Ventilator-induced Lung Injury (VILI) is the unwanted result of a complex interplay of multiple factors on mechanical ventilation. These factors are directly set on the ventilator by the clinician, such as tidal volume (VT), driving pressure (ΔP), respiratory rate (RR), and positive end-expiratory pressure (PEEP). The core of protective lung strategy is to minimize the volume and pressure (both plateau and driving pressures), and optimize PEEP to prevent volutrauma, atelectrauma, and barotrauma.
The concept of mechanical power (MP) of ventilation is derived from the work of breathing that the patient needs to do to get the inspiratory volume. Work of breathing is the product of ventilation multiplied by the transpulmonary pressure. Similarly, the ventilator delivers the tidal volume using a positive pressure and the energy that is expended is directly related to how large the volume and how much pressure is used. Therefore, we can define mechanical power as the total energy delivered to the lungs by the ventilator over a period of time and is usually expressed as joules per minute (J/min).
Before we dive into the complex formula for the mechanical power, lets understand it with a graphical representation of the equation of power. In the below graph, the upper left green rectangle (∆V × PEEP) represents the energy level needed to be overcome at each tidal volume delivery. The light pink triangle (1/2 × Ers × ∆V) represents the energy expended on the elasticity of the respiratory system. The red parallelogram (F × Raw × ∆V) represents the energy needed for the airway resistance. The lower blue triangle represents the static component of the PEEP but since it is delivered only once (at the start of the PEEP application), it is negligible and was not included in the equation of power.
Therefore, mechanical power includes three components, the resistive component of the airways, the static elastic component, and the dynamic elastic component of both the lungs and chest wall. The energy spent at each component is calculated for each breath using a slow flow PV curve, then these values are added together and multiplied by the respiratory rate. A conversion factor of 0.098 is used to convert from L × cmH2O to Joules/min. As you see, mechanical power includes all the factors contributing to VILI, the respiratory rate, tidal volume, PEEP, and airway pressure, therefore, it is a collection of traditional indicators affecting VILI and when are combined together, they better predict VILI than any single factor. The detailed formula for calculation is:
Power, rs= 0.098 × RR × {ΔV2 × [(0.5 × E,rs + RR × (1+I:E)/60 × I:E×Raw) + ΔV×PEEP]}
where 0.098 is the conversion factor from L × cmH2O to joule, ∆V is the tidal volume (L), Ers is the elastance of the respiratory system, I:E is the inspiratory-to-expiratory time ratio, Raw is the airway resistance and PEEP is the airway pressure at end-expiration.
This complex formula was simplified and validated experimentally by Gattinoni et al [2]. The minute ventilation is multiplied by the peak pressure subtracted from half of the driving pressure:
Power (J/min) = 0.089 X RR X VT X (Ppeak - ∆P/2)
However, this formula still requires the clinician to pause inspiration to calculate the plateau pressure in order to get the driving pressure (∆P =Plateau-PEEP). Giosa et al, tested a more simplified equation of mechanical power for volume-controlled ventilation that does not need any intervention from the clinician and can easily be applied to the ventilator software [1]:
Power (J/min) = (VE X (Ppeak + PEEP + F/6))/20
Several large retrospective studies have looked at the performance of mechanical power in predicting clinical outcome in patients on mechanical ventilation with ARDS. Guerin et al, found that MP is related to survival as there was a hazard ratio increase of 1.03 per unit of power in total of 787 ARDS patients in both the ACURASYS and PROSEVA trials [3]. Serpa Neto et al in a large retrospective study found that even at a low VT and a low ∆P, a high MP was associated with an increase in in-hospital mortality [OR: 1.70; 1.32-2.18] [4].
Similarly, the investigators of the Writing Group for the Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial found that a strategy with recruitment and higher PEEP (thus higher MP) compared with low PEEP increased 28-day all-cause mortality despite similar driving pressure between groups [5].
Zhang et all looked at data from eight randomized controlled trials conducted by the ARDSnet and found that a normalized MP to the predicted body weight was associated with an increase risk of death in moderate and severe ARDS and was a better predictor than the absolute MP [6].
On the other hand, mechanical power should not be taken as a sole determinant of VILI in patients with ARDS. The tidal volume can independently contribute to VILI regardless of the degree of mechanical power.
The value of MP is not well-determined but based the above explanation and studies, it seems crucial to keep MP at the lowest possible value. In the retrospective study by Serpa Neto, there was a consistent increase in the risk of death with MP higher than 17.0 J/min [4]. Therefore, the target would be to keep MP below 17 J/min provided that the PEEP is set appropriately to prevent atelectrauma.
Lets assume that you have patient (70 Kg IBW) who is ventilated with a tidal volume of 360 mL, respiratory rate of 28 beats/min, driving pressure of 15 cm H2O, and peak pressure of 29 at a PEEP of 14 and FiO2 of 60%. All those parameters would be within the acceptable range of protective lung strategy but the calculated MP is around 19 jJ/min putting this patient at risk for VILI. The clinician may opt to decrease his minute ventilation (or PEEP) to lower his MP below 17, provided that oxygenation and ventilation status is acceptable!
Finally, I just want to mention that I myself started to calculate the MP in my practice and I try to minimize it on the ventilator as it is very logical. However, more studies are needed to confirm that the power for the static elastic and for the resistive components should be included in the equation as this has been challenged by some scientists. Also, more clinical studies are needed to confirm its benefit. Please note that the above formulas apply only to volume-controlled mode of ventilation. For pressure-controlled mode of ventilation, please see the the formulas in this image taken from the paper by Giosa at al [1].
REFERENCES
1. Giosa, L., Busana, M., Pasticci, I. et al. Mechanical power at a glance: a simple surrogate for volume-controlled ventilation. ICMx7, 61 (2019). https://doi.org/10.1186/s40635-019-0276-8.
2. Gattinoni L, Tonetti T, Cressoni M, Cadringher P, Herrmann P, Moerer O, Protti A, Gotti M, Chiurazzi C, Carlesso E, Chiumello D, Quintel M (2016) Ventilator-related causes of lung injury: the mechanical power. Intensive Care Med 42:1567–1575.
3. Guérin C, Papazian L, Reignier J, Ayzac L, Loundou A, Forel JM; investigators of the Acurasys and Proseva trials. Effect of driving pressure on mortality in ARDS patients during lung protective mechanical ventilation in two randomized controlled trials. Crit Care. 2016 Nov 29;20(1):384. doi: 10.1186/s13054-016-1556-2. PMID: 27894328; PMCID: PMC5126997.
4. Serpa Neto A, Deliberato RO, Johnson AEW, Bos LD, Amorim P, Pereira SM, Cazati DC, Cordioli RL, Correa TD, Pollard TJ, Schettino GPP, Timenetsky KT, Celi LA, Pelosi P, Gama de Abreu M, Schultz MJ, PROVE Network Investigators. Intensive Care Med. 2018 Nov; 44(11):1914-1922.
5. Writing Group for the Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial (ART) Investigators, Cavalcanti AB, et al. Effect of Lung Recruitment and Titrated Positive End-Expiratory Pressure (PEEP) vs Low PEEP on Mortality in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA. 2017 Oct 10;318(14):1335-1345. doi: 10.1001/jama.2017.14171. PMID: 28973363; PMCID: PMC5710484.
6. Zhang Z, Zheng B, Liu N, Ge H, Hong Y. Mechanical power normalized to predicted body weight as a predictor of mortality in patients with acute respiratory distress syndrome. Intensive Care Med. 2019 Jun;45(6):856-864. doi: 10.1007/s00134-019-05627-9. Epub 2019 May 6. PMID: 31062050.