Setting Tidal Volume scaled on End Expiratory Lung Volume (TiVel): a safety and feasibility study
CCCF ePoster library. Grassi A. 11/12/19; 283430; EP92
Dr. Alice Grassi
Dr. Alice Grassi
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Abstract
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ePoster
Topic: Retrospective or Prospective Cohort Study or Case Series

Grassi, Alice1,2; Manzolini, Dario2;Giovannoni Cecilia2; Meroni Valeria2; Borgo Asia2; Rabboni Francesca2; Foti Giuseppe2,3; Bellani Giacomo2,3
1Department if Anesthesia and Pain Management, University Health Network, Toronto, Canada; 2Department of Medicine and Surgery, University of Milan-Bicocca; 3Department of Anesthesia and Critical Care Medicine, San Gerardo Hospital, ASST Monza, Italy 


INTRODUCTION: Protective ventilation with low Tidal Volume (Vt) improves outcome of acute respiratory distress syndrome (ARDS) patients. A Vt range between 6 to 8ml/kg of ideal body weight (IBW) was shown to improve survival, as compared to higher Vt [1]. However, in ARDS the amount of functional parenchyma, the “baby lung”, is reduced proportionally to the severity of disease [2]. In these patients the strain applied to the lung can be determined as Vt/EELV (End Expiratory Lung Volume, which is the volume of 'open' lung, so the volume of the alveoli exposed to ventilation) [3]. An increased strain is associated with a pro-inflammatory response [4]. Measuring EELV may allow to set protective Vt in order to maintain strain below a safety threshold [5].
 
OBJECTIVE: To determine the safety and feasibility of setting Vt=0,25*EELV in ARDS patients and maintain it for 24 hours.
 
METHODS: ARDS patients defined according to Berlin criteria [6], intubated and mechanically ventilated for less than 96 hours were enrolled. Exclusion criteria were conditions that did not allow to measure EELV (i.e. air leaks, extracorporeal membrane oxygenation) by the “oxygen wash-in wash-out technique” (GE Carescape R860 ventilator). Vt was set as 0.25*(measured EELV–PEEP related strain), up to a safety threshold of 8ml/kg IBW. Target Vt was set and kept for 24h unless one of the following events occurred: need to increase the RR>35 bpm to achieve the target pH, desaturation requiring an FiO2 change >20%, development of a plateau pressure>30cmH2O, necessity of administer neuromuscular blocking agents if not already administered. Data regarding hemodynamic and respiratory mechanics were collected at baseline, at the moment of Vt setting (T0) and then every 4 hours until the end of the study protocol (T24, 24 hours after enrolment). Primary end point was the safety and feasibility to maintain the target Vt for 24hours. As a secondary endpoint, the correlation between driving pressure (DP) and lung strain was investigated. Therefore at the time of enrolment (T0) we also measured DP at different levels of lung strain (increasing Vt/EELV). 
 
RESULTS: We enrolled fifteen mild to moderate ARDS patients (mean P/F at baseline 196,5 ±51,5). The target Vt was maintained for 24h in 8 out of 15 patients (53%), maintaining pH into a safe range and RR below 30 (Fig.1; red dots indicate the patients who dropped from the study). The main reason for drop out (3 out of 7 patients) was improvement of clinical conditions and switch to Pressure Support Ventilation; in 1 patient, the calculated Vt was higher than 8ml/kg; in 2 out of 7 patients the study was interrupted for safety concerns (need to increase RR above 35 to keep pH into normal range). In the overall population mean set Vt was 345,4 ±122,9ml, not different from baseline Vt (373,5 ±64,2ml), p=0,53. DP decreased from 8,8 ±1,6 at baseline to 8,1 ±1,1 cmH2O after optimized Vt setting (p=0,051, Fig.1). As a secondary result, we found a strict correlation between the strain applied to the lungs (Vt/EELV) and DP (R=0,87, Fig. 2).
 
CONCLUSION: Preliminary results show that targeting a TV set as 0.25*EELV is feasible in 53% of patients enrolled, and safety concerns were present in 20% of the patients. DP decreased after setting of the target Vt. Moreover, in these patients DP is a surrogate measurement of lung strain.


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  1. ARDS 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 May 4;342(18):1301-8
  2. Gattinoni L, Pesenti A. The concept of 'baby lung'. Intensive Care Med. 2005 Jun;31(6):776-84
  3. Chiumello D et al. Lung Stress and Strain during Mechanical Ventilation for Acute Respiratory Distress Syndrome Am J Respir Crit Care Med 2008 Aug 15;178(4):346-55
  4. Bellani G et al. Lung regional metabolic activity and gas volume changes induced by tidal ventilation in patients with acute lung injury. Am J Respir Crit Care Med. 2011 May 1;183(9):1193-9
  5. González-López A et al. Lung strain and biological response in mechanically ventilated patients. Intensive Care Med. 2012 Feb;38(2):240-7
  6. ARDS Definition Task Force, Acute respiratory Distress Syndrome. The Berlin Definition. JAMA. 2012;307(23):2526-2533
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