Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

2007 ◽  
Vol 102 (6) ◽  
pp. 2414-2414 ◽  
Author(s):  
E. Costa ◽  
M. Amato
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Saline Lavage

scholarly journals Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

2007 ◽  
Vol 102 (1) ◽  
pp. 331-339 ◽  
Author(s):  
Rebecca S. Syring ◽  
Cynthia M. Otto ◽  
Rebecca E. Spivack ◽  
Klaus Markstaller ◽  
James E. Baumgardner
Keyword(s):  
Cardiac Output ◽  
Lung Injury ◽  
Respiratory Rate ◽  
Pressure Control ◽  
Plateau Pressure ◽  
Control Mode ◽  
Intrinsic Peep ◽  
Mixed Venous Saturation ◽  
Mixed Venous ◽  
Saline Lavage

Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitment at end exhalation, but PEEPe depresses cardiac output and increases overdistension. Short exhalation times can also maintain end-expiratory recruitment, but if the mechanism of this recruitment is generation of intrinsic PEEP (PEEPi), there would be little advantage compared with PEEPe. In seven New Zealand White rabbits, we compared recruitment from increased respiratory rate (RR) to recruitment from increased PEEPe after saline lavage. Rabbits were ventilated in pressure control mode with a fraction of inspired O2 (FiO2) of 1.0, inspiratory-to-expiratory ratio of 2:1, and plateau pressure of 28 cmH2O, and either 1) high RR ( 24 ) and low PEEPe (3.5) or 2) low RR ( 7 ) and high PEEPe ( 14 ). We assessed cyclical lung recruitment with a fast arterial Po2 probe, and we assessed average recruitment with blood gas data. We measured PEEPi, cardiac output, and mixed venous saturation at each ventilator setting. Recruitment achieved by increased RR and short exhalation time was nearly equivalent to recruitment achieved by increased PEEPe. The short exhalation time at increased RR, however, did not generate PEEPi. Cardiac output was increased on average 13% in the high RR group compared with the high PEEPe group ( P < 0.001), and mixed venous saturation was consistently greater in the high RR group ( P < 0.001). Prevention of end-expiratory derecruitment without increased end-expiratory pressure suggests that another mechanism, distinct from intrinsic PEEP, plays a role in the dynamic behavior of atelectasis.

Open lung approach ventilation abolishes the negative effects of respiratory rate in experimental lung injury

2016 ◽  
Vol 60 (8) ◽  
pp. 1131-1141 ◽  
Author(s):  
J. Retamal ◽  
J. B. Borges ◽  
A. Bruhn ◽  
R. Feinstein ◽  
G. Hedenstierna ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Negative Effects ◽  
Open Lung ◽  
Open Lung Approach

Comparison of variable and conventional ventilation in a sheep saline lavage lung injury model*

2006 ◽  
Vol 34 (2) ◽  
pp. 439-445 ◽  
Author(s):  
Carissa L. Bellardine ◽  
Andrew M. Hoffman ◽  
Larry Tsai ◽  
Edward P. Ingenito ◽  
Stephen P. Arold ◽  
...  
Keyword(s):  
Lung Injury ◽  
Conventional Ventilation ◽  
Injury Model ◽  
Lung Injury Model ◽  
Saline Lavage

scholarly journals 0893. High respiratory rate favors pulmonary edema in an experimental model of acute lung injury

2014 ◽  
Vol 2 (S1) ◽  
Author(s):  
J Retamal ◽  
JB Borges ◽  
F Suarez-Sipmann ◽  
A Bruhn ◽  
G Hedenstierna ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Respiratory Rate ◽  
Experimental Model ◽  
High Respiratory Rate

Mechanical Power and Development of Ventilator-induced Lung Injury

2016 ◽  
Vol 124 (5) ◽  
pp. 1100-1108 ◽  
Author(s):  
Massimo Cressoni ◽  
Miriam Gotti ◽  
Chiara Chiurazzi ◽  
Dario Massari ◽  
Ilaria Algieri ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Transpulmonary Pressure ◽  
Lung Parenchyma ◽  
Plateau Pressure ◽  
Mechanical Power ◽  
Lung Edema ◽  
Lung Weight ◽  
Ventilator Induced Lung Injury ◽  
Power Threshold

Abstract Background The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung. Methods Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold. Results In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r2 = 0.41, P = 0.001) and lung elastance (r2 = 0.33, P &lt; 0.01) and decrease in Pao2/Fio2 (r2 = 0.40, P &lt; 0.001) at the end of the study. Conclusion In piglets, VILI develops if a mechanical power threshold is exceeded.

scholarly journals Effects of Nitric Oxide Donor on the Lung Functions in a Saline Lavage-Induced Model of ARDS

2019 ◽  
pp. S265-S273 ◽  
Author(s):  
P. KOSUTOVA ◽  
P. MIKOLKA ◽  
S. BALENTOVA ◽  
M. ADAMKOV ◽  
D. MOKRA
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Cell Count ◽  
Nitric Oxide Donor ◽  
Control Group ◽  
Lung Edema ◽  
Edema Formation ◽  
Respiratory Parameters ◽  
Lung Functions ◽  
Saline Lavage

Acute respiratory distress syndrome (ARDS) is characterized by acute hypoxemia, neutrophil-mediated inflammation, and lung edema formation. Whereas lung damage might be alleviated by nitric oxide (NO), goal of this study was to evaluate if intratracheal NO donor S-nitroso-N-acetylpenicillamine (SNAP) can positively influence the lung functions in experimental model of ARDS. New Zealand rabbits with respiratory failure induced by saline lavage (30 ml/kg, 9±3 times) were divided into: ARDS group without therapy, ARDS group treated with SNAP (7 mg/kg i.t.), and healthy Control group. During 5 h of ventilation, respiratory parameters (blood gases, ventilatory pressures) were estimated. After anesthetics overdosing, left lung was saline-lavaged and cell count, cell viability and protein content in bronchoalveolar lavage fluid (BALF) were measured. Right lung tissue was used for estimation of wet/dry weight ratio, concentration of NO metabolites, and histomorphological investigation. Repetitive lung lavage induced lung injury, worsened gas exchange, and damaged alveolar-capillary membrane. Administration of SNAP reduced cell count in BALF, lung edema formation, NO metabolites, and histopathological signs of injury, and improved respiratory parameters. Treatment with intratracheal SNAP alleviated lung injury and edema and improved lung functions in a saline-lavaged model of ARDS suggesting a potential of NO donors also for patients with ARDS.

Mild hypothermia reduces ventilator–induced lung injury, irrespective of reducing respiratory rate

2012 ◽  
Vol 159 (2) ◽  
pp. 110-117 ◽  
Author(s):  
Hamid Aslami ◽  
Maria T. Kuipers ◽  
Charlotte J.P. Beurskens ◽  
Joris J.T.H. Roelofs ◽  
Marcus J. Schultz ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Mild Hypothermia ◽  
Ventilator Induced Lung Injury
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