[Hemodynamic profile in patients presenting with cerebral arterial spasm after meningeal hemorrhage in the presence of preventive administration of i.v. nimodipine].
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Biomedical subjects
Publications and source records attributed to P Adnet.
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A moderate controlled hypotension has been performed with isoflurane in the presence of nimodipine (4 mg.h-1) on ten patients anesthetized for cerebral aneurysm clipping. The administration of both drugs induced a dose-dependent hypotension secondary to the reduction of the systemic vascular resistance without impairment of cardiac index. Nimodipine did not modify the cardiovascular effects of isoflurane. It is concluded that intravenous administration of nimodipine should be continued during the operative period.
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Calcium blockers (CB) are routinely used. This could lead to possible interference with anaesthetic drugs. CB prevent calcium from entering the cell by inhibiting the slow voltage-dependent calcium channels. They act mostly on heart and smooth muscle. Of all the possible indications, the three that are confirmed are coronary heart disease, arterial hypertension and supraventricular rhythm disturbances. Most of the work published and the cases reported concerns interactions between CB and halogenated anaesthetic agents; the latter's actions on the heart depend on cellular calcium exchange. Also, the cardiovascular effects of these anaesthetics are similar to that of CB. Experimentally, halothane and enflurane have direct cardiac inhibitory effects similar to verapamil and diltiazem, whereas isoflurane's properties seem closer to the dihydropyridines (nifedipine and nicardipine). Giving verapamil or diltiazem increases the number of sino-atrial and atrio-ventricular blocks when using a halogenated agent. Clinically, interpreting the effects of CB during anaesthetic induction is difficult because of the pathology (coronary heart disease, cardiac failure), the other drugs (beta-blockers and nitrates) and the type of anaesthesia (emergency or elective). Interactions can give rise to anything from a severe cardiovascular collapse, requiring catecholamines, to a mild fall in blood pressure which responds well to plasma expansion, or even no effect on blood pressure. Rebound is seen on stopping CB in patients with coronary heart disease or arterial hypertension; stopping them before surgery does not therefore seem justified. However, extreme care must be taken when using halogenated agents for patients under treatment with CB and/or beta-blockers. A wary anaesthetist will be able to adapt the technique to the patient. It has been suggested that CB could be used to treat preoperatively myocardial ischaemia (diltiazem), hypertensive crises (nifedipine, nicardipine) and ventricular rhythm disturbances (verapamil); this must be done with caution, the patient being closely monitored (haemodynamic and electrocardiographic monitoring). Postoperatively, intranasal nifedipine, continuous intravenous nicardipine or diltiazem have been used to treat increases in arterial blood pressure during recovery and to adapt the cardiovascular system to the increased metabolic needs. Here again, close patient monitoring is essential. In any case, treatment with CB which has been stopped should be started up again as soon as possible.
Twenty-seven patients, four of whom had presented with a crisis of malignant hyperthermia and the 23 other being close relatives of such patients, underwent a muscle biopsy so as to determine their susceptibility to malignant hyperthermia. Halothane-caffeine contracture tests, interpreted in accordance with the criteria of the European Group on Malignant Hyperthermia, yielded the following results: 13 positive (MHS), 10 negative (MHN), 4 equivocal (MHE). The history, clinical examination, CPK level, histoenzymatic morphology and electron microscopic study did not provide information sensitive enough to use for the detection of susceptibility to malignant hyperthermia. This confirmed the literature: the halothane-caffeine contracture test remains the only reliable diagnostic test to detect this susceptibility, despite the search for non invasive tests. If the mechanism of triggering a contracture to increasing doses of caffeine is well known in normal muscle, it is the smaller concentrations required which suggests malignant hyperthermia abnormality. The halothane effect is less well understood. A concentration less than or equal to 2 vol % yields a contracture only in MHS muscle. Differences in protocols used by American authors emphasize the importance of standardization as used by the European Group, which is the only way of collecting and comparing results on well over a thousand patients. This confrontation should reduce the number of equivocal diagnoses and allow a correct classification of patients at risk or their relatives as MHS or MHN.
The first results of the long-term treatment of chronic heart failure with inotrope positive medications are disappointing, especially in that survival is not prolonged and even a greater mortality is suggested. Is it because of the regular failure of specific medications, of a class of medications or because the overall concept of inotropism stimulation during chronic heart failure should be condemned? The mechanisms of inotropism of normal muscles or muscles in human chronic heart failure are reviewed as well as the various pharmacological means available to stimulate inotropism.
The in vitro halothane and caffeine contracture tests have been performed on muscle tissue from six survivors of the neuroleptic malignant syndrome. The results, which are expressed in accordance with the criteria of the European MH Group, defined five of the subjects as MHN and one patient as MHE. It is concluded that there is no common pathophysiological link between the neuroleptic malignant syndrome and malignant hyperthermia.
The familial nature of anaesthetic malignant hyperthermia must lead to the search for susceptibility in other members of the family of a sensitive subject. According to the literature, only in vitro studies of contraction characteristics of biopsied skeletal muscle fibres exposed to caffeine or halothane are of predictive value. Four members of the family of a patient who died as a result of malignant hyperthermia were investigated. The results expressed in accordance with the criteria defined by the European group on malignant hyperthermia, coupled with a histoenzymatic study, defined three of the subjects as HMN (negative) and one subject as HM (c) (equivocal or intermediate).
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The realisation and reliability of the halothane-caffeine contracture tests in children to detect the susceptibility to malignant hyperthermia (MH) is still controversial. The present study concerned 26 children aged 2 to 13 years, (mean 9.5 +/- 1.3 years) who were tested either because of a personal symptomatology (14 cases) or as a member of a susceptible MH family (12 cases). Half of the children had a positive test (MHS and MHE) as is found in adults. Furthermore comparison of threshold concentrations of halothane and caffeine as well as the 32 nmol caffeine-induced contractures dit not show significant differences related to age. These results support the possibility to perform under good conditions and with good reliability the diagnostic test of susceptibility to malignant hyperthermia in children from 2 years on.
A rare complication of general anesthesia, malignant hyperthermia is nonetheless very topical because it causes the death of young, healthy subjects who most often undergo surgery with no vital risk. Screening, an essential means of achieving riskless anesthesia, is based on testing on fresh biopsy specimens of muscle. The current state of knowledge, especially the progress made in genetics, will be commented.