Relative roles of vascular and airspace pressures in ventilator-induced lung injury

John R. Hotchkiss, Lluis Blanch, Alberto Naveira, Alexander B. Adams, Christopher Carter, Douglas A. Olson, Perry H. Leo, John J. Marini

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Objective: To determine whether elevations in pulmonary vascular pressure induced by mechanical ventilation are more injurious than elevations of pulmonary vascular pressure of similar magnitude occurring in the absence of mechanical ventilation, Design: Prospective comparative laboratory investigation, Setting: University research laboratory. Subjects: Male New Zealand white rabbits. Interventions: Three groups of isolated, perfused rabbit lungs were exposed to cyclic elevation of pulmonary artery pressures arising from either intermittent positive pressure mechanical ventilation or from pulsatile perfusion of lungs held motionless by continuous positive airway pressure. Peak, mean, and nadir pulmonary artery pressures and mean airway pressure were matched between groups (35, 27.4 ± 0.74, and 20.8 ± 1.5 mm Hg, and 17.7 ± 0.22 cm H2O, respectively). Measurements and Main Results: Lungs exposed to elevated pulmonary artery pressures attributable to intermittent positive pressure mechanical ventilation formed more edema (6.8 ± 1.3 vs. 1.1 ± 0.9 g/g of lung), displayed more perivascular (61 ± 26 vs. 15 ± 13 vessels) and alveolar hemorrhage (76 ± 11% vs. 26 ± 18% of alveoli), and underwent larger fractional declines in static compliance (88 ± 4.4% vs. 48 ± 25.1% decline) than lungs exposed to similar peak and mean pulmonary artery pressures in the absence of tidal positive pressure ventilation. Conclusions: Isolated phasic elevations of pulmonary artery pressure may cause less damage than those occurring during intermittent positive pressure mechanical ventilation, suggesting that cyclic changes in perivascular pressure surrounding extra-alveolar vessels may be important in the genesis of ventilator-induced lung injury.

Original languageEnglish (US)
Pages (from-to)1593-1598
Number of pages6
JournalCritical care medicine
Volume29
Issue number8
StatePublished - Aug 29 2001

Fingerprint

Ventilator-Induced Lung Injury
Blood Vessels
Pressure
Artificial Respiration
Pulmonary Artery
Lung
Intermittent Positive-Pressure Ventilation
Rabbits
Pulsatile Flow
Continuous Positive Airway Pressure
Positive-Pressure Respiration
Compliance
Edema
Research Design
Hemorrhage

Keywords

  • Acute lung injury
  • Blood-air barrier
  • Hemodynamics
  • Mechanical ventilation
  • Pulmonary circulation
  • Rabbits

Cite this

Hotchkiss, J. R., Blanch, L., Naveira, A., Adams, A. B., Carter, C., Olson, D. A., ... Marini, J. J. (2001). Relative roles of vascular and airspace pressures in ventilator-induced lung injury. Critical care medicine, 29(8), 1593-1598.

Relative roles of vascular and airspace pressures in ventilator-induced lung injury. / Hotchkiss, John R.; Blanch, Lluis; Naveira, Alberto; Adams, Alexander B.; Carter, Christopher; Olson, Douglas A.; Leo, Perry H.; Marini, John J.

In: Critical care medicine, Vol. 29, No. 8, 29.08.2001, p. 1593-1598.

Research output: Contribution to journalArticle

Hotchkiss, JR, Blanch, L, Naveira, A, Adams, AB, Carter, C, Olson, DA, Leo, PH & Marini, JJ 2001, 'Relative roles of vascular and airspace pressures in ventilator-induced lung injury', Critical care medicine, vol. 29, no. 8, pp. 1593-1598.
Hotchkiss JR, Blanch L, Naveira A, Adams AB, Carter C, Olson DA et al. Relative roles of vascular and airspace pressures in ventilator-induced lung injury. Critical care medicine. 2001 Aug 29;29(8):1593-1598.
Hotchkiss, John R. ; Blanch, Lluis ; Naveira, Alberto ; Adams, Alexander B. ; Carter, Christopher ; Olson, Douglas A. ; Leo, Perry H. ; Marini, John J. / Relative roles of vascular and airspace pressures in ventilator-induced lung injury. In: Critical care medicine. 2001 ; Vol. 29, No. 8. pp. 1593-1598.
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AU - Olson, Douglas A.

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AB - Objective: To determine whether elevations in pulmonary vascular pressure induced by mechanical ventilation are more injurious than elevations of pulmonary vascular pressure of similar magnitude occurring in the absence of mechanical ventilation, Design: Prospective comparative laboratory investigation, Setting: University research laboratory. Subjects: Male New Zealand white rabbits. Interventions: Three groups of isolated, perfused rabbit lungs were exposed to cyclic elevation of pulmonary artery pressures arising from either intermittent positive pressure mechanical ventilation or from pulsatile perfusion of lungs held motionless by continuous positive airway pressure. Peak, mean, and nadir pulmonary artery pressures and mean airway pressure were matched between groups (35, 27.4 ± 0.74, and 20.8 ± 1.5 mm Hg, and 17.7 ± 0.22 cm H2O, respectively). Measurements and Main Results: Lungs exposed to elevated pulmonary artery pressures attributable to intermittent positive pressure mechanical ventilation formed more edema (6.8 ± 1.3 vs. 1.1 ± 0.9 g/g of lung), displayed more perivascular (61 ± 26 vs. 15 ± 13 vessels) and alveolar hemorrhage (76 ± 11% vs. 26 ± 18% of alveoli), and underwent larger fractional declines in static compliance (88 ± 4.4% vs. 48 ± 25.1% decline) than lungs exposed to similar peak and mean pulmonary artery pressures in the absence of tidal positive pressure ventilation. Conclusions: Isolated phasic elevations of pulmonary artery pressure may cause less damage than those occurring during intermittent positive pressure mechanical ventilation, suggesting that cyclic changes in perivascular pressure surrounding extra-alveolar vessels may be important in the genesis of ventilator-induced lung injury.

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