Key result
Tourniquet release in total knee arthroplasty is linked to reduced pulmonary vascular resistance in ~91% of patients.
Why the study?
Embolic events after tourniquet release during total knee arthroplasty occur in all patients and may lead to lung injury, but mechanisms allowing lung tolerance are not well understood.
Does tourniquet release during total knee arthroplasty affect pulmonary capillary recruitment as measured by ACE substrate hydrolysis and pulmonary vascular resistance?
Observational (n=11)
Does tourniquet release during total knee arthroplasty affect pulmonary capillary recruitment as measured by ACE substrate hydrolysis and pulmonary vascular resistance?
Answers are grounded in this paper and cite their sources.
Pulmonary capillary recruitment, indicated by increased ACE substrate hydrolysis and decreased PVR, appears to be a key mechanism allowing patients to tolerate the embolic burden during tourniquet release in total knee arthroplasty.
In Brief Emboli after tourniquet release (TR) during total knee arthroplasty (TKA) occur in all patients. This may lead to fat embolism syndrome with lung injury. Angiotensin-converting enzyme (ACE) lines the pulmonary endothelium, and a decrease in ACE metabolism or hydrolysis of 3HBPAP (3H-benzoyl-Phe-Ala-Pro; a substrate specific for ACE) has been associated with lung injury. We evaluated the association of this assay with pulmonary changes during TKA. Eleven consecutive patients undergoing bilateral TKA had the ACE assay performed perioperatively. We determined substrate hydrolysis and pulmonary capillary surface area (capillary perfusion index; CPI) and correlated it with pulmonary vascular resistance (PVR) and clinical outcome. Ten of the 11 patients demonstrated an increase in substrate hydrolysis and CPI along with a decrease in PVR after first or second TR when compared with baseline values (P < 0.05). In the other patient, PVR continued to increase even after TR, whereas CPI and substrate hydrolysis decreased after surgery. Whereas all others did well clinically, this patient developed confusion and hypoxemia. In previous studies, a decrease in PVR with an increase in CPI, as exhibited by the 10 patients, has been associated with pulmonary capillary recruitment. We believe this to be an important mechanism by which the lungs are able to accommodate the burden of emboli at the time of TR. IMPLICATIONS: The embolic phenomenon to the heart and lungs occurs in all patients undergoing total knee arthroplasty at the time of tourniquet release. This study investigates possible mechanisms that allow most patients to tolerate such insults to their lungs without clinical complications.
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Jules-Elysee et al. (2004) conducted an observational in Total knee arthroplasty (n=11). Tourniquet release vs. Baseline was evaluated on Substrate hydrolysis, capillary perfusion index (CPI), and pulmonary vascular resistance (PVR) (p=< 0.05). Tourniquet release during total knee arthroplasty increased ACE substrate hydrolysis and capillary perfusion index, and decreased pulmonary vascular resistance in 10 of 11 patients (P<0.05).
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