• Siv M Hestenes, Per S Halvorsen, Helge Skulstad, Espen W Remme, Andreas Espinoza, Stefan Hyler, Jan F Bugge, Erik Fosse, Erik W Nielsen, and Thor Edvardsen.
• 1Intervention Centre, Oslo University Hospital, Oslo, Norway. 2Department of Anaesthesiology, Oslo University Hospital, Oslo, Norway. 3Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 4KG Jebsen Cardiac Research Centre, University of Oslo, Oslo, Norway. 5Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. 6Department of Emergency Medicine, Nordland Hospital, Bodø, Norway. 7University of Nordland, Bodø, Norway. 8Faculty of Health Sciences, University of Tromsø, Tromsø, Norway.
• Crit. Care Med.. 2014 Jun 1;42(6):e432-40.

ObjectivesCardiovascular failure is an important feature of severe sepsis and mortality in sepsis. The aim of our study was to explore myocardial dysfunction in severe sepsis.DesignProspective experimental study.SettingOperating room at Intervention Centre, Oslo University Hospital.SubjectsEight Norwegian Landrace pigs.InterventionsThe pigs were anesthetized, a medial sternotomy performed and miniature sensors for wall-thickness measurements attached to the epicardium and invasive pressure monitoring established, and an infusion of Escherichia coli started. Hemodynamic response was monitored and myocardial strain assessed by echocardiography.Measurements And Main ResultsLeft ventricular myocardial function was significantly reduced assessed by longitudinal myocardial strain (-17.2% ± 2.8% to -12.3% ± 3.2%, p = 0.04), despite a reduced afterload as expressed by the left ventricular end-systolic meridional wall stress (35 ± 13 to 18 ± 8 kdyn/cm, p = 0.04). Left ventricular ejection fraction remained unaltered (48% ± 7% to 49% ± 5%, p = 0.4) as did cardiac output (6.3 ± 1.3 to 5.9 ± 3 L/min, p = 0.7). The decline in left ventricular function was further supported by significant reductions in the index of regional work by pressure-wall thickness loop area (121 ± 45 to 73 ± 37 mm × mm Hg, p = 0.005). Left ventricular myocardial wall thickness increased in both end diastole (11.5 ± 2.7 to 13.7 ± 2.4 mm, p = 0.03) and end systole (16.1 ± 2.9 to 18.5 ± 1.8 mm, p = 0.03), implying edema of the left ventricular myocardial wall. Right ventricular myocardial function by strain was reduced (-24.2% ± 4.1% to -16.9% ± 5.7%, p = 0.02). High right ventricular pressures caused septal shift as demonstrated by the end-diastolic transseptal pressure gradient (4.1 ± 3.3 to -2.2 ± 5.8 mm Hg, p = 0.01).ConclusionsThe present study demonstrates myocardial dysfunction in severe sepsis. Strain echocardiography reveals myocardial dysfunction before significant changes in ejection fraction and cardiac output and could prove to be a useful tool in clinical evaluation of septic patients.

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