Influence of venous drainage and hemofiltration on hypercirculatory instability after high volume crystalloid cardioplegia during coronary artery bypass surgery.

ABSTRACT

AIM: The etiology of hypercirculatory instability following cardiac surgery with cardiopulmonary bypass has not yet been completely investigated and its clinical impact remains unclear. This prospective study was undertaken in order to investigate the impact of the systemic infusion of high volume crystalloid cardioplegia on the incidence of hypercirculatory instability and inflammatory mediator release in patients undergoing coronary artery bypass grafting. METHODS: Forty patients with single-atrial cannulation (group A), 40 patients with single-atrial cannulation and intraoperative hemofiltration (group B), and 40 patients with bicaval cannulation and complete removal of the cardioplegic solution from the right atrium (group C) were analyzed for hemodynamic changes and inflammatory mediator release until the postoperative day 2. Myocardial protection was performed using 2,000 mL cold crystalloid cardioplegia. RESULTS: A higher incidence of hypercirculatory instability in group A (39.2%) and B (42.8 %) was noted when compared to group C (18%, P = 0.032). Cardiac index was lower in group C when compared with group A (P = 0.001; 95% CI 4.1, 15.57) and group B (P = 0.02; 95% CI 1.13, 15.25). Systemic vascular resistance was higher in group C when compared with group A (P = 0.0001; 95% CI 7108.7, 3131) and group B (P < 0.005; 95% CI 7598.9; 2830.6). High levels of tumor necrosis factor alpha, interleukin-6, interleukin-8, interleukin-10, and intercellular adhesion molecule-1 with no significant differences between the groups were measured early postoperative. CONCLUSIONS: High volume crystalloid cardioplegia under use of single-atrial venous cannulation is associated with a higher incidence of hypercirculatory failure. Hemofiltration during cardiopulmonary bypass offers no benefit on the incidence of hypercirculatory instability and to the release of inflammatory mediators.