Question

What effect do beta-blockers have on cardiac output and hemodynamics?  Which specific structures do these medications affect?

Answer 1

Beta blockers (beta-blockers, β-blockers, etc.) are a class of medications that are predominantly used to manage abnormal heart rhythms, and to protect the heart from a second heart attack (myocardial infarction) after a first heart attack (secondary prevention). They are also widely used to treat high blood pressure (hypertension), although they are no longer the first choice for initial treatment of most patients.

Beta blockers are competitive antagoniststhat block the receptor sites for the endogenous catecholamines epinephrine(adrenaline) and norepinephrine(noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response.

Beta receptors are found on cells of theheart muscles, smooth muscles, airways,arteries, kidneys, and other tissues that are part of the sympathetic nervous systemand lead to stress responses, especially when they are stimulated by epinephrine(adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and other stress hormones, and weaken the effects of stress hormones.

They have the potential to worsen the condition due to their effect of decreasing cardiac contractility.

Beta blockers are known primarily for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure.[citation needed] Beta blockers, in addition to their sympatholytic β1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering extracellular volume and increasing the oxygen-carrying capacity of blood. Heart failure characteristically involves increased catecholamine activity on the heart, which is responsible for a number of deleterious effects, including increased oxygen demand, propagation of inflammatory mediators, and abnormal cardiac tissue remodeling, all of which decrease the efficiency of cardiac contraction and contribute to the low ejection fraction. Beta blockers counter this inappropriately high sympathetic activity, eventually leading to an improved ejection fraction, despite an initial reduction in ejection fraction.

administration of angiotensin-converting enzyme inhibitors (ACEIs) and beta-blockers, the natural history of chronic heart failure (HF) remains progressive, and many patients eventually develop decompensation. During decompensation, patients with HF are limited by dyspnea and fatigue at rest or with minimal exertion, require frequent hospitalizations, have a higher mortality rate, and both symptoms and prognosis become critically dependent on hemodynamic conditions. Treatment with inotropic agents may, thus, become necessary. In addition, beta-blockers, which are indicated for their long-term favorable actions , may be less well-tolerated in advanced HF patients because of their initial negative inotropic activity resulting from withdrawal of adrenergic support . The concomitant administration of an inotropic agent and a beta-blocker, therefore, may be necessary both in patients already on maintenance beta-blocker treatment who have progressed to decompensated HF and in patients with advanced HF who do not tolerate the initiation of beta-blockade.The most common inotropic agents presenting clinical practice are the beta-adrenergic receptor agonist dobutamine and the type III phosphodiesterase (PDE) inhibitors, milrinone and enoximone. These two classes of drugs have important differences.