TY - JOUR

T1 - Orthostatic intolerance and the cardiovascular response to early postoperative mobilization

AU - Bundgaard-Nielsen, M

AU - Jørgensen, Christoffer Calov

AU - Jørgensen, T B

AU - Ruhnau, B

AU - Secher, N H

AU - Kehlet, H

N1 - Keywords: Aged; Analgesics, Opioid; Anesthesia, General; Blood Pressure; Drug Administration Schedule; Early Ambulation; Fluid Therapy; Humans; Male; Middle Aged; Orthostatic Intolerance; Pain, Postoperative; Perioperative Care; Postoperative Care; Postoperative Complications; Prostatectomy

PY - 2009

Y1 - 2009

N2 - BACKGROUND: A 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. METHODS: Orthostatic 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. RESULTS: Before 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). CONCLUSIONS: The 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.

AB - BACKGROUND: A 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. METHODS: Orthostatic 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. RESULTS: Before 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). CONCLUSIONS: The 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.

U2 - 10.1093/bja/aep083

DO - 10.1093/bja/aep083

M3 - Journal article

C2 - 19398452

VL - 102

SP - 756

EP - 762

JO - British Journal of Anaesthesia

JF - British Journal of Anaesthesia

SN - 0007-0912

IS - 6

ER -