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  • 1.
    Batista Borges, João
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Santos, Arnoldo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Lucchetta, L.
    Hosp San Matteo, Pavia, Italy..
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Redistribution Of Regional Lung Perfusion During Mechanical Ventilation With An Open Lung Approach Impacts Pulmonary Vascular Mechanics2017Ingår i: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 195, artikel-id A3751Artikel i tidskrift (Övrigt vetenskapligt)
  • 2.
    Graf, J.
    et al.
    Univ Desarrollo, Fac Med, Clin Alemana, Santiago, Chile..
    Santos, Arnoldo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Silva, C.
    Clin Alemana Santiago, Santiago, Chile..
    Salazar, A.
    Clin Alemana Santiago, Santiago, Chile..
    Formenti, P.
    Polo Univ, Azienda Osped San Paolo, Milan, Italy..
    Marini, J. J.
    Univ Minnesota, St Paul, MN 55108 USA..
    Rapid Quantification Of Lung Inflation And Recruitment With Automatic Lung Segmentation Of Chest Computed Tomography In A Variable Lung Collapse Model2016Ingår i: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 193Artikel i tidskrift (Refereegranskat)
  • 3.
    Monge Garcia, Manuel Ignacio
    et al.
    Hosp SAS Jerez, Serv Cuidados Intens, C Circunvalac S-N, Jerez de la Frontera 11407, Spain.
    Santos, Arnoldo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. CIBER Enfermedades Resp CIBERES, Avd Monforte de Lemos 3-5,Pabellon 11,Planta 0, Madrid 28029, Spain.
    Diez Del Corral, Beatriz
    Hosp SAS Jerez, Serv Cuidados Intens, C Circunvalac S-N, Jerez de la Frontera 11407, Spain.
    Guijo Gonzalez, Pedro
    Hosp SAS Jerez, Serv Cuidados Intens, C Circunvalac S-N, Jerez de la Frontera 11407, Spain.
    Gracia Romero, Manuel
    Hosp SAS Jerez, Serv Cuidados Intens, C Circunvalac S-N, Jerez de la Frontera 11407, Spain.
    Gil Cano, Anselmo
    Hosp SAS Jerez, Serv Cuidados Intens, C Circunvalac S-N, Jerez de la Frontera 11407, Spain.
    Cecconi, Maurizio
    St Georges Univ London, London SW17 0QT, England;St Georges Healthcare NHS Trust, Dept Intens Core Med, London SW17 0QT, England.
    Noradrenaline modifies arterial reflection phenomena and left ventricular efficiency in septic shock patients: A prospective observational study2018Ingår i: Journal of critical care, ISSN 0883-9441, E-ISSN 1557-8615, Vol. 47, s. 280-286Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: To determine whether noradrenaline alters the arterial pressure reflection phenomena in septic shock patients and the effects on left ventricular (LV) efficiency.

    Material and methods: Thirty-seven septic shock patients with a planned change in noradrenaline dose. Timing and magnitude (Reflection Magnitude and Augmentation Index) of arterial reflections were evaluated. Total, steady, and oscillatory LV power (also expressed as fraction of the total power), subendocardial viability ratio (SEVR), energy efficiency and transmission ratios were used as a marker of LV efficiency.

    Results: An incremental change in noradrenaline increased Reflection Magnitude [0.28(0.09) to 0.31(0.1], Augmentation Index [-6.4(23.6) to 4.8(20.7)%], and LV total power [0.79(IQR:0.47-1) to 0.98(IQR:0.57-127) W], all p < 0.001; whereas decreased arrival time of reflected waves [from 95(87 to 121) to 83(79 to 101)ms; p < 0.001]. Variables of LV performance showed a decreased efficiency: oscillatory fraction and energy efficiency ratio increased [20.9(5.7) to 22.8(4.9)%, and 82(1.7) to 10.1(2) mW.min.litre(-1); p < 0.001, respectively]; and energy transmission ratio and SEVR decreased [73.8(9.9) to 72(9.8)% and 146(IQR:113-188) to 143 (IQR:109-172)%, p = 0.003 and p = 0.041, respectively].

    Conclusions: Noradrenaline increased reflection phenomena, increasing LV workload and worsening LV performance in septic shock patients. These conditions could explain the detrimental effects during long-term use of noradrenaline.

  • 4.
    Santos, Arnoldo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Hemodynamic Effects of Lung Function Optimization in Experimental Acute Respiratory Distress Syndrome2018Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Acute Respiratory Distress Syndrome (ARDS) is a severe pulmonary inflammation affecting thousands of patients every year in Sweden and has a mortality of 30-50%. Mechanical ventilation (MV) is usually necessary, but could per se augment the inflammation and contribute to mortality. MV strategies protective for the lung parenchyma have been developed but without considering the pulmonary circulation or the right heart ventricle (RV) that also are affected in ARDS. MV should ideally be optimized to protect both the lung parenchyma and the RV/pulmonary vasculature. My hypothesis was that MV that prevents alveolar collapse and overdistension, i.e., the “open lung approach (OLA)” would be optimal. The aims of this project were 1) to carefully describe the pulmonary vascular mechanics (PVM) in ARDS compared with healthy lungs, 2) to assess how different ventilatory methods influence PVM, and 3) to propose a ventilatory method that protects both lung parenchyma and circulation.

    In a porcine model, high fidelity pressure and flow sensors were applied directly on the main pulmonary artery to evaluate steady and oscillatory components of PVM.  In this way a complete PVM description was obtained for normal and injured lungs at different MV. In particular, the effects of OLA were compared with standard MV and, in addition, with MV methods where overdistension or collapse were present.

    Results: 1) Compared with collapse or overdistension, OLA provided better PVM. 2) The effects on PVM of OLA and the standard protective MV were similar. 3) Early ARDS augmented the effects of pulse wave reflection on PVM leading to a situation in which the RV had to increase its work to maintain adequate blood flow. Thus, a part of this work was wasted by the effect of wave reflections, making the RV/pulmonary vasculature inefficient. 4) Tidal breathing affected PVM cyclically and this effect was enhanced in ARDS compared with healthy lungs.

    In conclusion, ARDS and different ventilatory methods, as well as tidal ventilation per se, affected PVM. OLA improved PVM compared with other MV settings where significant collapse and overdistension were allowed. However, OLA was not superior to standard protective MV.

    Delarbeten
    1. The Open Lung Approach Improves Pulmonary Vascular Mechanics in an Experimental Model of Acute Respiratory Distress Syndrome
    Öppna denna publikation i ny flik eller fönster >>The Open Lung Approach Improves Pulmonary Vascular Mechanics in an Experimental Model of Acute Respiratory Distress Syndrome
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    2017 (Engelska)Ingår i: Critical Care Medicine, ISSN 0090-3493, E-ISSN 1530-0293, Vol. 45, nr 3, s. e298-e305Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    OBJECTIVE: To test whether positive end-expiratory pressure consistent with an open lung approach improves pulmonary vascular mechanics compared with higher or lower positive end-expiratory pressures in experimental acute respiratory distress syndrome.

    DESIGN: Experimental study.

    SETTING: Animal research laboratory.

    SUBJECTS: Ten pigs, 35 ± 5.2 kg.

    INTERVENTIONS: Acute respiratory distress syndrome was induced combining saline lung lavages with injurious mechanical ventilation. The positive end-expiratory pressure level resulting in highest compliance during a decremental positive end-expiratory pressure trial after lung recruitment was determined. Thereafter, three positive end-expiratory pressure levels were applied in a random order: hyperinflation, 6 cm H2O above; open lung approach, 2 cm H2O above; and collapse, 6 cm H2O below the highest compliance level. High fidelity pressure and flow sensors were placed at the main pulmonary artery for measuring pulmonary artery resistance (Z0), effective arterial elastance, compliance, and reflected pressure waves.

    MEASUREMENTS AND MAIN RESULTS: After inducing acute respiratory distress syndrome, Z0 and effective arterial elastance increased (from 218 ± 94 to 444 ± 115 dyn.s.cm and from 0.27 ± 0.14 to 0.62 ± 0.22 mm Hg/mL, respectively; p < 0.001), vascular compliance decreased (from 2.76 ± 0.86 to 1.48 ± 0.32 mL/mm Hg; p = 0.003), and reflected waves arrived earlier (0.23 ± 0.07 vs 0.14 ± 0.05, arbitrary unit; p = 0.002) compared with baseline. Comparing the three positive end-expiratory pressure levels, open lung approach resulted in the lowest: 1) Z0 (297 ± 83 vs 378 ± 79 dyn.s.cm, p = 0.033, and vs 450 ± 119 dyn.s.cm, p = 0.002); 2) effective arterial elastance (0.37 ± 0.08 vs 0.50 ± 0.15 mm Hg/mL, p = 0.04, and vs 0.61 ± 0.12 mm Hg/mL, p < 0.001), and 3) reflection coefficient (0.35 ± 0.17 vs 0.48 ± 0.10, p = 0.024, and vs 0.53 ± 0.19, p = 0.005), comparisons with hyperinflation and collapse, respectively.

    CONCLUSIONS: In this experimental setting, positive end-expiratory pressure consistent with the open lung approach resulted in the best pulmonary vascular mechanics compared with higher or lower positive end-expiratory pressure settings.

    Nyckelord
    Fluid responsiveness, Spontaneous breathing, Head-up tilt, Pulse pressure variation, Stroke volume variation, Systolic pressure variation
    Nationell ämneskategori
    Anestesi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-307915 (URN)10.1097/CCM.0000000000002082 (DOI)27763913 (PubMedID)
    Tillgänglig från: 2016-11-22 Skapad: 2016-11-22 Senast uppdaterad: 2018-12-05Bibliografiskt granskad
    2. Effects on Pulmonary Vascular Mechanics of Two Different Lung-Protective Ventilation Strategies in an Experimental Model of Acute Respiratory Distress Syndrome
    Öppna denna publikation i ny flik eller fönster >>Effects on Pulmonary Vascular Mechanics of Two Different Lung-Protective Ventilation Strategies in an Experimental Model of Acute Respiratory Distress Syndrome
    Visa övriga...
    2017 (Engelska)Ingår i: Critical Care Medicine, ISSN 0090-3493, E-ISSN 1530-0293, Vol. 45, nr 11, s. e1157-e1164Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    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.

    Nationell ämneskategori
    Lungmedicin och allergi
    Identifikatorer
    urn:nbn:se:uu:diva-334177 (URN)10.1097/CCM.0000000000002701 (DOI)000417107000007 ()28872540 (PubMedID)
    Forskningsfinansiär
    Vetenskapsrådet, K2015-99X-22731-01-4Hjärt-LungfondenEU, FP7, Sjunde ramprogrammet, 291820
    Tillgänglig från: 2017-11-21 Skapad: 2017-11-21 Senast uppdaterad: 2018-03-09Bibliografiskt granskad
    3. Acute Respiratory Distress Syndrome deteriorates pulmonary vascular efficiency and increases cardiac energy wasting in a porcine model.
    Öppna denna publikation i ny flik eller fönster >>Acute Respiratory Distress Syndrome deteriorates pulmonary vascular efficiency and increases cardiac energy wasting in a porcine model.
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    (Engelska)Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    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.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-337402 (URN)
    Tillgänglig från: 2017-12-25 Skapad: 2017-12-25 Senast uppdaterad: 2018-01-12
    4. Cyclic Changes of Pulmonary Vascular Mechanics During mechanical ventilation in acute respiratory distress syndrome. A porcine experimental model.
    Öppna denna publikation i ny flik eller fönster >>Cyclic Changes of Pulmonary Vascular Mechanics During mechanical ventilation in acute respiratory distress syndrome. A porcine experimental model.
    Visa övriga...
    (Engelska)Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    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.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-337405 (URN)
    Tillgänglig från: 2017-12-25 Skapad: 2017-12-25 Senast uppdaterad: 2018-01-12
  • 5.
    Santos, Arnoldo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. CIBER Enfermedades Resp CIBERES, Madrid, Spain.; CNIC, Ctr Nacl Invest Cardiovasc Carlos 3, Madrid, Spain.
    Gomez-Peñalver, Eva
    Hosp Gen Villalba, Intens Care Unit, Villalba, Spain.
    Monge-Garcia, M Ignacio
    Hosp SAS, Intens Care Unit, Jerez de la Frontera, Spain.
    Retamal, Jaime
    Pontificia Univ Catolica Chile, Dept Med Intens, Santiago, Chile.
    Batista Borges, João
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Univ Sao Paulo, Heart Inst InCor, Hosp Clin, Div Pulm, Sao Paulo, Brazil.
    Tusman, Gerardo
    Department of Anesthesia, Hospital Privado de Comunidad, Mar del Plata, Argentina.
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. CIBER de enfermedades respiratorias (CIBERES), Madrid, Spain..
    Effects on Pulmonary Vascular Mechanics of Two Different Lung-Protective Ventilation Strategies in an Experimental Model of Acute Respiratory Distress Syndrome2017Ingår i: Critical Care Medicine, ISSN 0090-3493, E-ISSN 1530-0293, Vol. 45, nr 11, s. e1157-e1164Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    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.

  • 6.
    Santos, Arnoldo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Ruiz-Cabello, Jesus
    Monge-Garcia, M. Ignacio
    Borges, Joao Batista
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Gomez-Peñalver, Eva
    Retamal, Jaime
    Lucchetta, Luca
    Tusman, Gerardo
    Hedenstierna, Goran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Cyclic Changes of Pulmonary Vascular Mechanics During mechanical ventilation in acute respiratory distress syndrome. A porcine experimental model.Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    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.

  • 7.
    Santos, Arnoldo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Lucchetta, Luca
    Monge-Garcia, M Ignacio
    Batista Borges, João
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Tusman, Gerardo
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    The Open Lung Approach Improves Pulmonary Vascular Mechanics in an Experimental Model of Acute Respiratory Distress Syndrome2017Ingår i: Critical Care Medicine, ISSN 0090-3493, E-ISSN 1530-0293, Vol. 45, nr 3, s. e298-e305Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: To test whether positive end-expiratory pressure consistent with an open lung approach improves pulmonary vascular mechanics compared with higher or lower positive end-expiratory pressures in experimental acute respiratory distress syndrome.

    DESIGN: Experimental study.

    SETTING: Animal research laboratory.

    SUBJECTS: Ten pigs, 35 ± 5.2 kg.

    INTERVENTIONS: Acute respiratory distress syndrome was induced combining saline lung lavages with injurious mechanical ventilation. The positive end-expiratory pressure level resulting in highest compliance during a decremental positive end-expiratory pressure trial after lung recruitment was determined. Thereafter, three positive end-expiratory pressure levels were applied in a random order: hyperinflation, 6 cm H2O above; open lung approach, 2 cm H2O above; and collapse, 6 cm H2O below the highest compliance level. High fidelity pressure and flow sensors were placed at the main pulmonary artery for measuring pulmonary artery resistance (Z0), effective arterial elastance, compliance, and reflected pressure waves.

    MEASUREMENTS AND MAIN RESULTS: After inducing acute respiratory distress syndrome, Z0 and effective arterial elastance increased (from 218 ± 94 to 444 ± 115 dyn.s.cm and from 0.27 ± 0.14 to 0.62 ± 0.22 mm Hg/mL, respectively; p < 0.001), vascular compliance decreased (from 2.76 ± 0.86 to 1.48 ± 0.32 mL/mm Hg; p = 0.003), and reflected waves arrived earlier (0.23 ± 0.07 vs 0.14 ± 0.05, arbitrary unit; p = 0.002) compared with baseline. Comparing the three positive end-expiratory pressure levels, open lung approach resulted in the lowest: 1) Z0 (297 ± 83 vs 378 ± 79 dyn.s.cm, p = 0.033, and vs 450 ± 119 dyn.s.cm, p = 0.002); 2) effective arterial elastance (0.37 ± 0.08 vs 0.50 ± 0.15 mm Hg/mL, p = 0.04, and vs 0.61 ± 0.12 mm Hg/mL, p < 0.001), and 3) reflection coefficient (0.35 ± 0.17 vs 0.48 ± 0.10, p = 0.024, and vs 0.53 ± 0.19, p = 0.005), comparisons with hyperinflation and collapse, respectively.

    CONCLUSIONS: In this experimental setting, positive end-expiratory pressure consistent with the open lung approach resulted in the best pulmonary vascular mechanics compared with higher or lower positive end-expiratory pressure settings.

  • 8.
    Santos, Arnoldo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Monge-Garcia, I
    Gomez Peñalver, E
    Borges, João Batista
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Lucchetta, L
    Retamal, Jaime
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Tusman, G
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    ARDS Decreases Pulmonary Artery Compliance in a Porcine Model2016Ingår i: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 93, artikel-id A7917Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    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)

  • 9.
    Santos, Arnoldo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Monge-Garcia, M.
    Hosp SAS, Jerez de la Frontera, Spain..
    Batista Borges, João
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Gomez-Penalver, E.
    Hosp Gen Villalba, Villalba, Spain..
    Retamal, J.
    Pontificia Univ Catolica Chile, Santiago, Chile..
    Lucchetta, L.
    Hosp San Matteo, Pavia, Italy..
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Pulmonary Vascular Efficiency Worsening And Cardiac Energy Wasting During Early Stages Of Experimental Acute Respiratory Distress Syndrome2017Ingår i: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 195, nr D27, artikel-id A7698Artikel i tidskrift (Övrigt vetenskapligt)
  • 10.
    Santos, Arnoldo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Monge-Garcia, M. Ignacio
    Borges, Joao Batista
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Gomez-Peñalver, Eva
    Retamal, Jaime
    Lucchetta, Luca
    Tusman, Gerardo
    Hedenstierna, Goran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Suarez-Sipmann, Fernando
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Acute Respiratory Distress Syndrome deteriorates pulmonary vascular efficiency and increases cardiac energy wasting in a porcine model.Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    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.

  • 11.
    Suarez Sipmann, Fernando
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Ciber Enfermedades Resp CIBERES Inst Invest Carlo, Madrid, Spain.;Univ Hosp La Fe, Dept Intens Care, Valencia, Spain..
    Santos, Arnoldo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Ciber Enfermedades Resp CIBERES Inst Invest Carlo, Madrid, Spain..
    Tusman, Gerardo
    Hosp Privado Comunidad Mar Del Plata, Dept Anesthesia, Mar Del Plata, Buenos Aires, Argentina..
    Heart-lung interactions in acute respiratory distress syndrome: pathophysiology, detection and management strategies2018Ingår i: Annals of Translational Medicine, ISSN 2305-5839, E-ISSN 2305-5847, Vol. 6, nr 2, artikel-id 27Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Acute respiratory distress syndrome (ARDS) is the most severe form of acute respiratory failure characterized by diffuse alveolar and endothelial damage. The severe pathophysiological changes in lung parenchyma and pulmonary circulation together with the effects of positive pressure ventilation profoundly affect heart lung interactions in ARDS. The term pulmonary vascular dysfunction (PVD) refers to the specific involvement of the vascular compartment in ARDS and is expressed clinically by an increase in pulmonary arterial (PA) pressure and pulmonary vascular resistance both affecting right ventricular (RV) afterload. When severe, PVD can lead to RV failure which is associated to an increased mortality. The effect of PVD on RV function is not only a consequence of increased pulmonary vascular resistance as afterload is a much more complex phenomenon that includes all factors that oppose efficient ventricular ejection. Impaired pulmonary vascular mechanics including increased arterial elastance and augmented wave-reflection phenomena are commonly seen in ARDS and can additionally affect RV afterload. The use of selective pulmonary vasodilators and lung protective mechanical ventilation strategies are therapeutic interventions that can ameliorate PVD. Prone positioning and the open lung approach (OLA) are especially attractive strategies to improve PVD due to their effects on increasing functional lung volume. In this review we will describe some pathophysiological aspects of heart-lung interactions during the ventilatory support of ARDS, its clinical assessment and discuss therapeutic interventions to prevent the occurrence and progression of PVD and RV failure.

  • 12.
    Suarez-Sipmann, Fernando
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Santos, Arnoldo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Hedenstiernalaboratoriet.
    Boehm, Stephan H.
    Borges, Joao Batista
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Tusman, Gerardo
    Corrections of Enghoffs dead space formula for shunt effects still overestimate Bohr's dead space2013Ingår i: Respiratory Physiology & Neurobiology, ISSN 1569-9048, E-ISSN 1878-1519, Vol. 189, nr 1, s. 99-105Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Dead space ratio is determined using Enghoffs modification (VDB-E/V-T) of Bohr's formula (V-DBohr/V-T) in which arterial is used as a surrogate of alveolar PCO2. In presence of intrapulmonary shunt Enghoffs approach overestimates dead space. In 40 lung-lavaged pigs we evaluated the Kuwabara's and Niklason's algorithms to correct for shunt effects and hypothesized that corrected VDB-E/V-T should provide similar values as V-DBohr/V-T. We analyzed 396 volumetric capnograms and arterial and mixed-venous blood samples to calculate V-DBohr/V-T and VDB-E/V-T. Thereafter, we corrected the latter for shunt effects using Kuwabara's (K) VDB-E/V-T and Niklason's (N) VDB-E/V-T algorithms. Uncorrected VDB-E/V-T (mean +/- SD of 0.70 +/- 0.10) overestimated V-DBohr/V-T (0.59 +/- 0.12) (p < 0.05), over the entire range of shunts. Mean (K) VDB-E/V-T was significantly higher than V-DBor/V-T (0.67 +/- 0.08, bias 0.085, limits of agreement 0.232 to 0.085; p< 0.05) whereas (N)VDB-E/V-T showed a better correction for shunt effects (0.64 +/- 0.09, bias 0.048, limits of agreement -0.168 to 0.072; p < 0.05). Neither Kuwabara's nor Niklason's algorithms were able to correct EnghofFs dead space formula for shunt effects. 

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