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Transesophageal echocardiographic hemodynamic monitoring during preoperative acute normovolemic hemodilution.
Hälsouniversitetet, Linköping University.
2000 (English)In: Anesthesiology, ISSN 0003-3022, E-ISSN 1528-1175, Vol. 92, no 5, 1250-6 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Preoperative acute normovolemic hemodilution may compromise oxygen transport. The aims of our study were to describe the hemodynamic effects of normovolemic hemodilution and to determine its effect on systolic and diastolic cardiac function by multiplane transesophageal echocardiography.

METHODS: In eight anesthetized patients (aged 13-51 yr) without heart disease, hemoglobin was reduced in steps from 123 +/- 8 (mean +/- SD) to 98 +/- 3 and to 79 +/- 5 g/l. Hemodynamic measurements (intravascular pressures, thermodilution cardiac output, and echocardiographic recordings) were obtained during a stabilization period and at each level of hemodilution. Left ventricular wall motion was monitored continuously, and Doppler variables, annular motion, and changes in ejection fractional area were analyzed off-line.

RESULTS: During hemodilution, cardiac output by thermodilution increased by 16 +/- 7% and 26 +/- 10%, corresponding well to the increase in cardiac output as measured by Doppler (difference, 0.32 +/- 1.2 l/min). Systemic vascular resistance fell 16 +/- 14% and 23 +/- 9% and pulmonary capillary wedge pressure increased slightly (2 +/- 2 mmHg), whereas other pressures, heart rate, wall motion, and diastolic Doppler variables remained unchanged. Ejection fractional area change increased from 44 +/- 7% to 54 +/- 10% and 60 +/- 9% as a result of reduced end-systolic and increased end-diastolic left ventricular areas.

CONCLUSIONS: A reduction in hemoglobin to 80 g/l during acute normovolemic hemodilution does not normally compromise systolic or diastolic myocardial function as determined by transesophageal echocardiography. Preload, left ventricular ejection fraction, and cardiac output increase with a concomitant fall in systemic vascular resistance.

Place, publisher, year, edition, pages
2000. Vol. 92, no 5, 1250-6 p.
National Category
Clinical Medicine
URN: urn:nbn:se:kth:diva-86343PubMedID: 10781269OAI: diva2:500637
NR 20140805Available from: 2012-02-13 Created: 2012-02-13 Last updated: 2012-02-13Bibliographically approved

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