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Acute Respiratory Distress Syndrome deteriorates pulmonary vascular efficiency and increases cardiac energy wasting in a porcine model.

Santos, Arnoldo (author)
Uppsala universitet,Hedenstiernalaboratoriet
Monge-Garcia, M. Ignacio (author)
Borges, Joao Batista (author)
Uppsala universitet,Hedenstiernalaboratoriet
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Gomez-Peñalver, Eva (author)
Retamal, Jaime (author)
Lucchetta, Luca (author)
Tusman, Gerardo (author)
Hedenstierna, Goran (author)
Uppsala universitet,Klinisk fysiologi
Larsson, Anders (author)
Uppsala universitet,Hedenstiernalaboratoriet
Suarez-Sipmann, Fernando (author)
Uppsala universitet,Hedenstiernalaboratoriet
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 (creator_code:org_t)
English.
  • Other publication (other academic/artistic)
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  • 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.

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