We have compared the incidence of CNS symptoms and changes in echocardiography and electrophysiology during i.v. infusions of ropivacaine, bupivacaine and placebo. Acute tolerance of i.v. infusion of 10 mg min-1 was studied in a crossover, randomized, double-blind study in 12 volunteers previously acquainted with the CNS effects of lignocaine. The maximum tolerated dose for CNS symptoms was higher after ropivacaine in nine of 12 subjects and higher after bupivacaine in three subjects. The 95% confidence limits for the difference in mean dose between ropivacaine and bupivacaine were -30 and 7 mg. The maximum tolerated unbound arterial plasma concentration was twice as high after ropivacaine (P < 0.001). Muscular twitching occurred more frequently after bupivacaine (P < 0.05). The time to disappearance of all symptoms was shorter after ropivacaine (P < 0.05). A threshold for CNS toxicity was apparent at a mean free plasma concentration of approximately 0.6 mg litre-1 for ropivacaine and 0.3 mg litre-1 for bupivacaine. Bupivacaine increased QRS width during sinus rhythm compared with placebo (P < 0.001) and ropivacaine (P < 0.01). Bupivacaine reduced both left ventricular systolic and diastolic function compared with placebo (P < 0.05 and P < 0.01, respectively), while ropivacaine reduced only systolic function (P < 0.01).

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Caffeine is a natural alkaloid methylxanthine that is found in various plants such as coffee or tea. Symptoms of a severe overdose may present with hypokalemia, hyponatremia, ventricular arrhythmias, hypertension followed by hypotension, respiratory failure, seizures, rhabdomyolysis, ventricular fibrillation and finally circulatory collapse. A 21-year-old woman called for the ambulance herself soon after the ingestion of about 10,000 mg of caffeine. At the arrival of the ambulance, the patient went into cardiac arrest almost immediately. After a total resuscitation period of 34 min including seven counter-shocks and 2 mg epinephrine, the patient was stable enough to be transferred to the hospital. The patient soon went into VF again and received two more counter-shocks and 1 mg epinephrine and finally an intravenous bolus dose of 300 mg amiodarone. The initial arterial blood gas showed pH at 6.47, lactate at 33 mmol/l and potassium level at 2.3 mmol/l. Unfortunately, no blood samples for caffeine analysis were taken. Three days after hospital admission, the patient developed myoclonus, which did not respond to medical treatment. Excessive intake of caffeine may produce arrhythmias and pronounced hypokalemia and ensuing ventricular fibrillation. In case of counter-shock-resistant VF, it can be necessary to give an early loading dose of amiodarone. Furthermore, it may be beneficial to replace the potassium as early as possible. Epinephrine and buffer solutions used during resuscitation may further decrease blood potassium levels and should be administrated cautiously. Epinephrine can be replaced by other vasopressor drugs, such as vasopressin without effects on beta-receptors.

Intoxication by GHB has substantial morbidity and abuse of GHB has substantial mortality. The acute prognosis is good but long-term prognosis is insecure with an increased risk for drug dependency and an early death.