beta(1)- or beta(2)-blockers to improve hemodynamics following endotracheal adrenaline administration Academic Article uri icon

abstract

  • Background: The recommended dose for endotracheal adrenaline (0.02 mg/kg) causes a pronounced initial decrease in diastolic blood pressure which is detrimental at the initial phase of cardiopulmonary resuscitation. This effect was previously attributed to an early and preferential stimulation of the β-adrenergic receptors causing vasodilatation unopposed by an α-adrenergic vasoconstriction. We hypothesized that inhibition of the β 2 -adrenoreceptors is responsible for prevention of the deleterious initial decrease in blood pressure that takes place following endotracheal administration of adrenaline. Methods: Adrenaline (0.02 mg/kg) diluted with normal saline (5 ml) was injected into the endobronchial tree of anesthetized dogs 3 min following pretreatment with the non-selective β-blocker propranolol, selective β 1 -blocker metoprolol (0.1 mg/kg, i.v.), or without pretreatment. Heart rate, blood pressure and arterial blood gases were monitored. Results: The selective β 1 -blocker metoprolol was almost as effective as the non-selective β-blocker propranolol in attenuating the initial decrease in blood pressure following endotracheally administered adrenaline, a phenomenon that was previously attributed to inhibition of β-adrenoreceptors. Conclusions: The outcome of this study might be explained by a dose-related loss of cardioselectivity of metoprolol. Further studies are warranted to refine the pharmacological means to abort the initial blood pressure-lowering effect of endotracheally administered adrenaline.

publication date

  • January 1, 2005