Over the last three decades since the introduction of the term ventilator-induced lung injury (VILI), we have recognized that mechanical ventilation can injure the lungs. VILI can be caused by excessive transpulmonary pressure (barotrauma), volume (volutrauma) or cyclic opening and closing of alveoli, particularly around collapsed alveolar units (atelectrauma). Publication of the ARMA trial helped define the pressure and volume threshold at which VILI is triggered, demonstrating that a maximum plateau pressure value of 30 cm H20 and tidal volume of 6 mL/kg predicted body weight is considered safe.¹ More recently, driving pressure has emerged as one of the best predictors of VILI and mortality in mechanical ventilation of patients with acute respiratory distress syndrome (ARDS). Amato et al. studied the relationship between respiratory system compliance (C_RS) and functional lung size. Rather than simply using predicted tidal volume based on ideal body weight, the authors assessed driving pressure to estimate the size of the functional (or baby) lung. Driving pressure can be calculated by subtracting PEEP from the plateau pressure (DP = Pplat – PEEP), or can be expressed as the ratio of tidal volume to respiratory system compliance (DP = V_t/C_RS). The authors found that adjusting PEEP to minimize driving pressure was associated with reduction in mortality.²

Lung protective ventilation has traditionally focused on tidal volume (Vt) and plateau pressure reduction with respiratory rate augmentation (up to 35 breaths per minute) to maintain minute ventilation within the context of permissive hypercapnia. Overall, there has been less focus on the impact of respiratory rate and flow on VILI. The concept of controlling respiratory rate to reduce VILI is intuitive, yet novel. If a given tidal volume is injurious at 16 breaths per minute (bpm), it is easy to understand that it would be more harmful if delivered 32 times per minute. This is similar to the concept of impulse control in medical management of aortic dissection where both the blood pressure and heart rate must be reduced to limit shear stress on the aorta and risk of propagation. Unlike excessive volume and pressure, we have less insight on the maximum allowable flow that is considered safe. However, clearly the rate of gas flow also contributes to the energy load on the lung. Flow during mechanical ventilation can be viewed as the rate of strain on the lung.³

To understand mechanical power, we need to define the relationship between pressure, volume and flow that represents the energy driving gas into the airways to inflate the lungs during mechanical ventilation. The mathematical model describing the total pressure in the respiratory system is termed the equation of motion, which is the sum of the pressure required to deliver flow into the rigid airways (resistance x flow) and tidal volume into the elastic lung compartment (elastance x tidal volume).⁵

Equation of Motion:

Transpulmonary pressure = elastic load + resistive load

Muscle pressure + ventilator pressure = (elastance  x volume) + (resistance x flow) + PEEP

P_m + P_vent = (1/Cst x vol) + (res x flow)

P_m + P_vent = (Vt/Cst + PEEP) + (res x flow)

P_m + P_vent = (Vt/Cst + PEEP) + (res x Vt/Ti)

Efforts to reduce VILI have traditionally been directed at lower driving pressure and tidal volume while ignoring the impact of flow and respiratory rate. In contrast, mechanical power describes the energy applied to the lung (work per unit time: J/min). Professional cyclists utilize power to gauge how much work an athlete can sustain during cycling as measured by watts (joules/second). Similarly, mechanical power is the amount of energy (or work) applied to the lung resulting from the product of transpulmonary pressure (stress), tidal volume (strain), positive end-expiratory pressure (PEEP), flow and respiratory rate.^6,7

Mechanical power = delivered energy per breath * respiratory rate

Excessive mechanical power is thought to mechanically disrupt the extracellular matrix of the lung parenchyma. As VILI leads to capillary leak, the damaged lung requires increased mechanical power to ventilate at a constant tidal volume. Specifically, the collapsed airways and fluid-filled alveoli require increased inflation pressure and flow, resulting in the delivery of greater mechanical power. While tidal volume is the greatest driver of mechanical power, the impact of respiratory rate and flow should not be underestimated. In an animal study examining the power threshold for VILI in mechanically ventilated pigs, a constant lung strain at high, fixed tidal volume was observed to be lethal when delivered at 15 bpm, but not fatal at 3 or 6 bpm. The authors observed that a five-fold increase in respiratory rate increased mechanical power by 11 times.⁴ Gattinoni studied mechanical power in ARDS patients and similarly found that mechanical power increases exponentially as the respiratory rate increases. 

Mechanical power unites the causes of ventilator-induced lung injury in a single variable that incorporates both the elastic and resistive loads of the positive pressure breath.⁶ In other words, mechanical power quantifies the energy load delivered to the lung during each positive pressure breath by assessing the relative contribution of pressure, volume, flow and respiratory rate. As clinicians, we must consider the mechanical power we are delivering to our patient’s respiratory system, not just when we set the tidal volume or airway pressure on the ventilator, but also the PEEP, respiratory rate and flow.⁷ To deliver truly “lung protective” mechanical ventilation, we must consider the relative impact of each variable in the equation of motion on the energy applied to the lung, not just pressure and volume. 

References: 

1. ARDSNet: ARMA trial. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New Engl J Med 2000;342(18):1301-1308. 

2. Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. New Engl J Med 2015;372(8):747-755. 

3. Tonetti T, et al. Driving pressure and mechanical power: New targets for VILI prevention. Annals of Translational Medicine 2017;5(14):286-296.

4. Cressoni M et al. Mechanical power and development of VILI. Anesthesiology 2016;124:1100-8.

5.  Chatburn R. Fundamentals of mechanical ventilation. Cleveland Heights: Mandu Press Ltd; 2003.

6. Gattinoni L et al. Ventilator-related causes of lung injury: the mechanical power. Int Care Med 2016;42:1567-1575. 

7.  Silva PL et al. Power to mechanical power to minimize VILI. Int Care Med 2019;7(38):1-11.