British Journal of Anaesthesia, 2003, Vol. 91, No. 2 224-232
© 2003 The Board of Management and Trustees of the British Journal of Anaesthesia
Laboratory Investigations |
Effects of sustained post-traumatic shock and initial fluid resuscitation on extravascular lung water content and pulmonary vascular pressures in a porcine model of shock
,21 MRC Trauma Group University of Manchester, University of Manchester, Oxford Road, Manchester M13 9PT, UK. 2 South Manchester University Hospitals, Manchester, UK.
Corresponding author: University Department of Anaesthesia and Intensive Care, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK. E-mail: mahesan.nirmalan@man.ac.uk Declaration of interest: Dr D. J. Edwards acted as a Medical Advisor to Maelor Pharmaceuticals, Ltd.
Background. The temporal evolution of lung injury following post-traumatic shock is poorly understood. In the present study we have tested the hypothesis that manifestations of pulmonary vascular dysfunction may be demonstrable within the first hour after the onset of shock.
Methods. Twenty-nine anaesthetized pigs (mean weight 27.4 kg; (SD) 3.2) were randomly allocated to three groups: control (C, n=9), shock resuscitated with either NaCl 0.9% (S, n=10), or 4% gelatine (G, n=10). Shock was maintained for 1 h followed by fluid resuscitation with either normal saline or 4% gelatine solution. Cardiac output (CO), mean arterial pressure (MAP), mixed venous saturation (SvO2), blood lactate concentration, mean pulmonary artery pressure (MPAP), MPAP/MAP, pulmonary vascular resistance (PVR), extravascular lung water index (EVLWi), PaO2/FIO2, venous admixture (Q·S/Q·T), and dynamic lung compliance (Cdyn) were measured at baseline, beginning of shock phase, end of shock phase, and post-resuscitation.
Results. At the end of volume resuscitation CO was restored to control values in both shock groups. MAP remained significantly below control values (95% CI: C=70–95, S=28–52, G=45–69 mm Hg) in both shock groups. MPAP/MAP was significantly greater in both shock groups at the end of the shock phase (95% CI; C=0.15–0.24, S=0.28–0.38, G=0.32–0.42) and at the post-resuscitation phase (95% CI: C=0.12–0.30, S=0.43–0.61, G=0.32–0.49) indicating the presence of relative pulmonary hypertension. This was associated with a significant increase in PVR in Group S (F=3.9; P<0.05). There were no significant changes in PaO2/FIO2, Q·S/Q·T, EVLWi, or Cdyn. In a small cohort of animals a measurable increase in EVLWi (>30%) and reduction in Cdyn (>10%) were observed.
Conclusions. Pulmonary vascular injury manifesting as relative pulmonary hypertension and increased PVR may occur within the first hour after the onset of shock. These changes may not be accompanied by overt changes in oxygenation, compliance, or EVLWi.
Br J Anaesth 2003; 91: 224–32
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