scholarly journals Haemodynamic Effects of Lung Recruitment Manoeuvres

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
András Lovas ◽  
Tamás Szakmány
Keyword(s):  
Left Ventricle ◽  
Lung Injury ◽  
Cardiovascular System ◽  
Haemodynamic Effects ◽  
Lung Recruitment ◽  
Venous Admixture ◽  
Intrapulmonary Shunt ◽  
Airway Pressures ◽  
Short Period

Atelectasis caused by lung injury leads to increased intrapulmonary shunt, venous admixture, and hypoxaemia. Lung recruitment manoeuvres aim to quickly reverse this scenario by applying increased airway pressures for a short period of time which meant to open the collapsed alveoli. Although the procedure can improve oxygenation, but due to the heart-lung and right and left ventricle interactions elevated intrathoracic pressures can inflict serious effects on the cardiovascular system. The purpose of this paper is to give an overview on the pathophysiological background of the heart-lung interactions and the best way to monitor these changes during lung recruitment.

Reversal of dependent lung collapse predicts response to lung recruitment in children with early acute lung injury

2012 ◽  
Vol 13 (5) ◽  
pp. 509-515 ◽  
Author(s):  
Gerhard K. Wolf ◽  
Camille Gómez-Laberge ◽  
John N. Kheir ◽  
David Zurakowski ◽  
Brian K. Walsh ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Recruitment ◽  
Dependent Lung ◽  
Lung Collapse

scholarly journals AIRWAY PRESSURES DURING IPPV BEFORE AND AFTER LUNG INJURY

1989 ◽  
Vol 26 (5) ◽  
pp. 508-508
Author(s):  
Anders Jonzon ◽  
Torgny Norsted ◽  
Gunnar Sedin
Keyword(s):  
Lung Injury ◽  
Airway Pressures ◽  
Before And After

Lung Recruitment in Localized Lung Injury

2002 ◽  
pp. 313-319
Author(s):  
L. Blanch ◽  
G. Murias ◽  
A. Nahum
Keyword(s):  
Lung Injury ◽  
Lung Recruitment

In the Loop—Left Ventricular Pressures

2011 ◽  
pp. 42-47
Author(s):  
James R. Munis
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Cardiovascular System ◽  
Aortic Root ◽  
Left Ventricular ◽  
Root Pressure ◽  
The Third

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.

scholarly journals Modeling the dynamics of recruitment and derecruitment in mice with acute lung injury

2008 ◽  
Vol 105 (6) ◽  
pp. 1813-1821 ◽  
Author(s):  
Christopher B. Massa ◽  
Gilman B. Allen ◽  
Jason H. T. Bates
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Recruitment ◽  
Mechanically Ventilated ◽  
Critical Opening ◽  
Injured Lung ◽  
Order Of Magnitude ◽  
Opening And Closing ◽  
Air Liquid Interface ◽  
Insight Into

Lung recruitment and derecruitment contribute significantly to variations in the elastance of the respiratory system during mechanical ventilation. However, the decreases in elastance that occur with deep inflation are transient, especially in acute lung injury. Bates and Irvin ( 8 ) proposed a model of the lung that recreates time-varying changes in elastance as a result of progressive recruitment and derecruitment of lung units. The model is characterized by distributions of critical opening and closing pressures throughout the lung and by distributions of speeds with which the processes of opening and closing take place once the critical pressures have been achieved. In the present study, we adapted this model to represent a mechanically ventilated mouse. We fit the model to data collected in a previous study from control mice and mice in various stages of acid-induced acute lung injury ( 3 ). Excellent fits to the data were obtained when the normally distributed critical opening pressures were about 5 cmH2O above the closing pressures and when the hyperbolically distributed opening velocities were about an order of magnitude greater than the closing velocities. We also found that, compared with controls, the injured mice had markedly increased opening and closing pressures but no change in the velocities, suggesting that the key biophysical change wrought by acid injury is dysfunction of surface tension at the air-liquid interface. Our computational model of lung recruitment and derecruitment dynamics is thus capable of accurately mimicking data from mice with acute lung injury and may provide insight into the altered biophysics of the injured lung.

scholarly journals Noninvasive quantification of macrophagic lung recruitment during experimental ventilation-induced lung injury

2019 ◽  
Vol 127 (2) ◽  
pp. 546-558
Author(s):  
Laurent Bitker ◽  
Nicolas Costes ◽  
Didier Le Bars ◽  
Franck Lavenne ◽  
Maciej Orkisz ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protective Ventilation ◽  
Lung Recruitment ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Dynamic Strain ◽  
Lung Uptake ◽  
Positron Emission ◽  
Ventilation Induced Lung Injury

Macrophagic lung infiltration is pivotal in the development of lung biotrauma because of ventilation-induced lung injury (VILI). We assessed the performance of [11C](R)-PK11195, a positron emission tomography (PET) radiotracer binding the translocator protein, to quantify macrophage lung recruitment during experimental VILI. Pigs ( n = 6) were mechanically ventilated under general anesthesia, using protective ventilation settings (baseline). Experimental VILI was performed by titrating tidal volume to reach a transpulmonary end-inspiratory pressure (∆PL) of 35–40 cmH2O. We acquired PET/computed tomography (CT) lung images at baseline and after 4 h of VILI. Lung macrophages were quantified in vivo by the standardized uptake value (SUV) of [11C](R)-PK11195 measured in PET on the whole lung and in six lung regions and ex vivo on lung pathology at the end of experiment. Lung mechanics were extracted from CT images to assess their association with the PET signal. ∆PL increased from 9 ± 1 cmH2O under protective ventilation, to 36 ± 6 cmH2O during experimental VILI. Compared with baseline, whole-lung [11C](R)-PK11195 SUV significantly increased from 1.8 ± 0.5 to 2.9 ± 0.5 after experimental VILI. Regional [11C](R)-PK11195 SUV was positively associated with the magnitude of macrophage recruitment in pathology ( P = 0.03). Compared with baseline, whole-lung CT-derived dynamic strain and tidal hyperinflation increased significantly after experimental VILI, from 0.6 ± 0 to 2.0 ± 0.4, and 1 ± 1 to 43 ± 19%, respectively. On multivariate analysis, both were significantly associated with regional [11C](R)-PK11195 SUV. [11C](R)-PK11195 lung uptake (a proxy of lung inflammation) was increased by experimental VILI and was associated with the magnitude of dynamic strain and tidal hyperinflation. NEW & NOTEWORTHY We assessed the performance of [11C](R)-PK11195, a translocator protein-specific positron emission tomography (PET) radiotracer, to quantify macrophage lung recruitment during experimental ventilation-induced lung injury (VILI). In this proof-of-concept study, we showed that the in vivo quantification of [11C](R)-PK11195 lung uptake in PET reflected the magnitude of macrophage lung recruitment after VILI. Furthermore, increased [11C](R)-PK11195 lung uptake was associated with harmful levels of dynamic strain and tidal hyperinflation applied to the lungs.

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