| 1. |
- Bachmann, M. Consuelo, et al.
(author)
-
Electrical impedance tomography in acute respiratory distress syndrome
- 2018
-
In: Critical Care. - : BioMed Central. - 1364-8535 .- 1466-609X. ; 22
-
Research review (peer-reviewed)abstract
- Acute respiratory distress syndrome (ARDS) is a clinical entity that acutely affects the lung parenchyma, and is characterized by diffuse alveolar damage and increased pulmonary vascular permeability. Currently, computed tomography (CT) is commonly used for classifying and prognosticating ARDS. However, performing this examination in critically ill patients is complex, due to the need to transfer these patients to the CT room. Fortunately, new technologies have been developed that allow the monitoring of patients at the bedside. Electrical impedance tomography (EIT) is a monitoring tool that allows one to evaluate at the bedside the distribution of pulmonary ventilation continuously, in real time, and which has proven to be useful in optimizing mechanical ventilation parameters in critically ill patients. Several clinical applications of EIT have been developed during the last years and the technique has been generating increasing interest among researchers. However, among clinicians, there is still a lack of knowledge regarding the technical principles of EIT and potential applications in ARDS patients. The aim of this review is to present the characteristics, technical concepts, and clinical applications of EIT, which may allow better monitoring of lung function during ARDS.
|
|
| 2. |
- Hurtado, Daniel E., et al.
(author)
-
Improving the Accuracy of Registration-Based Biomechanical Analysis : A Finite Element Approach to Lung Regional Strain Quantification
- 2016
-
In: IEEE Transactions on Medical Imaging. - 0278-0062 .- 1558-254X. ; 35:2, s. 580-588
-
Journal article (peer-reviewed)abstract
- Tissue deformation plays an important role in lung physiology, as lung parenchyma largely deforms during spontaneous ventilation. However, excessive regional deformation may lead to lung injury, as observed in patients undergoing mechanical ventilation. Thus, the accurate estimation of regional strain has recently received great attention in the intensive care community. In this work, we assess the accuracy of regional strain maps computed from direct differentiation of B-Spline (BS) interpolations, a popular technique employed in non-rigid registration of lung computed tomography (CT) images. We show that, while BS-based registration methods give excellent results for the deformation transformation, the strain field directly computed from BS derivatives results in predictions that largely oscillate, thus introducing important errors that can even revert the sign of strain. To alleviate such spurious behavior, we present a novel finite-element (FE) method for the regional strain analysis of lung CT images. The method follows from a variational strain recovery formulation, and delivers a continuous approximation to the strain field in arbitrary domains. From analytical benchmarks, we show that the FE method results in errors that are a fraction of those found for the BS method, both in an average and pointwise sense. The application of the proposed FE method to human lung CT images results in 3D strain maps are heterogeneous and smooth, showing high consistency with specific ventilation maps reported in the literature. We envision that the proposed FE method will considerably improve the accuracy of image-based biomechanical analysis, making it reliable enough for routine medical applications.
|
|
| 3. |
- Hurtado, Daniel E., et al.
(author)
-
Spatial patterns and frequency distributions of regional deformation in the healthy human lung
- 2017
-
In: Biomechanics and Modeling in Mechanobiology. - : SPRINGER HEIDELBERG. - 1617-7959 .- 1617-7940. ; 16:4, s. 1413-1423
-
Journal article (peer-reviewed)abstract
- Understanding regional deformation in the lung has long attracted the medical community, as parenchymal deformation plays a key role in respiratory physiology. Recent advances in image registration make it possible to noninvasively study regional deformation, showing that volumetric deformation in healthy lungs follows complex spatial patterns not necessarily shared by all subjects, and that deformation can be highly anisotropic. In this work, we systematically study the regional deformation in the lungs of eleven human subjects by means of in vivo image-based biomechanical analysis. Regional deformation is quantified in terms of 3D maps of the invariants of the right stretch tensor, which are related to regional changes in length, surface and volume. Based on the histograms of individual lungs, we show that log-normal distributions adequately represent the frequency distribution of deformation invariants in the lung, which naturally motivates the normalization of the invariant fields in terms of the log-normal score. Normalized maps of deformation invariants allow for a direct intersubject comparison, as they display spatial patterns of deformation in a range that is common to all subjects. For the population studied, we find that lungs in supine position display a marked gradient along the gravitational direction not only for volumetric but also for length and surface regional deformation, highlighting the role of gravity in the regional deformation of normal lungs under spontaneous breathing.
|
|
| 4. |
- Retamal, Jaime, et al.
(author)
-
Does Regional Lung Strain Correlate With Regional Inflammation in Acute Respiratory Distress Syndrome During Nonprotective Ventilation? : An Experimental Porcine Study
- 2018
-
In: Critical Care Medicine. - 0090-3493 .- 1530-0293. ; 46:6, s. e591-e599
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: It is known that ventilator-induced lung injury causes increased pulmonary inflammation. It has been suggested that one of the underlying mechanisms may be strain. The aim of this study was to investigate whether lung regional strain correlates with regional inflammation in a porcine model of acute respiratory distress syndrome.DESIGN: Retrospective analysis of CT images and positron emission tomography images using [18F]fluoro-2-deoxy-D-glucose.SETTING: University animal research laboratory.SUBJECTS: Seven piglets subjected to experimental acute respiratory distress syndrome and five ventilated controls.INTERVENTIONS: Acute respiratory distress syndrome was induced by repeated lung lavages, followed by 210 minutes of injurious mechanical ventilation using low positive end-expiratory pressures (mean, 4 cm H2O) and high inspiratory pressures (mean plateau pressure, 45 cm H2O). All animals were subsequently studied with CT scans acquired at end-expiration and end-inspiration, to obtain maps of volumetric strain (inspiratory volume - expiratory volume)/expiratory volume, and dynamic positron emission tomography imaging. Strain maps and positron emission tomography images were divided into 10 isogravitational horizontal regions-of-interest, from which spatial correlation was calculated for each animal.MEASUREMENTS AND MAIN RESULTS: The acute respiratory distress syndrome model resulted in a decrease in respiratory system compliance (20.3 ± 3.4 to 14.0 ± 4.9 mL/cm H2O; p < 0.05) and oxygenation (PaO2/FIO2, 489 ± 80 to 92 ± 59; p < 0.05), whereas the control animals did not exhibit changes. In the acute respiratory distress syndrome group, strain maps showed a heterogeneous distribution with a greater concentration in the intermediate gravitational regions, which was similar to the distribution of [18F]fluoro-2-deoxy-D-glucose uptake observed in the positron emission tomography images, resulting in a positive spatial correlation between both variables (median R2 = 0.71 [0.02-0.84]; p < 0.05 in five of seven animals), which was not observed in the control animals.CONCLUSION: In this porcine acute respiratory distress syndrome model, regional lung strain was spatially correlated with regional inflammation, supporting that strain is a relevant and prominent determinant of ventilator-induced lung injury.
|
|
| 5. |
- Retamal, Jaime, et al.
(author)
-
Feasibility of 68Ga-labeled Siglec-9 peptide for the imaging of acute lung inflammation : a pilot study in a porcine model of acute respiratory distress syndrome
- 2016
-
In: American Journal of Nuclear Medicine and Molecular Imaging. - 2160-8407. ; 6:1, s. 18-31
-
Journal article (peer-reviewed)abstract
- There is an unmet need for noninvasive, specific and quantitative imaging of inherent inflammatory activity. Vascular adhesion protein-1 (VAP-1) translocates to the luminal surface of endothelial cells upon inflammatory challenge. We hypothesized that in a porcine model of acute respiratory distress syndrome (ARDS), positron emission tomography (PET) with sialic acid-binding immunoglobulin-like lectin 9 (Siglec-9) based imaging agent targeting VAP-1 would allow quantification of regional pulmonary inflammation. ARDS was induced by lung lavages and injurious mechanical ventilation. Hemodynamics, respiratory system compliance (Crs) and blood gases were monitored. Dynamic examination using [(15)O]water PET-CT (10 min) was followed by dynamic (90 min) and whole-body examination using VAP-1 targeting (68)Ga-labeled 1,4,7,10-tetraaza cyclododecane-1,4,7-tris-acetic acid-10-ethylene glycol-conjugated Siglec-9 motif peptide ([(68)Ga]Ga-DOTA-Siglec-9). The animals received an anti-VAP-1 antibody for post-mortem immunohistochemistry assay of VAP-1 receptors. Tissue samples were collected post-mortem for the radioactivity uptake, histology and immunohistochemistry assessment. Marked reduction of oxygenation and Crs, and higher degree of inflammation were observed in ARDS animals. [(68)Ga]Ga-DOTA-Siglec-9 PET showed significant uptake in lungs, kidneys and urinary bladder. Normalization of the net uptake rate (Ki) for the tissue perfusion resulted in 4-fold higher uptake rate of [(68)Ga]Ga-DOTA-Siglec-9 in the ARDS lungs. Immunohistochemistry showed positive VAP-1 signal in the injured lungs. Detection of pulmonary inflammation associated with a porcine model of ARDS was possible with [(68)Ga]Ga-DOTA-Siglec-9 PET when using kinetic modeling and normalization for tissue perfusion.
|
|
| 6. |
- Retamal, Jaime, et al.
(author)
-
High PEEP levels are associated with overdistension and tidal recruitment/derecruitment in ARDS patients
- 2015
-
In: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 59:9, s. 1161-1169
-
Journal article (peer-reviewed)abstract
- BackgroundPositive end-expiratory pressure (PEEP) improves gas exchange and respiratory mechanics, and it may decrease tissue injury and inflammation. The mechanisms of this protective effect are not fully elucidated. Our aim was to determine the intrinsic effects of moderate and higher levels of PEEP on tidal recruitment/derecruitment, hyperinflation, and lung mechanics, in patients with acute respiratory distress syndrome (ARDS). MethodsNine patients with ARDS of mainly pulmonary origin were ventilated sequential and randomly using two levels of PEEP: 9 and 15cmH(2)O, and studied with dynamic computed tomography at a fix transversal lung region. Tidal recruitment/derecruitment and hyperinflation were determined as non-aerated tissue and hyperinflated tissue variation between inspiration and expiration, expressed as percentage of total weight. We also assessed the maximal amount of non-aerated and hyperinflated tissue weight. ResultsPEEP 15cmH(2)O was associated with decrease in non-aerated tissue in all the patients (P<0.01). However, PEEP 15cmH(2)O did not decrease tidal recruitment/derecruitment compared to PEEP 9cmH(2)O (P=1). In addition, PEEP 15cmH(2)O markedly increased maximal hyperinflation (P<0.01) and tidal hyperinflation (P<0.05). Lung compliance decreased with PEEP 15cmH(2)O (P<0.001). ConclusionIn this series of patients with ARDS of mainly pulmonary origin, application of high levels of PEEP did not decrease tidal recruitment/derecruitment, but instead consistently increased tidal and maximal hyperinflation.
|
|
| 7. |
- Retamal, Jaime, et al.
(author)
-
High respiratory rate is associated with early reduction of lung edema clearance in an experimental model of ARDS
- 2016
-
In: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 60:1, s. 79-92
-
Journal article (peer-reviewed)abstract
- BACKGROUND: The independent impact of respiratory rate on ventilator-induced lung injury has not been fully elucidated. The aim of this study was to investigate the effects of two clinically relevant respiratory rates on early ventilator-induced lung injury evolution and lung edema during the protective ARDSNet strategy. We hypothesized that the use of a higher respiratory rate during a protective ARDSNet ventilation strategy increases lung inflammation and, in addition, lung edema associated to strain-induced activation of transforming growth factor beta (TGF-β) in the lung epithelium.METHODS: Twelve healthy piglets were submitted to a two-hit lung injury model and randomized into two groups: LRR (20 breaths/min) and HRR (40 breaths/min). They were mechanically ventilated during 6 h according to the ARDSNet strategy. We assessed respiratory mechanics, hemodynamics, and extravascular lung water (EVLW). At the end of the experiment, the lungs were excised and wet/dry ratio, TGF-β pathway markers, regional histology, and cytokines were evaluated.RESULTS: No differences in oxygenation, PaCO2 levels, systemic and pulmonary arterial pressures were observed during the study. Respiratory system compliance and mean airway pressure were lower in LRR group. A decrease in EVLW over time occurred only in the LRR group (P < 0.05). Wet/dry ratio was higher in the HRR group (P < 0.05), as well as TGF-β pathway activation. Histological findings suggestive of inflammation and inflammatory tissue cytokines were higher in LRR.CONCLUSION: HRR was associated with more pulmonary edema and higher activation of the TGF-β pathway. In contrast with our hypothesis, HRR was associated with less lung inflammation.
|
|
| 8. |
- Retamal, Jaime, et al.
(author)
-
Non-lobar atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation
- 2014
-
In: Critical Care. - : Springer Science and Business Media LLC. - 1364-8535 .- 1466-609X. ; 18:5, s. 505-
-
Journal article (peer-reviewed)abstract
- IntroductionWhen alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation.MethodsA total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (VT) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH2O (VT10/PEEP3); and 2) VT = 20 ml/kg and PEEP = 0 cmH2O (VT20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls.ResultsAtelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm3. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the VT20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1β and cytokine-induced neutrophil chemoattractant-1 between regions.ConclusionsThe present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.
|
|
| 9. |
- Retamal, Jaime, et al.
(author)
-
Physiological and inflammatory consequences of high and low respiratory rate in acute respiratory distress syndrome
- 2021
-
In: Acta Anaesthesiologica Scandinavica. - : John Wiley & Sons. - 0001-5172 .- 1399-6576. ; 65:8, s. 1013-1022
-
Research review (peer-reviewed)abstract
- Using protective mechanical ventilation strategies with low tidal volume is usually accompanied by an increment of respiratory rate to maintain adequate alveolar ventilation. However, there is no robust data that support the safety of a high respiratory rate concerning ventilator-induced lung injury. Several experimental animal studies have explored the effects of respiratory rate over lung physiology, using a wide range of frequencies and different models. Clinical evidence is scarce and restricted to the physiological impact of increased respiratory rate. Undoubtedly, the respiratory rate can influence respiratory mechanics in various ways as a factor of multiplication of the power of ventilation, and gas exchange, and also on alveolar dynamics. In this narrative review, we present our point of view over the main experimental and clinical evidence available regarding the effect of respiratory rate on ventilator-induced lung injury development.
|
|
| 10. |
- Retamal, Jaime, et al.
(author)
-
Regional pulmonary deformation is positively correlated with regional lung inflammation assessed by 18F-FDG positron emission tomography / computed tomography
-
Other publication (other academic/artistic)abstract
- Objective: Lung deformation beyond of physiological capacity is associated with cell death and inflammation. Lung strain has been estimated as a global strain, but uneven strain distribution may lead to regional stress concentrations and lung damage. Local lung inflammation can be estimated using PET imaging of [18F]fluoro-2-deoxy-D-glucose. We hypothesized that local lung deformation correlates well with local inflammation. The aim of this study was to assess local tidal deformations by using a new mathematical model of finite-elements to analyze CT images, and to correlate them with local inflammation in a porcine experimental model of early acute respiratory distress syndrome.Design: Retrospective images analysis, laboratory investigation.Setting: University animal research laboratory.Subjects: Seven piglets submitted to experimental ventilator-induced lung injury and five healthy ventilated controls.Intervention: Lung injury was induced by repeated lung lavages and 210 minutes of injurious mechanical ventilation using low positive end-expiratory pressure and high inspiratory pressures. All animals were subsequently studied with dynamic PET imaging of [18F]fluoro-2-deoxy-D-glucose. CT scans were acquired at end expiration and end inspiration. Then maps of deformation were constructed and regional deformation was estimated. We divided the lung parenchyma in 10 horizontal ROIs, and correlations of local volumetric strain and [18F]fluoro-2-deoxy-D-glucose uptake were analyzed in each ROI.Measurements and Main Results: The deformation maps showed a heterogeneous distribution with a greater concentration in the intermediate gravitational regions. We found a strong correlation between local strain and inflammation (R2 > 0.5) for the whole lung, when we eliminate the 3/10 dorsal ROIs R2 increased until>0.8.Conclusion: the present findings suggest that the greater local stretches were mainly concentrated in the intermediate gravitational zones of injured heterogeneous lungs. Additionally, local lung deformations correlated well with local inflammation in this experimental model of VILI. And the new proposed image-based estimation of regional volumetric strain based on finite element interpolations has the potential to give new insights of local pathogenic mechanisms of VILI and how best design protective-ventilations strategies.
|
|
| 11. |
- Retamal Montes, Jaime, 1978-
(author)
-
Aspects on ventilation induced stress and strain on regional and global inflammation in experimental acute respiratory distress syndrome
- 2016
-
Doctoral thesis (other academic/artistic)abstract
- Mechanical ventilation (MV) is a life-saving therapy in acute respiratory distress syndrome (ARDS), a condition that affects 3000 patients/year in Sweden with a mortality rate of about 40%. However, MV may induce or worsen lung injury causing “ventilator-induced lung injury (VILI)”. From a mechanical perspective strain (deformation, or relative change in lung volume) and stress (tension) have been postulated as main determinants of VILI. High respiratory rate is potentially another factor that may exacerbate VILI by amplifying the total energy transmitted to the lungs during MV. In this thesis in animal ARDS models the hypotheses were that 1) lung parenchyma inhomogeneities concentrate stress and amplify lung damage and inflammation, 2) higher respiratory rates increase lung inflammation and lung edema in heterogeneous ARDS, and 3) local lung deformation is related to local inflammation.First, in a rat model the effect on inflammation and structural damage of regional lung collapse on the healthy surrounding lung tissue was assessed. Second, in porcine models the effect of respiratory rate on lung edema and inflammation was studied during two ventilatory modes; a) a permissive collapse mode and b) a homogenized lung parenchyma mode. Finally, lung deformation was correlated with lung inflammation assessed by positron emission tomography using 18F-FDG uptake.It was found that; 1) local inhomogeneities can act as stress amplifiers, increasing lung tissue inflammation and damage in the healthy surrounded lung. 2) high respiratory rate increases lung edema but decreases lung inflammation when permissive lung collapse is used and that these effects are prevented with lung parenchyma homogenization; 3) local lung deformation and inflammation are well correlated.In conclusion, lung inhomogeneities may aggravate VILI, respiratory rate may affect in different ways VILI progression depending on the ventilatory strategy, and finally, lung deformation is closely related to lung inflammation. With the caveat that the studies are performed in animal models, the results suggest that using ventilator strategies that homogenize the lungs, i.e., open collapsed lung regions and prevent re-collapse in ARDS will reduce VILI and in the end may decrease morbidity and the high mortality in this condition.
|
|
| 12. |
- Retamal Montes, Jaime, 1978-, et al.
(author)
-
Open lung approach ventilation abolishes the negative effects of respiratory rate in experimental lung injury
- 2016
-
In: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 60:8, s. 1131-1141
-
Journal article (peer-reviewed)abstract
- BACKGROUND: We recently reported that a high respiratory rate was associated with less inflammation than a low respiratory rate, but caused more pulmonary edema in a model of ARDS when an ARDSNet ventilatory strategy was used. We hypothesized that an open lung approach (OLA) strategy would neutralize the independent effects of respiratory rate on lung inflammation and edema. This hypothesis was tested in an ARDS model using two clinically relevant respiratory rates during OLA strategy.METHODS: Twelve piglets were subjected to an experimental model of ARDS and randomized into two groups: LRR (20 breaths/min) and HRR (40 breaths/min). They were mechanically ventilated for 6 h according to an OLA strategy. We assessed respiratory mechanics, hemodynamics, and extravascular lung water (EVLW). At the end of the experiment, wet/dry ratio, regional histology, and cytokines were evaluated.RESULTS: After the ARDS model was established, Cdyn,rs decreased from 21 ± 3.3 to 9.0 ± 1.8 ml/cmH2 O (P < 0.0001). After the lung recruitment maneuver, Cdyn,rs increased to the pre-injury value. During OLA ventilation, no differences in respiratory mechanics, hemodynamics, or EVLW were observed between groups. Wet/dry ratio and histological scores were not different between groups. Cytokine quantification was similar and showed a homogeneous distribution throughout the lung in both groups.CONCLUSION: Contrary to previous findings with the ARDSNet strategy, respiratory rate did not influence lung inflammatory response or pulmonary edema during OLA ventilation in experimental ARDS. This indicates that changing the respiratory rate when OLA ventilation is used will not exacerbate lung injury.
|
|
| 13. |
- Santos, Arnoldo, et al.
(author)
-
Acute Respiratory Distress Syndrome deteriorates pulmonary vascular efficiency and increases cardiac energy wasting in a porcine model.
-
Other publication (other academic/artistic)abstract
- Background: Right ventricle failure worsen outcomes in acute respiratory distress syndrome (ARDS). However, the pathophysiology of right ventricle failure and vascular dysfunction in ARDS is not completely understood. In this study we aim to evaluate the effects of early ARDS on pulmonary vascular efficiency for transmission of flow and pressure in an experimental animal model. Methods: ARDS was induced in 10 pigs (32.5±4.3 kg) combining saline lung-lavages with injurious mechanical ventilation. Pressure and flow sensors were placed at the main pulmonary artery for pulmonary vascular function evaluation, including arterial load parameters, cardiac power and energy transmission ratio.Results: Compared to baseline healthy conditions, ARDS increased pulmonary vascular resistance (199±62 versus 524±154 dyn.s.cm-5, p <0.001), effective arterial elastance (0.65±0.26 versus 1.13±0.36 mmHg/ml, p <0.001) and total hydraulic power (195±60 to 266±87 mW, p =0.015), decreased pulmonary arterial compliance (from 2.34±0.86 to 1.00±0.25 ml/mmHg, p <0.001) and energy transmission ratio (68±15 versus 55±14%, p = 0.014), whereas oscillatory power did not change (17±6 versus 16±6%, p = 0.359).Conclusions: In this experimental ARDS model, an increase in pulmonary arterial load was associated with a higher cardiac power and a decrease in the energy transmission ratio. These results suggest that right ventricle energy consumption is increased and part of this energy is wasted in pulmonary circulation worsening pulmonary vascular efficiency in the early course of ARDS. These findings may help to explain primary mechanisms leading to right ventricle dysfunction in ARDS.
|
|
| 14. |
- Santos, Arnoldo, et al.
(author)
-
ARDS Decreases Pulmonary Artery Compliance in a Porcine Model
- 2016
-
In: American Journal of Respiratory and Critical Care Medicine. - 1073-449X .- 1535-4970. ; 93
-
Journal article (peer-reviewed)abstract
- Rationale: Importance of pulmonary hemodynamic disarrangements in ARDS has been remarked recently. In this study we describe the effect of ARDS on pulmonary artery compliance and the related effect on pulmonary hemodynamics. In this way we highlight the importance of pulsatile hemodynamic evaluation beyond the classic evaluation based only on resistance.Methods: 17 anesthetized and muscle relaxed pigs were monitored with a transonic flow probe and high fidelity micro-tip pressure sensor placed in the pulmonary artery through a small thoracotomy. An experimental model of ARDS was induced in these animals by means of lung saline lavages followed by two hours of injurious mechanical ventilation. Pulmonary artery compliance was measured as the stroke volume divided by the pulse pressure. Waveform analysis of pulmonary artery pressure and flow signal was applied to calculate the following variables: first harmonic impedance magnitude (inversely related with arterial compliance), characteristic impedance, wave reflections (which are affected by arterial compliance) magnitude and peak and foot arrival time (normalized to cardiac period). These variables are related to the pulmonary vessels efficiency to transmit pressure and flow produced by the right ventricle. In addition, pulmonary vascular resistance was evaluated as usual. Variables were evaluated before (Baseline) and after (ARDS) development of the model.Results: Comparing with Baseline, ARDS provoked a decrease in pulmonary artery compliance (3.03±0.99 vs 1.53±0.41 ml/mmHg, p<0.001), and in the wave reflections arrival time of foot (0.18±0.09 vs 0.11±0.05, p<0.001) and peak (0.50±0.12 vs 0.39±0.10, p< 0.001) and an increase in the impedance magnitude of the first harmonic (80±29 vs 145±38 dyn.s.cm-5, p<0.001) and in the pulmonary vascular resistance (230±79 vs 504±129 dyn.s.cm-5, p<0.001). Characteristic impedance and wave reflections magnitude showed no differences.Conclusions: In this porcine model, ARDS provoked a decrease in pulmonary artery compliance. This effect was followed by a deterioration of pulmonary vascular efficiency. Our findings can be relevant for the pathophysiology of right ventricle failure during ARDS. This abstract is funded by: European Society of Intensive Care Medicine (ESICM), Basic Science Award 2012, the Swedish Heart and Lung foundation and the Swedish Research Council (K2015-99X-22731-01-4)
|
|
| 15. |
- Santos, Arnoldo, et al.
(author)
-
Cyclic Changes of Pulmonary Vascular Mechanics During mechanical ventilation in acute respiratory distress syndrome. A porcine experimental model.
-
Other publication (other academic/artistic)abstract
- Objective: To test the hypothesis that acute respiratory syndrome (ARDS) worsens pulmonary vascular mechanics during the respiratory cycle under mechanical ventilation in an animal model. Design: Experimental study.Setting: Animal research laboratory.Subjects: 6 pigs, 31.7 ± 5.4 kg.Interventions: ARDS was induced by combining saline lung-lavages with injurious mechanical ventilation. Pressure and flow sensors were placed at the main pulmonary artery (PA) and signals were collected simultaneously with airway pressure and flow. Pulmonary vascular mechanics and cardiac function parameters were calculates beat by beat during 2-3 minutes. We designed a novel method to quantify how the calculated variables behave during the whole respiratory cycle, i.e., during expiration and during inspiration. Results are expressed as the mean value during the corresponding phase of the respiratory cycle.Measurements and Main Results: During the whole respiratory cycle and at expiration ARDS decreased SV and arterial compliance while increased mean and pulse PA pressure, effective arterial elastance and Dp/Dtmax when compared to baseline. At baseline and after ARDS, inspiration in positive pressure ventilation caused a decrease in stroke volume (-3±1ml, p<0.001 and -3±1ml, p<0.001), pulmonary mean (-0.5±0.3, p=0.007 and -0.7±0.3mmHg, p=0.002) and pulse pressure (-0.8±0.4, p=0.003 and -1,5±0.7mmHg, p=0.003) and compliance (-0.07±0.04 and -0.04±0.00ml/mmHg, p<0.001) and an increase in resistance (34±13, p=0.001 and 50±32dyn.s.cm-5, p=0.012) and in effective arterial elastance (0.04±0.01, p=0.001 and 0.08±0.04mmHg/ml, p=0.003). ARDS produced a more pronounced inspiratory increase in effective arterial elastance (p=0.041) when compared to baseline. Positive pressure ventilation caused a decrease in Dp/Dtmax at baseline (-15±9mmHg/s, p=0.010) but this was not significant during ARDS (-27±28mmHg/s, p=0.068). Conclusions: We found in this experimental model that MV induced tidal increase in arterial load and that this effect was higher during ARDS. This finding if transferred to patients, might partly explain the high rate of right heart failure clinically in ARDS.
|
|
| 16. |
- Santos, Arnoldo, et al.
(author)
-
Effects on Pulmonary Vascular Mechanics of Two Different Lung-Protective Ventilation Strategies in an Experimental Model of Acute Respiratory Distress Syndrome
- 2017
-
In: Critical Care Medicine. - 0090-3493 .- 1530-0293. ; 45:11, s. e1157-e1164
-
Journal article (peer-reviewed)abstract
- OBJECTIVES: To compare the effects of two lung-protective ventilation strategies on pulmonary vascular mechanics in early acute respiratory distress syndrome.DESIGN: Experimental study.SETTING: University animal research laboratory.SUBJECTS: Twelve pigs (30.8 ± 2.5 kg).INTERVENTIONS: Acute respiratory distress syndrome was induced by repeated lung lavages and injurious mechanical ventilation. Thereafter, animals were randomized to 4 hours ventilation according to the Acute Respiratory Distress Syndrome Network protocol or to an open lung approach strategy. Pressure and flow sensors placed at the pulmonary artery trunk allowed continuous assessment of pulmonary artery resistance, effective elastance, compliance, and reflected pressure waves. Respiratory mechanics and gas exchange data were collected.MEASUREMENTS AND MAIN RESULTS: Acute respiratory distress syndrome led to pulmonary vascular mechanics deterioration. Four hours after randomization, pulmonary vascular mechanics was similar in Acute Respiratory Distress Syndrome Network and open lung approach: resistance (578 ± 252 vs 626 ± 153 dyn.s/cm; p = 0.714), effective elastance, (0.63 ± 0.22 vs 0.58 ± 0.17 mm Hg/mL; p = 0.710), compliance (1.19 ± 0.8 vs 1.50 ± 0.27 mL/mm Hg; p = 0.437), and reflection index (0.36 ± 0.04 vs 0.34 ± 0.09; p = 0.680). Open lung approach as compared to Acute Respiratory Distress Syndrome Network was associated with improved dynamic respiratory compliance (17.3 ± 2.6 vs 10.5 ± 1.3 mL/cm H2O; p < 0.001), driving pressure (9.6 ± 1.3 vs 19.3 ± 2.7 cm H2O; p < 0.001), and venous admixture (0.05 ± 0.01 vs 0.22 ± 0.03, p < 0.001) and lower mean pulmonary artery pressure (26 ± 3 vs 34 ± 7 mm Hg; p = 0.045) despite of using a higher positive end-expiratory pressure (17.4 ± 0.7 vs 9.5 ± 2.4 cm H2O; p < 0.001). Cardiac index, however, was lower in open lung approach (1.42 ± 0.16 vs 2.27 ± 0.48 L/min; p = 0.005).CONCLUSIONS: In this experimental model, Acute Respiratory Distress Syndrome Network and open lung approach affected pulmonary vascular mechanics similarly. The use of higher positive end-expiratory pressures in the open lung approach strategy did not worsen pulmonary vascular mechanics, improved lung mechanics, and gas exchange but at the expense of a lower cardiac index.
|
|
| 17. |
- Santos, Arnoldo, et al.
(author)
-
Impact of respiratory cycle during mechanical ventilation on beat-to-beat right ventricle stroke volume estimation by pulmonary artery pulse wave analysis
- 2024
-
In: Intensive Care Medicine Experimental. - : Springer. - 2197-425X. ; 12
-
Journal article (peer-reviewed)abstract
- Background: The same principle behind pulse wave analysis can be applied on the pulmonary artery (PA) pressure waveform to estimate right ventricle stroke volume (RVSV). However, the PA pressure waveform might be influenced by the direct transmission of the intrathoracic pressure changes throughout the respiratory cycle caused by mechanical ventilation (MV), potentially impacting the reliability of PA pulse wave analysis (PAPWA). We assessed a new method that minimizes the direct effect of the MV on continuous PA pressure measurements and enhances the reliability of PAPWA in tracking beat-to-beat RVSV.Methods: Continuous PA pressure and flow were simultaneously measured for 2-3 min in 5 pigs using a high-fidelity micro-tip catheter and a transonic flow sensor around the PA trunk, both pre and post an experimental ARDS model. RVSV was estimated by PAPWA indexes such as pulse pressure (SVPP), systolic area (SVSystAUC) and standard deviation (SVSD) beat-to-beat from both corrected and non-corrected PA signals. The reference RVSV was derived from the PA flow signal (SVref).Results: The reliability of PAPWA in tracking RVSV on a beat-to-beat basis was enhanced after accounting for the direct impact of intrathoracic pressure changes induced by MV throughout the respiratory cycle. This was evidenced by an increase in the correlation between SVref and RVSV estimated by PAPWA under healthy conditions: rho between SVref and non-corrected SVSD - 0.111 (0.342), corrected SVSD 0.876 (0.130), non-corrected SVSystAUC 0.543 (0.141) and corrected SVSystAUC 0.923 (0.050). Following ARDS, correlations were SVref and non-corrected SVSD - 0.033 (0.262), corrected SVSD 0.839 (0.077), non-corrected SVSystAUC 0.483 (0.114) and corrected SVSystAUC 0.928 (0.026). Correction also led to reduced limits of agreement between SVref and SVSD and SVSystAUC in the two evaluated conditions.Conclusions: In our experimental model, we confirmed that correcting for mechanical ventilation induced changes during the respiratory cycle improves the performance of PAPWA for beat-to-beat estimation of RVSV compared to uncorrected measurements. This was demonstrated by a better correlation and agreement between the actual SV and the obtained from PAPWA.
|
|
| 18. |
|
|
