I - PAV+ Clinical Summary - Georgopoulos Et Al

MEDTRONIC REVIEW:
CLINICAL PAPER
Medtronic provides the following synopsis of a clinical publication involving PAV™*+

software.
TITLE “Driving pressure during assisted mechanical ventilation: Is it controlled by patient brain?”
AUTHORS Georgopoulos D, Xirouchaki N, Tzanakis N, Younes M

JOURNAL Respir Physiol Neurobiol. 2016; 228: 69-75
INTRODUCTION
When patients are ventilated with conventional mechanical ventilation, their lungs are subjected to the degree of stretch (ΔP or VT)
that is set by the caregiver and applied by the ventilator. Conventional mechanical ventilation strategies that employ sedation and
analgesia to diminish respiratory drive (commonly called passive ventilation) and limit tidal volume (VT) delivery according to ideal
body weight are a recognized means of avoiding ventilator-induced lung injury (VILI). However, Amato’s (2015) re-analysis of
individual data from more than 3500 ARDS patients who had been enrolled in previous randomized control studies revealed that for
patients who are ventilated passively, controlling driving pressure [ΔP; static end-inspiratory plateau pressure (Pplat) minus PEEP,
or VT to respiratory system compliance (Crs) ratio] so that VT is normalized to functional lung size rather than to ideal body weight
is more strongly associated with survival than is controlling VT alone. In other words, for these patients, a reduction in VT increases
survival when associated with a decrease in ΔP.
When patients are ventilated with patient-directed, proportional forms of mechanical ventilation (proportional assist ventilation
[PAV™*+] and neurally adjusted ventilatory assist [NAVA]) sedation is limited so that the patient’s respiratory drive remains intact
and neither ΔP or VT are set by the caregiver. Instead, the patient’s intrinsic reflexes and instantaneous muscle activity control
ventilation.
Georgopoulos et al. hypothesized that when patients are allowed to direct spontaneous breathing (as is the case with PAV™*+ and
NAVA), their own feedback mechanisms may naturally act to restrict ΔP but not necessarily restrict VT. In the current study, they
sought to compare the ΔP applied during passive controlled mechanical ventilation (CMV) using the currently accepted lung
protective strategy (The ARDSnet, 2000; Malhotra, 2007) with the ΔP measured when the same patients are ventilated with the
patient-directed, proportional form of mechanical ventilation called PAV™*+.
PURPOSE OF THE STUDY
The authors hypothesized that “the patients’ control of breathing system is adept at protecting the lungs by preventing high ΔP
using appropriate feedback mechanisms, while not unnecessarily restricting tidal volume when this has no protective value”
(Georgopoulos et al., 2016 pg. 70). They sought to determine which variable, VT or ΔP, is controlled by spontaneously breathing,
critically ill patients when ventilated with PAV™*+ rather than with passive CMV.
METHODS
 Re-analyzed data from 108 patients who had been ventilated passively > 36 h with VC or PC CMV then switched to
PAV™*+ (Puritan-BennettTM 840 ventilator) with PEEP and FIO2 values set similarly to those during CMV and PAV™*+
assist settings adjusted using pre-defined written algorithms.
 Averaged the VT, Crs, and ΔP collected during the initial 8-h PAV™*+ period and compared those values to the
corresponding values obtained during CMV within 8-h before switching to PAV™*+.
RESULTS
 During lung protective passive CMV, VT was tightly controlled and as a result ΔP was less than 15 cmH2O in the majority
of the patients.
 When patients were switched to spontaneous breathing with PAV™*+, ΔP (but not VT) was tightly controlled by the
patients.
 During PAV™*+, the average ΔP did not differ from ΔP used during CMV [10.2 cmH2O (8.1–12.4) vs. 10.7 cmH2O (9.0–
12.9), respectively],
 VT and Crs were higher with PAV™*+ than during CMV.
CONCLUSION
The main findings of this study were:
1. When critically ill patients were switched from conventional passive, lung protective mechanical ventilation to PAV™*+
assisted spontaneous ventilation which permits them to direct their own depth of breathing, they controlled their driving
pressure as well as it had been controlled by the passive, lung protective strategy but they did not constrain VT to the
narrow limits used during passive ventilation.
2. The majority of measurements showed that when the lung protective strategy resulted in high driving pressure (ΔP ≥15
cmH2O), switching to PAV™*+ resulted patients spontaneously reducing driving pressure.
3. When switched to PAV™*+, patients were able to increase VT without compromising driving pressure because
respiratory system compliance increased as a result in the change of ventilation mode.
REFERENCES
1. Amato, MBP et al (2015). Driving Pressure and Survival in the Acute Respiratory Distress Syndrome. N Engl J Med 2015;372:747-55.
2. Georgopoulos D, Xirouchaki N, Tzanakis N, Younes M. Driving pressure during assisted mechanical ventilation: Is it controlled by patient
brain? Respir Physiol Neurobiol. 2016 Jul;228:69-75.
3. The Acute Respiratory Distress Syndrome Network, 2000. Ventilation with lower tidal volumes as compared with traditional tidal volumes
for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N. Engl. J. Med.
342, 1301–1308.
4. Malhotra, A., 2007. Low-tidal-volume ventilation in the acute respiratory distress syndrome. N. Engl. J. Med. 357, 1113–1120.
**THIS CONCLUDES THE CLINICAL SYNOPSIS OF THIS PUBLICATION**
© 2016 Medtronic. All rights reserved. Medtronic, Medtronic logo and Further, Together
are trademarks of Medtronic. TM*Proportional Assist and PAV are registered trademarks of
The University of Manitoba, Canada. Used under license. All other brands are trademarks of
a Medtronic company. M/Y 16-VE-0011b

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MEDTRONIC REVIEW:

Medtronic provides the following synopsis of a clinical publication involving PAV™*+

AUTHORS Georgopoulos D, Xirouchaki N, Tzanakis N, Younes M

PURPOSE OF THE STUDY

 VT and Crs were higher with PAV™*+ than during CMV.

The main findings of this study were:

THIS CONCLUDES THE CLINICAL SYNOPSIS OF THIS PUBLICATION

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