NO RELEASE OF CARDIAC TROPONIN-I DURING MAJOR ORTHOPEDIC-SURGERY AFTER ACUTE NORMOVOLEMIC HEMODILUTION

Background: Normovolemic hemodilution is a well-accepted method for in traoperative blood salvage. However, some controversy exists concernin g the possible risk of myocardial fiber injury as a consequence of the reduced oxygen content. Laboratory diagnosis of perioperative myocard ial fiber injury is difficult, since biochemical markers are elevated postoperatively due to the surgical trauma. Cardiac troponin I (cTnI) is a new, highly sensitive and specific cardiac marker for the detecti on of myocardial injury. The aim of our study was to investigate wheth er normovolemic hemodilution in patients with major orthopedic surgery (13 hemodiluted patients, 15 controls) induces a release of cTnI. Met hods: cTnI as a highly specific and sensitive cardiac parameter, as we ll as total creatine kinase (CK), creatine kinase isoenzyme MB mass (C KMB mass) and myoglobin were measured after induction of anesthesia, a fter normovolemic hemodilution, prior to retransfusion of blood compon ents, 3 h after surgery, and on the first and third postoperative days . Results: Prior to retransfusion of blood components the hematocrit w as decreased to 25.4+/-1.2% (mean+/-SEM; range: 18%-34%) in the contro l group and to 20.2+/-0.8% (mean+/-SEM; range: 17%-24%) in the hemodil ution group. Total CK, CKMB mass as well as myoglobin concentration in creased significantly in both groups, reaching their maxima within the first day of surgery. In contrast, cTnI was below the detection limit of the assay (<0.5 mu g/L) at any time. Conclusions: We suggest that pre- and intraoperative hemodilution to a hematocrit of approximately 20% by maintaining normovolemia does not induce myocardial fiber injur y in patients without preexisting cardiac diseases.