Cardiovascular Beta-Blockers

Cardiovascular Beta-Blockers

      Cardiovascular Beta-Blockers, selective and non-selective Beta-Blockers, how and when to use in management of the patient with cardiovascular problems

      Cardiovascular Beta-Blockers cause the inhibition of chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation. This drug class decreases activation of B1 adrenoceptors on the heart and decreases cardiac output which decreases blood pressure. Cardiovascular Beta-Blockers decrease renin, angiotensin II, aldosterone,  sodium and water retention, blood volume and peripheral resistance. Commonly used Cardiovascular Beta-Blockers are: propranolol, atenolol, metoprolol, carvedilol and labetolol.

      Beta-Blockers are classified by their Beta-Blocking selectivity: Nonselective beta-blockers and Beta 1 selective Beta-Blockers. Non-selective Beta-Blockers (Carvedilol & Labetalol) should not be used in patients with asthma. Selective Beta-Blockers diminishes with high doses. Beta-Blockers are used in the treatment of angina, post myocardial infarction, chronic heart failure, hypertension, arrhythmias, migraines, essential tremors, and hyperthyroidism. Beta-Blockers are contraindicated in acute heart failure, sick sinus syndrome without pacer, cardiogenic shock,heart block greater than first degree, and severe bradycardia.


Drug Overview Cardiovascular Beta-Blockers

Nonselective beta-blockers

  • propranolol, carteolol, nadolol, penbutolol, sotalol, timolol


B1-selective beta-blockers

  • atenolol, acebutolol, betaxolol, bisoprolol, metoprolol, esmolol



  • labetalol and carvedilol


Indications for Cardiovascular Beta-Blockers

  • Hypertension
  • Angina (atenolol, metoprolol, nadolol, propranolol)
  • CHF (metoprolol, carvedilol, bisoprolol)
  • Arrythmias (aacebutolol, esmolol, propranolol, sotalol,)
  • Migraines (propranolol)


Beta 1 receptors

  • Beta 1 receptors are in the heart
  • B 1 receptors stimulate catecholamine, which increases HR, BP, myocardial contractility, AV conduction, and decrease in AV node refractoriness.

Beta 2 receptors:

  • Beta 2 receptors are in the lungs and peripheral vascular smooth muscle
  • Beta 2 receptors stimulate catecholamine, causing vasodilation and bronchodilation
  • When beta 2 receptors are stimulated, it causes bronchoconstriction and reflex peripheral vasoconstriction


Mechanism of action of Beta-blockers

  • slows atrioventricular conduction system
  • Decreases sympathetic peripheral outflow
  • Renin release is antagonized by decreasing vasoconstrictor properties of the renin-angiotensin system
  • BP is lowered by decreasing cardiac output, pvr, venous return, plasma volume, and renin release.
  • In anginacompetitive inhibition of sympathetic stimulation. Beta-blockers block the effect of adrenaline on the heart and reduces the risk of developing angina during periods of stress and exercise.
  • Beta-blockers in CHF- decrease catecholamine levels and reduce cardiac congestion and LVF, increases beta 1 receptor sensitivity and restore inotropic response and promotes peripheral vasodilation.
  • Beta-blocker use for arrhythmias- blocks abnormal cardiac pacemaker potentials, decreases myocardial oxygen demand, prolongs ventricular filling time, and decreases microvascular damage to the myocardium


Treatment Principles of beta-blockers

  • Use with caution in patients with heart block, sinus bradycardia, cardiogenic shock, or heart failure
  • Beta-Blockers are never used as first line agents in the treatment of hypertension (JNC 8 Guidelines)
  • Beta-Blockers are effective for hypertension and one of these comorbid conditions: angina, arrhythmias, CHF, post-myocardial infarction, tremors, glaucoma, and migraine headache.
  • Avoid use of Beta-Blockers in the following patients: asthma, COPD, severe PVD, Raynaud’s phenomenon, depression, bradycardia, second or third-degree heart block, hypoglycemic prone diabetic patients, and elderly unless the elderly patient has CAD, MI, CHF
  • Beta-Blockers are the treatment of choice for chronic long-term stable and unstable angina
  • Beta-Blockers re-used for secondary prevention post MI. All patients post MI should receive Beta-blocker therapy because Beta-Blockers have been shown to improve survival in post MI patients by reducing the incidence of sudden death.
  • Beta-Blockers are used for symptomatic improvement and enhanced survival in chronic heart failure by increasing ejection fraction and decreasing ventricular size and mass (carvedilol, metoprolol, and bisoprolol are the drugs used for heart failure)
  • Beta-Blockers (metoprolol) may have some benefit in maintaining normal sinus rhythm after cardioversion of a-fibrillation
  • Beta-Blockers are used for migraine prophylaxis (only propranolol and timolol are FDA approved for migraine prophylaxis)
  • Beta-Blockers are used for essential tremor
  • Beta-Blockers are used for Hyperthyroidism
  • Beta-Blockers are also used in, tachycardias, mitral valve prolapse, LVH, and pheochromocytoma


Monitoring Beta-Blockers

  • BP and pulse weekly until stable then q3-4 months
  • Baseline ECG, as needed and annual thereafter
  • Baseline lipids, blood glucose, renal and hepatic function,TSH, CBC, BMP


Signs and symptoms of toxicity

  • Bradycardia
  • Hypotension
  • Progression of heart failure
  • Exacerbation of bronchospasm
  • Hypoglycemia episodes
  • Depression


Considerations for Beta-Blocker use

  • Geriatrics– potential for hepatic and renal failure. Drug levels may accumulate quickly in the elderly. Therapeutic doses need to be half the normal dosage and titrated slowly. Sedation and sleep disturbances have been associated with use in this population
  • Pregnancy and lactation– benefits of Beta-Blocker use in pregnancy should clearly outweigh risk. Low birth weight infants have been reported in mothers with Beta-blocker use during pregnancy. If the mother is breastfeeding the drug should be discontinued
  • Race– avoid use in African American patients as first-line therapy


Patient Education

  • Report shortness of breath, difficulty breathing, nocturnal cough, and/or lower extremity edema
  • Do not discontinue abruptly
  • Report use to ophthalmologist
  • Monitor pulse and contact provider if pulse less than 50 bpm
  • Diabetic patient must monitor blood sugar for masked signs of hypoglycemia
  • Use caution when performing hazardous tasks because of CNS side effects


Drug interactions

  • Calcium channel blockers, oral contraceptives, quinidine, diphenhydramine, flecainide, cipro, and hydroxychloroquine all increase the action of Beta-blockers
  • Aluminum salts, barbiturates, calcium salts, cholestyramine, colestipol, ampicillin, NSAIDs, salicylates, and sulfinpyrazone decrease the action of Beta-blockers
  • Beta-Blockers increase the action of clonidine, epinephrine, lidocaine, and prazosin
  • Propranolol increases the action of phenothiazines, haloperidol, anticoagulants, and gabapentin
  • Metoprolol and propranolol increase the action of benzodiazepines and hydralyzine


Key points

  • When patients are taking Beta-blockers they should not push themselves to physical extremes.
  • Hypotension, bradycardia ,fatigue, sexual dysfunction, and masking of hypoglycemic symptoms are some adverse effects
  • Asthmatic patients should avoid Beta-Blockers (non-selective)
  • Beta-Blockers are the drug of choice for patients with angina
  • OTC NSAIDS should be avoided in patients taking a Beta-blocker
  • Cardio-selective Beta-Blockers (Toprol XL) are used to prevent increased HR that results from sympathetic stimulation which occurs as compensation for reduced CO of HF
  • Coreg is an alpha and beta blocker
  • Cardioselective Beta-Blockers (metorpolol xl) are indicated for HF with a low ejection fraction
  • Compensatory increases in heart rate and renin release may be alleviated by metoprolol (Toprol XL)



Nonselective Beta
Cardio selective Beta
-Act at both B1 (heart) and B2 (lungs) receptors:
- Carvdilol -B1,
B2, and α1
-Labetalol- B1,
B2 and α1
Block only B1 (heart)
- Esmolol
-Do not give to COPD patients
-Attenuate normal response to hypoglycemia
-Cardio: ↓ CO, ↓Cardiac work, ↓O2 consumption by blockade of B1 receptors

-Peripheral Vasoconstriction: ↓CO=↓Blood flow to periphery

-Bronchoconstriction: blocking B2=contraction of bronchiolar SM

↑Na+ Retention: ↓BP= ↓renal perfusion=↑Na+ retention and plasma volume

Disturbances in Glucose Metabolism: B-blockade =↓glycogenolysis and ↓glucagon secretion
Blocked action of isoproterenol
↓Renin Secretion
Therapeutic Effects

Propranolol DOC for stable Angina and Migraines

Timolol used in tx of open-angle glaucoma
Therapeutic Effects

- ↓ B/P (by ↓CO)

-Glaucoma (by ↓ICP)



-Angina Pectoris (↓o2 requirement of heart muscle)

-MI (given during MI will reduce infarct size and ↑recovery)
Side Effects
-Contraindicated in COPD/Asthma patients

-Can cause sexual impairment
Side Effects
A- Asthma
B- heart block
D-Diabetes mellitus
E- Electrolytes (↑K+)



Edmunds, M. W., & Mayhew, M. S. (2014). Pharmacology for the primary care provider (4th ed.). St. Louis, MO: Elsevier Mosby.

Harvey, R. A., Clark, M. A., Finkel, R., Rey, J. A., & Whalen, K. (2012). Pharmacology (5th ed.). Baltimore, MD: Lippincott.

JNC8 Guidlines 2014. (2014). JNC 8 Guidlines. Retreived from: