopathology
Respiratory Mechanics*
Respiratory Muscles / innervation,  physiopathology
Work of Breathing*
Reg. No./Substance:
124-38-9/Carbon Dioxide
Comment In:
Crit Care Med. 1995 Jan;23(1):213-4   [PMID:  8001378 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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