Measurement of Pressure–Time Product during Spontaneous Assisted Breathing by Rapid Interrupter Technique

2007 ◽  
Vol 106 (3) ◽  
pp. 484-490 ◽  
Author(s):  
Giacomo Bellani ◽  
Nicolò Patroniti ◽  
Dieter Weismann ◽  
Lucia Galbiati ◽  
Francesco Curto ◽  
...  

Background Measuring the work of breathing of patients undergoing spontaneous assisted ventilation can be useful to monitor and titrate ventilatory support. The aim of this study was to obtain measurements of the pressure generated by the respiratory muscles (PMUSC) and the derived pressure-time product (PTP; a good indicator of the metabolic work of breathing), performing the rapid interrupter technique with a commercial ventilator. Methods A Draeger Evita 4 ventilator (Draeger Medical, Lubeck, Germany) was controlled by a personal computer to rapidly interrupt the airway flow at different times and volumes of the respiratory cycle during pressure-support ventilation. From the airway pressure tracing after the occlusion, the authors estimated the alveolar pressure and PMUSC; the integration of PMUSC values over the inspiratory time yields the measurement of PTP. Esophageal pressure measurements were used as a reference. After a bench study of the valves' performance, the authors performed 11 measurement sequences in eight patients. Results The closure times for the inspiratory and expiratory valves were 74 +/- 10 and 61 +/- 13 ms, respectively. The interrupter technique provided a reliable estimate of PMUSC (PMUSC, occl = 1.00 . PMUSC, pes + 0.19; r = 0.88; 95% confidence interval for agreement, +5.49/-5.32 cm H2O). PTPoccl tightly correlated with PTPpes (PTPoccl = 0.95 . PTPpes + 0.13; r = 0.96; 95% confidence interval, 1.94/-1.61 cm H2O . s). Conclusion The rapid interrupter technique can be performed by means of a commercial ventilator, providing reliable measurement of PMUSC and PTP.

1996 ◽  
Vol 81 (1) ◽  
pp. 426-436 ◽  
Author(s):  
V. M. Ranieri ◽  
R. Giuliani ◽  
L. Mascia ◽  
S. Grasso ◽  
V. Petruzzelli ◽  
...  

The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.


1996 ◽  
Vol 22 (S1) ◽  
pp. S120-S120
Author(s):  
D. Chiumello ◽  
P. Pelosi ◽  
M. Croci ◽  
L. Gattinoni

1998 ◽  
Vol 5 (6) ◽  
pp. 485-490 ◽  
Author(s):  
Robert J Smyth

Asthma continues to pose a significant medical problem in terms of both morbidity and mortality. A number of patients with a severe exacerbation of asthma fail medical therapy and require urgent intubation and mechanical ventilation. New modalities of ventilatory support, including noninvasive ventilation, have been shown to provide effective ventilation even in the presence of severe bronchoconstriction. An intrinsically high level of auto positive end-expiratory pressure in these patients requires a precise balance between respiratory frequency, tidal volume and inspiratory flow rates. Pressure support ventilation reduces the risk of barotrauma and lowers the work of breathing in these patients. Adjuvant therapy with inhaled anesthetics and bronchoalveolar lavage may also be indicated in patients requiring high pressures to achieve adequate ventilation.


Author(s):  
Antonella LoMauro ◽  
Andrea Aliverti ◽  
Gaetano Perchiazzi ◽  
Peter Frykholm

Phrenic nerve damage may occur as a complication of specific surgical procedures, prolonged mechanical ventilation, or physical trauma. The consequent diaphragmatic paralysis or dysfunction can lead to major complications. To elucidate the role of the non-diaphragmatic respiratory muscles during partial or complete diaphragm paralysis induced by unilateral and bilateral phrenic nerve damage at different levels of ventilatory pressure support in an animal model. Ten pigs were instrumented, the phrenic nerve exposed from the neck and spontaneous respiration preserved at three levels of pressure support: high, low and null at baseline condition, after left phrenic nerve damage and bilateral phrenic nerve damage. Breathing pattern, thoraco-abdominal volumes and asynchrony and pressures were measured at each condition. Physiological breathing was predominantly diaphragmatic, homogeneously distributed between right and left sides. After unilateral damage, the paralyzed hemidiaphragm was passively dragged by the ipsilateral ribcage muscles and the contralateral hemidiaphragm. After bilateral damage, the drive to and the work of breathing of ribcage and abdominal muscles increased, to compensate for diaphragmatic paralysis, ensuing paradoxical thoraco-abdominal breathing. Increasing level of pressure support ventilation replaces this muscle group compensation. When the diaphragm is paralyzed (unilaterally and/or bilaterally), there is a coordinated reorganization of non-diaphragmatic respiratory muscles as compensation that might be obscured by high level of pressure support ventilation. Non-invasive thoraco-abdominal volume and asynchrony assessment could be useful in phrenic nerve injured patients to estimate the extent and type of inspiratory muscle dysfunction.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Robert G. T. Blokpoel ◽  
Alette A. Koopman ◽  
Jefta van Dijk ◽  
Martin C. J. Kneyber

Abstract Background Patient–ventilator asynchrony is associated with increased morbidity and mortality. A direct causative relationship between Patient–ventilator asynchrony and adverse clinical outcome have yet to be demonstrated. It is hypothesized that during trigger errors excessive pleural pressure swings are generated, contributing to increased work-of-breathing and self-inflicted lung injury. The objective of this study was to determine the additional work-of-breathing and pleural pressure swings caused by trigger errors in mechanically ventilated children. Methods Prospective observational study in a tertiary paediatric intensive care unit in an university hospital. Patients ventilated > 24 h and < 18 years old were studied. Patients underwent a 5-min recording of the ventilator flow–time, pressure–time and oesophageal pressure–time scalar. Pressure–time–product calculations were made as a proxy for work-of-breathing. Oesophageal pressure swings, as a surrogate for pleural pressure swings, during trigger errors were determined. Results Nine-hundred-and-fifty-nine trigger errors in 28 patients were identified. The additional work-of-breathing caused by trigger errors showed great variability among patients. The more asynchronous breaths were present the higher the work-of-breathing of these breaths. A higher spontaneous breath rate led to a lower amount of trigger errors. Patient–ventilator asynchrony was not associated with prolonged duration of mechanical ventilation or paediatric intensive care stay. Conclusions The additional work-of-breathing caused by trigger errors in ventilated children can take up to 30–40% of the total work-of-breathing. Trigger errors were less common in patients breathing spontaneously and those able to generate higher pressure–time–product and pressure swings. Trial registration Not applicable.


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