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An analysis of respiratory drive components during flow-resistive respiratory loading

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Abstract

Inspiratory flow-resistive loading normally causes an additional respiratory drive that limits the resistance-induced decrease in minute ventilation (load compensation). Occlusion pressures (P100) were measured during CO2 rebreathing with and without added inspiratory loads in normal persons and persons with obstructive sleep apnea (OSA). At each point obtained during loaded breathing, the additional drive due to resistive loading was determined by subtracting CO2-dependent drive (estimated from the nonloaded run) from total drive. In normal subjects, the additional drive correlated with each of four different estimates of load magnitude. In OSA subjects, there was no significant increase in drive due to loading and ventilation decreased markedly during loading. The relationships among ventilation rate, load, and drive, with and without load compensation, were analyzed using a 4-quadrant feedback control diagram. The diagram enables the prediction of ventilation rate for any end-tidal CO2 in the loaded and nonloaded cases, and the flow decrement that will occur as a result of added inspiratory resistance.

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Authors and Affiliations

  1. Department of Physiology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, 20814, Bethesda, Maryland

    Peter H. Abbrecht, Krishnan R. Rajagopal & Howard J. Bryant

  2. Department of Internal Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, 20814, Bethesda, Maryland

    Peter H. Abbrecht, Krishnan R. Rajagopal & Howard J. Bryant

  3. Pulmonary Disease and Clinical Investigation Services, Walter Reed Army Medical Center, Washington, DC

    Peter H. Abbrecht, Krishnan R. Rajagopal & Howard J. Bryant

Authors
  1. Peter H. Abbrecht
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  2. Krishnan R. Rajagopal
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  3. Howard J. Bryant
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Abbrecht, P.H., Rajagopal, K.R. & Bryant, H.J. An analysis of respiratory drive components during flow-resistive respiratory loading. Ann Biomed Eng 11, 417–433 (1983). https://doi.org/10.1007/BF02584217

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  • DOI: https://doi.org/10.1007/BF02584217

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