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Georg Ertl - One of the best experts on this subject based on the ideXlab platform.
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Angiotensin II subtype 1 (AT1) receptors contribute to ischemic contracture and regulate chemomechanical energy transduction in isolated transgenic rat (αMHC-hAT1)594–17 hearts
European journal of heart failure, 2002Co-Authors: Hong Han, Sigrid Hoffmann, Georg ErtlAbstract:Background: The role of AT1 receptors in myocardial ischemia/reperfusion injury is unclear. We, therefore, investigated the effects of the AT1 receptor antagonist irbesartan (Irb) in isolated hearts of selective myocardial AT1 overexpressing transgenic [transgenic(αMHC-hAT1)594–17] and Sprague–Dawley rats (SD) subjected to ischemia/reperfusion injury. Methods and results: Hearts of 4-week-old male SD or transgenic rats were isolated and perfused with Krebs–Henseleit buffer with or without 10 μM Irb in Langendorff mode. After 15 min of stabilization, pressure–volume Curves were obtained and the hearts subjected to 20 min ischemia followed by 30 min reperfusion. A second set of pressure–volume Curves was obtained thereafter. Left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), total coronary flow (CF) and oxygen consumption (MVO2) were recorded continuously. Myocardial efficiency was derived from the slope of relations of MVO2 to pressure/volume area. After 20 min ischemia, LVEDP was significantly higher in transgenic than in SD (35.7±1.8 vs. 29.2±1.0 mmHg, P
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angiotensin ii subtype 1 at1 receptors contribute to ischemic contracture and regulate chemomechanical energy transduction in isolated transgenic rat αmhc hat1 594 17 hearts
European Journal of Heart Failure, 2002Co-Authors: Hong Han, Sigrid Hoffmann, Georg ErtlAbstract:Background: The role of AT1 receptors in myocardial ischemia/reperfusion injury is unclear. We, therefore, investigated the effects of the AT1 receptor antagonist irbesartan (Irb) in isolated hearts of selective myocardial AT1 overexpressing transgenic [transgenic(αMHC-hAT1)594–17] and Sprague–Dawley rats (SD) subjected to ischemia/reperfusion injury. Methods and results: Hearts of 4-week-old male SD or transgenic rats were isolated and perfused with Krebs–Henseleit buffer with or without 10 μM Irb in Langendorff mode. After 15 min of stabilization, pressure–volume Curves were obtained and the hearts subjected to 20 min ischemia followed by 30 min reperfusion. A second set of pressure–volume Curves was obtained thereafter. Left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), total coronary flow (CF) and oxygen consumption (MVO2) were recorded continuously. Myocardial efficiency was derived from the slope of relations of MVO2 to pressure/volume area. After 20 min ischemia, LVEDP was significantly higher in transgenic than in SD (35.7±1.8 vs. 29.2±1.0 mmHg, P<0.05) or Irb treated transgenic hearts (24.3±1.6 mmHg, P<0.05). Myocardial efficiency was increased by Irb before ischemia. Ischemia increased efficiency in SD but not in transgenic rats, Irb increased efficiency in transgenic hearts post-ischemia. Conclusion: Transgenic hearts developed ischemic contracture more rapidly than SD hearts as indicated by higher LVEDP during ischemia. This response was antagonized by Irb, indicating a role of AT1 receptors in ischemic contracture, AT1-receptors also appear to be involved in the control of myocardial efficiency.
Lluis Blanch - One of the best experts on this subject based on the ideXlab platform.
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Static Pressure-Volume Curves of the respiratory system: were they just a passing fad?
Current opinion in critical care, 2008Co-Authors: Guillermo M Albaiceta, Lluis Blanch, Umberto LucangeloAbstract:Purpose of reviewThe aim of this article is to describe the physiologic utility, correlation with lung morphology, difficulties in interpretation and current clinical applications of static respiratory system pressure–volume Curves at the bedside in patients with acute lung injury or acute respirato
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Bedside evaluation of Pressure-Volume Curves in patients with acute respiratory distress syndrome.
Current opinion in critical care, 2007Co-Authors: Lluis Blanch, Josefina López-aguilar, Ana VillagráAbstract:Purpose of review To describe the physiologic and diagnostic utility of static Pressure-Volume Curves of the respiratory system at the bedside in patients with acute lung injury or acute respiratory distress syndrome. Recent findings The Pressure-Volume curve of the respiratory system is a useful tool for the measurement of respiratory system mechanics in patients with acute lung injury or acute respiratory distress syndrome. The Pressure-Volume curve has a sigmoid shape, with lower and upper points on the inspiratory limb and a point of maximum curvature on the expiratory limb. Visual and mathematical Pressure-Volume curve analysis may be useful for understanding individual lung mechanics and for selecting ventilator settings. Among the different techniques for acquiring Pressure-Volume Curves at the bedside, the constant slow flow method is the simplest to perform, the most clinically reliable and has the fewest limitations. Summary Measurement of Pressure-Volume Curves at the bedside in critically ill patients with acute lung injury or acute respiratory distress syndrome should be considered a useful respiratory monitoring tool to assess physiologic lung status and to adjust ventilator settings, when appropriate, to minimize superimposed lung injury associated with mechanical ventilators.
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application of continuous positive airway pressure to trace static pressure volume Curves of the respiratory system
Critical Care Medicine, 2003Co-Authors: Guillermo M Albaiceta, Ana Villagrá, Enrique Piacentini, Josefina Lopezaguilar, Francisco Taboada, Lluis BlanchAbstract:Objective: To evaluate a new technique for Pressure-Volume curve tracing. Design: Prospective experimental study. Setting: Animal research laboratory. Subjects: Six anesthetized rats. Interventions: Two Pressure-Volume Curves were obtained by means of the super-syringe method (gold standard) and the continuous positive airway pressure (CPAP) method. For the CPAP method, the ventilator was switched to CPAP and the pressure level was raised from 0 to 50 cm H 2 O in 5 cm H 2 O steps and then decreased, while we measured lung volume using respiratory inductive plethysmography. Thereafter, lung injury was induced using very high-volume ventilation. Following injury, two further Pressure-Volume Curves were traced. Pressure-Volume pairs were fitted to a mathematical model. Measurements and Main Results: Pressure-Volume Curves were equivalent for each method, with intraclass correlation coefficients being higher than .75 for each pressure level measured. Bias and precision for volume values were 0.46 ± 0.875 mL in basal measurements and 0.31 ± 0.67 mL in postinjury conditions. Lower and upper inflection points on the inspiratory limb and maximum curvature point on the deflation limb obtained using both methods and measured by regression analysis also were correlated, with intraclass correlation coefficients (95% confidence interval) being .97 (.58, .99), .85 (.55, .95), and .94 (.81, .98) (p <.001 for each one). When inflection points were estimated by observers, the correlation coefficient between methods was.90 (.67,.98) for lower inflection points (p <.001). However, estimations for upper inflection points and maximum curvature point were significantly different. Conclusions: The CPAP method for tracing Pressure-Volume Curves is equivalent to the super-syringe method. It is easily applicable at the bedside, avoids disconnection from the ventilator, and can be used to obtain both the inspiratory and the deflation limbs of the Pressure-Volume curve. Use of regression techniques improves determination of inflection points.
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Application of continuous positive airway pressure to trace static Pressure-Volume Curves of the respiratory system.
Critical care medicine, 2003Co-Authors: Guillermo M Albaiceta, Josefina López-aguilar, Ana Villagrá, Enrique Piacentini, Francisco Taboada, Lluis BlanchAbstract:Objective: To evaluate a new technique for Pressure-Volume curve tracing. Design: Prospective experimental study. Setting: Animal research laboratory. Subjects: Six anesthetized rats. Interventions: Two Pressure-Volume Curves were obtained by means of the super-syringe method (gold standard) and the continuous positive airway pressure (CPAP) method. For the CPAP method, the ventilator was switched to CPAP and the pressure level was raised from 0 to 50 cm H 2 O in 5 cm H 2 O steps and then decreased, while we measured lung volume using respiratory inductive plethysmography. Thereafter, lung injury was induced using very high-volume ventilation. Following injury, two further Pressure-Volume Curves were traced. Pressure-Volume pairs were fitted to a mathematical model. Measurements and Main Results: Pressure-Volume Curves were equivalent for each method, with intraclass correlation coefficients being higher than .75 for each pressure level measured. Bias and precision for volume values were 0.46 ± 0.875 mL in basal measurements and 0.31 ± 0.67 mL in postinjury conditions. Lower and upper inflection points on the inspiratory limb and maximum curvature point on the deflation limb obtained using both methods and measured by regression analysis also were correlated, with intraclass correlation coefficients (95% confidence interval) being .97 (.58, .99), .85 (.55, .95), and .94 (.81, .98) (p
Björn Jonson - One of the best experts on this subject based on the ideXlab platform.
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Elastic Pressure-Volume Curves in acute lung injury and acute respiratory distress syndrome
Intensive care medicine, 2004Co-Authors: Björn JonsonAbstract:Background The principal features of elastic Pressure-Volume Curves of lungs or the respiratory system (Pel/V Curves) recorded during reexpansion of collapsed lungs and subsequent deflation have been known since the 1950s. In acute respiratory failure and acute respiratory distress syndrome such Curves have recently attracted increasing interest because new knowledge can be acquired from them, and because such Curves may be useful as guidelines in setting the ventilator so as to avoid ventilator-induced lung injury.
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Seminal Studies in Intensive Care Elastic Pressure-Volume Curves in acute lung injury and acute respiratory distress syndrome
2004Co-Authors: Björn JonsonAbstract:Background The principal features of elastic Pressure-Volume Curves of lungs or the respiratory system (Pel/V Curves) recorded during reexpansion of collapsed lungs and subsequent deflation have been known since the 1950s. In acute respiratory failure and acute respiratory distress syndrome such Curves have recently attracted increasing interest because new knowledge can be acquired from them, and because such Curves may be useful as guidelines in setting the ventilator so as to avoid ventilator-induced lung injury. Discussion This article reviews recording methods, underlying physiology and utility of Pel/V Curves in research and clinical work.
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pressure volume Curves and compliance in acute lung injury evidence of recruitment above the lower inflection point
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Björn Jonson, François Lemaire, Jeanchristophe Richard, Christian Straus, Jordi Mancebo, Laurent BrochardAbstract:Measuring elastic pressure–volume (Pel-V) Curves of the respiratory system and the volume recruited by a positive end-expiratory pressure (PEEP) allows one to study the pressure range over which recruitment occurs in acute lung injury (ALI), and to explain how recruitment affects the compliance. Pel-V Curves were measured with the low flow inflation technique in 11 patients mechanically ventilated for ALI. Curve I was recorded during inflation from the volume attained after a prolonged expiration (6 s) at PEEP (9.0 ± 2.2 cm H2O), and Curve II after expiration to the elastic equilibrium volume at zero end-expiratory pressure (ZEEP). By using the end-expiratory volume of the breaths, the Curves were aligned on a common volume axis to determine the effect of a single complete expiration. In each patient, Curve II (from ZEEP) was shifted toward lower volumes than Curve I. The volume shift, probably due to derecruitment, was 205 ± 100 ml at 15 cm H2O (p < 0.01) and 78 ± 93 ml at 30 cm H2O (p < 0.01); thus, dur...
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pressure volume Curves and compliance in acute lung injury evidence of recruitment above the lower inflection point
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Björn Jonson, François Lemaire, Jeanchristophe Richard, Christian Straus, Jordi Mancebo, Laurent BrochardAbstract:Measuring elastic Pressure-Volume (Pel-V) Curves of the respiratory system and the volume recruited by a positive end-expiratory pressure (PEEP) allows one to study the pressure range over which recruitment occurs in acute lung injury (ALI), and to explain how recruitment affects the compliance. Pel-V Curves were measured with the low flow inflation technique in 11 patients mechanically ventilated for ALI. Curve I was recorded during inflation from the volume attained after a prolonged expiration (6 s) at PEEP (9.0 +/- 2.2 cm H2O), and Curve II after expiration to the elastic equilibrium volume at zero end-expiratory pressure (ZEEP). By using the end-expiratory volume of the breaths, the Curves were aligned on a common volume axis to determine the effect of a single complete expiration. In each patient, Curve II (from ZEEP) was shifted toward lower volumes than Curve I. The volume shift, probably due to derecruitment, was 205 +/- 100 ml at 15 cm H2O (p < 0.01) and 78 +/- 93 ml at 30 cm H2O (p < 0.01); thus, during inflation from ZEEP, the volume deficit was successively regained over a pressure range up to at least 30 cm H2O. At any pressure, compliance was higher on the curve from ZEEP than from PEEP, by 10.0 +/- 8.7 ml/cm H2O at 15 cm H2O (p < 0.01), and by 5.4 +/- 5.5 at 30 cm H2O (p < 0.01). It is concluded that in ALI, a single expiration to ZEEP leads to lung collapse. High compliance during insufflation from ZEEP indicates that lung recruitment happens far above the lower inflection point of the Pel-V curve.
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Elastic pressure–volume Curves: what information do they convey?
Thorax, 1999Co-Authors: Björn Jonson, Cecilia SvantessonAbstract:In 1929 von Neergaard demonstrated that surface forces are responsible for a large part of the elastic recoil pressure of the lungs.1 This was evidenced by recordings of elastic recoil during deflation of air- and liquid-filled lungs. On the basis of similar experiments, extended to include inflation (fig 1), Radford laid down concepts which still form the basis for the interpretation of elastic pressure–volume (Pel–V) Curves in today’s intensive care units.2 In this review these concepts will be analysed. The relevance of Pel–V Curves as guidelines in managing ventilation to avoid lung trauma will be discussed. Furthermore, techniques for recording and analysis of Pel–V Curves will be briefly commented upon. Figure 1 Pulmonary pressure–volume Curves obtained during inflation and deflation with air and saline.2 The higher elastic recoil pressure during air deflation shows that surface tension contributes to lung recoil. It can be seen that during inflation with air a lower inflection point is followed by a steep, nearly linear, segment. Pel–V Curves are often recorded during an insufflation of gas which is preceded by an expiration to the elastic equilibrium volume. An example of an inspiratory Pel–V curve recorded from a patient with acute lung injury (ALI) is shown in fig 2. The features of the curve are well known.3 4 The curve can be considered to consist of three segments: an initial flat segment reflects a very low compliance, indicating collapse of peripheral airways and/or lung units preventing lung inflation; there then follows a segment with a steeper slope (that is, greater compliance); the transition between these two segments, which may be more or less abrupt, can be denoted the lower inflection point (LIP). Compliance remains stable over the second “linear” segment, as shown in …
Guillermo M Albaiceta - One of the best experts on this subject based on the ideXlab platform.
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Static Pressure-Volume Curves of the respiratory system: were they just a passing fad?
Current opinion in critical care, 2008Co-Authors: Guillermo M Albaiceta, Lluis Blanch, Umberto LucangeloAbstract:Purpose of reviewThe aim of this article is to describe the physiologic utility, correlation with lung morphology, difficulties in interpretation and current clinical applications of static respiratory system pressure–volume Curves at the bedside in patients with acute lung injury or acute respirato
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inspiratory vs expiratory pressure volume Curves to set end expiratory pressure in acute lung injury
Intensive Care Medicine, 2005Co-Authors: Guillermo M Albaiceta, Luis H Luyando, Diego Parra, Rafael Menendez, Juan Calvo, P R Pedreira, Francisco TaboadaAbstract:Objective To study the effects of two levels of positive end-expiratory pressure (PEEP), 2 cmH2O above the lower inflection point of the inspiratory limb and equal to the point of maximum curvature on the expiratory limb of the Pressure-Volume curve, in gas exchange, respiratory mechanics, and lung aeration.
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application of continuous positive airway pressure to trace static pressure volume Curves of the respiratory system
Critical Care Medicine, 2003Co-Authors: Guillermo M Albaiceta, Ana Villagrá, Enrique Piacentini, Josefina Lopezaguilar, Francisco Taboada, Lluis BlanchAbstract:Objective: To evaluate a new technique for Pressure-Volume curve tracing. Design: Prospective experimental study. Setting: Animal research laboratory. Subjects: Six anesthetized rats. Interventions: Two Pressure-Volume Curves were obtained by means of the super-syringe method (gold standard) and the continuous positive airway pressure (CPAP) method. For the CPAP method, the ventilator was switched to CPAP and the pressure level was raised from 0 to 50 cm H 2 O in 5 cm H 2 O steps and then decreased, while we measured lung volume using respiratory inductive plethysmography. Thereafter, lung injury was induced using very high-volume ventilation. Following injury, two further Pressure-Volume Curves were traced. Pressure-Volume pairs were fitted to a mathematical model. Measurements and Main Results: Pressure-Volume Curves were equivalent for each method, with intraclass correlation coefficients being higher than .75 for each pressure level measured. Bias and precision for volume values were 0.46 ± 0.875 mL in basal measurements and 0.31 ± 0.67 mL in postinjury conditions. Lower and upper inflection points on the inspiratory limb and maximum curvature point on the deflation limb obtained using both methods and measured by regression analysis also were correlated, with intraclass correlation coefficients (95% confidence interval) being .97 (.58, .99), .85 (.55, .95), and .94 (.81, .98) (p <.001 for each one). When inflection points were estimated by observers, the correlation coefficient between methods was.90 (.67,.98) for lower inflection points (p <.001). However, estimations for upper inflection points and maximum curvature point were significantly different. Conclusions: The CPAP method for tracing Pressure-Volume Curves is equivalent to the super-syringe method. It is easily applicable at the bedside, avoids disconnection from the ventilator, and can be used to obtain both the inspiratory and the deflation limbs of the Pressure-Volume curve. Use of regression techniques improves determination of inflection points.
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Application of continuous positive airway pressure to trace static Pressure-Volume Curves of the respiratory system.
Critical care medicine, 2003Co-Authors: Guillermo M Albaiceta, Josefina López-aguilar, Ana Villagrá, Enrique Piacentini, Francisco Taboada, Lluis BlanchAbstract:Objective: To evaluate a new technique for Pressure-Volume curve tracing. Design: Prospective experimental study. Setting: Animal research laboratory. Subjects: Six anesthetized rats. Interventions: Two Pressure-Volume Curves were obtained by means of the super-syringe method (gold standard) and the continuous positive airway pressure (CPAP) method. For the CPAP method, the ventilator was switched to CPAP and the pressure level was raised from 0 to 50 cm H 2 O in 5 cm H 2 O steps and then decreased, while we measured lung volume using respiratory inductive plethysmography. Thereafter, lung injury was induced using very high-volume ventilation. Following injury, two further Pressure-Volume Curves were traced. Pressure-Volume pairs were fitted to a mathematical model. Measurements and Main Results: Pressure-Volume Curves were equivalent for each method, with intraclass correlation coefficients being higher than .75 for each pressure level measured. Bias and precision for volume values were 0.46 ± 0.875 mL in basal measurements and 0.31 ± 0.67 mL in postinjury conditions. Lower and upper inflection points on the inspiratory limb and maximum curvature point on the deflation limb obtained using both methods and measured by regression analysis also were correlated, with intraclass correlation coefficients (95% confidence interval) being .97 (.58, .99), .85 (.55, .95), and .94 (.81, .98) (p
Hong Han - One of the best experts on this subject based on the ideXlab platform.
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Angiotensin II subtype 1 (AT1) receptors contribute to ischemic contracture and regulate chemomechanical energy transduction in isolated transgenic rat (αMHC-hAT1)594–17 hearts
European journal of heart failure, 2002Co-Authors: Hong Han, Sigrid Hoffmann, Georg ErtlAbstract:Background: The role of AT1 receptors in myocardial ischemia/reperfusion injury is unclear. We, therefore, investigated the effects of the AT1 receptor antagonist irbesartan (Irb) in isolated hearts of selective myocardial AT1 overexpressing transgenic [transgenic(αMHC-hAT1)594–17] and Sprague–Dawley rats (SD) subjected to ischemia/reperfusion injury. Methods and results: Hearts of 4-week-old male SD or transgenic rats were isolated and perfused with Krebs–Henseleit buffer with or without 10 μM Irb in Langendorff mode. After 15 min of stabilization, pressure–volume Curves were obtained and the hearts subjected to 20 min ischemia followed by 30 min reperfusion. A second set of pressure–volume Curves was obtained thereafter. Left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), total coronary flow (CF) and oxygen consumption (MVO2) were recorded continuously. Myocardial efficiency was derived from the slope of relations of MVO2 to pressure/volume area. After 20 min ischemia, LVEDP was significantly higher in transgenic than in SD (35.7±1.8 vs. 29.2±1.0 mmHg, P
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angiotensin ii subtype 1 at1 receptors contribute to ischemic contracture and regulate chemomechanical energy transduction in isolated transgenic rat αmhc hat1 594 17 hearts
European Journal of Heart Failure, 2002Co-Authors: Hong Han, Sigrid Hoffmann, Georg ErtlAbstract:Background: The role of AT1 receptors in myocardial ischemia/reperfusion injury is unclear. We, therefore, investigated the effects of the AT1 receptor antagonist irbesartan (Irb) in isolated hearts of selective myocardial AT1 overexpressing transgenic [transgenic(αMHC-hAT1)594–17] and Sprague–Dawley rats (SD) subjected to ischemia/reperfusion injury. Methods and results: Hearts of 4-week-old male SD or transgenic rats were isolated and perfused with Krebs–Henseleit buffer with or without 10 μM Irb in Langendorff mode. After 15 min of stabilization, pressure–volume Curves were obtained and the hearts subjected to 20 min ischemia followed by 30 min reperfusion. A second set of pressure–volume Curves was obtained thereafter. Left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), total coronary flow (CF) and oxygen consumption (MVO2) were recorded continuously. Myocardial efficiency was derived from the slope of relations of MVO2 to pressure/volume area. After 20 min ischemia, LVEDP was significantly higher in transgenic than in SD (35.7±1.8 vs. 29.2±1.0 mmHg, P<0.05) or Irb treated transgenic hearts (24.3±1.6 mmHg, P<0.05). Myocardial efficiency was increased by Irb before ischemia. Ischemia increased efficiency in SD but not in transgenic rats, Irb increased efficiency in transgenic hearts post-ischemia. Conclusion: Transgenic hearts developed ischemic contracture more rapidly than SD hearts as indicated by higher LVEDP during ischemia. This response was antagonized by Irb, indicating a role of AT1 receptors in ischemic contracture, AT1-receptors also appear to be involved in the control of myocardial efficiency.