Beta-Blockers vs. Beta-Agonists

Beta-Adrenergic Drugs

The category of beta-adrenergic drugs includes both beta-adrenergic blockers and beta-adrenergic agonists (also known as beta-blockers and beta-agonists). 

The term “adrenergic” references the sympathetic nervous system. A beta-adrenergic blocker stops stimulation from the sympathetic nervous system, whereas a beta-adrenergic agonist intensifies the effects of the sympathetic nervous system.

Beta-Blockers

Medications that are beta-adrenergic blockers, or beta-blockers, have names that end in “-lol” and include drugs like metoprolol, carvedilol, propranolol, and atenolol. These beta-adrenergic blockers act on beta-receptors in the heart, smooth muscle and sometimes the lungs.

To understand how beta-blockers fit into the broader context of emergency cardiovascular pharmacology, watch our Introduction to ACLS Medications video.

Cardiovascular diseases are often treated with beta-blockers.

Cardioselectivity

The more cardioselective beta-blockers, like metoprolol, predominantly target beta-1 adrenergic receptors in the heart, which is ideally what providers desire for cardiac treatment.

If the beta-blocker is non-cardioselective, it also affects the lungs. An easy memory hook to differentiate these targets is:

• Beta-1 receptors are mainly located in the heart. Think “1 heart.” (While also present in the kidneys, their cardiac role is most critical here).
• Beta-2 receptors are predominantly located in the lungs and vascular smooth muscle. Think “2 lungs.”

Non-cardioselective beta-blockers, like propranolol, affect both the beta-1 receptors in the heart as well as the beta-2 receptors in the lungs. The provider may not want this outcome, as the beta-blockers should only affect the heart.

Why Cardioselectivity Matters for COPD/Asthma Risk: When a patient with asthma or chronic obstructive pulmonary disease (COPD), a common pulmonary disease, relies on an inhaled beta-agonist (like Albuterol) to keep their airways open, administering a non-selective beta-blocker creates a direct conflict. The non-selective beta-blocker will bind to the beta-2 receptors in the lungs, physically blocking the albuterol from working and potentially triggering severe, life-threatening bronchoconstriction.

Beta-Blockers Used in Cardiovascular Diseases

Beta-blockers are used for several purposes beyond hypertension. A provider may give beta-blockers for many reasons, including, but not limited to:

• Hypertension (high blood pressure)
• Premature ventricular contractions (PVC)
• Congestive heart failure (CHF)

A clinician administers beta-blockers to patients with congestive heart failure because they slow down, or “block,” conduction through the AV node, slowing the heart rate and giving the ventricles more time in diastole. The heart then has more filling time, ideal for a CHF patient.

Beta-blockers slow the heart rate.

Beta-blockers also decrease contractility, so they have a negative inotropic effect on the heart, providing it with rest and slowing down the heart rate. 

Providers will not give beta-blockers if a patient is in an acute exacerbation of CHF, with elevated brain natriuretic peptides (BNP). The provider should not decrease this patient’s heart rate. They already have an issue pumping enough blood and the beta-blocker will further reduce cardiac output.

A few beta-blockers work on the smooth muscles in the periphery, causing vasodilation. Vasodilation decreases preload, another word for venous return. This reduces the blood volume that  returns to the right side of the heart, a positive for the patient with CHF because it decreases the volume the heart must manage.

Vasodilation also decreases afterload, the force the left ventricle has to overcome to pump blood out to the body. Decreasing afterload decreases the overall workload on the heart.

Beta-blockers decrease myocardial oxygen consumption, aiding the heart and decreasing its workload. Diagnosis and treatment aren’t solely about hypertension, it’s about decreasing preload and afterload. Beta-blockers provide the heart with rest in patients with chronic CHF.

Non-cardioselective beta-blockers, like propranolol, also target beta-2 receptors in the lungs, which may result in very dangerous bronchoconstriction in patients with pre-existing asthma or COPD. Providers must exercise extreme caution when administering beta-blockers to respiratory patients. 

Beta-blockers interact with the sodium-potassium pump, so they may increase potassium levels, presenting a potential risk for hyperkalemia. Clinicians must watch for hyperkalemia when administering beta-blockers.

Read: Cardiac Tamponade

Beta-Adrenergic Agonists

Beta-adrenergic agonists act on the sympathetic nervous system’s fight or flight response. The names of beta-agonist drugs often follow a pattern and typically end in “-terol” (e.g., Albuterol, Formoterol) instead of “-lol”. There are two main categories:

• Short-acting beta-agonists
• Long-acting beta-agonists

Short-acting vs. Long-acting Beta-Agonists

Albuterol is a common short-acting beta-agonist. Albuterol is a rescue inhaler. When a patient experiences an acute asthma attack, albuterol is the standard rapid treatment.

Formoterol, a long-acting beta-adrenergic agonist, is not a rescue inhaler. It won’t act immediately on the airways or help an asthma patient’s respiration right away during a crisis. It might be used as a daily maintenance medication for patients with asthma or COPD to prevent attacks.

Albuterol is a fast-acting beta-agonist.

A beta-adrenergic agonist’s main therapeutic use is bronchodilation. The beta-adrenergic agonists mimic the sympathetic nervous system, preparing the body for fight or flight. They open the airways, allowing a patient to take in more oxygen.

Why Beta-Agonists Increase Heart Rate: While drugs like albuterol are primarily beta-2 selective (targeting the lungs), giving large or frequent doses causes “receptor spillover.” This means the drug begins stimulating the beta-1 receptors in the heart as well, leading to the unfortunate side effect of tachycardia.

If the tachycardia becomes too severe, the patient’s cardiac output may drop. The patient will then experience hypotension, dizziness, and lightheadedness. In this case, a clinician should look for alternative interventions or other medications.

Monitoring Mini-List During Beta-Agonist Administration:

• Heart Rate: Monitor for severe tachycardia and palpitations.
• Tremors: Muscle tremors are a common, harmless side effect of sympathetic stimulation.
• Potassium Levels: Albuterol is quite powerful and pushes potassium into cells. The provider needs to watch for hypokalemia when using beta-adrenergic agonists.

Because of this potassium shift, some doctors will prescribe albuterol to patients with incredibly elevated potassium levels, such as one who’s missed a dialysis treatment. It’s paramount that providers monitor potassium levels when administering significant amounts of a beta-adrenergic agonist.

Summary

Beta-blockers block the heart’s beta-1 receptors to slow down a patient’s heart rate, and providers use them to treat a variety of cardiovascular diseases. Beta-blockers may also raise potassium levels, so clinicians must watch for hyperkalemia. Beta-blockers that also block beta-2 receptors in the lungs should be used with caution in patients with underlying respiratory disease

Beta-agonists trigger beta-2 receptors in the body’s lungs, opening up the patient’s airways. They also activate beta-1 receptors and cause an increase in the heart rate, so clinicians must monitor for potential tachycardic episodes.