How can very low dose beta adrenergic blockers be used in the treatment of heart failure?
In heart failure there is sympathetic stimulation in a trial to increase the COP. This stimulation may be initially (in the compensated stage of heart failure) of value because 1) increasing the heart rate (beta-1 receptor stimulation) — > increases the COP 2) the venoconstriction (alpha receptor stimulation) — > increases the venous return which stretches the heart and according to Starling law increases the COP 3) the aretrioconstriction (alpha receptor stimulation) — > increases the peripheral resistance (PR) to maintain the ABP However, when the heart failure enters the de-compensated stage; this over sympathetic stimulation is useless (since the number of cardiac beta adrenergic receptors is down regulated) and even may be deleterious because: 1) much increase in the heart rate occurs on the expense of shorting the diastole — > decreases cardiac filling time and subsequently the COP 2) much venoconstriction — > over-stretches the heart and further decreases the contractility
