Final answer:
Beta-blockers such as metoprolol and propranolol act on beta-1 receptors in the heart to slow HR and reduce contractility, offering therapeutic benefits in hypertension and HFrEF. They lead to reduced mortality in HFrEF by decreasing the heart's workload. However, careful dosing is needed to avoid bradycardia and cardiac arrest.
Step-by-step explanation:
Beta-Blockers and Their Role in Reducing Mortality in HFrEF Patients:
Beta-blockers are a class of medications that target G-protein-linked receptors in the heart muscle, antagonizing the effects of adrenaline and noradrenaline (NE) by blocking the beta-1 receptors. This results in a slower heart rate (HR) and reduced force of contraction, which are beneficial effects for patients with heart failure with reduced ejection fraction (HFrEF). Certain beta-blockers have been associated with reduced mortality in these patients due to their negative inotropic and chronotropic effects, which lessen the workload on the compromised heart.
Examples and Mechanism of Action:
By blocking beta-1 receptors, these drugs prevent NE from increasing the heart rate and the strength of cardiac muscle contraction. Metoprolol and propranolol are common examples of beta-blockers; metoprolol is selective for beta-1 receptors, while propranolol non-selectively blocks all beta receptors. Such medications not only manage hypertension but are also vital in improving outcomes in patients with HFrEF, potentially preventing episodes of acute heart failure or sustaining life after heart attacks.
Over prescription of beta-blockers, however, can lead to adverse effects such as bradycardia or even cardiac arrest due to excessive inhibition of cardiac function. Hence, precise dosing is critical to balance therapeutic benefits with potential risks.