Advantages of strain echocardiography in assessment of myocardial function in severe sepsis: an experimental study

• Published in: Critical care medicine Vol. 42; no. 6; p. e432
• Main Authors: Hestenes, Siv M, Halvorsen, Per S, Skulstad, Helge, Remme, Espen W, Espinoza, Andreas, Hyler, Stefan, Bugge, Jan F, Fosse, Erik, Nielsen, Erik W, Edvardsen, Thor
• Format: Journal Article
• Language: English
• Published: United States 01.06.2014
• Subjects: Animals; Cardiac Output - physiology; Echocardiography, Doppler - methods; Escherichia coli Infections; Heart Ventricles - diagnostic imaging; Hemodynamics - physiology; Myocardium - pathology; Prospective Studies; Sepsis - diagnostic imaging; Sepsis - physiopathology; Stroke Volume - physiology; Swine; Ventricular Function, Left - physiology
• ISSN: 1530-0293
• DOI: 10.1097/CCM.0000000000000310

Cardiovascular 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. Prospective experimental study. Operating room at Intervention Centre, Oslo University Hospital. Eight Norwegian Landrace pigs. The 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. Left 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). The 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.