• M Bundgaard-Nielsen, C C Jørgensen, T B Jørgensen, B Ruhnau, N H Secher, and H Kehlet.
• Section of Surgical Pathophysiology, Rigshospitalet, University of Copenhagen, Copenhagen DK-2100, Denmark. morten.bundgaard-nielsen@rh.regionh.dk
• Br J Anaesth. 2009 Jun 1;102(6):756-62.

BackgroundA key element in enhanced postoperative recovery is early mobilization which, however, may be hindered by orthostatic intolerance, that is, an inability to sit or stand because of symptoms of cerebral hypoperfusion as intolerable dizziness, nausea and vomiting, feeling of heat, or blurred vision. We assessed orthostatic tolerance in relation to the postural cardiovascular responses before and shortly after open radical prostatectomy.MethodsOrthostatic tolerance and the cardiovascular response to sitting and standing were evaluated on the day before surgery and 6 and 22 h after operation in 16 patients. Non-invasive systolic (SAP) and diastolic arterial pressure (DAP) (Finometer), heart rate, cardiac output (CO, Modelflow), total peripheral resistance (TPR), and central venous oxygen saturation (Scv(O2)) were monitored.ResultsBefore surgery, no patients had symptoms of orthostatic intolerance. In contrast, 8 (50%) and 2 (12%) patients were orthostatic intolerant at 6 and approximately 22 h after surgery, respectively. Before surgery, SAP, DAP, and TPR increased (P<0.05), whereas CO did not change (P>0.05) and Scv(O2) decreased (P<0.05) upon mobilization. At 6 h after operation, SAP and DAP declined with mobilization (P<0.05) and the arterial pressure response differed from the preoperative response both upon sitting (P<0.05) and standing (P<0.05) due to both impaired TPR and CO. At approximately 22 h, the SAP and DAP responses to mobilization did not differ from the preoperative evaluation (P>0.05).ConclusionsThe early postoperative postural cardiovascular response is impaired after radical prostatectomy with a risk of orthostatic intolerance, limiting early postoperative mobilization. The pathogenic mechanisms include both impaired TPR and CO responses.

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