Patients on propranolol are at increased risk for all of the following EXCEPT which?

Patients on propranolol are at increased risk for all of the following EXCEPT which?

• A. Blunted response to hypoglycemia
• B. Bronchoconstriction
• C. Rebound tachycardia after discontinuation
• D. Orthostatic hypotension

Answer: (D)

Propranolol is a nonselective beta-adrenergic blocker, so it blocks both beta-1 receptors in the heart and beta-2 receptors in the lungs and other tissues. This produces several well-known effects. First, it blunts the body’s warning signs of low blood sugar. Normally, during hypoglycemia, adrenaline triggers symptoms like tremor, palpitations, and, importantly, stimulates glycogenolysis and gluconeogenesis to raise glucose. Blocking beta receptors dampens these adrenergic symptoms and can impair the liver’s ability to mobilize glucose, making hypoglycemia harder to detect and manage in patients, especially those with diabetes. Second, blocking beta-2 receptors in the airways causes bronchoconstriction. This is why nonselective beta-blockers like propranolol can precipitate or worsen bronchospasm in patients with asthma or COPD. Third, stopping a nonselective beta-blocker suddenly can lead to rebound tachycardia. With chronic blockade, beta receptors become upregulated, and a rapid discontinuation removes the blockade, allowing a surge in heart rate and potential for tachyarrhythmias. Orthostatic hypotension is not a primary or typical risk associated with propranolol. While any antihypertensive can contribute to low blood pressure in susceptible individuals, the characteristic concerns with propranolol center on masking hypoglycemia, bronchoconstriction, and withdrawal-induced tachycardia rather than a specific predisposition to orthostatic hypotension.

Propranolol is a nonselective beta-adrenergic blocker, so it blocks both beta-1 receptors in the heart and beta-2 receptors in the lungs and other tissues. This produces several well-known effects.

First, it blunts the body’s warning signs of low blood sugar. Normally, during hypoglycemia, adrenaline triggers symptoms like tremor, palpitations, and, importantly, stimulates glycogenolysis and gluconeogenesis to raise glucose. Blocking beta receptors dampens these adrenergic symptoms and can impair the liver’s ability to mobilize glucose, making hypoglycemia harder to detect and manage in patients, especially those with diabetes.

Second, blocking beta-2 receptors in the airways causes bronchoconstriction. This is why nonselective beta-blockers like propranolol can precipitate or worsen bronchospasm in patients with asthma or COPD.

Third, stopping a nonselective beta-blocker suddenly can lead to rebound tachycardia. With chronic blockade, beta receptors become upregulated, and a rapid discontinuation removes the blockade, allowing a surge in heart rate and potential for tachyarrhythmias.

Orthostatic hypotension is not a primary or typical risk associated with propranolol. While any antihypertensive can contribute to low blood pressure in susceptible individuals, the characteristic concerns with propranolol center on masking hypoglycemia, bronchoconstriction, and withdrawal-induced tachycardia rather than a specific predisposition to orthostatic hypotension.