Pathophysiologic Hemodynamics After Primary Unilateral Total Hip Arthroplasty

Early postoperative mobilization is a cornerstone in the so-called fast track multimodal perioperative approach and is essential in preventing postoperative morbidity and reducing hospital length-of-stay. Intact orthostatic blood pressure regulation is essential for early postoperative mobilization. However, early postoperative mobilization can be delayed due to postoperative orthostatic hypotension (POH) defined as a fall in systolic pressure > 20 mmHg and/or diastolic pressure > 10 mmHg or due to postoperative orthostatic intolerance (POI), characterized by dizziness, nausea, vomiting, blurred vision or syncope during mobilization. Although these conditions are well-known clinical problems that can delay early mobilization, relatively few data are available on pathophysiological mechanisms and possible treatments.

Several prospective studies with standardized mobilization procedures have already established that the incidence of POI and POH after THA is 38-42% at 6 hours after surgery.

Previous studies on patients undergoing prostatectomy and THA have also demonstrated that attenuated vasopressor response and a concomitant reduction in cardiac output (CO) and cerebral perfusion during postural changes after surgery contributes to POI and POH. Strategies aiming to reduce the incidence of POI and POH by pain management, vasoconstrictive treatment with alpha-1 receptor agonist, optimized fluid management with goal-directed fluid therapy and reduction of surgical stress-response with pre-operative high-dose glucocorticoid did not solve the problem.

The precise pathophysiological mechanisms of POI and POH remain to be elucidated and this is therefore the aim of the current prospective observational study.