Adrenaline dysrhythmias

Small quantities of adrenaline, such as are present as an additive in local anesthetic formulations, can be dangerously potentiated by beta-adrenoceptor blockers propranolol should be discontinued at least 3 days in advance of administering such products for local anesthesia. A combined infusion of adrenaline and propranolol has been used for diagnosing insulin resistance, but it can evoke cardiac dysrhythmias, even in patients without signs of coronary disease (17). 

Halothane and some other anesthetics sensitize patients to the risk of adrenaline-induced ventricular dysrhythmias and acute pulmonary edema, especially if hypoxia is present (18,19). 

Bupivacaine can cause ventricular extra beats (8). Ventricular dysrhythmias and seizures were reported in a patient who received 0.5% bupivacaine 30 ml with adrenaline 5 micrograms/ml for lumbar plexus block, after a negative aspiration test (9). The patient developed ventricular fibrillation and required advanced cardiac life support for 1 hour, including 15 defibrillations, and adrenaline 40 mg before sinus rhythm could be restored. There were no neurological sequelae. 

Adrenaline used during anesthesia can cause ventricular dysrhjdhmias. The threshold dose of adrenaline for dysrhythmias is reduced by halothane, but not by desflurane the dose of adrenaline required to produce dysrhythmias in 50% of patients was three times that needed when anesthesia was with halothane (17). 

Cardiac dysrhythmias are generally considered to be less frequent, or at least less severe, with enflurane than with halothane (5,6). However, caution in the use of adrenaline is advisable, especially in patients with cardiac disease or hjrperthyroidism. Isorhythmic atrioventricular dissociation was seen in 16 of 105 patients after the use of 1.0-1.5% enflurane (7). 

Current concepts of resuscitation after local anesthetic cardiotoxicity have been reviewed (17). Vasopressin may be a logical vasopressor in the setting of hypotension, rather than adrenaline, in view of the dysrhythmogenic potential of the latter. Amiodarone is probably of use in the treatment of dysrhythmias. Calcium channel blockers, phenytoin, and bretyllium should be avoided. In terms of new modes of therapy targeted at the specific action of local anesthetics, lipid infusions, propofol, and insulin/ glucose/potassium infusions may all have a role, but further research is necessary. 

For acute anaphylaxis, immediate treatment is essential, with adrenaline followed by intravenous histamine Hi receptor antagonists, glucocorticoids, fluids, and electrolytes. In view of the frequency of cardiac dysrhythmias and conduction disturbances in patients with anaphylactic shock, they should immediately be monitored (198,199). 

Sevoflurane has a similar effect on regional blood flow to other halogenated anesthetics, although it is perhaps slightly less of a coronary artery vasodilator than isoflurane. It reduces myocardial contractility and does not potentiate adrenaline-induced cardiac dysrhythmias (5). 

Following inhalation overexposure, a calm environment with no physical exertion is imperative to avoid an endogenous adrenaline surge. Exogenous adrenergic drugs should not be used to prevent induction of sensitized myocardial dysrhythmias. Dip-henylhydantoin and countershock may be effective for ventricular dysrhythmias. 

Cardiovascular The incidences of intraoperative critical dysrhythmias related to adrenaline in patients who have received inhalational anesthesia with halogenated agents have been analysed in a retrospective questionnaire study of Japanese Anesthesiologists in 583 institutions critical dysrhythmias were recorded in 1.2 case per 100 000 cases [59 ]. 

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