Adrenergic Blockers

Adrenergic blockers reduce the effects of catecholamines such as epinephrine and norepinephrine, but the clinical result depends on which receptor is blocked. The most important pattern for this lesson is beta-adrenergic blockade. Beta-blockers are competitive antagonists at β1 and β2 receptors. Blocking β1 receptors slows the heart rate and reduces myocardial contractility, so cardiac workload and oxygen demand fall. Blocking β2 receptors reduces catecholamine-mediated vasodilator and bronchodilator responses. This is why a non-selective beta-blocker such as propranolol can produce bronchospasm, particularly in a patient with asthma or COPD. The mechanism gives you the bedside pattern before you memorize adverse effects: a slower pulse, lower blood pressure, reduced exercise tolerance, conduction slowing, fatigue, and—when β2 receptors are blocked—an increased risk of bronchospasm. In a patient with diabetes, the drug may also blunt warning signs of hypoglycemia, especially tachycardia and palpitations. A normal pulse therefore does not prove that glucose is safe. The family label is not enough to guide administration. An adrenergic blocker’s receptor target, indication, formulation, and prescribed parameters must be checked individually. Do not transfer a beta-blocker hold parameter...