Radial traction in pulmonary physiology
Radial traction is the outward mechanical force exerted by the lung parenchymal extracellular matrix on the alveolar septal region to maintain alveolar expansion and patency. [1] In alveolar mechanics, this parenchymal “tethering” counteracts inward collapsing forces so that alveoli remain open across the respiratory cycle. [1] Radial traction also supports airway-parenchymal interdependence by tethering airway walls to surrounding alveoli, which dilates small airways as lung volume increases. [2]
Alveolar stability determined by alveolar tension and parenchymal recoil
Alveolar stability is governed by the balance between inward collapsing forces driven primarily by surface tension and outward recoil forces provided by lung tissue properties. [1] Disruption of surfactant function or alveolar structural integrity in ARDS increases alveolar surface tension, which predisposes to heterogeneous collapse and ventilation-induced injury. [1] The parenchymal matrix contributes radial traction that helps maintain inflation, and loss of effective traction can permit greater end-expiratory collapse. [1]
Relationship between radial traction and ARDS alveolar collapse
ARDS involves heterogeneous dependent atelectasis, which reflects impaired maintenance of alveolar patency at end-expiration. [3] PEEP is used to counteract compressive forces that promote derecruitment and cyclic opening and closing of lung units in ARDS. [3] This pathophysiology aligns with a reduction in effective mechanical stabilization of alveoli, including diminished ability of parenchymal tethering to keep alveoli open at end-expiration. [1][3]
PEEP management through stabilization of alveoli at end-expiration
Higher PEEP strategies increase end-expiratory lung volume and reduce cyclic recruitment/derecruitment, which decreases shear stress generated by repetitive alveolar opening and closing. [3] Higher PEEP can improve oxygenation by reducing atelectasis and intrapulmonary shunt. [3] Higher PEEP also mitigates ventilator-induced lung injury risk in recruitable ARDS by reducing atelectrauma. [3]
Selection algorithm for PEEP strategy in moderate–severe ARDS
Higher levels of PEEP are recommended in adult patients with moderate or severe ARDS rather than lower levels of PEEP. [4] A reasonable starting point is implementation of a higher PEEP strategy consistent with large randomized trials used in the evidence base. [4] Clinical monitoring of adverse effects is required because higher PEEP can increase risks including end-inspiratory overdistention, increased intrapulmonary shunt, increased dead space, and increased pulmonary vascular resistance. [4]
Key evidence supporting higher PEEP in ARDS
Higher PEEP strategies were evaluated in eight RCTs including 2,728 patients with mean PEEP values of 15.1 cm H2O versus 9.1 cm H2O on day 1. [4] Across six studies with 2,580 patients, no significant difference in mortality was found for higher versus lower PEEP in the primary pooled analysis. [4] In an individual patient data meta-analysis restricted to moderate or severe ARDS (PaO2/FiO2 < 200), higher PEEP was associated with significantly lower mortality with adjusted RR 0.90 (95% CI 0.81–1.00). [4] Higher PEEP increased PaO2/FiO2 by about 61 mm Hg compared with lower PEEP in pooled analysis. [4]
Initiation and adjustment considerations for PEEP
Increasing PEEP changes inspiratory plateau pressure, so the risks and benefits of further PEEP escalation should be assessed when plateau pressure reaches greater than or equal to 30 cm H2O. [4] Evidence-based starting points for PEEP escalation use trial-based higher PEEP protocols included in the higher-versus-lower PEEP evidence base. [4] PEEP titration should target stabilization of atelectatic lung units by reducing end-expiratory collapse and minimizing cyclic derecruitment. [3]
Common pitfalls in PEEP titration
PEEP adjusted only to oxygenation targets can produce suboptimal outcomes when recruitment is limited or when hemodynamic compromise from increased intrathoracic pressure worsens perfusion matching. [3] Insufficient PEEP permits derecruitment at end-expiration in newly recruited lung units, which promotes surfactant depletion and further alveolar injury. [3] Excessive PEEP can overdistend already aerated regions, increasing stress and strain in non-target lung units. [3]
Target goals of PEEP-based alveolar stabilization
The therapeutic goal of higher PEEP is improved alveolar stability at end-expiration by reducing the magnitude of cyclic opening and closing of lung units. [3] A secondary goal is improved oxygenation through reduced atelectasis and reduced intrapulmonary shunt. [3] A safety goal is avoidance of overdistention-related lung injury and prevention of clinically important adverse hemodynamic and pulmonary vascular consequences. [4]