Objective: We aimed to identify the impact of re-exploration for bleeding after coronary artery bypass grafting (CABG) and the effect of time delay, re-exploration within 12 h (<12 h) versus 12 h or later (12 h). Methods: Analyses of prospective clinical data on 3220 consecutive patients who underwent CABG between 2003 and 2005 were performed. Pearson x 2 tests, Fisher's exact tests, Student's t-tests, Mann-Whitney U tests, or univariate logistic regression analysis were used to assess the effects of pre-operative and operative characteristics on re-exploration, and the effects of re-exploration and time delay on adverse outcomes. Predictors of re-exploration and its effect on adverse outcomes were further evaluated using multiple logistic regression analysis. Results: One hundred ninety-one patients (5.9%) underwent re-exploration for bleeding. Reexplored patients as a group in comparison to the non-re-explored group had increased postoperative blood loss, transfusion requirements, duration of mechanical ventilation, ICU stay, intra-aortic balloon pump (IABP) and haemofiltration support, and mortality (all p < 0.001). One hundred fifty-seven (82%) of the 191 patients were re-explored <12 h. The group of patients who were re-explored <12 h in comparison to 12 h group had shorter ICU stay (median 3 vs 8.5 days; p < 0.001), less IABP support (22.3 vs 44.1%; p = 0.009) and a lower mortality (7 vs 29.4%; p = 0.001). There was no significant difference in blood loss or transfusion requirements between the two groups. The predicted EuroSCORE risks of the <12 h group was 6.66% and the observed mortality was 7% ( p = 0.865). The observed mortality of 29.4% in the 12 h group was significantly higher than the predicted EuroSCORE risks of 7.59% ( p < 0.001). Conclusions: Patients requiring re-exploration for bleeding are at higher risk of adverse outcomes and this risk is increased if time to re-exploration is prolonged for 12 h or longer. #

Lung diffusing capacity for nitric oxide (DLNO) is used to measure alveolar membrane conductance (DMNO), but disagreement remains as to whether DMNO=DLNO, and whether blood conductance (thetaNO)=infinity. Our previous in vitro and in vivo studies suggested that thetaNO

To model lung nitric oxide (NO) and carbon monoxide (CO) uptake, a membrane oxygenator circuit was primed with horse blood flowing at 2.5 l/min. Its gas channel was ventilated with 5 parts/million NO, 0.02% CO, and 22% O2 at 5 l/min. NO diffusing capacity (Dno) and CO diffusing capacity (Dco) were calculated from inlet and outlet gas concentrations and flow rates: Dno = 13.45 ml.min(-1).Torr(-1) (SD 5.84) and Dco = 1.22 ml.min(-1).Torr(-1) (SD 0.3). Dno and Dco increased (P = 0.002) with blood volume/surface area. 1/Dno (P < 0.001) and 1/Dco (P < 0.001) increased with 1/Hb. Dno (P = 0.01) and Dco (P = 0.004) fell with increasing gas flow. Dno but not Dco increased with hemolysis (P = 0.001), indicating Dno dependence on red cell diffusive resistance. The posthemolysis value for membrane diffusing capacity = 41 ml.min(-1).Torr(-1) is the true membrane diffusing capacity of the system. No change in Dno or Dco occurred with changing blood flow rate. 1/Dco increased (P = 0.009) with increasing Po2. Dno and Dco appear to be diffusion limited, and Dco reaction limited. In this apparatus, the red cell and plasma offer a significant barrier to NO but not CO diffusion. Applying the Roughton-Forster model yields similar specific transfer conductance of blood per milliliter for NO and CO to previous estimates. This approach allows alteration of membrane area/blood volume, blood flow, gas flow, oxygen tension, red cell integrity, and hematocrit (over a larger range than encountered clinically), while keeping other variables constant. Although structurally very different, it offers a functional model of lung NO and CO transfer.

A simple model lung has been designed using a membrane oxygenator circuit comprising two membrane oxygenators primed with one to two litres of equine blood, giving reproducible results over several hours. Normoxia and normocapnia were achieved consistently over the duration of the test with a blood flow of 2.5 l/min, oxygenator ventilation gas flow of 5 l/min air with 0.3 l/min O2 and deoxygenator ventilation gas flow of 5 l/min 5% CO2 in N2 with 0.2 l/min CO2. The measured PaO2 was 81.3 (SD 3.35 mmHg), PvO2 38.3 (SD 1.38 mmHg), PvCO2 60.6 (SD 1.13 mmHg) and PaCO2 36.1 (SD 0.69mmHg). MO2 and MCO2 were 116 ml/min and 169 ml/min, respectively. An increasing linear relationship was observed for FiO2 and the corresponding PaO2 and, similarly, with FiCO2 and PvCO2, providing reference ranges for this model.

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