A New Method for Measurement of Airway Occlusion Pressure

doi:10.1378/chest.98.2.421

Chest

Volume 98, Issue 2, August 1990, Pages 421-427

https://doi.org/10.1378/chest.98.2.421 Get rights and content

Airway occlusion pressure correlates with central respiratory drive. The airway occlusion pressure (P0.1) may be an excellent predictor of the ability of patients with obstructive lung disease to wean from mechanical ventilation. We describe a new method for measuring P0.1 using digitized signals generated from standard respiratory equipment and a computer program to automatically determine P0.1 values. The accuracy of this new method was tested by comparison with standard analog recorder methods using a mechanical lung model, in ventilated patients in an intensive care unit, and in normal volunteers. In all settings, excellent correlation was obtained between P0.1 measurements by the digital Servo and standard analog methods (r = 0.99). This new method permits accurate and automatic determination of P0.1 in ventilated patients using standard respiratory equipment. The rapid response and ease of use of this method should enable evaluation of a number of physiologic variables involved in respiratory control in ventilated and nonventilated patients.

Section snippets

Occlusion Pressure Measurements

Analog Pressure Recording Standard Methods: The standard method for measuring P0.1 employed a ± 10 cm pressure transducer (model MP45-1, Validyne Co, Northridge, CA) with a probe placed in the respiratory tubing at the endotracheal tube connector site. The pressure transducer was connected to a carrier demodulator (model CD19, Validyne Co, Northridge, CA). The demodulator outputs were sent to an X-Y recorder (model 750A, Cardiopulmonary Instruments, Houston, TX). The pressure transducer was

Lung Model Results

The mechanical lung model was used to generate breathing patterns with P0.1 values ranging from 1.5 to 10.5 cm H₂O. Occlusion pressure values obtained by the servo ventilator method at the same lung model flow settings correlated extremely well with those obtained by the standard method (r = 0.99, slope = 1.00, p<0.001) (Fig 2). Using the standard analog measurement methods and proximal airway tubing occlusion, P0.1 values obtained at each pressure level yielded an average variance of 0.067 cm H

DISCUSSION

Airway occlusion pressure appears to correlate well with the ability of patients with lung disease to tolerate weaning from mechanical ventilation.4, 5 The use of P0.1 in ventilated patients has been limited by technical complexity of the measurement procedure. We have developed a new method for measuring P0.1 using standard ventilatory equipment. This method is accurate in a mechanical lung model, in patients receiving ventilatory support in the intensive care unit, and in nonventilated

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Cited by (17)

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1997, Journal of Critical Care
$Purpose$ : To assess the short-term effects of pressure support ventilation in adult respiratory distress syndrome (ARDS), we studied 17 patients with moderate to severe ARDS using mandatory rate ventilation (MRV), a servocontrolled mode of PSV having respiratory rate as the targeted parameter.
$Materials and Methods$ : Based on the duration of ARDS, the patients were divided into two groups: Group 1, early ARDS (duration up to 1 week), 10 patients; Group 2, intermediate ARDS (duration between 1 and 2 weeks). The patients were initially ventilated with assisted mechanical ventilation then with MRV, and finally with controlled mechanical ventilation. After a 20-minute period allowed for stabilization in each mode, ventilatory variables, gas exchange, hemodynamics, and patient's inspiratory effort were evaluated.
$Results$ : During MRV blood gases, airway pressures and hemodynamic variables remained within acceptable limits in all patients. Compared with assisted mechanical ventilation, during MRV, patients of group 1 decreased their Vt and V̇ (from 0.64 ± 0.04 to 0.42 ± 0.03 L/sec) and increased their Ti/Tt (from 0.39 ± 0.03 to 0.52 ± 0.03). f did not change. PAO₂ - PaO₂ and Q̇s/Q̇t decreased (from 306 ± 16 to 269 ± 15 mm Hg, and from 20.2 ± 1.4 to 17.5 ± 1.1, respectively), while PaCO₂ increased (from 44 ± 3 to 50 ± 3 mm Hg). On the contrary, patients of group 2 increased their Vt (from 0.69 ± 0.02 to 0.92 ± 0.09 L), decreased their f (from 22.3 ± 0.5 to 19.3 ± 0.3 b/min), although they did not change their V̇ and Ti/Tt. PAO₂ - PaO₂ and Q̇s/Q̇t remained stable. PaCO₂ diminished (from 39 ± 3 to 34 ± 3 mm Hg). Pressure support level was higher in group 2 than in group 1 (29.4 ± 3.0 v 19.8 ± 2.9 cm H₂O).
$Conclusions$ : We conclude that (1) PSV delivered by MRV may adequately ventilate patients with moderate to severe ARDS, preserving gas exchange and hemodynamics, at least for the short period tested; (2) early and intermediate ARDS respond in a different manner to MRV in terms of breathing pattern, gas exchange, and level of pressure assistance; and (3) patients with early ARDS are those who have an improvement in intrapulmonary oxygenation probably due, at least in part, to alveolar recruitment augmented by active diaphragmatic contraction.
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1993, Chest
We investigated the effects of short-term oxygenation changes upon the neuromuscular respiratory drive (airway occlusion pressure [P0.1]), minute ventilation ${\dot{V}}_{E}$ , and respiratory rate (RR) in 12 acute lung injury patients undergoing pressure support ventilation. We ventilated the patients first at a high level (H1) of oxygenation, then at intermediate (I), at low, and again at the high (H2) level. The H1 and H2 periods showed no differences. In the H1, I, and L periods, PaO₂ was 158 ± 68, 75 ± 12, and 55 ± 6 mm Hg, respectively. Decreasing oxygenation caused very significant increases in ${\dot{V}}_{E}$ , RR, and P0.1. Differences in RR, ${\dot{V}}_{E}$ , and rapid shallow breathing index were significant at step H1 versus I. Changes in P0.1 appeared to be higher when the H1 value was higher than normal. An arterial oxygenation target higher than the generally accepted 60 mm Hg level may decrease both RR and VE.
A method for digitized flow-volume curves and expiratory resistance measurements using standard ventilatory equipment
1992, Journal of Critical Care
Pulmonary resistance may be assessed in ventilated patients by analysis of passive expiratory pressure and flow properties of the respiratory system. Such measurements are generally complex and require specialized equipment. To facilitate expiratory airway mechanics measurements, we have developed a method for automatically recording and analyzing expiratory pressure flow curves in mechanically ventilated patients using standard ventilatory equipment and a personal computer. Simultaneous digital pressure, flow, and volume recordings are obtained with this system during exhalation. These values allow continuous calculation of ventilator circuitry and total system resistance, which could be used for assessing expiratory airway resistance in intubated patients. The accuracy of these methods was tested by comparison to standard analog recorder pressure-flow methods using two lung models as well as by testing in normal volunteers ventilated through a mouthpiece. In all situations (flows, pressures, and volumes) there was excellent correlation between data generated from the automatic digital method and standard analog methods (all r values > .9, slopes 0.9 to 1.02, P < .001, flow bias −0.02 L/min, flow precision 0.08 L/min, volume bias 0.008 L, volume precision 0.027 L). Expiratory resistance (using expiratory time-constant cord methods) also correlated well between automatic digital and standard analog analyses (r = .9, slope 0.98, P < .001). We found that expiratory flow limb resistances (airway, tubing, filters, and valves) were substantial (range, 5.5 to 14.0 cm H₂O/L/s) and are varied throughout the expiratory cycle. Therefore, measurement of expiratory-flow limb resistance is necessary for accurate clinical assessment of pulmonary resistance for any system analyzing expiratory flow mechanics in ventilated patients. We conclude that this simple and convenient method allows automatic and accurate construction of pulmonary expiratory flow properties and may enable measurement of passive expiratory resistance. Rapid and accurate measurements of expiratory lung mechanics may be possible at the bedside of ventilated patients using standard ventilatory equipment with these methods.
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1992, Chest
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Citation Excerpt :
The conventional measurement of P0.1 is based on the analysis of an end-expiratory occlusion maneuver, and hence allows just an intermittent monitoring of P0.1. In mechanically ventilated patients, the occlusion maneuver can be performed easily by manual activation of the end-expiratory occlusion function provided by modern ventilators: when exhalation is finished and the patient attempts to trigger an inspiration, both the inspiratory and expiratory valve of the ventilator fully close, thus generating an occlusion condition.4 On a recording of airway pressure during the occlusion period, we can identify the point of occlusion start and the point corresponding to 100 ms later: P0.1 is the difference in pressure between these two points.16

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: St. Joseph Hospital is a Beta Test Site for Siemens ventilators. There is no payment from Siemens Co. to St. Joseph Hospital or any of the authors as part of the test site arrangement.

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