TY - JOUR
T1 - Adverse heart–lung interactions in ventilator-induced lung injury
AU - Katira, Bhushan H.
AU - Giesinger, Regan E.
AU - Engelberts, Doreen
AU - Zabini, Diana
AU - Kornecki, Alik
AU - Otulakowski, Gail
AU - Yoshida, Takeshi
AU - Kuebler, Wolfgang M.
AU - McNamara, Patrick J.
AU - Connelly, Kim A.
AU - Kavanagh, Brian P.
N1 - Publisher Copyright:
Copyright © 2017 by the American Thoracic Society.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - Rationale: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high VT with zero positive end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to lung shear stress. Objectives: To reproduce the lung injury and edema examined in the Webb and Tierney study and to investigate the underlying mechanism thereof. Methods: Sprague-Dawley rats weighing approximately 400 g received mechanical ventilation for 60 minutes according to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H2O). Additional series of experiments (20 min in duration to ensure all animals survived) were studied to assess permeability (n = 4 per group), echocardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respectively). Measurements and Main Results: The original Webb and Tierney results were replicated in terms of lung/body weight ratio (45/0 . 45/10 30/0 14/0; P, 0.05) and histology. In 45/0, pulmonary edema was overt and rapid, with survival less than 30 minutes. In 45/0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preload, and progressive dilation of the right ventricle. Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 45/0. Conclusions: In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately resulting in right ventricular failure and dilation. Pulmonary edema was due to increased permeability, which was augmented by a modest (approximately 40%) increase in hydrostatic pressure. The lung injury and acute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertain, but which may be due to cyclic interruption and exaggeration of pulmonary blood flow.
AB - Rationale: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high VT with zero positive end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to lung shear stress. Objectives: To reproduce the lung injury and edema examined in the Webb and Tierney study and to investigate the underlying mechanism thereof. Methods: Sprague-Dawley rats weighing approximately 400 g received mechanical ventilation for 60 minutes according to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H2O). Additional series of experiments (20 min in duration to ensure all animals survived) were studied to assess permeability (n = 4 per group), echocardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respectively). Measurements and Main Results: The original Webb and Tierney results were replicated in terms of lung/body weight ratio (45/0 . 45/10 30/0 14/0; P, 0.05) and histology. In 45/0, pulmonary edema was overt and rapid, with survival less than 30 minutes. In 45/0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preload, and progressive dilation of the right ventricle. Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 45/0. Conclusions: In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately resulting in right ventricular failure and dilation. Pulmonary edema was due to increased permeability, which was augmented by a modest (approximately 40%) increase in hydrostatic pressure. The lung injury and acute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertain, but which may be due to cyclic interruption and exaggeration of pulmonary blood flow.
KW - Cor pulmonale
KW - Lung injury
KW - Microvascular injury
KW - Preload
UR - http://www.scopus.com/inward/record.url?scp=85038086478&partnerID=8YFLogxK
U2 - 10.1164/rccm.201611-2268OC
DO - 10.1164/rccm.201611-2268OC
M3 - Article
C2 - 28795839
AN - SCOPUS:85038086478
SN - 1073-449X
VL - 196
SP - 1411
EP - 1421
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 11
ER -