Positive End-expiratory Pressure and Mechanical Power

Abstract

EDITOR’S PERSPECTIVE What We Already Know about This Topic Positive end-expiratory pressure protects against ventilation-induced lung injury by improving homogeneity of ventilation, but positive end-expiratory pressure contributes to the mechanical power required to ventilate the lung What This Article Tells Us That Is New This in vivo study (36 pigs mechanically ventilated in the prone position) suggests that low levels of positive end-expiratory pressure reduce injury associated with atelectasis, and above a threshold level of power, positive end-expiratory pressure causes lung injury and adverse hemodynamics Background Positive end-expiratory pressure is usually considered protective against ventilation-induced lung injury by reducing atelectrauma and improving lung homogeneity. However, positive end-expiratory pressure, together with tidal volume, gas flow, and respiratory rate, contributes to the mechanical power required to ventilate the lung. This study aimed at investigating the effects of increasing mechanical power by selectively modifying its positive end-expiratory pressure component. Methods Thirty-six healthy piglets (23.3 ± 2.3 kg) were ventilated prone for 50 h at 30 breaths/min and with a tidal volume equal to functional residual capacity. Positive end-expiratory pressure levels (0, 4, 7, 11, 14, and 18 cm H2O) were applied to six groups of six animals. Respiratory, gas exchange, and hemodynamic variables were recorded every 6 h. Lung weight and wet-to-dry ratio were measured, and histologic samples were collected. Results Lung mechanical power was similar at 0 (8.8 ± 3.8 J/min), 4 (8.9 ± 4.4 J/min), and 7 (9.6 ± 4.3 J/min) cm H2O positive end-expiratory pressure, and it linearly increased thereafter from 15.5 ± 3.6 J/min (positive end-expiratory pressure, 11 cm H2O) to 18.7 ± 6 J/min (positive end-expiratory pressure, 14 cm H2O) and 22 ± 6.1 J/min (positive end-expiratory pressure, 18 cm H2O). Lung elastances, vascular congestion, atelectasis, inflammation, and septal rupture decreased from zero end-expiratory pressure to 4 to 7 cm H2O (P < 0.0001) and increased progressively at higher positive end-expiratory pressure. At these higher positive end-expiratory pressure levels, striking hemodynamic impairment and death manifested (mortality 0% at positive end-expiratory pressure 0 to 11 cm H2O, 33% at 14 cm H2O, and 50% at 18 cm H2O positive end-expiratory pressure). From zero end-expiratory pressure to 18 cm H2O, mean pulmonary arterial pressure (from 19.7 ± 5.3 to 32.2 ± 9.2 mmHg), fluid administration (from 537 ± 403 to 2043 ± 930 ml), and noradrenaline infusion (0.04 ± 0.09 to 0.34 ± 0.31 μg · kg−1 · min−1) progressively increased (P < 0.0001). Lung weight and lung wet-to-dry ratios were not significantly different across the groups. The lung mechanical power level that best discriminated between more versus less severe damage was 13 ± 1 J/min. Conclusions Less than 7 cm H2O positive end-expiratory pressure reduced atelectrauma encountered at zero end-expiratory pressure. Above a defined power threshold, sustained positive end-expiratory pressure contributed to potentially lethal lung damage and hemodynamic impairment.

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

“…MP is the energy delivered to the respiratory system over time, which is the product of the absolute proximal airway pressure and related changes in volume and respiratory rate [10]. Animal data showed that increasing MP was associated with an increase in lung edema and lung damage [11][12][13]. Furthermore, two studies in patients with and without ARDS found that MP computed during the first days of mechanical ventilation was independently associated with mortality, which rose significantly above a certain level of MP [14,15].…”

Which component of mechanical power is most important in causing VILI?

“…Regarding the monitored variables of ventilation that relate to total inflation pressure, active debate has developed as to whether the element with most influence is endinspiratory static (plateau) pressure or its difference from PEEP, known as the driving pressure (ΔP) [6][7][8]. PEEP bears a U-shaped relationship to VILI risk, with low levels tending to reduce atelectasis and distribute stress [9,10]. On the other hand, high PEEP sets an elevated platform from which widespread tidal overstretching of the parenchyma as well as hemodynamic compromise become increasingly likely [10].…”

“…PEEP bears a U-shaped relationship to VILI risk, with low levels tending to reduce atelectasis and distribute stress [9,10]. On the other hand, high PEEP sets an elevated platform from which widespread tidal overstretching of the parenchyma as well as hemodynamic compromise become increasingly likely [10]. Finally, neither PEEP, plateau pressure, nor their difference (ΔP) reflect the dynamics and dissipated energy of the tidal cycle.…”

“…It must be recognized that VILI may manifest in various ways: e.g., as inflammation, cellular disruption, or focal hyperinflation, with different tidal pressure components contributing unequally to each [9,10]. For an individual lung, thresholds for stress, strain, energy, and power must exist, below which their applications pose little threat of whichever kind (Fig.…”

Should we titrate positive end-expiratory pressure based on an end-expiratory transpulmonary pressure?

“…These hemodynamic problems recede quickly after release of the recruiting pressure. Sustained high transpulmonary pressures have been shown to be potentially tissue damaging in both pre-injured rodents (39) and healthy pigs (40). The durability of benefit from the RM also depends on the tidal ventilation pattern (PEEP and tidal volume) that follows its application (24).…”