Normothermic versus hypothermic cardiopulmonary bypass during repair of congenital heart disease.

OBJECTIVE: To compare normothermic cardiopulmonary bypass (CPB) versus hypothermic CPB in pediatric patients undergoing repair of congenital heart disease with focus on biochemical markers for brain damage. DESIGN: Prospective randomized interventional study. SETTING: Postgraduate teaching hospital. PARTICIPANTS: Twenty patients undergoing repair of congenital heart disease. INTERVENTIONS: Patients were randomized to normothermic (36 degrees C) versus hypothermic (25 degrees C) CPB. Serum levels of neuron-specific enolase (NSE) and S-100beta protein were measured in all patients before surgery, immediately after CPB, and 12 and 24 hours after surgery. Blood loss and time for extubation of the trachea were recorded. MEASUREMENTS AND MAIN RESULTS: Before operation, the S-100beta protein and NSE levels were similar in the 2 groups. The S-100beta protein serum level increased significantly after CPB in both groups, whereas no change was found in the NSE level. There was no difference in the change of NSE and S-100beta protein levels between normothermic and hypothermic CPB. Blood loss was significantly less after hypothermic CPB (25 mL/kg/24 h v 42 mL/kg/24 h). Time for extubation was similar. CONCLUSION: No difference was found in the release of brain-specific proteins between normothermic and hypothermic CPB, but blood loss was higher after normothermic CPB.

Central cardiovascular and oxygen variables during haemorrhage in the pig.

BACKGROUND: We evaluated the ability of the standards issued by the Danish Society of Anaesthesiologists to reflect a blood loss. METHODS: In 9 pigs bled (0-24 ml kg-1 and retransfused (to 28 ml kg-1) during halothane anaesthesia central cardiovascular, thoracic electrical impedance (TI), oxygen, acid-base and temperature variables were recorded. RESULTS: With the recommendation for minor surgery (mean arterial pressure (MAP) and heart rate (HR)), the correlation to the blood loss was 0.74 (P < 0.001) and with that for major surgery (MAP, HR, central venous pressure (CVP) and rectal temperature (Tempr)) it was 0.79 (P < 0.001). With the recommendation for extensive surgery (MAP, HR, CVP, pulmonary artery catheter variables and the central-peripheral temperature difference (delta Tempr-t)), the correlation was 0.84 (P < 0.001). Non-invasive monitoring (MAP, HR, delta Tempr-t, TI and near-infrared spectroscopy of the brain (SinvosO2)) was only slightly better than basal monitoring (r = 0.76, P < 0.001). However, adding arterial base excess (BE), TI, and peripheral temperature (Tempt) to the recommendation for major surgery resulted in a correlation of 0.87 (P < 0.001), while adding BE and TI to the recommendation for extensive surgery raised correlation to only 0.88 (P < 0.001). CONCLUSION: When the recommendations were followed the correlation to the blood loss ranged from 0.74-0.84. However, with the recording of MAP, HR, CVP, delta Tempr-t, BE and TI a correlation of 0.87 was achieved, indicating that a pulmonary artery catheter may not be in need for patients undergoing surgical procedures with expected haemorrhage.

Timing of tracheal intubation: monitoring the orbicularis oculi, the adductor pollicis or use a stopwatch?

The most suitable time for tracheal intubation, following vecuronium 0.1 mg kg-1, was estimated in 120 patients. The trachea was intubated at cessation of the visually observed response of the orbicularis oculi muscle to facial nerve stimulation (group 1; n = 30), or of the manually detected response of the adductor pollicis to ulnar nerve stimulation (group 2; n = 30), or after waiting 3 min (group 3; n = 30), or 4 min (group 4; n = 30). There were no significant differences in intubation scores between the four groups of patients. Loss of response to train-of-four stimulation occurred significantly sooner in group 1 (orbicularis oculi) than in group 2 (adductor pollicis) P = 0.021). However, intubating conditions were poor in four patients (14%) in group 1, compared with none in group 2 and one in groups 3 and 4, respectively. Thus, contrary to expectations, the cessation of the response of the orbicularis oculi muscle did not guarantee good or even satisfactory intubating conditions. The results suggest that in fit adult patients it is as good to wait 3 min after injection of vecuronium 0.1 mg kg-1 before tracheal intubation, as to use a nerve stimulator.

Purine metabolite washout and platelet aggregation at reflow after tourniquet ischemia: effect of intravenous regional lidocaine.

Tourniquet ischemia will influence the biochemical milieu of tissue cells and affect the metabolism of purines in skeletal muscle distal to the occlusion. At reperfusion, generation of oxygen radicals by the hypoxanthine-xanthine oxidase system may ensue, influencing white blood cell and thrombocyte aggregation, causing damage to the endothelial cell barrier and inducing non-reflow type phenomena. Amide-type local anaesthetics are known to affect local vasotone, leukocyte adherence and platelet function but the influence of lidocaine on purine metabolite washout and platelet aggregation following tourniquet ischemia for lower limb surgery is not known in detail. Therefore, the effects of regional intravenous lidocaine during tourniquet ischemia for knee surgery on purine catabolite washout and platelet function following reflow were assessed. Eight patients served as control (C-group) and 8 (L-group) received 100 ml of lidocaine (2.5 mg/ml) in the emptied venous bed of the leg to be operated. All patients had spinal anaesthesia (0.5% bupivacaine). Effluent venous blood from the leg and radial arterial blood was collected and analysed for xanthine (X), hypoxanthine (HX), base excess (BE), pH and potassium before and after reperfusion. Platelet ADP-induced aggregation (ADP-agg.) and secretion of beta-thromboglobulin (beta-TG) were measured in the effluent blood as well as systemically. After tourniquet release (TR), X and HX were significantly increased in effluent venous blood but the washout was enhanced in the L-group during the initial reperfusion phase. BE was significantly higher in the L-group both before and after TR whereas pH and potassium washout was comparable between the groups. No systemic effects on platelets were detected after tourniquet release but ADP-agg. in effluent venous blood was attenuated in 6 out of 8 patients in the L-group (NS). It is concluded that HX and X are generated during leg ischemia. Regional intravenous lidocaine, most probably through a vasodilatory mechanism and inhibition of white blood cell activation, may attenuate non-reflow phenomena and thereby exert beneficial effects on post-ischemic recovery by enhancing post-ischemic tissue reperfusion.

Enhanced heart rate response to haemorrhage by ileus in the pig.

Effects of ileus on cardiovascular and hormonal responses to haemorrhage were evaluated in 10 anaesthetized pigs. Ileus was induced and the bleeding sequence repeated on the following day. Before ileus, a resting heart rate (HR) of 105 (range 83-140) beats min-1 remained unchanged until haemorrhage amounted to 15% of the blood volume. With a blood loss of 28% HR increased to a maximum of 162 (126-245) beats min-1. In contrast, ileus increased HR upon initiation of haemorrhage from a similar resting value to a maximum of 200 (152-250) beats min-1 (P < 0.0005). There were neither statistical differences in mean arterial pressure, cardiac output, central venous pressure, thoracic electrical impedance, pulmonary arterial mean pressure, pulmonary wedge pressure, pulmonary and systemic vascular resistances, nor in plasma concentrations of dopamine, adrenaline, vasopressin and aldosterone during haemorrhage before and after ileus. Plasma noradrenaline increased more with haemorrhage after than before ileus: from 2.8 (1.2-5.0) to 13 (2.3-59.0) vs. 3.0 (1.5-4.2) to 3.6 (2.7-17.5) nmol l-1 (P < 0.005). Also, the pancreatic polypeptide response to haemorrhage was enlarged with ileus (29 (0-60) to 90 (45-145) vs. 23 (0-64) to 57 (27-106) pmol l-1 (P < 0.005)). No significant differences could be detected in cardiovascular and hormonal responses to haemorrhage before and after a sham-operation in three pigs. Results demonstrate an immediate and enhanced HR response to haemorrhage in the pig with ileus, reflected in sympathetic activation as indicated by plasma noradrenaline.

The effect of epidural anaesthesia with 1% lidocaine on the pressor response to dynamic exercise in man.

1. In order to examine the sensitivity to local anaesthetics of afferent neural feedback from working muscle during dynamic exercise, sixteen subjects cycled for 12 min before and after epidural anaesthesia using 1% lidocaine. The presence of afferent neural blockade was verified by elimination of the blood pressure response to a cold pressor test, laser-induced evoked potentials and increases in pain detection and tolerance thresholds of the foot. Conversely, epidural anaesthesia had no effect on these variables in the unblocked skin areas or on electrically evoked potentials in blocked or unblocked skin. 2. During dynamic exercise, heart rate increased as did mean arterial pressure and cardiac output. Mean arterial pressure remained at the exercise level during post-exercise ischaemia, but heart rate and cardiac output decreased while total peripheral resistance increased. Epidural anaesthesia did not significantly affect these variables during rest, dynamic exercise, post-exercise ischaemia or recovery. 3. The results of this study show that, in order to affect blood pressure during dynamic exercise, epidural anaesthesia must block the pressor response to post-exercise ischaemia. The implication of these data is that complete or almost complete block of group III and/or group IV muscle afferents is necessary to inhibit the pressor response to dynamic exercise in man.

Reversal of benzodiazepine intoxication by flumazenil.

In order to firstly evaluate the efficacy of flumazenil in reversing benzodiazepine-induced sedation because of drug overdose and secondly to register adverse events, 13 patients admitted to the intensive care unit because of drug intoxication, were given flumazenil intravenously to a maximum of 1.0 mg. Sedation state was scored on a modified Glasgow Coma Scale and arterial blood pressure, heart rate and arterial blood gases were recorded before and after flumazenil was given, and every 30 min for 2 h. Results showed that flumazenil reversed the sedation due to benzodiazepines effectively increasing the coma score significantly (P less than 0.005). We found no change in arterial blood pressure (apart from one patient), heart rate or arterial blood gases. Two patients gave further information about drug intake after flumazenil was given. Six patients became resedated, only one needed additional flumazenil. One patient developed a hypertensive crisis after flumazenil was given as a result of the unmasking of an untreated hypertension. Another patient aspirated gastric content to the trachea during resedation and needed respiratory support.

Ultrasonically guided percutaneous treatment of liver abscesses.

Twenty-two patients with liver abscesses demonstrated by ultrasonography (US) were treated over a nine-year period. The diagnosis was in all cases verified by puncture. The patients were treated by US-guided puncture or catheter drainage. Seventeen patients (77%) were cured without surgical drainage. Four patients were cured after subsequent surgical intervention. One patient died later of pancreatic carcinoma. There were no complications from the US-guided therapy. For the treatment of liver abscesses we recommend US-guided drainage as the first choice. Close collaboration between surgeon and radiologist is mandatory since some of these patients still need surgical treatment.