[Right extrapericardial post-traumatic hernia of the heart: a peculiar symptomatology].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Freysz.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Myocardial ischemia sensitizes the cardiotoxic effects of bupivacaine, especially the propensity to ventricular fibrillation. To investigate this sensitization and to elucidate its mechanism, the influence of bupivacaine alone, or associated with ischemia, was studied on electrical fibrillation threshold in anesthetized, open chest pigs. Determination of fibrillation threshold was performed with impulses of 100 ms duration at the rate of 180 bpm, in the absence of ischemia and at the end of increasing periods of ischemia (30, 60, 120, 180 s) obtained by complete occlusion of the left anterior descending coronary artery close to its origin. The effect of bupivacaine (1.00 mg/kg initial dose plus 0.04 mg.kg-1.min-1 over 25 min) was compared to the control in the same animals. This effect corresponded to 1.4-1.8 micrograms/mL plasma concentrations likely to be observed in humans after regional anesthesia. Bupivacaine significantly increased the fibrillation threshold before coronary occlusion from approximately 7.0 to 9.5 mA. In contrast, during ischemia the fibrillation threshold was shifted to the left and down, with a hastening of spontaneous fibrillation. Recording of monophasic action potentials in the ischemic area revealed that conduction time was prolonged by more than 100% under the combined influence of ischemia and bupivacaine, whereas the major enhancement of excitability due to ischemia was not attenuated by bupivacine. Therefore, bupivacaine should be used with caution in the condition of ischemia, especially if heart rate is rapid. In the present experiments, tachycardia is another factor in the enhancement of bupivacaine effects on conduction.
Because recent clinical studies have failed to show evidence of the benefit of lidocaine in the arrhythmias occurring in the early stage of myocardial infarction and have even shown an increased mortality in patients thus treated, we investigated the value of lidocaine as a protective agent against ventricular fibrillation related to myocardial ischemia in the in situ heart of anesthetized open-chest pigs subjected to transient total occlusion of the proximal left anterior descending coronary artery (LAD) under ventricular pacing at a constant high rate. Vulnerability to the fibrillatory process induced by coronary occlusion was assessed both by time to onset of ventricular fibrillation (TF) and by electrical ventricular fibrillation threshold (EFT) determined after coronary occlusions of increasing duration (30, 60, 120, 180 s). Monophasic action potential (MAP) was recorded concurrently in the nonischemic and ischemic areas. Lidocaine, even in relatively high doses (2-4 mg.kg-1), did not prolong TF, nor did it increase EFT. On the contrary, TF was significantly shortened and EFT was significantly decreased (15-30%) at the maximal concentrations of lidocaine, with return to control values in 40-60 min. Therefore, lidocaine tends to increase the risk of ischemic ventricular fibrillation (VF): It fails to control the extreme enhancement of excitability and worsens conduction disorders, even though it decreases normal conduction only slightly. Use of lidocaine against rhythm disorders in acute myocardial infarction (AMI), is at least debatable and probably contraindicated.
The success of transplantations relies on uninjured organs i.e., harvested before circulatory failure. At present, french law concerning cerebral death criteria (circulaire ministérielle n. 3 du 21.01.91) requires the association of clinical patterns and 2 repeated, unreactive and flat electroencephalographic (EEG) tracings. Blood and urinary samples also need to be free from any nervous system depressant drug, the patient has not to be hypothermic. These obligations are not always compatible with patients status or local organization. The consequence might be organ loss or delay in harvesting schedule. A review of the literature points out the trap in realization and analysis of EEG in this kind of intensive care patients. Angiogram, on the opposite, is influenced neither by nervous system depressant drug nor by hypothermia. As it is in some other western countries, it should be proposed as the reference.
Explore the source record for details and available documents.
The impairment of intraventricular conduction by bupivacaine may result in reentrant arrhythmias including ventricular fibrillation. The concentrations responsible for serious accidents are high (5.0 to 8.0 micrograms/ml), but likely to be lowered by myocardial ischemia which gives rise to similar disorders. Therefore we did an electrophysiological study of bupivacaine's effects in an ischemic area of the myocardium. Monophasic action potential (MAP) of the ventricular myocardium was recorded in 30 anesthetized, open-chest pigs. Conduction time and effective refractory period were also measured. Data were obtained during short periods (10-15 s) of pacing at 180 beats/min, but ventricular beats remained governed by the sinus node in the intervals. Ischemia was produced by occluding the left anterior descending coronary artery completely but transiently (up to 8 min), not far from its origin. Comparison was made between the effects of bupivacaine i.v. (n = 10), ischemia (n = 10) and both factors (n = 10). Two min after injection of bupivacaine 2.0 mg/kg (plasma levels 2.0-3.0 micrograms/ml), the duration of MAP was only slightly (7.5-15%) prolonged and its ischemia-induced shortening only slightly attenuated by bupivacaine. At the same time, conduction time was considerably (75-150%) lengthened and its ischemia-induced lengthening enhanced, so that ventricular fibrillation induced by coronary occlusion occurred sooner (about 100 instead of 300 s) in the presence of bupivacaine. Consequently, bupivacaine should be used only with caution in individuals whose myocardium is ischemic or liable to ischemia episodes.
Sedation for patients during surgery under local or regional anaesthesia may induce ventilatory depression. All sedated patients must be monitored with a pulse oximeter. Routine administration of supplementary oxygen is necessary. General anaesthesia must be rapidly performed when regional anaesthesia is unsuccessful.
Explore the source record for details and available documents.
This study compared the efficacy and side effects of equianalgesic doses of nalbuphine and fentanyl as intravenous (IV) analgesics for medically compromised patients undergoing oral surgery with local anesthesia. A total of 24 inpatients scheduled for oral surgery and with an ASA physical status of 3 or 4 were randomly assigned to two treatment groups and received IV analgesia with an injection of either 0.2 mg/kg nalbuphine or 2 micrograms/kg fentanyl. Three minutes later, local anesthesia was administered. Respiratory rate, heart rate, arterial blood pressure, and oxyhemoglobin saturation (SpO2) were recorded before and during surgery. After the operation, the patient, surgeon, and anesthesiologist were asked to complete questionnaires regarding drug effects. Analgesia and sedation appeared sufficient and comparable according to the surgeon, anesthesiologists, and patients in the two groups, and there were no significant differences in blood pressure or heart rate. Respiratory rate and SpO2 were lower in patients treated with fentanyl (P < 0.05), and eight patients of this group experienced episodes of oxygen desaturation (SpO2 < 90%) compared with only two patients who received nalbuphine (P < 0.05). Nalbuphine produced less respiratory depression and should be considered a suitable alternative to fentanyl for use in medically compromised patients undergoing oral surgery.
Explore the source record for details and available documents.
A case is reported of a severe neurological deficit occurring after axillary blockade. The 37-year-old ASA I patient underwent an axillary block for hand surgery using 20 ml of lignocaine 1% with adrenaline and 20 ml of lignocaine 2%. In order to elicit paraesthesia, several attempts were required. Injection of the local anaesthetic was not painful. The tourniquet remained at 250 mmHg for only 35 min. The following day, the patient's arm remained numb. As there was no improvement, epineurotomy was carried out on day 19, to liberate the median nerve which was severely stenosed at the axilla. The patient then started to improve slowly, so that he was able to return to part-time work 6 months later. Prevention of such an accident relies on avoiding intraneural injection and repeated punctures when searching for paraesthesia. When using axillary blockade in day-care surgery, the patient's must be informed upon the possibility of persistent paraesthesia. Should such a rare incident occur, rapid consultation with the anaesthesiologist is essential.
Explore the source record for details and available documents.
Regional anesthesia with bupivacaine in pediatric patients is often accompanied by light levels of halothane general anesthesia. To determine the potential cardiotoxicity of these two drugs when used together, we defined the interaction between moderate plasma bupivacaine concentrations (1270-1760 ng/mL) and halothane (end-tidal concentrations, 0.5%-1.0%) on ventricular contractility and conduction in 22 closed-chest dogs anesthetized with chloralose. Bupivacaine alone (1-mg/kg intravenous bolus plus a 0.1-mg.kg-1.min-1 constant rate infusion) resulted in significant increases in ventricular conduction time (VCT) and effective refractory period (VERP) and nonsignificant decreases in dP/dtmax and blood pressure. The addition of halothane resulted in hypotension and in progressively increasing plasma bupivacaine levels secondary to reduced hepatic clearance, which led to further dose-related significant increases in VCT and VERP and to significant decreases in dP/dtmax and blood pressure. In other dogs given halothane but in which bupivacaine levels were held constant (1400 ng/mL), VCT remained constant and VERP lengthened slightly, whereas dP/dtmax decreased. We conclude that the combination of bupivacaine and halothane can cause adverse effects on ventricular contractility and intraventricular conduction.
The heparinization of multiple trauma patients during hemofiltration involves a high risk of bleeding. We report here two continuous hemofiltration cases -15 and 60 days in duration-using a low molecular weight heparin, enoxaparine. No major bleeding or clotting was observed. However, continuous infusion of the heparin is needed and the rate of delivery of the hemofiltration pump must be taken into consideration since it influences the clearance of the drug through the hemofiltration membrane. Anti-Xa activity measurement is not sufficient to adjust the heparin dose.
Severe head injury (Glasgow Coma Score less than or equal to 7) is associated with high mortality and morbidity which can be improved by early energetic therapy. Such patients must be picked up by prehospital/EMS service with three aims: controlling ventilation, controlling haemodynamics, avoiding any increased intracranial pressure. After initial neurological assessment, management involves endotracheal intubation, mechanical ventilation following benzodiazepine sedation, early compensation of hypovolemia avoiding any overloading, analgesia for painful injuries; according to the clinical status other pharmacological agents can be used. At admission to emergency unit, intensive care must be continued while X-rays and CT-scan are achieved. Imperative indications of transport to neuro-intensive care unit are discussed for hospitals without a neuro-surgeon.
Explore the source record for details and available documents.
Creatinine clearance (Ccr) is a good predictor of renal dysfunction. However, numerous analytical interferences have been observed with the classical measurement of creatinine by Jaffé's procedure. This prospective study was conducted to compare 4 methods for determining creatinine; and also endogenous creatinine clearance with inulin clearance (Cin) to estimate the glomerular filtration rate. The 4 different techniques for measuring creatinine were: 1) 2 techniques using Jaffé's colorimetric reaction: one with rapid and the other with slow kinetics: 2) 2 more selective methods: enzymatic procedure and high performance liquid chromatography (HPLC). Measurements were performed in 13 multiple trauma patients after stabilization and in 5 comatose patients (control group) over a 3-day period, with strict 24-h urine collection. On the second day, inulin clearance and para-aminohippuric acid clearance (Cpah) were measured. Measurement of creatinine by Jaffé's procedure yields significantly higher levels than those obtained by the other methods. Higher levels of both plasma and urinary creatinine were observed in the multiple trauma patients with all the methods used. There were no significant differences in Ccr, Cin, Cpah between the multiple trauma patients and the control patients. The best correlations between inulin clearance and creatinine clearance were observed for Jaffé's rapid kinetics (r = 0.90) in the control group and for the enzymatic procedure in the multiple trauma group (r = 0.55). Plasma creatinine is not a useful indicator in multiple trauma. The correlation between creatinine clearance and inulin clearance is not very strong in multiple trauma, indicating that the relative evolution (not the absolute values) of creatinine clearance is of interest.