[Heart arrest in children after intravenous injection of succinylcholine in the ENT operating room]. / Herzstillstand bei Kindern nach intravenöser Injektion von Succinylcholin im HNO-Operationssaal.

Acute rhabdomyolysis with hyperkalemia has been followed by ventricular dysrhythmia, cardiac arrest and death after the administration of succinylcholine to apparently healthy children who were subsequently found to have undiagnosed skeletal muscle myopathies. Boys have mostly been affected. Reports of anesthesia emergencies from the United States and Germany have indicated that serious side effects of succinylcholine are not as rare as previously thought. This disorder often presents as sudden cardiac arrest within minutes after the administration of the drug. The tragedy is that an apparently healthy child dies abruptly during what was considered to be a relatively uncomplicated surgical procedure (most often in ENT surgery). Due to the abrupt onset of rhabdomyolysis, routine resuscitative measures are likely to be unsuccessful. Extraordinary measures (including institution of extracorporeal circulation) and prolonged efforts have resulted in successful resuscitation of some cases. Since there are usually no signs or symptoms to alert the practitioner to patients at risk, the use of succinylcholine in children should be reserved for emergency intubations or instances in which immediate securing of the airway is necessary.

[Anesthesia for surgery in ambulatory patients: organizational aspects of the hospital physician]. / Anästhesie für Operationen bei ambulanten Patienten: Organisatorische Aspekte des Krankenhausarztes.

At first sight it seems impossible to put into practice the 1992 resolution of the German Federal Council recommending increased frequency of hospital based operative care for ambulatory patients and the duty to do so under full financial coverage. A detailed analysis of the current situation suggests that this may be possible even today--with some reservations regarding the infrastructure of the hospitals. Selection and preparation of the patient is a process in which the anaesthesiologist must play an important role. Delegation of this duty to the surgeon or the general practitioner is not permitted. The anaesthesiologist must have sufficient time, prior to the procedure, to meet the patient; meeting the patient for the first time a few minutes before induction of anaesthesia is unacceptable. Even if one concedes freedom of methods, one drug and one procedure should be avoided while caring for surgical ambulatory patients: this drug is succinylcholine, because of life-threatening hyperkaliaemia in children with occult myopathy and severe and frequent myalgia especially in ambulatory patients. The procedure not suitable in ambulatory patients is subarachnoidal analgesia--due to an unacceptably high percentage of headaches in young ambulatory patients. The postoperative care and observation must be delegated to especially qualified persons only--and these persons should not be distracted by duties outside the recovery area. The anaesthetist must--in addition--be available at all times without delay. Pain, nausea and emesis molest the ambulatory patient during the postoperative course to a particular extent. The anaesthesiologist must take care of these complaints--even if the patient is discharged.(ABSTRACT TRUNCATED AT 250 WORDS)

[Should the use of succinylcholine in pediatric anesthesia be re-evaluated?]. / Sollte die Verwendung von Succinylcholin in der Kinderanästhesie neu überdacht werden?

We report on the occurrence of cardiac arrests within a few minutes following succinylcholine in 9 children, all of whom were later shown to have occult neuromuscular disease. Five of the children did not survive the catastrophic event. The anaesthetist in most cases, when discussing premedication, got the impression that the patients were in good health; just in 2 children were there indications of myopathy. Myopathic children coming to surgery and anaesthesia are rare. In these cases the administration of succinylcholine is contraindicated. But the anaesthetist must be aware of the fact that a small number of paediatric patients with unknown/subclinical myopathies might be referred to him. In these cases, without warning muscle rigor, bradycardia and hyperkalemia cardiac arrest may develop within minutes following administration of succinylcholine. The anaesthetist must be prepared for such a challenging event--particularly mentally. Misinterpretation of the symptoms as signs of malignant hyperthermia should be excluded. Resuscitation must start without delay and must continue for more than 30 minutes. Therapeutic attempts to lower extracellular potassium with glucose and insulin must fail for pharmacokinetic reasons. Therapy with intravenous calcium under control of the e.c.g. seems to be the only rational approach to the problem. It is suggested that in every healthy child coming to anaesthesia the physician should consider whether relaxation could not be achieved by other agents. Succinylcholine may well be defined as a "membrane poison"--especially considering the efflux of potassium, myoglobin and creatine kinase from the intracellular space into the bloodstream. The answer to the question asked in the title must therefore be: definitely--yes.

[An attempt to reconcile differences of opinion in the field of malignant hyperthermia]. / Ein Beitrag zur Beseitigung von Meinungsverschiedenheiten auf dem Gebiet der Malignen Hyperthermie.

Two of the persisting controversies concerning malignant hyperthermia (MH) are discussed: storing and dosage of dantrolene and preoperative tactics to be followed with patients who are MH-susceptible. Reasons are presented for the obligation to store sufficient amounts of dantrolene in every operating suite. The second part discusses the question of pretreatment of MH-susceptible patients with dantrolene.

[Reasons for the persistent lethality of malignant hyperthermia and recommendations for its reduction]. / Gründe für die persistierende Letalität der Malignen Hyperthermie und Empfehlungen zu deren Senkung.

Dantrolene is the only known specific treatment of malignant hyperthermia (MH). Following official approval an intravenous formulation of dantrolene became clinically available for emergency treatment of MH. At that time it had been anticipated, that with dantrolene therapy combined with constant vigilance each case of MH could be treated successfully and the mortality rate should be close to zero. Surprisingly enough, reports of death due to MH continue to be published up to the present. Analysis of case reports revealed the following reasons for the discrepancy between the expectations and the clinical reality: 1. Delay in early diagnosis due to preoccupation with the name-giving symptom hyperthermia: lack of MH-sensitive monitoring (i.e. capnometry, pulse oximetry, blood gas analysis). 2. Preoccupation with non specific facets of therapy: measures such as cooling, change of the anaesthesia machine, transfer of the patient to the intensive care unit or the administration of drugs which have been shown to be ineffective in treating MH may not only be a waste of time, but fully disregard the prime factor in therapy--intravenous administration of dantrolene. 3. Administration of an insufficient amount of dantrolene and delayed start of specific therapy due to failure to have immediate access to intravenous dantrolene. 4. Failure to increase minute ventilation immediately after making the diagnosis to meet elevated metabolic demands. A recommendation is presented how to diagnose, to treat and prevent MH, considering present day diagnostic and therapeutic measures in the presence of the presumptive diagnosis of MH.

["Round the clock"--an information service for malignant hyperthermia emergencies]. / "Rund um die Uhr"--Informationsdienst für maligne Hyperthermie-Notfälle.

A 24-hour 7-day telephone service has been created for emergency consultation: MH-hotline 030/3035504 (daytime) or 030/30351 (after office hours). In emergencies callers should ask for a consultant, indicating the code word "malignant hyperthermia" and give their name, the name of the institution and the telephone number.

Effects of short-term infusion of nifedipine or verapamil on systemic hemodynamics and left ventricular myocardial contractility in patients prior to coronary artery bypass surgery.

The effects of short-term infusion (10 min) of nifedipine (7.5 micrograms . kg-1) or verapamil (0.15 mg . kg-1) on left ventricular (LV) contractility and on systemic hemodynamics in patients with coronary artery disease, chronically treated with low-dose beta-adrenergic blocking drugs, exhibiting a normal LV function at rest, are presented. In order to analyze the interaction between calcium entry blocking drugs and halothane, the results are discussed in light of data, obtained in similar patients during halothane anesthesia, using identical experimental conditions, which have already been reported. LV dP/dtmax and LV end-diastolic pressure (LVEDP) remained unaffected when nifedipine was infused in the awake patients. Verapamil significantly decreased LV dP/dtmax in patients while awake, but LVEDP did not change. Both calcium entry blocking drugs caused decreases in blood pressure and systemic vascular resistance, accompanied by increases in heart rate. The only significant differences between the awake and the anesthetized patients were the absence of changes in heart rate and the greater reduction in LV dP/dtmax following administration of the calcium entry blocking drugs during anesthesia. Possible explanations for this may include the drugs' combined interference with calcium ion fluxes within the myocardial and smooth muscle fibers, the ability of halothane to modify the response of the autonomic nervous system to the calcium entry blocking drugs and altered kinetics of the calcium entry blocking drugs induced by the volatile anesthetic. It is impossible to determine from the present investigation which of these mechanisms is predominant.

Isoflurane improves the tolerance to pacing-induced myocardial ischemia.

Fourteen patients with normal, global, left ventricular function scheduled for elective myocardial revascularization were studied at rest and during atrial pacing before and during isoflurane anesthesia (0.5% end-tidal) plus 50% nitrous oxide. Rapid atrial pacing was performed in a stepwise fashion until the onset of angina pectoris in the awake patients. The same step increase in pacing rate was applied in the anesthetized patients. Compared with prepacing baseline values, isoflurane significantly decreased systemic blood pressure, coronary perfusion pressure, the rate-pressure product, and cardiac index. No patient had ST-segment depression while awake or during isoflurane anesthesia before pacing was started. Prepacing left and right ventricular filling pressures and wave forms were normal, both while awake and during isoflurane anesthesia. The mean pacing rate at which first signs of myocardial ischemia appeared (V5 ST-segment depression greater than or equal to 0.1 mV, increase in pulmonary capillary wedge pressure (PCWP) to greater than or equal to 15 mmHg, and prominent PCWP v-waves greater than or equal to 20 mmHg) was significantly higher during isoflurane anesthesia than in the awake patients (128 +/- 4 vs. 115 +/- 5 beats/min). With the exception of one patient, the individual pacing rates inducing first signs of ischemia in the awake patients were below the anginal threshold. None of the patients had a reduced ischemic threshold during anesthesia. Eleven anesthetized patients tolerated a higher pacing rate until initial signs of ischemia appeared. In four of these patients, the pacing rate required to induce first signs of ischemia was above the heart rate at which chest pain had been induced while they were awake. At a peak atrial pacing rate of 129 +/- 5 beats/min, which had induced angina pectoris in the awake patients, the increase in PCWP was significantly smaller during pacing with isoflurane than during control pacing. Prominent PCWP v-waves (greater than or equal to 20 mmHg) appeared in 12 of the 14 patients during initial pacing to angina and in eight patients paced during isoflurane anesthesia. In six of these eight patients, the abnormal v-waves were less prominent than those observed during control pacing. Ischemic ST-segment changes developed in 13 of 14 patients during initial pacing and in nine patients during pacing with isoflurane. Mean V5 ST-segment depression during the two pacing periods was significantly different, averaging 0.19 and 0.11 mV, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

[New findings and experiences in the field of malignant hyperthermia]. / Neue Erkenntnisse und Erfahrungen auf dem Gebiet der malignen Hyperthermie.

New publications on malignant hyperthermia (MH), with direct clinical importance, are reported. Since even in the recent past patients have died from MH in spite of therapy with dantrolene, the effectiveness of dantrolene is discussed in particular. Atypical clinical pictures of MH are presented. Special psychiatric syndromes (malignant neuroleptic syndrome and acute febrile catatonia), rhabdomyolysis with myoglobinuria following strenuous exercise or exposure to heat are mentioned, as these disorders appear to be related to MH, in that they are hypermetabolic syndromes implying a muscle membrane dysfunction. The role of slow calcium channel blockers and 5-hydroxytryptamine antagonists as prophylactic or therapeutic agents in MH is discussed. A schedule describing how to diagnose, treat and prevent MH, considering recent advances, is presented.

[Circulatory effects of vecuronium as well as pancuronium under different conditions of anesthesia]. / Untersuchungen der Kreislaufwirkungen von Vecuronium sowie von Pancuronium unter verschiedenen Anästhesie-Bedingungen.

The cardiovascular effects of equipotent doses (1,25 X ED95) of vecuronium (70 micrograms/kg iv) and pancuronium (80 micrograms/kg iv) were studied in 16 patients scheduled for elective coronary artery bypass surgery during steady-state conditions of isoflurane (0,4-0,5 vol% end-tidal)-nitrous oxide anaesthesia. All patients were chronically treated with oral beta receptor-blocking agents. Vecuronium did not cause any significant cardiovascular changes whereas pancuronium produced increases in heart rate (13%), cardiac index (15%) and mean arterial pressure (4%) while systemic vascular resistance decreased (8%). In a second part of this study we analysed whether the magnitude of the vagolytic effects of pancuronium is influenced by the anaesthetic procedure and/or by preoperative beta-blocker therapy. A group of 8 patients who were pretreated with beta-receptor blockers and received fentanyl (7 micrograms/kg) during the anaesthetic procedure showed low control values of heart rate (HR), cardiac index (CI), mean arterial pressure (MAP) and the rate-pressure product (RPP) which were due to both, the antisympathetic effects of beta-blocker therapy and the central vagomimetic properties of fentanyl. The administration of pancuronium (80 micrograms/kg) caused the greatest percentage increases in HR (20%), CI (22%), MAP (8%) and RPP (31%) in this group of patients. In contrast, patients (n = 8) anaesthetized with isoflurane-nitrous oxide who were not on preoperative beta-receptor blocker medication, demonstrated higher haemodynamic control values and less increases in HR (10%), CI (10%) and RPP (15%), MAP did not change. The clinical significance of these findings is discussed.

Comparison of phentolamine and urapidil in controlling acute intra-operative hypertension in patients subjected to coronary artery bypass surgery.

Intra-operative hypertensive episodes are a frequent problem in patients undergoing coronary artery bypass grafting. The haemodynamic effects of the alpha-adrenergic blocking drugs phentolamine and urapidil, two alpha-adrenergic blocking drugs with a different alpha-receptor subtype specificity, when used to control intra-operative hypertension were evaluated. Ten patients received phentolamine (about 25 micrograms kg-1 min-1) and ten patients received urapidil (about 100 micrograms kg-1 min-1) to return arterial blood pressure to control levels. Both drugs decreased arterial pressure to baseline values within 2-3 minutes by reducing the elevated systemic vascular resistance. Treatment with phentolamine was accompanied by a marked increase in heart rate with a concomitant increase in cardiac index and the rate-pressure product. Urapidil caused no change in heart rate, but the cardiac index increased. Urapidil lowered the rate-pressure product significantly. Both drugs reduced mean pulmonary artery and pulmonary capillary wedge pressures. The different selectivity of phentolamine and urapidil to alpha 1-and alpha 2-adrenergic receptors induces the diverse haemodynamic effects. We conclude that the use of urapidil is the superior regimen when an alpha-adrenergic blocking agent is favoured as a vasodilator.