Pulmonary impedance and alveolar instability during injurious ventilation in rats

Allen, Gilman B.; Pavone, Lucio A.; DiRocco, Joseph D.; Bates, Jason H. T.; Nieman, Gary F.

doi:10.1152/japplphysiol.01339.2004

Cited by 61 publications

(71 citation statements)

References 47 publications

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“…It was concluded that simultaneous increase in both H and are reflective of lung injury in the form of alveolar instability, whereas an increase in just H reflects merely derecruitment of alveoli. [Published with permission (4)]. …”

Section: Ards Is a Disease That Progresses In Stagesmentioning

confidence: 99%

“…However, trauma, sepsis, or hemorrhagic shock can result in a serious systemic inflammatory response syndrome (SIRS) that initiates a pathological tetrad (Fig. 3) (4,62,67,86), which significantly disrupts normal homogeneous ventilation resulting in stress concentrators (Fig. 8) (104,109) and dynamic strain (Fig.…”

Section: Synthesis Reviewmentioning

confidence: 99%

“…Impact of Mechanical Ventilation on Acute Lung Injury • Nieman GF et al 4) alveolar instability ( Fig. 3) (1,25,32,83,117,122,135).…”

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confidence: 99%

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Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury

Nieman

Gatto

Habashi

2015

Journal of Applied Physiology

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Nieman GF, Gatto LA, Habashi NM. Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury. J Appl Physiol 119: 1245-1261. First published October 15, 2015 doi:10.1152/japplphysiol.00659.2015The earliest description of what is now known as the acute respiratory distress syndrome (ARDS) was a highly lethal double pneumonia. Ashbaugh and colleagues (Ashbaugh DG, Bigelow DB, Petty TL, Levine BE Lancet 2: 319-323, 1967) correctly identified the disease as ARDS in 1967. Their initial study showing the positive effect of mechanical ventilation with positive end-expiratory pressure (PEEP) on ARDS mortality was dampened when it was discovered that improperly used mechanical ventilation can cause a secondary ventilator-induced lung injury (VILI), thereby greatly exacerbating ARDS mortality. This Synthesis Report will review the pathophysiology of ARDS and VILI from a mechanical stress-strain perspective. Although inflammation is also an important component of VILI pathology, it is secondary to the mechanical damage caused by excessive strain. The mechanical breath will be deconstructed to show that multiple parameters that comprise the breath-airway pressure, flows, volumes, and the duration during which they are applied to each breath-are critical to lung injury and protection. Specifically, the mechanisms by which a properly set mechanical breath can reduce the development of excessive fluid flux and pulmonary edema, which are a hallmark of ARDS pathology, are reviewed. Using our knowledge of how multiple parameters in the mechanical breath affect lung physiology, the optimal combination of pressures, volumes, flows, and durations that should offer maximum lung protection are postulated. acute lung injury; lung; pathophysiology ventilator; VILI THE POLIO EPIDEMIC OF 1916 inspired many treatment attempts including vitamin C therapy, hydrotherapy, and electrotherapy, but no effective therapy was found until Philip Drinker's group invented negative pressure mechanical ventilation-the iron lung. Their landmark paper, "The use of a new apparatus for the prolonged administration of artificial respiration: I. A fatal case of poliomyelitis," published in 1929, demonstrated the effective clinical use of this device (Fig. 1) (38). The concept of conversion from negative to positive pressure ventilation was based on technical advances that were made during World War II to deliver pressurized oxygen to high-altitude fighter and bomber pilots. Concomitant with these technologic advances in mechanical ventilation was the realization that what was originally thought to be a universally fatal form of double pneumonia was indeed a unique clinical entity that we now call the acute respiratory distress syndrome (ARDS). In a 1967 seminal paper published in The Lancet, Ashbaugh et al. (10) first identified and described ARDS as a collection of pathologic abnormalities that can be caused by many unrelated insults such as sepsis, hemorrhagic shock, pneumonia, and trauma to name a few. The disease and the ventil...

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Section: Ards Is a Disease That Progresses In Stagesmentioning

confidence: 99%

Section: Synthesis Reviewmentioning

confidence: 99%

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Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury

Nieman

Gatto

Habashi

2015

Journal of Applied Physiology

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“…The increased rises in H over time in the injured animals relative to naive controls were not accompanied by any significant differences in hysteresivity () between groups, (Fig. 1, B and E), signifying active temporal derecruitment of lung volume from air space instability as opposed to any changes in heterogeneity or intrinsic tissue properties (6,9).…”

Section: Lung Mechanical Functionmentioning

confidence: 84%

Neither fibrin nor plasminogen activator inhibitor-1 deficiency protects lung function in a mouse model of acute lung injury

Allen

Cloutier²,

Larrabee³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Allen GB, Cloutier ME, Larrabee YC, Tetenev K, Smiley ST, Bates JH. Neither fibrin nor plasminogen activator inhibitor-1 deficiency protects lung function in a mouse model of acute lung injury. Am J Physiol Lung Cell Mol Physiol 296: L277-L285, 2009. First published December 5, 2008 doi:10.1152/ajplung.90475.2008.-Fibrin impairs surfactant function in vitro, and inhibition of fibrinolysis by plasminogen activator inhibitor (PAI-1) is thought to promote fibrin accumulation in acute lung injury (ALI). This has led to speculation that impaired PAI-1 and fibrin accumulation should protect lung function in ALI. We tested this hypothesis by investigating ALI severity in fibrinogen-deficient (FgnϪ/Ϫ) and PAI-1-deficient (PAI-1Ϫ/Ϫ) mice. PAI-1Ϫ/Ϫ, C57BL/6, FgnϪ/Ϫ, and Fgnϩ/Ϫ females were anesthetized and allowed to aspirate 4 l/g of hydrochloric acid (pH 1.0) and then reanesthetized and connected to a ventilator 48 h later. Naive C57BL/6 and Fgnϩ/Ϫ females served as controls. Following deep inflation (DI), forced oscillations were delivered periodically over 8 min to measure changes in elastance (H) as a surrogate of lung derecruitment, at positive end-expiratory pressures (PEEP) of 6, 3, and 1 cmH 2O. Increases in H following DI in acid-injured mice were greater than naive strain-matched controls. Increases in H were no different between injured PAI-1Ϫ/Ϫ and C57BL/6, or between injured FgnϪ/Ϫ and ϩ/Ϫ mice, at any PEEP. Pressure-volume curves were no different between injured groups. Total lung fibrin was lower in injured PAI-1Ϫ/Ϫ and FgnϪ/Ϫ mice relative to injured C57BL/6 and Fgnϩ/Ϫ mice, respectively, but indices of permeability were no different between strains. Unexpectedly, neither fibrin nor PAI-1 deficiency protects lung mechanical function in mice with acid-induced ALI. We speculate that in vivo lung function may be more closely tied to permeability and alveolar protein in general, rather than being linked specifically to fibrin. lung mechanics; respiratory impedance; acid aspiration; coagulation ACUTE LUNG INJURY (ALI) is a severe form of noncardiogenic pulmonary edema and hypoxemic respiratory failure stemming from numerous causes (60). Current treatment of ALI rests largely on supportive care with mechanical ventilation, and its prognosis remains poor with a mortality of 30 -40% in the general population, and higher in the elderly (49). The pathology of ALI typically progresses through an initial exudative phase characterized by neutrophil infiltration, edema, and accumulation of hyaline membranes, the latter consisting primarily of necrotic debris and fibrin (58). In this regard, the coagulation pathway and its end product fibrin have excited particular interest, in part due to the ability of fibrin to inhibit surfactant function in vitro (52,54), and the increasingly recognized interplay between coagulation and innate immunity (17,63). Fibrin formation and clearance in the lung are governed by the relative quantity and activity of fibrinolysis promoters such as plasminogen activators and fibrinolysis inh...

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“…The result equals the part of area in the observed video frame that is characterized by showing no visible structures and is, because of that, associated with alveolar collapse and atelectasis (1,12). Because the optical appearance of the recorded tissue only showed little variability during the CPAP maneuvers, a single representative image taken at an end-expiratory point during normal ventilation (PEEP ϭ 7 mbar) in between the CPAP maneuvers was evaluated for each animal.…”

Section: Experimental Protocolmentioning

confidence: 99%

Locally measured shear moduli of pulmonary tissue and global lung mechanics in mechanically ventilated rats

Schwenninger

Runck

Schumann

et al. 2012

Journal of Applied Physiology

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Schwenninger D, Runck H, Schumann S, Haberstroh J, Guttmann J. Locally measured shear moduli of pulmonary tissue and global lung mechanics in mechanically ventilated rats. J Appl Physiol 113: 273-280, 2012. First published May 24, 2012 doi:10.1152/japplphysiol.01620.2011.-This study was aimed at measuring shear moduli in vivo in mechanically ventilated rats and comparing them to global lung mechanics. Wistar rats (n ϭ 28) were anesthetized, tracheally intubated, and mechanically ventilated in supine position. The animals were randomly assigned to the healthy control or the lung injury group where lung injury was induced by bronchoalveolar lavage. The respiratory system elastance Ers was analyzed based on the single compartment resistance/elastance lung model using multiple linear regression analysis. The shear modulus (G) of alveolar parenchyma was studied using a newly developed endoscopic system with adjustable pressure at the tip that was designed to induce local mechanostimulation. The data analysis was then carried out with an inverse finite element method. G was determined at continuous positive airway pressure (CPAP) levels of 15, 17, 20, and 30 mbar. The resulting shear moduli of lungs in healthy animals increased from 3.3 Ϯ 1.4 kPa at 15 mbar CPAP to 5.8 Ϯ 2.4 kPa at 30 mbar CPAP (P ϭ 0.012), whereas G was ϳ2.5 kPa at all CPAP levels for the lung-injured animals. Regression analysis showed a negative correlation between G and relative Ers in the control group (r ϭ Ϫ0.73, P ϭ 0.008 at CPAP ϭ 20 mbar) and no significant correlation in the lung injury group. These results suggest that the locally measured G were inversely associated with the elastance of the respiratory system. Rejecting the study hypothesis the researchers concluded that low global respiratory system elastance is related to high local resistance against tissue deformation.

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Pulmonary impedance and alveolar instability during injurious ventilation in rats

Cited by 61 publications

References 47 publications

Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury

Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury

Neither fibrin nor plasminogen activator inhibitor-1 deficiency protects lung function in a mouse model of acute lung injury

Locally measured shear moduli of pulmonary tissue and global lung mechanics in mechanically ventilated rats

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