Secondary Logo

Journal Logo

The Effect of Ventilator Performance on Airway Pressure Release Ventilation

A Model Lung Study

Yoshida, Takeshi, MD; Uchiyama, Akinori, MD, PhD; Mashimo, Takashi, MD, PhD; Fujino, Yuji, MD, PhD

doi: 10.1213/ANE.0b013e31821d72d0
Technology, Computing, and Simulation: Research Reports
Free
SDC

BACKGROUND: Using a model lung connected to six different ventilators, with each ventilator in the airway pressure release ventilation mode, we measured differences in intrinsic positive end-expiratory pressure (PEEPi) during the expiratory phase and calculated the inspiratory and expiratory pressure time product (PTP) as an index of work of breathing during the inspiratory phase.

METHODS: We compared 6 ventilators: Puritan–Bennett 840, Evita XL, Servo i, Avea, Hamilton G5, and Engström. With a constant inspiratory pressure level of 25 cm H2O and expiratory pressure level of 0 cm H2O, PEEPi was measured as the expiratory time was decremented from 1.0 second to 0.2 second in steps of 0.1 second. The inspiratory and expiratory PTPs were measured during the ventilator’s inspiratory phase by simulating spontaneous breathing with a tidal volume of 300 mL, with a respiratory rate of 30 breaths/min and with expiratory flow rates of 0.5 L/s, 1.0 L/s, and 1.5 L/s.

RESULTS: In all ventilators, the progressive diminution of the expiratory time caused a significant increase in PEEPi (P< 0.001). With a 0.2-second expiratory time, PEEPi ranged from 9.4± 0.07 cm H2O for the Servo i to 15.7± 0.04 cm H2O for the Avea. The Servo i had a significantly lower inspiratory PTP than did the other ventilators (P< 0.001). When the expiratory flow rate was 0.5 L/s and 1.0 L/s, the expiratory PTP was lower with the Servo i and Evita XL than with the other ventilators (P< 0.001).

CONCLUSIONS: PEEPi varied significantly among ventilators. Inspiratory and expiratory work of breathing varied between ventilators when spontaneous breathing occurred during the ventilator’s inspiratory phase.

Published ahead of print April 25, 2011

From the Department of Anesthesiology and Intensive Care Medicine, Osaka University Graduate School of Medicine, Suita, Japan.

Funding: None.

The authors declare no conflicts of interest.

Reprints will not be available from the authors.

Address correspondence Takeshi Yoshida, MD, Department of Anesthesiology and Intensive Care Medicine, Osaka University Graduate School of Medicine, 2-15 Yamadaoka, Suita, Osaka, Japan 565-0871. Address e-mail to doctor@mvj.biglobe.ne.jp.

Accepted March 23, 2011

Published ahead of print April 25, 2011

Airway pressure release ventilation (APRV) enables long inspiration with a continuous positive airway pressure phase and brief expiration with an intermittent pressure release phase.1,2Unrestricted spontaneous breathing can occur during any phase of the ventilatory cycle.13 Accordingly, APRV has been shown to improve gas exchange46 and decrease atelectasis79 in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). However, several problems with APRV have to be resolved before its application can become a standard for all patients with ALI/ARDS.1

According to previous papers,1,2,10 a brief expiratory time is set to ensure intrinsic positive end-expiratory airway pressure (PEEPi) and avoid derecruitment by terminating the expiratory phase when the expiratory flow decreases to 50%–75% of the peak expiratory flow rate (PEFR). Because the characteristics of the exhalation valve are different for each type of ventilator, the relationship between expiratory time and PEEPi would be different for each ventilator. Furthermore, actual values for PEEPi are unknown when the expiratory phase is terminated at 50%–75% of PEFR. The work of breathing (WOB) associated with spontaneous breathing could be different for each ventilator. Therefore we connected a model lung to each APRV ventilator and measured PEEPi and pressure time product (PTP) as an index of WOB during spontaneous breathing.

Back to Top | Article Outline

METHODS

Model Lung and Experimental Setup

A Puritan–Bennett™840 ventilator (Nellcor Puritan Bennett, Carlsbad, CA) was used to ventilate the drive chamber of a double-chamber TTL model lung (Michigan Instruments, Grand Rapids, MI) (Fig. 1).11 Each APRV ventilator was sequentially connected to the test chamber of the TTL model lung. The 2 chambers were connected to each other to simulate spontaneous breathing during APRV. The alveolar pressure (Palv) transducer inside the test chamber measured PEEPi. Flow was measured with a pneumotachometer (model 4700; Hans–Rudolph Inc, Kansas City, MO) placed at the proximal end of the endotracheal tube (ETT). Pressure in the test chamber of the model lung (Palv) and at the proximal end of the ETT (Paw) was measured using a differential pressure transducer (model TP603T; Nihon Kohden, Tokyo, Japan). Pressure signals and flow were sampled at a rate of 100 Hz with 12-bit resolution. WINDAQ software (Dataq Instruments Inc., Akron, OH) computed flow, Paw, and Palv.

Figure 1

Figure 1

To measure a simulated patient’s expiratory PTP during the ventilator’s inspiratory phase, we generated spontaneous expiratory flow using a 2-L syringe driven by a stepping motor (Oriental Motor Co., Tokyo, Japan) (Fig. 2).12 The syringe was attached to the expiratory limb of the ventilator’s breathing circuit through a one-way valve. During the high inspiratory pressure phase, the syringe “exhales” gas into the APRV ventilator.

Figure 2

Figure 2

We evaluated 6 APRV ventilators in this study: Puritan–Bennett (PB) 840 (Nellcor Puritan Bennett, Carlsbad, CA); Evita XL (Dräger Medical AG & Co., Lübeck, Germany); Servo i (Maquet, Bridgewater, NJ); Avea (Cardinal/Viasys Healthcare, Yorba Linda, CA); Hamilton G5 (Hamilton Medical AG, Rhäzüns, Switzerland); and Engström Carestation (GE Healthcare, Helsinki, Finland).

The APRV ventilators were connected to the test chamber via an 8-mm internal diameter endotracheal tube (ETT) and a standard ventilator circuit (RT105, Fisher & Paykel Healthcare, Auckland, New Zealand) without a humidifier. The APRV ventilators were set as follows: high inspiratory pressure level 25 cm H2O, expiratory pressure level 0 cm H2O; inspiratory time 4.5 seconds, expiratory time 0.5 second. The imposition of pressure support above inspiratory phase was not used and Fio 2was 0.21. Apart from the Evita XL, which does not allow trigger setting, inspiratory triggering sensitivity was set at –2 cm H2O. To measure a simulated patient’s inspiratory PTP during the ventilator’s inspiratory phase, the PB 840 ventilator was set in a volume-controlled mode: quasisinusoidal flow pattern; inspiratory:expiratory time ratio 0.3; PEEP 25 cm H2O; tidal volume 300 mL; and respiratory rate 30 breaths/min.

PEEPi and percentage of PEFR termination were measured as the expiratory time was decremented from 1.0 second to 0.2 second in steps of 0.1 second, and in parallel, inspiratory time was incremented from 4.0 seconds to 4.8 seconds in steps of 0.1 second. Because the Engström can be set with a minimum expiratory time of 0.25 second and allows inspiratory time steps of 0.25 second, it was tested with the following settings: inspiratory time/expiratory time 4.0/1.0, 4.0/0.9, 4.25/0.8, 4.25/0.7, 4.5/0.6, 4.5/0.5, 4.5/0.4, 4.75/0.3, and 4.75/0.25.

The expiratory flow from the 2-L syringe was set at 0.5, 1.0, and 1.5 L/s and held for 1.0 second. The PTP for 3 simulated breaths was calculated at each flow rate.

Compliance of the model lung was set at 0.02 L/cm H2O by adjusting springs on the bellows (settings were checked with a calibration syringe and calibrated manometer). The resistance of the model lung was imposed with a parabolic airway resistor (5 cm H2O/L/s, Pneuflo resistor Rp5; MI Instruments). An additional model 4700 pneumotachometer was placed between the one-way valve and the expiratory limb, and a model TP603T pressure transducer was moved to the same location to evaluate added expiratory PTP during the inspiratory phase, owing to the insertion of a one-way valve to regulate expiratory flow from a syringe to the APRV ventilators, to measure expiratory flow and Paw.

Back to Top | Article Outline

Data Analysis

We defined PEEPi as Palvat the end of the expiratory phase. Figure 3 is a sample waveform showing PEEPi when the expiratory phase was terminated at 50% of PEFR. The PTP, as an index of WOB, is the area between Palvand the pressure during the inspiratory phase.13 As Figure 3 shows, we calculated the inspiratory and expiratory PTP.14

Figure 3

Figure 3

Back to Top | Article Outline

Statistical Analysis

Statistical analyses were performed using SPSS 16.0J for windows (SPSS, Chicago, IL). Results are expressed as mean± SD. Differences among the 6 ventilators under identical test conditions and within-group differences were evaluated with one-way analysis of variance (ANOVA). Post hoc analysis was performed with Tukey’s pairwise multiple comparison test. All statistical tests were two-tailed, with P< 0.01 indicating statistical significance.

Back to Top | Article Outline

RESULTS

PEEPi

Table 1 shows PEEPi and percentage of PEFR termination for each expiratory time. The progressive diminution of expiratory time caused PEEPi and percentage of PEFR termination to increase (P< 0.001).When the expiratory phase was terminated at 50%–75% of PEFR, PEEPi ranged from 6 to 13 cm H2O. To keep PEEPi above 10 cm H2O, it was necessary to terminate the expiratory phase at >70% of PEFR (Table 1). Small changes in the PEFR termination result in large changes in PEEPi.

Table 1

Table 1

Back to Top | Article Outline

Inspiratory and Expiratory Work of Breathing

Table 2 shows inspiratory PTP was lowest with Servo i and highest with Hamilton G5 and Avea (P< 0.001), which had values almost twice those of the other ventilators. Although there were no statistically significant differences in expiratory PTP among ventilators at an expiratory flow of 1.5 L/s, expiratory PTP was lower with expiratory flows of 0.5 L/s and 1.0 L/s with the Servo i and Evita XL (P< 0.001) (Table 3).

Table 2

Table 2

Table 3

Table 3

Back to Top | Article Outline

DISCUSSION

Three main findings have emerged from this study. First, even when ventilators had the same expiratory time, PEEPi varied among different makes of ventilator. Second, when the expiratory phase was terminated at 50%–75% of PEFR, PEEPi was generated at between 6 and 13 cm H2O. Third, inspiratory and expiratory WOB during the inspiratory phase also varied depending on the ventilator.

Our findings show that both the expiratory time setting and the type of ventilator could greatly affect PEEPi. In this study, with all other features being the same, including lung compliance and use of the same flow circuits, the different level of PEEPi in each ventilator was most likely mainly due to the characteristics of the exhalation valve used in the ventilator.15

In previous clinical studies of patients with ALI/ARDS,7,16 PEEP of more than approximately 10 cm H2O is often applied. Our results, however, show that it was necessary to terminate the expiratory phase at >70% of PEFR to ensure PEEPi of >10 cm H2O, which suggests a very restricted range for PEFR termination to ensure substantial PEEPi and prevent derecruitment. Moreover, small changes in PEFR termination can cause large changes in PEEPi, for instance, changes of 15% in PEFR termination caused changes of 4 cm H2O in PEEPi. This makes it difficult to deliver a specific PEEPi by setting the PEFR termination percentage. Intensivists need to recognize the potential risks hidden in a routine setting of expiratory time, the variability of PEEPi, which is greatly affected by small changes in PEFR termination, and interventilator differences.

Even though spontaneous breathing of 10% to 70% of total minute ventilation was preserved during APRV,46,8,9,17 we should not lose sight of the fact that the primary goal of partial ventilatory support is to reduce WOB.18 According to previous studies,13,14,19,20 the triggering operation and support function are important to reduce the inspiratory WOB. On the other hand, to reduce the expiratory WOB, APRV ventilators have a servocontrolled active exhalation valve that floats at the target pressure (high inspiratory pressure phase) and thus, through partial opening of the exhalation valve, avoids pressure increase, even if patients exhale or cough during the inspiratory phase.21 We surmise that the interventilator differences in inspiratory and expiratory WOB observed in this study were mainly due to these different functions. It is important to note that the lowest inspiratory and expiratory WOBs were always observed in Servo i. Accordingly, Servo i had the lowest resistance of the exhalation valve and the best performance to reduce inspiratory and expiratory WOB.

Our study had several limitations. First, although we tried to set our ventilators as similarly as possible to those commonly used in clinical practice, this was an in vitro study using a model lung, and our observations should not be considered directly applicable to patients. Second, because not all of the APRV ventilators provided automatic tube compensation (ATC) functions, we did not investigate the effect of ATC on WOB. It is important to note that previous studies13,19,20 concluded that commercially available ATC systems did not adequately compensate for WOB. Third, we did not evaluate the detailed working of exhalation valve and the detailed mechanism to reduce WOB. In future studies, therefore, we should evaluate the mechanism to explain this interventilator variation.

In conclusion, our results demonstrate that the different strengths and weaknesses of currently available APRV ventilators affect PEEPi during the expiratory phase and WOB during the inspiratory phase. We hope that our results might help intensivists make more informed decisions about appropriate ventilatory settings for APRV for individual ARDS patients.

Back to Top | Article Outline

DISCLOSURES

Name: Takeshi Yoshida, MD.

Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.

Attestation: Takeshi Yoshida has seen the original study data, reviewed the analysis of the data, approved the final manuscript, and is the author responsible for archiving the study files.

Name: Akinori Uchiyama, MD, PhD.

Contribution: This author helped design the study and analyze the data.

Attestation: Akinori Uchiyama has seen the original study data, reviewed the analysis of the data, and approved the final manuscript.

Name: Takashi Mashimo, MD, PhD.

Contribution: This author helped design the study, analyze the data, and write the manuscript.

Attestation: Takashi Mashimo has seen the original study data, reviewed the analysis of the data, and approved the final manuscript.

Name: Yuji Fujino, MD, PhD.

Contribution: This author helped design the study, and analyze the data.

Attestation: Yuji Fujino has seen the original study data, reviewed the analysis of the data, and approved the final manuscript.

Back to Top | Article Outline

REFERENCES

1. Myers TR, MacIntyre NR. Respiratory controversies in the critical care setting. Does airway pressure release ventilation offer important new advantages in mechanical ventilator support? Respir Care 2007; 52: 452–8
2. Habashi NM. Other approaches to open-lung ventilation: airway pressure release ventilation. Crit Care Med 2005; 33 (suppl 3): 228s–40s
3. Putensen C, Muders T, Varelmann D, Wrigge H. The impact of spontaneous breathing during mechanical ventilation. Curr Opin Crit Care 2006; 12: 13–8
4. Putensen C, Mutz NJ, Putensen-Himmer G, Zinserling J.Spontaneous breathing during ventilatory support improves ventilation–perfusion distributions in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 159: 1241–8
5. Putensen C, Zech S, Wrigge H, Zinserling J, Stuber F, Von Spiegel T, Mutz N. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med 2001; 164: 43–9
6. Varelmann D, Muders T, Zinserling J, Guenther U, Magnusson A, Hedenstierna G, Putensen C, Wrigge H. Cardiorespiratory effects of spontaneous breathing in two different models of experimental lung injury: a randomized controlled trial. Crit Care 2008; 12: R135
7. Yoshida T, Rinka H, Kaji A, Yoshimoto A, Arimoto H, Miyaichi T, Kan M. The impact of spontaneous ventilation on distribution of lung aeration in patients with acute respiratory distress syndrome: airway pressure release ventilation versus pressure support ventilation. Anesth Analg 2009; 109: 1892–900
8. Wrigge H, Zinserling J, Neumann P, Defosse J, Magusson A, Putensen C, Hedenstierna G. Spontaneous breathing improves lung aeration in oleic acid-induced lung injury. Anesthesiology 2003; 99: 376–84
9. Neumann P, Wrigge H, Zinserling J, Hinz J, Maripuu E, Andersson LG, Putensen C, Hedenstierna G. Spontaneous breathing affects the spatial ventilation and perfusion distribution during mechanical ventilatory support. Crit Care Med 2005; 33: 1090–5
10. Neumann P, Golisch W, Strohmeyer A, Buscher H, Burchardi H, Sydow M. Influence of different release times on spontaneous breathing pattern during airway pressure release ventilation. Intensive Care Med 2002; 28: 1742–9
11. Chatmongkolchart S, Schettino GP, Dillman C, Kacmarek RM, Hess DR. In vitro evaluation of aerosol bronchodilator delivery during noninvasive positive pressure ventilation: effect of ventilator settings and nebulizer position. Crit Care Med 2002; 30: 2515–9
12. Uchiyama A, Nishimura M, Amata M, Mashimo T, Fujino Y. A new expiratory support system for resolving air trapping in lungs during mechanical ventilation: a lung model study. Technol Health Care 2007; 15: 213–20
13. Fujino Y, Uchiyama A, Mashimo T, Nishimura M. Spontaneously breathing lung model comparison of work of breathing between automatic tube compensation and pressure support. Respir Care 2003; 48: 38–45
14. Bunburaphong T, Imanaka H, Nishimura M, Hess D, Kacmarek RM. Performance characteristics of bilevel pressure ventilators: a lung model study. Chest 1997; 111: 1050–60
15. Guttmann J, Eberhard L, Fabry B, Bertschmann W, Zeravik J, Adolph M, Eckart J, Wolff G. Time constant/volume relationship of passive expiration in mechanically ventilated ARDS patients. Eur Respir J 1995; 8: 114–20
16. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301–8
17. Neumann P, Hedenstierna G. Ventilatory support by continuous positive airway pressure breathing improves gas exchange as compared with partial ventilatory support with airway pressure release ventilation. Anesth Analg 2001; 92: 950–8
18. Putensen C, Hering R, Wrigge H. Controlled versus assisted mechanical ventilation. Curr Opin Crit Care 2002; 8: 51–7
19. Elsasser S, Guttmann J, Stocker R, Mols G, Priebe HJ, Haberthür C. Accuracy of automatic tube compensation in new-generation mechanical ventilators. Crit Care Med 2003; 31: 2619–26
20. Maeda Y, Fujino Y, Uchiyama A, Taenaka N, Mashimo T, Nishimura M. Does the tube-compensation function of two modern mechanical ventilators provide effective work of breathing relief? Crit Care 2003; 7: R92–7
21. Jiao GY, Newhart JW. Bench study on active exhalation valve performance. Respir Care 2008; 53: 1697–702
© 2011 International Anesthesia Research Society