Airway Occlusion Pressure As an Estimate of Respiratory Drive and Inspiratory Effort during Assisted Ventilation

Changes in length of costal and crural segments of the canine diaphragm were measured by sonomicrometry within the first 100–300 ms of inspiration during CO2 rebreathing in anesthetized animals. Both segments showed small but significant decreases in end-expiratory length during progressive hypercapnia. Although both costal and crural segments showed electromyographic activity within the first 100 ms of inspiration, in early inspiration crural shortening predominated with minimal costal shortening. Neither segment contracted isometrically early in inspiration in the presence of airway occlusion. The amount of crural shortening during airway occlusion exceeded costal shortening; both segments showed increased shortening with prolonged occlusion and increasing CO2. Costal and crural shortening at 100 ms was not different for unoccluded and occluded states. These observations suggest that neural control patterns evoke discrete and unequal contributions from the diaphragmatic segments at the beginning of an inspiration; the crural segment may be predominately recruited in early inspiration. Despite traditional assumptions about occlusion pressure measurement (P0.1), diaphragm segments do not contract isometrically during early inspiratory effort against an occluded airway.

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Effect of chest wall distortion on occlusion pressure and the preterm diaphragm

Journal of Applied Physiology ◽

10.1152/jappl.1983.55.2.359 ◽

1983 ◽

Vol 55 (2) ◽

pp. 359-364 ◽

Cited By ~ 20

Author(s):

P. N. LeSouef ◽

J. M. Lopes ◽

S. J. England ◽

M. H. Bryan ◽

A. C. Bryan

Keyword(s):

Chest Wall ◽

Preterm Infants ◽

Face Mask ◽

Respiratory Drive ◽

Occlusion Pressure ◽

Transdiaphragmatic Pressure ◽

Airway Occlusion ◽

Mouth Pressure ◽

Gastric Pressure ◽

Mouth Occlusion Pressure

We studied the effect of chest wall distortion (CWD) on transdiaphragmatic pressure (Pdi) and/or mouth pressure during end-expiratory airway occlusions in seven preterm infants. We measured mouth occlusion pressure (Pmo) with a face mask and pressure transducer, gastric pressure (Pga) with a fluid-filled catheter, diaphragmatic electromyogram (Edi) using surface electrodes, and rib cage and abdominal motion using magnetometers. We reasoned that Pdi = Pmo - Pga on airway occlusion. Periods with maximal and periods with minimal CWD were compared. We found that 1) when CWD was minimal, an increase in Edi produced an increase in Pmo and Pdi in all infants; when CWD was greatest, large increases in Edi produced no increase in Pmo or Pdi in four infants; 2) when breaths with the same Pmo or Pdi from each period in each infant were compared, those from the period with greatest CWD had an increased Edi (mean increase 76%, P less than 0.005, and 144%, P less than 0.01, for Pmo and Pdi, respectively). We conclude that in preterm infants, Pmo can be a poor indicator of respiratory drive, and CWD markedly limits the effectiveness of the diaphragm as a force generator.

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Relationship between inspiratory drive and perceived inspiratory effort in normal man

Clinical Science ◽

10.1042/cs0780493 ◽

1990 ◽

Vol 78 (5) ◽

pp. 493-496 ◽

Cited By ~ 4

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.

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