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INTRODUCTION: The α2-adrenoceptor agonist dexmedetomidine is an effective postoperative sedative without clear advantages over midazolam or propofol. We hypothesized that routine use of dexmedetomidine allows early extubation in cardiac surgery patients. Secondary outcomes included the use of narcotic and non-narcotic analgesics during the first 48 hours, early postoperative functional status, and the incidence of bradycardia or hypotension. METHODS: We retrospectively analyzed patients admitted to a cardiothoracic intensive care unit after cardiac surgery. Patient charts and the Society of Thoracic Surgery National database were reviewed. Patients who received no sedation were compared to those who received dexmedetomidine. RESULTS: Ninety-nine patients (52 receiving no sedation and 47 receiving dexmedetomidine) were included in this study. The median time to extubation was 3.9 (2.8-5.4) hours in the control group versus 4.7 (3.45-6.52) hours in the dexmedetomidine (P=.16). The incidence of bradycardia, hypotension, the ability to ambulate, and Glascow Coma Scores = 15 on postoperative day 0 did not differ significantly. Acetaminophen was used more frequently in the first 48 hours postoperatively in dexmedetomidine patients (P=.02) and a trend toward higher opioid (P=.09) and ketorolac use (P=.30) over the first 48 hours was noted. CONCLUSIONS: The use of dexmedetomidine did not allow earlier extubation or less use of analgesics when compared to no sedation. Bradycardia and hypotension were not a problem with the use of dexmedetomidine.

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The current study sought to elucidate the relationship between myocardial pH and function during a significant but not absolute reduction in coronary flow. In a canine model, a partial coronary arterial stenosis was created, with the left anterior descending coronary artery (LAD) flow reduced by 50% compared to prestenosis levels, and maintained at that level for the duration of the study. During the experiment, interstitial myocardial pH and regional myocardial function, as assessed by the regional preload recruitable work area (PRWA), were measured. PRWA was depressed to 60% of baseline values, on average, for the entire period of reduced LAD flow. In contrast to the pattern observed with myocardial blood flow and systolic function, metabolic evidence of myocardial ischemia, that is, reduced myocardial pH did not become significantly different from baseline levels until after LAD flow had been reduced for 15 min. Thus, measurable changes in myocardial pH appeared slowly over time despite the fact that regional myocardial blood flow was decreased immediately. Therefore, myocardial pH cannot be used to anticipate alterations in myocardial contractile function.

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The current study examined the effects of temperature on myocardial pH, contractile function and adenosine triphosphate metabolism, particularly the production of adenosine. We matched intermittent delivery of blood cardioplegia in two groups (hypothermia 15 degrees C; normothermia 37 degrees C), for 2 h of cardioplegic arrest. Hypothermic perfusion resulted in a markedly alkalotic pH, and nearly a threefold increase in adenosine and adenosine monophosphate levels compared to normothermic hearts. Tissue levels of adenosine triphosphate were preserved to the same extent in each group, despite the increased energy requirements of normothermia. Myocardial contractile function was not statistically different between the two groups at 30 min and 2 h after the cross clamp was removed. These data suggest that both methods, hypothermia via its reduced energy demands, and normothermia through continued glycolytic metabolic activity, allow the myocardium to maintain energy stores and resume adequate function. However, hypothermic perfusion results in an accumulation of adenosine, demonstrating that temperature should be considered when attempting to manipulate the generation and accumulation of the compound.

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UNLABELLED: Excessive postoperative bleeding after heart operations continues to be a source of morbidity. This prospective double-blind study evaluated epsilon-aminocaproic acid as an agent to reduce postoperative bleeding and investigated its mode of action. One hundred three patients were randomly assigned to receive either 30 gm epsilon-aminocaproic acid (51 patients) or an equivalent volume of placebo (52 patients). In a subset of these patients (14 epsilon-aminocaproic acid, 12 placebo), tests of platelet function and fibrinolysis were performed. RESULTS: By multivariate analysis, three factors were associated with decreased blood loss in the first 24 hours after operation: epsilon-aminocaproic acid versus placebo (647 ml versus 839 ml, p = 0.004), surgeon 1 versus all other surgeons (582 ml versus 978 ml, p = 0.002), and no intraaortic balloon versus intraaortic balloon pump use (664 ml versus 1410 ml, p = 0.02). No significant differences in platelet function could be demonstrated between the two groups. Inhibited fibrinolysis, as reflected by less depression of the euglobulin clot lysis and no rise in D-dimer levels, was significant in the epsilon-aminocaproic acid group compared with the placebo group. CONCLUSION: The intraoperative use of epsilon-aminocaproic acid reduces postoperative cardiac surgical bleeding.

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BACKGROUND: It is proposed that retrograde abdominal perfusion be used in combination with retrograde cerebral perfusion to provide total body visceral protection during aortic reconstruction; however, its physiologic effects remain unknown. METHODS: We compared the effect of superior vena caval perfusion alone with that of combined superior and inferior vena caval perfusion on the liver and kidney in 6 mongrel dogs. Organ blood flow was measured using ultrasonic flow probes on the hepatic artery, the portal vein, and the renal artery. Regional tissue blood flow to the liver and the kidney was assessed using colored microspheres and pH probes. Anesthetized dogs were placed on total cardiopulmonary bypass. After cooling to 20 degrees C, retrograde perfusion was begun with 30 minutes of superior vena caval perfusion followed by another 30 minutes of bicaval perfusion, or vice versa. RESULTS: Very little renal blood flow was measured with either method of retrograde perfusion. Although the liver received more blood flow in comparison to the kidney, there was no significant difference between superior vena caval perfusion alone and bicaval perfusion. The addition of inferior vena caval perfusion results in portal hypertension, hepatic congestion, ascites, and bowel edema. CONCLUSIONS: In the canine model, bicaval perfusion does not provide superior protection to the liver and kidneys when compared with superior vena caval perfusion alone.

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Warm continuous retrograde cardioplegia is thought to prevent myocardial ischemia. We tested this hypothesis by subjecting canine hearts to 2 hours of either antegrade or retrograde perfusion with normothermic blood cardioplegia. Ischemic alterations were evaluated through the measurement of myocardial pH, tissue levels of adenosine triphosphate and lactate, and the preservation of left ventricular contractility. Antegrade perfusion resulted in uniformly positive changes in the myocardial pH in both ventricles, preserved levels of adenosine triphosphate, and small increases in the myocardial lactate levels. In contrast, retrograde perfusion caused the myocardial pH to decrease, especially in the right ventricle. Tissue lactate levels rose to a significantly greater extent during retrograde perfusion and adenosine triphosphate levels declined, although not to a statistically significant degree. Finally, myocardial function, as assessed by the preload recruitable work area, was preserved (103% +/- 20% of baseline) in the antegrade group but was markedly diminished (33% +/- 6%) in retrogradely perfused left ventricles 35 minutes after the aortic cross-clamp was removed. These data suggest that ischemic metabolism and the subsequent alteration of myocardial function take place despite continuous retrograde perfusion with normothermic blood cardioplegia.

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The ability of retrograde cardioplegia to protect the right ventricle has been questioned. Canine myocardial circulation was assessed by infusing colored microspheres through the coronary sinus. The relative flow index (RFI), a normalized measure of tissue blood flow, was determined for 76 sections of myocardium. Three distinct flow regions were evident from these measurements. A paucity of blood flow through some basal sections of the right ventricle (RFI = 0.23 +/- 0.19) was found to be significantly different (p < 0.005) from regions of the heart with normal flow (RFI = 1.12 +/- 0.06). Sections from the right ventricular apex demonstrated augmented flow (RFI = 3.72 +/- 1.18). These data indicate that retrograde coronary perfusion provides nonuniform flow and under some conditions may provide inadequate perfusion to portions of the right ventricle.

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Activated leukocytes are thought to contribute to respiratory dysfunction, alterations in microvascular permeability, disseminated intravascular coagulation, and thrombosis, all of which can complicate extracorporeal circulation. The purpose of this work was to determine the effects of extracorporeal circulation on leukocyte functions likely to mediate organ damage. White blood cell counts in the bubble circuits (n = 5) fell to 51% +/- 7% (mean +/- standard error of the mean; p less than 0.05) of initial levels within 2 hours of recirculation. In contrast, counts from both the spiral coil (n = 5) and hollow-fiber (n = 5) groups remained at 91% +/- 12% and 100%, respectively. Plasma levels of human neutrophil elastase rose from 0.28 +/- 0.06 micrograms/ml to 3.14 +/- 0.36 micrograms/ml (p less than 0.05) and 0.20 +/- 0.02 micrograms/ml to 1.61 +/- 0.35 micrograms/ml (p less than 0.05) in bubble and spiral coil circuits, respectively, but from only 0.20 +/- 0.03 micrograms/ml to 0.96 +/- 0.42 micrograms/ml in the hollow-fiber circuit despite 2 hours of recirculation. Consistently, in response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine, a chemotactic peptide, cells from spiral coil and bubble circuits released and generated significantly less elastase and superoxide anion, respectively. In contrast, neutrophils from the hollow-fiber circuits demonstrated enhancement of N-formyl-L-methionyl-L-leucyl-L-phenylalanine-induced elastase release and superoxide generation. Finally, mixed leukocytes from all circuits expressed procoagulant activity reaching statistical significance in bubble circuits. In conclusion, extracorporeal circulation has pronounced effects on neutrophil elastase release, superoxide anion generation, and leukocyte procoagulant activity. Spiral coil and bubble oxygenators cause granule release and, subsequently, reduced sensitivity to soluble agonists. In contrast, hollow-fiber oxygenators "prime" cells, actually enhancing reactivity. Recirculation through all circuits induces leukocyte procoagulant activity that is likely to contribute to surface-induced thromboses and excessive bleeding.

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Truly effective prevention of reperfusion myocardial damage is precluded in part by a lack of understanding of the earliest events which accompany ischemia. The purpose of this study was to assess the coronary endothelial response to two forms of ischemic injury in an isolated crystalloid perfused rabbit heart. Global cardiac ischemia, confirmed by NADH fluorescence photography, was induced either by mechanically reducing coronary flow by 90% (MRCF, N = 11) or by an infusion of N-formyl-methionyl-leucyl-phenylalanine (fMLP, N = 11), a known stimulus for leukotriene synthesis and coronary vasospasm. Compared with control, MRCF resulted in an increase in effluent concentrations of both prostacyclin (152 +/- 22 pg/ml vs 951 +/- 214 pg/ml, P less than 0.05) and plasminogen activator (0.8 +/- .3 IU/ml vs 1.4 +/- 0.5, P less than 0.05) but no detectable increase in effluent thromboxane B2 or leukotriene C4 concentrations. fMLP infusion resulted in an immediate reduction in coronary flow coincident with diffuse myocardial ischemia. In contrast to MRCF, however, fMLP-induced ischemia resulted in a significant but smaller increase in effluent prostacyclin concentration (210 +/- 47 pg/ml vs 606 +/- .55 pg/ml, P = 0.05) and a marked increase in both thromboxane B2 (less than or equal to 33 +/- 4 pg/ml vs 1141 +/- 375 pg/ml, P less than 0.05) and leukotriene C4 (less than 0.25 ng/ml vs 3.3 +/- 1.2 ng/ml, P less than 0.05) concentrations. Additionally, fMLP caused a reduction in effluent plasminogen activator activity (0.5 +/- 0.1 IU/ml vs 0.39 +/- 0.1 IU/ml, N = 4).(ABSTRACT TRUNCATED AT 250 WORDS)

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