Metoprolol (Lopressor, Toprol)



Sinus Bradycardia (see Sinus Bradycardia)

  • Metoprolol May Exacerbate Bradycardia

Atrioventricular Heart Blocks

Hypotension (see Hypotension)

  • Metoprolol May Exacerbate Hypotension

Moderate-Severe Congestive Heart Failure (CHF) (see Congestive Heart Failure)

  • Metoprolol May Exacerbate CHF

Pulmonary Hypertension (see Pulmonary Hypertension)

  • Although used commonly to treat supraventricular arrhythmias, beta blockers should be used cautiously in pulmonary hypertension (due to their negative inotropic and chronotropic effects)


Cardioselective (β1-Selective) β-Adrenergic Receptor Antagonist (see β-Adrenergic Receptor Antagonists)

  • However, at higher plasma concentrations, metoprolol’s cardioselectivity is less and it can inhibit β2-adrenergic receptors (located predominantly in the bronchial and vascular musculature)

Physiologic Effects

  • Decreased Blood Pressure
    • Possible Mechanisms of Decreased Blood Pressure (exact mechanism is not well-defined)
      • Competitive Antagonism of Catecholamines at Peripheral (Especially Cardiac) Adrenergic Neuron Sites: results in decreased cardiac output
      • Central Decreased Sympathetic Outflow to the Periphery
      • Suppression of Renin Activity
  • Negative Chronotropy: decreased resting and exercise heart rate (due to antagonism of catecholamine-induced increases in heart rate)
  • Negative Inotropy: decreased velocity and force of myocardial contraction
  • Decreased Myocardial Oxygen Consumption
    • Mechanisms
      • Negative Chronotropy
      • Negative Inotropy
      • Decreased Afterload: due to decrease in blood pressure



Oral (PO)

  • Dose (Lopressor): start 25 mg BID
    • PO/IV Equivalence: 2.5 mg PO = 1 mg IV (Example: 25 mg PO BID = 5 mg IV q6hrs)

Intravenous (IV)

  • Dose: start 5 mg q6hrs
    • PO/IV Equivalence: 2.5 mg PO = 1 mg IV (Example: 25 mg PO BID = 5 mg IV q6hrs)

Dose Reduction

  • Hepatic: hepatic impairment may prolong the half-life of metoprolol -> it is recommended to start with lower dose and titrate up (as tolerated)
  • Renal: none

Adverse Effects

Cardiovascular Adverse Effects

Atrioventricular Heart Blocks

Sinus Bradycardia (see Sinus Bradycardia)

  • May especially occur when used in conjunction with other negative chronotropes which slow heart rate and atrioventricular nodal conduction (such as digoxin or calcium channel blockers)

Congestive Heart Failure (CHF) (see Congestive Heart Failure): due to negative inotropy

  • May occur in some cases, especially when used in conjunction with other negative inotropes and chronotropes (such as calcium channel blockers)

Hypotension (see Hypotension)

  • May Occur

Masking of Hypoglycemia-Induced Tachycardia (see Hypoglycemia)

  • Beta blockers may mask tachycardia (but not necessarily the diaphoresis or dizziness) which occur in hypoglycemia

Masking of Hyperthyroidism-Induced Tachycardia (see Hyperthyroidism)

  • Abrupt withdrawal of beta blockers in this setting may precipitate thyroid storm

Paradoxical Increase in Blood Pressure in Pheochromocytoma (see Pheochromocytoma)

  • When used alone and not in combination with alpha blockers, beta blockers may paradoxically increase blood pressure (due to attenuation of the beta receptor-mediated vasodilatation in skeletal muscle)
  • Therefore, in pheochromocytoma, beta blockers should only be initiated after alpha blockers have been initiated

Potentiation of the Hypertensive Response that Occurs with Clonidine Withdrawal (in Patients on Concomitant Clonidine and Beta Blockers)

  • In such cases, it is advised to withdraw the beta blocker at least several days before withdrawing the clonidine

Neurologic Adverse Effects

Pulmonary Adverse Effects

Other Adverse Effects

Beta Blocker Intoxication

Beta Blocker Withdrawal