Sonoclot analysis in elderly compared with younger patients undergoing coronary surgery.

BACKGROUND: The Sonoclot analyzer is a point-of-care method for assessment of the clotting mechanism in whole blood. The results are available within 20 min. The aim of the present study was to investigate whether repeated Sonoclot analyses could identify peri-operative differences in hemostatic function between elderly and younger patients undergoing coronary artery bypass grafting (CABG). In addition, we investigated whether Sonoclot analyses could identify disturbances in hemostatic function leading to post-operative bleeding. METHODS: Twenty-five elderly and 25 younger patients undergoing CABG were included. Blood samples for Sonoclot analyses were drawn pre-operatively, during surgery, and during the first 20 post-operative hours. The Sonoclot variables sonACT, clot rate, time-to-peak, amplitude of the peak, and R3 were analyzed, and the results were compared between the two groups. Post-operative blood loss volumes were recorded and correlated to the Sonoclot variables. The Sonoclot variables were also correlated to previously reported results on various hemostatic variables measured in the same patient population. RESULTS: There was a significant difference in sonACT between the two groups (P=0.018). There were no differences between the groups in any of the other Sonoclot variables. There were no significant correlations between any of the Sonoclot variables and post-operative bleeding, or between the Sonoclot variables and other hemostatic variables. CONCLUSIONS: The difference in sonACT between the two groups indicates a reduced hemostatic function in the elderly patients. However, repeated Sonoclot analyses were not able to identify more specific disturbances in hemostatic function, and did not predict increased post-operative bleeding.

Effects of autotransfusion of mediastinal shed blood on biochemical markers of myocardial damage in coronary surgery.

BACKGROUND: Previous studies have shown conflicting results regarding the effect of autotransfusion of mediastinal shed blood after coronary artery bypass grafting (CABG) on the serum levels of myocardial band (MB) isoenzymes of creatine kinase (CK-MB) and cardiac troponins. The effect of autotransfusion on serum levels of human heart fatty acid binding protein (H-FABP), another marker of myocardial necrosis, has not been studied. The aim of the present study was to investigate the effects of autotransfusion of mediastinal shed blood on the serum levels of CK-MB, cardiac troponin T (cTnT), and H-FABP after uncomplicated primary CABG. METHODS: Fifty patients were randomized to post-operative autotransfusion of mediastinal shed blood or no autotransfusion. Blood samples for the analysis of the biochemical markers of myocardial damage were drawn pre-operatively and 1, 4, 12, 24, 48, and 72 h after the termination of cardiopulmonary bypass. Samples from the mediastinal shed blood were collected after 1 and 4 h. RESULTS: The levels of the biochemical markers of myocardial injury were all markedly elevated in mediastinal shed blood. Autotransfusion did not significantly affect the serum levels of cTnT or H-FABP. However, during the early post-operative hours, there was a trend towards a higher level of cTnT and H-FABP in the autotransfusion group. During the first 24 h after surgery, the autotransfusion group had a significantly higher serum level of CK-MB. CONCLUSION: Post-operative autotransfusion of mediastinal shed blood may contribute to elevated serum levels of biochemical markers of myocardial injury.

Effects of thoracic epidural analgesia on pulmonary function after coronary artery bypass surgery.

OBJECTIVE: A substantial reduction in lung volumes and pulmonary function follows cardiac surgery. Pain may prevent effective breathing and coughing, and as thoracic epidural analgesia may reduce postoperative pain, we investigated the effect of epidural analgesia on pulmonary function. METHODS: Fifty-four male patients, under 65 years and with an ejection fraction of more than 0.5, were randomized into two groups: a control group receiving high-dose fentanyl anaesthesia and an epidural group receiving low-dose fentanyl anaesthesia + thoracic epidural analgesia. Time to awakening and time to extubation were recorded. Further, spirometric data, arterial oxygenation, pulmonary shunt, haemodynamics, use of vasoactive drugs and fluid balance were followed for up to 6 days postoperatively. RESULTS: Patients with low-dose fentanyl and epidural analgesia awoke (1.6 vs 3.6 h) and were extubated (5.4 vs 10.8 h) significantly earlier than control group patients. A 50-70% reduction in forced vital capacity, forced expiratory volume in 1 s (FEV1.0) and peak expiratory flow rate (PEFR) was seen after surgery, but higher FEV1.0 and PEFR on days 2 and 3 were seen in the epidural group than in the control group. Pulmonary shunt and alveolo-arterial oxygen difference increased similarly in both groups, whereas oxygen delivery and mixed venous oxygen saturation were higher in the epidural group. Epidural analgesia gave better control of the postoperative hyperdynamic circulation. CONCLUSIONS: Thoracic epidural analgesia yields a slight, but significant, improvement in pulmonary function, most likely due to a more profound postoperative analgesia.

Effects of thoracic epidural analgesia on coronary hemodynamics and myocardial metabolism in coronary artery bypass surgery.

OBJECTIVE: A possible influence of thoracic epidural analgesia on coronary hemodynamics and myocardial metabolism in coronary artery bypass grafting was investigated. DESIGN: The study was prospective and randomized. SETTING: The study was performed in a university hospital. PARTICIPANTS: Thirty male patients less than 65 years of age and with ejection fraction greater than 0.5 participated. They were randomized into 3 groups: the high fentanyl (HF) group receiving high-dose fentanyl (55 micrograms/kg) anesthesia, the HF + thoracic epidural analgesia (TEA) group receiving the same general anesthesia plus thoracic epidural analgesia, and the low-fentanyl (LF) + TEA group receiving low-dose fentanyl (15 micrograms/kg) anesthesia plus thoracic epidural analgesia. INTERVENTIONS: A thoracic epidural catheter, a peripheral and central venous catheter, a radial artery catheter, a thermodilution pulmonary artery catheter, and a coronary sinus reverse thermodilution catheter were inserted. MEASUREMENTS AND MAIN RESULTS: Coronary circulatory parameters, myocardial oxygenation, and myocardial substrate utilization were investigated before bypass and for 9 hours after bypass. Before bypass, the most striking finding was a reduction in myocardial lactate extraction in all groups, but also coronary flow and myocardial oxygen consumption decreased compared with baseline. After bypass, the only significant finding was a lower coronary vascular resistance early postoperatively in the epidural groups, but coronary blood flow was adequate in all groups. Myocardial metabolism was essentially unchanged both with and without epidural analgesia after bypass. CONCLUSION: With regard to the coronary circulation and myocardial metabolism, no hard data supporting the use of thoracic epidural analgesia in coronary artery bypass grafting were found.

Thoracic epidural analgesia in aortocoronary bypass surgery. II: Effects on the endocrine metabolic response.

Thoracic epidural analgesia (TEA) may offer haemodynamic benefits for patients with coronary heart disease going through major surgery. This may-in part-be secondary to an effect on the endocrine and metabolic response to surgery. We therefore investigated the effect of TEA on the endocrine metabolic response to aortocoronary bypass surgery (ACBS). Thirty male patients (age < 65 years, ejection fraction > 0.5) were randomized into 3 groups; the HF group receiving a high dose fentanyl (55 micrograms.kg-1) anaesthesia, the HF+TEA group with the same fentanyl dose+TEA with 10 ml bupivacain 5 mg.ml-1, followed by 4 ml every hour, and the LF+TEA group receiving fentanyl 15 micrograms.kg-1 + TEA. Adrenalin, noradrenalin, systemic vascular resistance (SVR), glucose, cortisol, lactate and free fatty acids were followed during the operation and for 20 h postoperatively. A significant increase in adrenalin, noradrenalin and SVR was found in the HF group whereas this increase was blocked in both epidural groups. An increase in glucose and cortisol was noticed in all groups, but the increase was delayed in the epidural groups. Our results suggest that a more effective blockade of the stress response during ACBS is obtained when TEA is added to general anaesthesia than with high dose fentanyl anaesthesia alone.

Thoracic epidural analgesia in aortocoronary bypass surgery. I: Haemodynamic effects.

Tachycardia and hypertension may cause myocardial ischaemia in patients with coronary heart disease going through major surgery. Thoracic epidural analgesia (TEA) has been reported to be beneficial in this situation. The haemodynamic effects of TEA in aortocoronary bypass surgery were investigated in 30 male patients < 65 years old and with ejection fraction > 0.5. They were randomized into 3 groups: the high dose fentanyl (HF) group receiving high-dose fentanyl (55 micrograms.kg-1) anaesthesia, the HF+TEA group receiving the same fentanyl dose+TEA with 10 ml bupivacaine 5 mg.ml-1 followed by 4 ml every hour, and the low dose fentanyl (LF) + TEA group receiving low-dose fentanyl (15 micrograms.kg-1) anaesthesia+TEA. Haemodynamic parameters, the use of vasoactive and inotropic drugs and fluid balance were followed during the operation and for 20 h postoperatively. Before bypass the only significant difference between groups was a higher mean pulmonary arterial pressure in the HF+TEA group and a lower systemic vascular resistance (SVR) in the LF+TEA group, both compared to the HF group. 89% of epidural group patients needed small doses of ephedrine whereas more HF group patients were given nitroglycerine. During bypass SVR and mean arterial pressure (MAP) were significantly higher and pump flow lower in the HF group compared to the LF+TEA group. More ketanserin to HF group patients and methoxamine to epidural group patients were given. After bypass heart rate increased in all groups. Lower MAP 0.5 h after bypass and higher filling pressures in the early post bypass period in the epidural groups, most pronounced in the HF+TEA group, were noted.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of thoracic epidural analgesia alone and in combination with general anesthesia on cardiovascular function and myocardial metabolism in patients receiving beta-adrenergic blockers.

Thoracic epidural analgesia combined with chronic beta-adrenergic blocker medication may cause cardiac depression. We investigated the cardiovascular and myocardial metabolic effects of a T1-T12 epidural block in 18 patients (age < 65 yr, ejection fraction > 0.5), receiving chronic beta-adrenergic blocker medication and scheduled for aortocoronary bypass surgery. After randomization into a light or deeper general anesthetic group, the cardiovascular and myocardial metabolic effects of a subsequent general anesthesia induction were investigated. Thoracic epidural analgesia induced a moderate decrease in mean arterial pressure, coronary perfusion pressure, free fatty acids, and myocardial consumption of free fatty acids. General anesthesia with thiopental (2-4 mg/kg) and a low fentanyl dose (5 micrograms/kg) increased heart rate, coronary perfusion pressure, and coronary vascular resistance, whereas mean pulmonary arterial pressure and pulmonary capillary wedge pressure decreased. After thiopental (2-4 mg/kg) and a high fentanyl dose (30 micrograms/kg), mean arterial pressure and left ventricular stroke work index decreased. We conclude that a T1-T12 epidural block in well sedated, beta-adrenergic blocked patients does not induce clinically significant cardiovascular effects. Induction of general anesthesia was well tolerated, but the light general anesthetic could not prevent an increase in heart rate and coronary vascular resistance, whereas the deeper anesthetic induced slight myocardial depression. No effect on the atrioventricular conduction, as measured by the PQ-time, was noted.