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Journal Article
Research Support, Non-U.S. Gov't
Validation of pulse contour derived stroke volume variation during modifications of cardiac afterload.
British Journal of Anaesthesia 2007 May
BACKGROUND: Left ventricular stroke volume variation (SVV) or its surrogates are useful tools to assess fluid responsiveness in mechanically ventilated patients. So far it is unknown, how changes in cardiac afterload affect SVV. Therefore, this study compared left ventricular SVV derived by pulse contour analysis with SVV measured using an ultrasonic flow probe and investigated the influence of cardiac afterload on left ventricular SVV.
METHODS: In 13 anaesthetized, mechanically ventilated pigs [31(SD 6) kg], we compared cardiac output (CO), stroke volume (SV), and SVV determined by pulse contour analysis and by an ultrasonic aortic flow signal (Bland-Altman analysis). After obtaining baseline measurements, cardiac afterload was increased using phenylephrine and decreased using adenosine (both continuously administered). Measurements were performed with a constant tidal volume (12 ml kg-1) without PEEP.
RESULTS: Neither increasing mean arterial pressure (MAP) [from 59 (7) to 116 (19)] nor decreasing MAP [from 63 (7) to 39 (4)] affected CO, SV, and SVV (both methods). Method comparison revealed a bias for SVV of 0.1% [standard error of the mean (SE) 0.8] at baseline, -1.2% (SE 0.8) during decreased and 4.0% (SE 0.7) during increased afterload, the latter being significantly different from the others (P<0.05). Thereby, pulse contour analysis tended to underestimate SVV during decreased afterload and to overestimate SVV during increased afterload. Limits of agreement were approximately 6% for all points of measurement.
CONCLUSIONS: Left ventricular SVV is not affected by changes in cardiac afterload. There is a good agreement of pulse contour with flow derived SVV. The agreement decreases, if afterload is extensively augmented.
METHODS: In 13 anaesthetized, mechanically ventilated pigs [31(SD 6) kg], we compared cardiac output (CO), stroke volume (SV), and SVV determined by pulse contour analysis and by an ultrasonic aortic flow signal (Bland-Altman analysis). After obtaining baseline measurements, cardiac afterload was increased using phenylephrine and decreased using adenosine (both continuously administered). Measurements were performed with a constant tidal volume (12 ml kg-1) without PEEP.
RESULTS: Neither increasing mean arterial pressure (MAP) [from 59 (7) to 116 (19)] nor decreasing MAP [from 63 (7) to 39 (4)] affected CO, SV, and SVV (both methods). Method comparison revealed a bias for SVV of 0.1% [standard error of the mean (SE) 0.8] at baseline, -1.2% (SE 0.8) during decreased and 4.0% (SE 0.7) during increased afterload, the latter being significantly different from the others (P<0.05). Thereby, pulse contour analysis tended to underestimate SVV during decreased afterload and to overestimate SVV during increased afterload. Limits of agreement were approximately 6% for all points of measurement.
CONCLUSIONS: Left ventricular SVV is not affected by changes in cardiac afterload. There is a good agreement of pulse contour with flow derived SVV. The agreement decreases, if afterload is extensively augmented.
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