Does Iso-mechanical Power Lead to Iso-lung Damage?

Abstract

Background Excessive tidal volume, respiratory rate, and positive end-expiratory pressure (PEEP) are all potential causes of ventilator-induced lung injury, and all contribute to a single variable: the mechanical power. The authors aimed to determine whether high tidal volume or high respiratory rate or high PEEP at iso-mechanical power produce similar or different ventilator-induced lung injury. Methods Three ventilatory strategies—high tidal volume (twice baseline functional residual capacity), high respiratory rate (40 bpm), and high PEEP (25 cm H2O)—were each applied at two levels of mechanical power (15 and 30 J/min) for 48 h in six groups of seven healthy female piglets (weight: 24.2 ± 2.0 kg, mean ± SD). Results At iso-mechanical power, the high tidal volume groups immediately and sharply increased plateau, driving pressure, stress, and strain, which all further deteriorated with time. In high respiratory rate groups, they changed minimally at the beginning, but steadily increased during the 48 h. In contrast, after a sudden huge increase, they decreased with time in the high PEEP groups. End-experiment specific lung elastance was 6.5 ± 1.7 cm H2O in high tidal volume groups, 10.1 ± 3.9 cm H2O in high respiratory rate groups, and 4.5 ± 0.9 cm H2O in high PEEP groups. Functional residual capacity decreased and extravascular lung water increased similarly in these three categories. Lung weight, wet-to-dry ratio, and histologic scores were similar, regardless of ventilatory strategies and power levels. However, the alveolar edema score was higher in the low power groups. High PEEP had the greatest impact on hemodynamics, leading to increased need for fluids. Adverse events (early mortality and pneumothorax) also occurred more frequently in the high PEEP groups. Conclusions Different ventilatory strategies, delivered at iso-power, led to similar anatomical lung injury. The different systemic consequences of high PEEP underline that ventilator-induced lung injury must be evaluated in the context of the whole body. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Fluid administration and monitoring in ARDS: which management?

“…Indeed, for the same fluid input, the water retention in a 46-h experiment was twice as much important in animals treated with PEEP than without PEEP [54]. Similarly, for the same mechanical power, we found that the positive fluid balance was dramatically higher in animals treated with high levels of PEEP [55]. Nevertheless, fluid retention ceases when a new equilibrium is reached after 2-3 days [54].…”

“…Fluid retention is the unavoidable "price" to pay to allow the use of positive-pressure mechanical ventilation. Importantly, the consequences of positive fluid balance are not limited to the lung (partly protected by the high intra-alveolar pressure) but also involve other organs which interstitial edema may deeply affect the function [55]. Consequently, excessive fluid retention must be ideally prevented, or corrected.…”

Bedside calculation of mechanical power during volume- and pressure-controlled mechanical ventilation

“…Clinicians are used to use low tidal volumes (6 mL/kg, driving pressure < 14 cmH 2 O), and to maintain a viable CO 2 clearance, they ramp up the respiratory frequency. It is therefore of paramount importance to sensitize the intensivists to consider that high respiratory rate does injure the lung as it is part of the whole energy package delivered by the ventilator [11,25].…”

Estimating the Damaging Power of High-Stress Ventilation

“…7,8 Recent experimental data suggest that, indeed, this may be the case when high, VILI-inducing power levels are sustained for long enough periods. 9 Whatever its components, the same numerical value of total power calculated from airway pressure implies different hazards for different patients. The chest wall, for example, also requires energy and power to expand, and its compliance is degraded by massive obesity.…”

“…It must be acknowledged that, although cumulative energy load and total power have been experimentally or clinically linked to VILI, exactly which delivered component or subcomponent of power correlates best with damage has not been clearly identified. 9,20,21 For example, it might be argued that only energy that relates to driving pressure or total elastic pressure {ie, the product of volume and absolute alveolar pressure, or (V T Â [DP + PEEP])} would best track lung stretch and VILI risk. 13 Alternatively, the total kinetic energy applied in excess of PEEP {ie, the product of volume and the sum of DP + P res .…”