ESTIMATION OF ACUTE LEFT-VENTRICULAR AFTE RLOAD ALTERATIONS IN VENTILATED PATIENTS BY TRANSESOPHAGEAL ECHOCARDIOGRAPHY

Left ventricular afterload is most accurately represented by left vent ricular end-systolic wall stress, but in clinical practice is commonly estimated by the systemic vascular resistance (SVR). End-systolic wal l stress can be derived from M-mode and two-dimensional (2D) echocardi ograms in combination with systolic arterial pressure (SAP). We tested transoesophageal echocardiography for the assessment of acute left ve ntricular afterload alterations in ventilated patients requiring cardi ovascular support with noradrenaline or nitroglycerine. Method. With a pproval from the local ethics committee, we studied afterload alterati ons in 11 hypotensive patients who were treated by increasing the dosa ge of IV noradrenaline by 2-5 mu g/min in order to raise mean arterial pressure (MAP) by 20 mmHg. In another 10 patients with MAP over 95 mm Hg, nitroglycerine was raised from 2 to 4 mg/h, aiming at a 20 mmHg MA P reduction. MAP and SAP were monitored via a radial artery cannula, c ardiac output (CO) was measured with the thermodilution technique usin g a Swan-Ganz catheter, and SVR was calculated from CO, MAP, and right atrial pressure. M-mode and 2D echocardiograms were obtained from the cross-sectional short-axis view of the left ventricle and recorded sh ortly before and during treatment when MAP had changed by 20 mmHg. Lef t ventricular total area (TA) and cavity area (A) including the papill ary muscles were obtained from end-systolic 2D echocardiograms, while end-systolic internal diameter (ID) and posterior wail thickness (HW) were measured in the M-mode. Wall stress was calculated in the M-mode as: WSM = 0.33 . SAP . ID/(HW . (1 + HW/ID)), and in the 2D mode as: W S2D = 1.33 SAP . A/(TA-A). Statistics: paired t-test (P < 0.05), regre ssion analysis. Results. Afterload alterations were reflected by signi ficant changes of WS2D (-41%, +68%), WSM (-26%, +38%), and SVR (-15%, +50%). WSM and SVR underestimated changes of WS2D by 15%-30%. WSM chan ges due to SAP rather than to left-ventricular dimensional changes. No correlation was found between WS2D or WSM and SVR. Inter-observer var iability for echocardiographInter-observer variability for echocardiog raphic wall stress was reasonable (WS2D 4%, WSM 10%). Conclusions. Acu te changes of left ventricular afterload and dimensions were clearly i ndicated by 2D measurements. As M-mode measures were not conclusive fo r left ventricular dimensional changes, WSM was not an appropriate par ameter for acute afterload alterations. WS2D is an afterload index sup erior to WSM that cannot be estimated by SVR.