LOWER ENERGY

High energy dissipation is associated with ventilator-induced lung injury (VILI)

Conventional mechanical ventilation, even when applied for only a few hours, has been shown to be a source of lung injury, so-called ‘ventilator-induced lung injury’ (VILI) ^4,5. In combination with previously existing inflammatory responses, which are present in more than 90% of intensive care unit (ICU) patients¹, this extra burden plays an important role in the morbidity and mortality of these patients ^2,3. Thus, it is of utmost importance to minimize the risk of ventilation hampering recovery or, even worse, leading to a lethal outcome ^2,8-15.

Over the last decades, innovative ‘lung-protective ventilation’ approaches have been developed to reduce VILI in the context of the two current golden standard ventilation techniques Pressure Controlled Ventilation (PCV) and Volume Controlled Ventilation (VCV). Up to now, these strategies are limited to suggested values for tidal volume settings (6 mL/kg of body mass), positive end expiratory pressure (PEEP) and plateau pressure in a “one size fits all” fashion ^3,6. In fact, the ‘golden standard’ of 6 mL/kg of body mass is based on one large randomized controlled trial focusing on a specific patient group, namely patients suffering from the relatively rare lung disease Acute Respiratory Distress Syndrome (ARDS) ³. The study showed a statistically significant reduction in mortality from 39.8% in the control group to 31.0% in the intervention group. However, later studies aiming to reduce ICU mortality of ARDS patients by setting high or low PEEP failed to show significant effects and reported unchanged high mortality rates of 22–40% ^16-19. A similarly high mortality rate of 35% was confirmed in the LUNG SAFE study analyzing data from 29,144 ICU patients in 50 countries ²⁰. Also, a recent study revealed no difference in ICU stay, mortality and morbidity between patients ventilated with low (4–6 mL/kg) versus intermediate (8–10 mL/kg) tidal volumes, raising further doubts as to whether low tidal volume ventilation represents the actual ‘holy grail’ ²¹.

The literature describes effects of mechanical power as well as mechanical energy during ventilation, where the energy dissipation is the overall power dissipation per unit of time. Mechanical power/energy derives from flow/volume and pressures provided by the ventilator in relation to the compliance and resistance of the patient’s thoracic wall and lungs. In general, more power is generated than is needed to induce inspiration and expiration. The net overspill of energy is dissipated in the lungs, which has been shown to have deleterious effects ² and is increasingly accepted as one of the causes for VILI ^7,8. While current ‘protective’ ventilation strategies mainly focus on optimizing inspiratory ventilation, the passive and abrupt expiration that occurs with conventional methods is considerably relevant ²² and potentially a key factor in inducing lung damage ²³. Moreover, controlling expiration has been shown to reduce lung damage in porcine ARDS ²⁴. Of note, a recent study revealed that mechanical power is associated with worse outcomes in critically ill patients receiving mechanical ventilation for more than 48 hours ⁹. As energy dissipation can be calculated based on factors such as pressures, flow and respiratory rate, independent top leaders in the field postulated that the ideal ventilator should monitor and display energy dissipation in order to really apply ‘safe’ ventilation ¹⁰.

FCV^® results in lower energy dissipation

FCV^® is based on the generation of a constant flow into and out of the lungs, resulting in linear increases and decreases of intratracheal pressures that are just high or low enough to facilitate mechanical breathing with efficient gas exchange. The sudden alveolar pressure drop during passive expiration with conventional ventilation is prevented. In other words, the amount of energy generated by the ventilator is just enough to facilitate respiration. Thereby, the impact on the lung tissue by dissipated energy is kept to a minimum, enabling ventilation with a markedly reduced risk of lung damage. 

Figure 1. Left: Idealized PV loops (the enclosed area of each loop is the dissipated energy) during PCV (red line), VCV (blue line) and FCV^®  (blue line during inspiration, green line during expiration). The dashed line is the static compliance curve of the lung/chest system in this example. Right: Real-time measured PV loops of a patient ventilated with FCV^®, demonstrating minimized hysteresis area of the PV loops (=energy dissipation) ²⁶.

Recently, clear theoretical evidence was provided for lower energy dissipation in the lungs by FCV^® as compared to VCV or PCV. A relatively simple analysis and numerical calculations indicated that energy dissipation is minimized by controlling the ventilation flow to be constant and continuous during both inspiration and expiration, and by ventilating at an I:E ratio close to 1:1. In other words, by using FCV^® 25. Energy dissipation can be calculated from the hysteresis area of pressure-volume loops obtained during ventilation. PV loops calculated based on routine ventilation protocols showed a 53% reduction in energy dissipation by FCV^® as compared to PCV and a 32% reduction as compared to VCV ²⁵. Additionally, it was emphasized that accurate measurement of intratracheal pressures is crucial for calculating energy dissipation. Where other VCV and PCV ventilators rely on calculated airway pressures, Evone is the only device that actually measures intratracheal pressures and is thus capable of measuring energy dissipation accurately.

This theory was further validated on a patient. Pressure-volume (PV) loops were recorded in real time, and the energy dissipated in the patient’s lungs was calculated from the hysteresis area of the PV loops. Strikingly, the energy dissipation was just 0.17 J/L, which is even lower than values reported for spontaneous breathing (0.2–0.7 J/L) ²⁶. Figure 1 outlines schematic PV loops obtained for PCV, VCV and FCV^® and the PV loops obtained during FCV^® ventilation of a patient.

Figure 2. Stained lung tissue samples retrieved after VCV or FCV® ventilation of ARDS pigs, revealing less thickening of alveolar walls in FCV group. Adapted from Schmidt et al. 2018.²⁷.

In porcine ARDS, FCV^® ventilation had a higher efficiency as compared to VCV with similar tidal volumes and PEEP, resulting in a 46% increased oxygenation (P=0.035) while using a 26% lower minute volume (P<0.001) ²⁷. Moreover, FCV^®  resulted in lower mechanical power ²⁶. Strikingly, histologic results demonstrated a significantly increased alveolar wall thickness in the control group as compared to the FCV^® group (7.8±0.2 μm vs. 5.5±0.1 μm; P<0.001), which was indicative of a worsened lung condition (Figure 2). Also, cell infiltrates, a marker for inflammation, were much less in the FCV group (32±2 vs 20±2/field; P<0.001). The authors state that they herewith provided evidence for attenuated lung injury after FCV^® 27.