Beta1- or beta2-blockers to improve hemodynamics following endotracheal adrenaline administration.

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 beta-adrenergic receptors causing vasodilatation unopposed by an alpha-adrenergic vasoconstriction. We hypothesized that inhibition of the beta2-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 beta-blocker propranolol, selective beta1-blocker metoprolol (0.1 mg/kg, i.v.), or without pre-treatment. Heart rate, blood pressure and arterial blood gases were monitored.

RESULTS

The selective beta-blocker metoprolol was almost as effective as the non-selective beta-blocker propranolol in attenuating the initial decrease in blood pressure following endotracheally administered adrenaline, a phenomenon that was previously attributed to inhibition of beta-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.