beta -Adrenergic blocking agents are standard treatment for patients with m
ild-to-moderate heart failure. When patients receiving beta -blockers decom
pensate they often need treatment with a positive inotropic agent. The beta
-agonist dobutamine may not produce much increase in cardiac output during
full-dose beta -blocker treatment and may increase systemic vascular resis
tance via a-adrenergic stimulation. In contrast, phosphodiesterase inhibito
rs (PDEIs) such as milrinone or enoximone retain full hemodynamic effects d
uring complete beta -blockade because the site of action of PDEIs is beyond
the beta -adrenergic receptor and because beta -blockade reverses some of
the desensitization phenomena that account for the attenuation of PDEI resp
onse in heart failure related to upregulation in G(alphai). Inotrope-requir
ing subjects with decompensated heart failure who are undergoing long-term
therapy with beta -blocking agents should be treated with a type III-specif
ic PDEI, not a beta -agonist such as dobutamine.