The parallel rise in diamine oxidase activity and the serum lactate concentration in Group I implies that ischemic injury to the mucosa of the small intestine occurs during cardiopulmonary bypass, and the rise in the serum peptidoglycan concentration indicates that bacteremia did occur. Thus, cardiopulmonary bypass causes hypoperfusion of small intestinal mucosa and consequently bacterial translocation.
Cardiopulmonary bypass causes a systemic inflammatory response, which can lead to capillary leak syndrome. In 15 adults undergoing elective cardiac surgery with cardiopulmonary bypass, we determined the volume and peak time of capillary leakage from the measurements of extracellular fluid volume and circulating blood volume taken preoperatively, at various intervals up to 24 hours after surgery, and on the 7th postoperative day. Extracellular fluid volume rose from 15.5 +/- 2.7 L preoperatively to a peak 4 hours after surgery of 18.3 +/- 3.2 L and remained elevated at 24 hours. Circulating blood volume fell from 4.10 +/- 0.68 L preoperatively to 3.20 +/- 0.58 L at the end of surgery. Fluid administered intraoperatively did not raise the circulating blood volume. Intraoperative fluid balance was positive at 2.62 +/- 0.72 L but negative at all time points postoperatively. There was significant postoperative capillary leakage, increasing from 4.7% +/- 2.3% of body weight at the end of surgery to a peak 4 hours later of 5.4% +/- 2.0% and falling to 2.8% +/- 3.3% at 24 hours. This knowledge of the pattern of change in capillary leakage after cardiac surgery with cardiopulmonary bypass might serve as a valuable guide for postoperative management.
Using a new method based on pulse dye densitometry, circulating blood volume (BV) was measured without direct sampling in patients undergoing open-heart surgery, and the effects of phosphodiesterase (PDE) III inhibitor administration during cardiopulmonary bypass (CPB) were evaluated. Sixteen patients scheduled for elective coronary artery bypass grafting were randomly assigned to the PDE III inhibitor group or control group. BV was determined before CPB, and immediately, and 4 and 12h after operation. After declamping of the aorta, the PDE III inhibitor amrinone (1 mg/kg) was infused as a single bolus into the venous reservoir in the PDE III inhibitor group. BV decreased significantly soon after the operation in the control group. It did not decrease in the PDE III inhibitor group (48.6 +/- 44 and 60.6 +/- 8.0 ml/kg for the control and PDE III inhibitor groups. respectively). Four hours after surgery and beyond no significant changes in BV were observed in either group. The body fluid balance was negative in both groups. In conclusion, a single administration of PDE III inhibitor during CPB was found to sustain BV soon after operation and, therefore, is useful for postoperative management of open-heart surgery.
Cardiac surgery with cardiopulmonary bypass is associated with a systemic inflammatory response. We examined combined use of heparin coating of the cardiopulmonary bypass circuit and a leukocyte-depleting arterial line filter to reduce this response. Thirty patients were allocated randomly to equal groups with a conventional circuit and arterial line filter (C group), a heparin-coated circuit with a conventional filter (H group), or a heparin-coated circuit with a leukocyte-depleting arterial line filter (HF group). Cytokines and respiratory function were repeatedly measured perioperatively. Plasma interleukin (IL)-6 concentrations in the HF group were lower than in the C group immediately following bypass and operation, at 4 h, and 12 h (p < 0.05). Plasma IL-8 was lower in the HF group than in the C group at 4 h (p < 0.05). The respiratory index was lower immediately after bypass in the HF group than the C group (0.61 +/- 0.2 versus 1.05 +/- 0.4, p < 0.05). Heparin-coated circuits with leukocyte-depleting filters decrease inflammatory responses and improve pulmonary function during operation.
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