Cardiovascular effects of local adrenaline infiltration during neurolept analgesia and adrenergic beta-receptor blockade in man.
The adrenergic beta-receptor blocking drug, alprenolol, was given together with atropine to 15 patients during neurolept analgesia (NLA) in order to prevent adrenaline-induced cardiac arrhythmias. Four patients operated on without adrenergic beta-receptor blockade formed the control group. Three of them developed tachyarrhythmias, ventricular tachycardia, multifocal ventricular extrasystoles and supraventricular tachycardia. All these arrhythmias were terminated by the adrenergic beta-receptor blocking drug, propranolol. The fourth patient developed a temporary sinus tachycardia which did not require any treatment. The adrenergic beta-receptor blockade induced a slight increase in pulse rate with almost no change in arterial blood pressure. The incidence of arrhythmias due to adrenaline infiltration was much less in this group. There was one supraventricular tachycardia and scattered ventricular extrasystoles in two other patients. NLA alone does not protect the heart against adrenaline-induced arrhythmias. It does, however, seem to be compatible with an adrenergic beta-receptor blockade, which in turn provides partial protection against adrenaline-induced arrhythmias. The occasionally developing arrhythmias can then be terminated with specific adrenergic beta blockers.
Cardiovascular effects of local adrenaline infiltration during neurolept analgesia and adrenergic beta-receptor blockade in man. The adrenergic beta-receptor blocking drug, alprenolol, was given together with atropine to 15 patients during neurolept analgesia (NLA) in order to prevent adrenaline-induced cardiac arrhythmias. Four patients operated on without adrenergic beta-receptor blockade formed the control group. Three of them developed tachyarrhythmias, ventricular tachycardia, multifocal ventricular extrasystoles and supraventricular tachycardia. All these arrhythmias were terminated by the adrenergic beta-receptor blocking drug, propranolol. The fourth patient developed a temporary sinus tachycardia which did not require any treatment. The adrenergic beta-receptor blockade induced a slight increase in pulse rate with almost no change in arterial blood pressure. The incidence of arrhythmias due to adrenaline infiltration was much less in this group. There was one supraventricular tachycardia and scattered ventricular extrasystoles in two other patients. NLA alone does not protect the heart against adrenaline-induced arrhythmias. It does, however, seem to be compatible with an adrenergic beta-receptor blockade, which in turn provides partial protection against adrenaline-induced arrhythmias. The occasionally developing arrhythmias can then be terminated with specific adrenergic beta blockers.