Version October 2024
Dosage guidance:
Safety: Accumulation can occur with high-dose continuous infusions and may result in severe hypotension and bradycardia (Ref). There is limited documentation of prolonged continuous infusions (Ref).
Acute aortic syndromes/acute aortic dissection (alternative agent) (off-label use):
Note: Manage patients on an emergency basis (including operative assessment) by first controlling pain with IV opioids and heart rate (target 60 to 80 beats per minute) with a parenteral beta blocker (eg, labetalol) while targeting systolic BP of ≤120 mm Hg (or lowest tolerated pressure without compromising perfusion). If systolic BP remains elevated after heart rate is controlled at 60 to 80 beats per minute with beta-blockade, may consider adding an additional parenteral vasodilator (ie, nitroprusside or nicardipine). Invasive BP monitoring, preferably via arterial line, in a critical care unit is recommended for appropriate dose titration (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in select patients, while monitoring for accumulation (Ref).
Intermittent IV: Initial: 20 mg over 2 minutes followed by 20 to 80 mg every 10 minutes until target heart rate and BP are reached; may transition to continuous infusion if unable to obtain target goals (Ref).
Continuous IV infusion: Initial loading dose: 20 mg over 2 minutes (loading dose is optional if intermittent dose is used prior to continuous infusion), followed by 0.5 to 2 mg/minute; some patients may require titration up to 10 mg/minute for optimal response (Ref).
Acute ischemic stroke, BP management with reperfusion therapy (off-label use):
Note: Prior to reperfusion therapy (thrombolytic and/or mechanical thrombectomy), maintain a target BP of ≤185/110 mm Hg. If BP remains >185/110 mm Hg, do not administer thrombolytic. During and 24 hours after start of thrombolytic therapy, maintain a target BP of ≤180/105 mm Hg; if hypertension is refractory or diastolic BP >140 mm Hg, consider alternative therapy (Ref).
Prior to reperfusion therapy:
IV: 10 to 20 mg over 1 to 2 minutes; may repeat once (Ref).
During and after reperfusion therapy:
IV: 10 mg over 1 to 2 minutes, followed by 2 to 8 mg/minute continuous infusion (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in select patients, while monitoring for accumulation (Ref).
Hypertension, chronic/resistant:
Note: Not recommended for initial management of hypertension, but may be considered as additional therapy in patients who do not respond adequately to combination therapy with preferred agents (Ref).
Oral: Initial: 100 mg twice daily; may increase as needed every 2 to 3 days by 100 mg twice daily (titration increments not to exceed 200 mg twice daily) until desired response is obtained; usual dosage range: 200 to 800 mg/day in 2 divided doses (Ref). In patients with resistant hypertension, doses up to 1.2 to 2.4 g/day in 2 or 3 divided doses may be required; however, combination therapy is preferred over dose escalation beyond the usual dosage range (Ref).
Hypertensive emergency:
Note: In general, reduce mean arterial blood pressure gradually by ~10% to 20% over the first hour, then by an additional 5% to 15% over the next 23 hours, unless there is a compelling indication (eg, acute aortic dissection, severe preeclampsia, eclampsia) for more rapid blood pressure and heart rate control (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in select patients, while monitoring for accumulation (Ref).
Intermittent IV: Initial: 10 to 20 mg over 1 to 2 minutes followed by 20 to 80 mg every 10 minutes until target blood pressure is reached; consider a continuous infusion if unable to obtain target blood pressure (Ref).
Continuous IV infusion: Initial loading dose: 10 to 20 mg over 2 minutes (loading dose is optional if intermittent dose is used prior to continuous infusion), followed by 0.5 to 2 mg/minute; some patients may require titration up to 10 mg/minute (Ref).
Hypertensive emergency in pregnancy or postpartum (including acute-onset severe hypertension in preeclampsia/eclampsia) (off-label use):
Note: For acute-onset, severe, persistent hypertension (eg, systolic BP ≥160 mm Hg or diastolic BP ≥110 mm Hg) (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in selected patients, while monitoring for accumulation (Ref).
Intermittent IV: Initial: 20 mg over 2 minutes; if blood pressure exceeds thresholds after 10 to 30 minutes, increase dose in increments of 20 to 40 mg every 10 to 30 minutes; maximum single dose: 80 mg. Note: If blood pressures remain above threshold after several intermittent doses, another agent should be used (Ref).
Continuous IV infusion: Initial loading dose: 20 mg over 2 minutes (loading dose is optional if intermittent dose is used prior to continuous infusion), followed by 0.5 to 2 mg/minute titrated to response (Ref).
Oral (alternative route): Initial: 200 mg every 60 minutes for up to 3 doses. Note: May use as alternative route to other ineffective oral therapy; IV therapy (intermittent or continuous infusion) may be needed for more acute treatment (Ref).
Intracerebral hemorrhage, acute, BP management (off-label use):
Note: For use in patients with mild to moderate intracerebral hemorrhage with a presenting systolic BP ≥150 mm Hg; acute lowering to <130 mm Hg is potentially harmful (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in select patients, while monitoring for accumulation (Ref).
Patients who present with systolic BP 150 to 220 mm Hg:
Intermittent IV: Initial: 5 to 20 mg IV push over 2 minutes. May repeat every 10 to 15 minutes; repeat doses may be increased incrementally up to 80 mg as needed based on response and tolerability until target systolic BP is reached; may consider a continuous infusion if unable to obtain target goals (Ref).
Patients who present with systolic BP >220 mm Hg (alternative agent):
Continuous IV infusion: Initial loading dose: 20 mg over 2 minutes, followed by 0.5 to 2 mg/minute; titrate to target systolic BP (Ref).
Perioperative hypertension:
Note: For patients with chronic hypertension prior to surgery, restart oral therapies as soon as appropriate once hemodynamically stable (Ref).
Intermittent IV: Initial: 5 to 20 mg over 2 minutes; followed by 5 to 40 mg every 5 to 10 minutes as needed until target BP is reached; may increase up to a maximum single dose of 80 mg if needed (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in selected patients, while monitoring for accumulation (Ref).
Continuous IV infusion: Initial loading dose: 5 to 20 mg IV bolus over 2 minutes (loading dose is optional if intermittent dose is used prior to continuous infusion), followed by 0.5 to 2 mg/minute continuous IV infusion titrated to target BP; some patients may require titration up to 10 mg/minute (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in selected patients, while monitoring for accumulation (Ref).
Subarachnoid hemorrhage, acute, BP management (off-label use):
Note: Optimal therapy is not well established. Cautious use of antihypertensive therapy to decrease the risk of rebleeding, while avoiding hypotension and blood pressure variability, may be appropriate in some patients presenting with severe hypertension (Ref). Although manufacturer's labeling recommends against exceeding a cumulative IV dose of 300 mg, it may be reasonable to exceed this dose in selected patients, while monitoring for accumulation (Ref).
Intermittent IV: Initial: 10 to 20 mg over 2 minutes; followed by 20 to 80 mg every 10 to 15 minutes until systolic BP <160 mm Hg or mean arterial pressure <100 mm Hg (Ref).
Continuous IV infusion: 0.5 to 2 mg/minute titrated to response; based on very limited data (Ref).
IV to oral conversion:
Upon discontinuation of continuous IV infusion, may initiate oral dose of 200 mg followed in 6 to 12 hours with an additional dose of 200 to 400 mg; adjust dose based on response at ≥1-day intervals to a range of 400 mg/day to 2.4 g/day in 2 to 3 divided doses. Note: For hypertension, the usual dosage range is 200 to 800 mg/day in 2 divided doses (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
IV, Oral:
Altered kidney function: Mild to severe impairment: No dosage adjustment necessary (Ref).
Hemodialysis, intermittent (thrice weekly): Poorly dialyzed (manufacturer’s labeling); no supplemental dose or dosage adjustment necessary (expert opinion).
Peritoneal dialysis: Poorly dialyzed (manufacturer’s labeling); no dosage adjustment necessary (expert opinion).
CRRT: No dosage adjustment necessary (expert opinion).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (expert opinion).
There are no dosage adjustments provided in the manufacturer’s labeling. However, dosage reduction may be necessary in hepatic impairment due to decreased metabolism and increased oral bioavailability, use with caution.
Refer to adult dosing.
Hypertension: Oral:
Manufacturer's labeling: Initial: 100 mg twice daily; may titrate in increments of 100 mg twice daily; usual maintenance: 100 to 200 mg twice daily
ACCF/AHA Expert Consensus recommendations: Consider lower initial doses and titrating to response (Ref)
(For additional information see "Labetalol: Pediatric drug information")
Dosage guidance:
Dosing: Use care with labetalol continuous IV infusions; the rate of administration is different for pediatric patients (mg/kg/hour) versus adult patients (mg/minute).
Hypertension:
Acute severe hypertension with life-threatening symptoms: Limited data available:
IV (intermittent bolus): Children and Adolescents: 0.2 to 1 mg/kg/dose; maximum dose: 40 mg/dose (Ref).
Continuous IV infusion: Infants, Children, and Adolescents: 0.25 to 3 mg/kg/hour; initiate at lower end of range and titrate up slowly to effect (Ref). In one retrospective study in infants and children ≤24 months of age, reductions in blood pressure were observed at doses up to 0.59 mg/kg/hour, with little additional benefit at higher doses (Ref).
Chronic hypertension: Limited data available: Children and Adolescents: Oral: Initial: 1 to 3 mg/kg/day in 2 divided doses; maximum daily dose: 10 to 12 mg/kg/day, up to 1,200 mg/day (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling. <1% removed by hemo- or peritoneal dialysis.
There are no dosage adjustments provided in the manufacturer’s labeling; however, dosage reduction may be necessary in hepatic impairment due to decreased metabolism and increased oral bioavailability; use with caution.
Beta-blockers may cause bradycardia and heart block, including first-degree atrioventricular (AV) block, second-degree AV block, or complete AV block (Ref). At maintenance dosing, second- or third-degree AV block are less likely (Ref). Beta-blocking agents with intrinsic sympathomimetic activity (ISA) (eg, pindolol) may cause fewer AV conduction abnormalities than those without intrinsic sympathomimetic activity (eg, carvedilol) due to their partial agonist effects (Ref); labetalol possesses a very small degree of ISA and exhibits a slight, but irregular effect on AV conduction (Ref). In most cases (up to 72%), AV block associated with a beta-blocker will resolve upon discontinuation; however, there are reported cases of recurrent AV block and nearly 50% of patients with more severe AV block may require a permanent pacemaker (Ref).
Mechanism: Dose-related; related to the pharmacologic action. Blockade of cardiac beta-1 adrenergic receptors results in slowed conduction and prolongation of the refractory period of the AV node. Slowing of AV conduction can lead to AV block (Ref).
Onset: Varied; one study included patients who were on a beta-blocker for more than 1 month (Ref); however, other studies noted prolongation AV nodal refractory period occurring anywhere from 1 dose to several days following treatment initiation (Ref).
Risk factors:
• Impaired AV node conduction or sinus node function (Ref)
• Concurrent use of other agents that impair AV nodal conduction (eg, nondihydropyridine calcium channel blockers, digoxin, ivabradine, select antiarrhythmic agents) (Ref)
• Older patients (Ref)
Nonselective beta-blockers (eg, labetalol) have a higher risk of bronchospasm compared to cardioselective beta-blockers and may lead to drug discontinuation in patients with chronic obstructive pulmonary diseases (COPD) or asthma (Ref). Use of labetalol in patients with hypertension and COPD or asthma has been associated with varying degrees of impact on FEV1, forced expiratory flow, and/or forced vital capacity (Ref). Based on the use of other beta-blockers in this setting, concurrent use of inhaled bronchodilators and/or corticosteroids are protective against beta-blocker-induced bronchospasm in patients with COPD or asthma (Ref). Bronchospasm is reversible upon discontinuation (Ref).
Mechanism: Dose-related; related to pharmacologic action. Beta-blocking agents can lead to airway smooth muscle constriction by antagonism of beta-2 receptors (Ref).
Onset: Varied; changes in pulmonary function tests have occurred after 1 dose (Ref).
Risk factors:
• Reactive airway disease (asthma) (Ref)
Beta-blockers may cause CNS effects such as fatigue, sleep disorder, insomnia, and vivid dreams (Ref). Lipophilic beta-blockers (including labetalol) penetrate the blood-brain barrier to a greater extent than hydrophilic beta-blockers, possibly leading to a greater incidence of CNS effects; however, other studies have refuted this theory (Ref). Sexual disorders may occur; however, patients who require beta-blocker therapy have risk factors for erectile dysfunction (eg, coronary artery disease, heart failure) (Ref). Memory impairment has been reported with the use of other lipophilic beta-blockers (eg, carvedilol); however newer data suggests carvedilol may be helpful for patients with Alzheimer disease (Ref). CNS effects generally resolve with dose reduction or discontinuation (Ref).
Mechanism: Dose-related; exact mechanism is not fully understood. Proposed mechanisms include presence of beta receptors in the brain, affinity and in some instances, inhibition of beta-blocking agents towards serotonin (5-HT) receptors in the brain (affecting mood and sleep), and beta-blocker-induced decreases in central sympathetic output (Ref). Beta-1 blockade may also impact sleep by blocking sympathetic signaling to the pineal gland, resulting in suppression of nighttime levels of melatonin (Ref). Beta-blockers may cause erectile dysfunction through decreased sympathetic nervous system output and subsequent decreases in luteinizing hormone secretion and testosterone stimulation (Ref).
Onset: Intermediate; CNS effects often occur within the first few weeks of treatment (Ref).
Risk factors:
• Higher starting doses (Ref)
• Older patients (Ref)
Beta-blockers may worsen, prolong, or cause hypoglycemia (Ref). Additionally, beta-blockers may mask symptoms of hypoglycemia (tremor, irritability, palpitations), making diaphoresis the only symptom unaffected by beta-blockers (Ref). It is unclear if nonselective or selective beta-blockers are more likely to cause hypoglycemia; as data are conflicting (Ref).
Mechanism: Dose-related; related to the pharmacologic action. Beta-blockers inhibit hepatic gluconeogenesis and glycogenolysis (Ref). Beta-blockers also reduce activation of the sympathetic nervous system, therefore masking hypoglycemic symptoms that are catecholamine-mediated (Ref).
Onset: Varied; hypoglycemia (<70 mg/dL) was reported significantly more after 24 hours of nonselective beta-blocker (ie, carvedilol) use compared to patients not on beta-blockers (Ref). In another study, episodes of severe hypoglycemia (<50 mg/dL) were reported over the course of 4 years (Ref).
Risk factors:
• Insulin-dependent diabetes (Ref)
• Type 2 diabetes mellitus (Ref)
• Patients who are hospitalized and not requiring basal insulin (Ref)
Beta-blocker therapy should not be withdrawn abruptly, but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia in patients with underlying cardiovascular disease (Ref). Some studies have found an increase in propensity-adjusted mortality and cardiovascular events; however, one study did not find changes in infarct size and left ventricular function when beta-blocker was abruptly withdrawn in patients with myocardial infarction (Ref).
Mechanism: Dose-dependent; related to the pharmacologic action. Beta blockade causes upregulation of beta-receptors, enhanced receptor sensitivity, and decreased sympathetic nervous system response. Abrupt withdrawal leads to a transient sympathetic hyper-response (Ref). Another proposed mechanism involves increased platelet aggregability to epinephrine and thrombin (Ref).
Onset: Rapid/varied and transient; increases in heart rate and blood pressure appear 24 hours after abrupt withdrawal, peak after 48 hours, and subside after 7 days (Ref). In other nonselective beta-blockers (propranolol), anginal symptoms reported to begin 12 to 24 hours after discontinuation. Development of adverse reactions also reported to occur 1 to 21 days after withdrawal (Ref).
Risk factors:
• Abrupt withdrawal in chronic users (Ref)
• Past medical history of coronary artery disease (including chronic stable angina) (Ref)
• Past medical history of hypertension (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%:
Cardiovascular: Orthostatic hypotension (IV: 58%; oral: 1%)
Gastrointestinal: Nausea (≤19%)
Nervous system: Dizziness (1% to 16%)
1% to 10%:
Cardiovascular: Edema (oral: 1% to 2%), flushing (IV: 1%), hypotension (IV: 1%), ventricular arrhythmia (IV: 1%)
Dermatologic: Diaphoresis (IV: 4%; oral: <1%), pruritus (IV: 1%), skin rash (oral: 1%)
Gastrointestinal: Dysgeusia (1%), dyspepsia (IV: 1%; oral: 1% to 4%), vomiting (oral: ≤4%)
Genitourinary: Ejaculatory failure (oral: 1% to 5%), impotence (oral: 1% to 4%)
Hepatic: Increased serum transaminases (oral: 4%)
Nervous system: Drowsiness (IV: ≤3%), fatigue (oral: 1% to 10%) (table 1), headache (oral: 2%), hypoesthesia (IV: 1%), paresthesia (≤7%), vertigo (1% to 2%), yawning (IV: ≤3%)
|
Drug (Labetalol) |
Comparator (Propranolol) |
Comparator (Metoprolol) |
Placebo |
Dose |
Number of Patients (Labetalol) |
Number of Patients (Propranolol) |
Number of Patients (Metoprolol) |
Number of Patients (Placebo) |
|---|---|---|---|---|---|---|---|---|
|
10% |
N/A |
N/A |
N/A |
2,400 mg/day |
175 |
N/A |
N/A |
N/A |
|
7% |
N/A |
N/A |
N/A |
1,200 mg/day |
411 |
N/A |
N/A |
N/A |
|
6% |
N/A |
N/A |
N/A |
1,600 mg/day |
242 |
N/A |
N/A |
N/A |
|
5% |
12% |
12% |
0% |
N/A |
227 |
84 |
49 |
98 |
|
5% |
N/A |
N/A |
N/A |
800 mg/day |
503 |
N/A |
N/A |
N/A |
|
4% |
N/A |
N/A |
N/A |
400 mg/day |
606 |
N/A |
N/A |
N/A |
|
4% |
N/A |
N/A |
N/A |
600 mg/day |
608 |
N/A |
N/A |
N/A |
|
3% |
N/A |
N/A |
N/A |
900 mg/day |
117 |
N/A |
N/A |
N/A |
|
2% |
N/A |
N/A |
N/A |
200 mg/day |
522 |
N/A |
N/A |
N/A |
|
1% |
N/A |
N/A |
N/A |
300 mg/day |
181 |
N/A |
N/A |
N/A |
Ophthalmic: Visual disturbance (oral: 1%)
Renal: Increased blood urea nitrogen (≤8%), increased serum creatinine (IV: 8%)
Respiratory: Dyspnea (oral: 2%), nasal congestion (oral: 1% to 6%), wheezing (IV: 1%)
<1%: Gastrointestinal: Diarrhea
Postmarketing:
Cardiovascular: Bradycardia, heart block, heart failure, syncope
Dermatologic: Facial erythema, lichen planus (bullous), lichenoid eruption, maculopapular rash, psoriasiform eruption, transient alopecia, urticaria
Genitourinary: Acute urinary retention, difficulty in micturition, Peyronie disease
Hematologic & oncologic: Positive ANA titer
Hepatic: Cholestatic jaundice, hepatic injury, hepatic necrosis, hepatitis
Hypersensitivity: Angioedema, hypersensitivity reaction, nonimmune anaphylaxis
Immunologic: Antibody development (antimitochondrial)
Neuromuscular & skeletal: Muscle cramps, myopathy (Willis 1990), systemic lupus erythematosus
Ophthalmic: Dry eye syndrome
Respiratory: Bronchospasm
Miscellaneous: Fever
Hypersensitivity (eg, anaphylaxis) to labetalol or any component of the formulation; severe sinus bradycardia; heart block greater than first degree; cardiogenic shock; bronchial asthma or obstructive airway disease; decompensated heart failure (oral only); administration of non-dihydropyridine calcium channel blockers (eg, verapamil).
Canadian labeling: Additional contraindications (not in the US labeling): Sick sinus syndrome (except in patients with a functioning artificial pacemaker); state of hypoperfusion; severe peripheral arterial circulatory disorders.
Concerns related to adverse effects:
• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.
• Floppy iris syndrome: Intraoperative floppy iris syndrome has been observed in cataract surgery patients who were treated with alpha1-blockers. There appears to be no benefit in discontinuing alpha-blocker therapy prior to surgery.
• Hepatic injury: Severe hepatocellular injury has been reported (rare). The hepatic injury is usually reversible, but hepatic necrosis and death have been reported. Injury has occurred after both short- and long-term treatment and may be slowly progressive despite minimal symptomatology.
Disease-related concerns:
• Angina: Use with caution in patients suspected of having vasospastic angina.
• Heart failure (HF): Use with extreme caution in patients with compensated heart failure and monitor for a worsening of the condition.
• Hepatic impairment: Use with caution in patients with hepatic impairment; bioavailability is increased due to decreased first-pass metabolism.
• Myasthenia gravis: Use beta blockers with caution in patients with myasthenia gravis.
• Peripheral vascular disease (PVD) and Raynaud disease: Beta blockers may precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud disease; use with caution and monitor for progression of arterial obstruction.
• Pheochromocytoma: Labetalol may be effective in lowering blood pressure and relieving symptoms in patients with pheochromocytoma; however, patients may experience paradoxical hypertensive responses due to inadequate alpha-1 blockade (Manger 2002; Mazza 2014). Adequate alpha-1 blockade should be initiated prior to use of any beta-blocker in this setting; use with caution in patients with pheochromocytoma or consider alternative therapy. If possible, obtain diagnostic tests for pheochromocytoma prior to use since labetalol may spuriously cause falsely elevated levels of plasma catecholamine and urinary metanephrine (Bravo 2002; MacCarthy 1983).
• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.
• Thyroid disease: Beta blockers may mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.
Special populations:
• Older adult: Bradycardia may be observed more frequently in elderly patients (>65 years of age); dosage reductions may be necessary.
Dosage form specific issues:
• Benzyl alcohol and derivatives: Some dosage forms may contain sodium benzoate/benzoic acid; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol derivative with caution in neonates. See manufacturer’s labeling.
• Injection: Patients who are tilted during administration or allowed to assume the upright position within 3 hours of administration may experience symptomatic postural hypotension.
Other warnings/precautions:
• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous, as hydrochloride:
Generic: 5 mg/mL (4 mL, 20 mL, 40 mL); 100 mg/100 mL (1 mg/mL) with NaCl 0.72% (100 mL); 200 mg/200 mL (1 mg/mL) with NaCl 0.72% (200 mL); 200 mg/200 mL (1 mg/mL) with dextrose 5% (200 mL); 300 mg/300 mL (1 mg/mL) in NaCl 0.72% (300 mL)
Solution Prefilled Syringe, Intravenous, as hydrochloride [preservative free]:
Generic: 10 mg/2 mL (2 mL)
Tablet, Oral, as hydrochloride:
Generic: 100 mg, 200 mg, 300 mg
Yes
Solution (Labetalol HCl Intravenous)
5 mg/mL (per mL): $0.13 - $0.69
Solution (Labetalol HCl-Dextrose Intravenous)
200 mg/200 mL 5% (per mL): $0.17
Solution (Labetalol HCl-Sodium Chloride Intravenous)
100MG/100ML 0.72% (per mL): $0.17
200MG/200ML 0.72% (per mL): $0.17
300MG/300ML 0.72% (per mL): $0.17
Solution Prefilled Syringe (Labetalol HCl Intravenous)
10 mg/2 mL (per mL): $3.60
Tablets (Labetalol HCl Oral)
100 mg (per each): $0.17 - $0.67
200 mg (per each): $0.26 - $1.14
300 mg (per each): $0.35 - $1.15
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous, as hydrochloride:
Generic: 5 mg/mL (20 mL, 40 mL)
Tablet, Oral, as hydrochloride:
Trandate: 100 mg [contains sodium benzoate]
Trandate: 200 mg [contains fd&c yellow #6 (sunset yellow), sodium benzoate]
Generic: 100 mg, 200 mg
Oral: Administer without regard to food; however, the absolute bioavailability of labetalol is increased when administered with food. Administer in a consistent manner with regards to meals.
Parenteral: Bolus dose of 10 mg may be administered IV push at a rate of 10 mg/minute; bolus doses of ≥20 mg may be administered IV push over 2 minutes; may follow with continuous IV infusion if clinically indicated (Ref). Orthostatic hypotension may occur with IV administration; patient should remain supine during and for up to 3 hours after IV administration; patient’s ability to tolerate an upright position should be established before permitting ambulation or assuming an upright position.
Oral: Administer without regard to food; however, the absolute bioavailability of labetalol is increased when administered with food. Administer in a consistent manner with regards to meals.
Parenteral:
IV bolus: Based on adult information, may administer undiluted over 2 minutes; maximum: 10 mg/minute.
Continuous IV infusion: Administer as a continuous IV infusion with the use of an infusion pump.
Note: Premixed solutions are available.
IV infusion: 200 mg in 200 mL (concentration: 1 mg/mL) or 400 mg in 200 mL (concentration: 2 mg/mL) or 500 mg in 250 mL (concentration: 2 mg/mL) of D5W.
IV infusion: 1 mg/mL, 5 mg/mL.
Hypertension: Management of hypertension (IV indicated for severe hypertension only [eg, hypertensive emergencies]). Note: Beta-blockers are not recommended as first-line therapy (ACC/AHA [Whelton 2018]).
Acute aortic syndromes/Acute aortic dissection; Acute ischemic stroke, BP management with reperfusion therapy; Hypertensive emergency in pregnancy or postpartum (including acute-onset severe hypertension in preeclampsia/eclampsia); Intracerebral hemorrhage, acute, blood pressure management; Subarachnoid hemorrhage, acute, blood pressure management
Labetalol may be confused with betaxolol, LaMICtal, lamoTRIgine, Lipitor
Normodyne may be confused with Norpramin
Trandate may be confused with traMADol, Trental
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drug classes (adrenergic antagonist, IV) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Acute Care Settings).
Labetalol is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age). Some disease states of concern include bradycardia, heart block, and severe symptomatic aortic stenosis. Use is not recommended as monotherapy for the treatment of uncomplicated hypertension (O’Mahony 2023).
Significant differences exist between oral and IV dosing. Use caution when converting from one route of administration to another.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Alpha2-Agonists: May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider therapy modification
Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider therapy modification
Amiodarone: May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. Risk C: Monitor therapy
Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Antidiabetic Agents: Beta-Blockers (Nonselective) may enhance the hypoglycemic effect of Antidiabetic Agents. Beta-Blockers (Nonselective) may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Antipsychotic Agents (Phenothiazines): May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. Risk C: Monitor therapy
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy
Arginine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Beta2-Agonists: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2-Agonists. Risk X: Avoid combination
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy
Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Risk C: Monitor therapy
Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination
Cannabis: Beta-Blockers may enhance the adverse/toxic effect of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification
Cholinergic Agonists: Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor therapy
Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy
Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Risk C: Monitor therapy
DOBUTamine: Beta-Blockers may diminish the therapeutic effect of DOBUTamine. Risk C: Monitor therapy
Dronedarone: May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider therapy modification
DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy
EPHEDrine (Systemic): Beta-Blockers may diminish the therapeutic effect of EPHEDrine (Systemic). Risk C: Monitor therapy
EPINEPHrine (Nasal): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of EPINEPHrine (Nasal). Risk C: Monitor therapy
EPINEPHrine (Oral Inhalation): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Risk C: Monitor therapy
EPINEPHrine (Systemic): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of EPINEPHrine (Systemic). Risk C: Monitor therapy
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor therapy
Etilefrine: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may diminish the therapeutic effect of Etilefrine. Risk C: Monitor therapy
Etofylline: Beta-Blockers may diminish the therapeutic effect of Etofylline. Risk X: Avoid combination
Etrasimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination
Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification
Flunarizine: May enhance the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider therapy modification
Herbal Products with Blood Pressure Increasing Effects: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Iloperidone: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Indoramin: May enhance the hypotensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Insulins: Beta-Blockers (Nonselective) may enhance the hypoglycemic effect of Insulins. Beta-Blockers (Nonselective) may diminish the therapeutic effect of Insulins. Risk C: Monitor therapy
Iobenguane Radiopharmaceutical Products: Labetalol may diminish the therapeutic effect of Iobenguane Radiopharmaceutical Products. Management: Discontinue all drugs that may inhibit or interfere with catecholamine transport or uptake for at least 5 biological half-lives before iobenguane administration. Do not administer labetalol until at least 7 days after each iobenguane dose. Risk X: Avoid combination
Isocarboxazid: May enhance the antihypertensive effect of Antihypertensive Agents. Risk X: Avoid combination
Isoproterenol: Beta-Blockers may diminish the therapeutic effect of Isoproterenol. Risk C: Monitor therapy
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy
Levodopa-Foslevodopa: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Foslevodopa. Risk C: Monitor therapy
Loop Diuretics: May enhance the hypotensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Mavacamten: Beta-Blockers may enhance the adverse/toxic effect of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor therapy
Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Risk C: Monitor therapy
Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Mivacurium: Beta-Blockers may enhance the therapeutic effect of Mivacurium. Risk C: Monitor therapy
Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Risk C: Monitor therapy
Nitrendipine: May enhance the therapeutic effect of Beta-Blockers. Risk C: Monitor therapy
Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Beta-Blockers. Risk C: Monitor therapy
Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider therapy modification
Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification
Prazosin: Antihypertensive Agents may enhance the hypotensive effect of Prazosin. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Reserpine: May enhance the bradycardic effect of Beta-Blockers. Reserpine may enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Risk X: Avoid combination
Silodosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification
Succinylcholine: Beta-Blockers may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
Sulfonylureas: Beta-Blockers (Nonselective) may enhance the hypoglycemic effect of Sulfonylureas. Beta-Blockers (Nonselective) may diminish the therapeutic effect of Sulfonylureas. Risk C: Monitor therapy
Tasimelteon: Beta-Blockers may diminish the therapeutic effect of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider therapy modification
Terazosin: Antihypertensive Agents may enhance the hypotensive effect of Terazosin. Risk C: Monitor therapy
Theophylline Derivatives: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. Risk C: Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Urapidil: Antihypertensive Agents may enhance the hypotensive effect of Urapidil. Risk C: Monitor therapy
White Birch Allergen Extract: Beta-Blockers may enhance the adverse/toxic effect of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid combination
Labetalol serum concentrations may be increased if taken with food. Management: Administer with food.
Medications considered acceptable for the treatment of chronic hypertension during pregnancy may generally be continued in patients trying to conceive. Labetalol is one of the medications patients can transition to if currently taking an agent that is ineffective or should be avoided during pregnancy (ACC/AHA [Whelton 2018]; ACOG 2019; NICE 2019).
Erectile dysfunction and inhibition of sperm motility are noted in product labeling following use of beta-blockers, including labetalol. As a class, outcomes from available studies evaluating beta-blockers and sexual dysfunction are inconsistent, and the negative effects on erectile function are considered controversial. A clear relationship between use of beta-blockers and erectile dysfunction has not been established. Hypertension itself is associated with erectile dysfunction. Patients on a beta-blocker presenting with sexual dysfunction should be evaluated for underlying disease (Farmakis 2021; Levine 2012; Semet 2017; Terentes-Printzios 2022; Viigimaa 2020).
Labetalol crosses the placenta.
Exposure to beta-blockers during pregnancy may increase the risk for adverse events in the neonate. If maternal use of a beta-blocker is needed, monitor fetal growth during pregnancy; monitor the newborn for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).
Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to the duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 2019).
Due to pregnancy-induced physiologic changes, some pharmacokinetic properties of labetalol may be altered (Mulrenin 2021; van de Vusse 2022). Dose adjustments may be required; close monitoring is recommended (Mulrenin 2021; SOGC [Magee 2022]).
Patients with preexisting hypertension may continue their medication during pregnancy unless contraindications exist (ESC [Regitz-Zagrosek 2018]). When treatment for hypertension is initiated during pregnancy, oral labetalol is one of the preferred agents (ACOG 2019; ESC [Cífková 2020]; ESC [Regitz-Zagrosek 2018]; SOGC [Magee 2022]). IV labetalol is recommended for use in the management of hypertensive emergencies in pregnant or postpartum patients (including acute-onset severe hypertension in preeclampsia/eclampsia) (ACOG 2020a; SOGC [Magee 2022]).
Labetalol is present in breast milk.
Data related to the presence of labetalol in breast milk are available following maternal administration of oral labetalol 300 mg twice daily to a woman for preeclampsia. Delivery was at 26 weeks' gestation; breast milk concentrations ~8 days postpartum were 0.71 mcg/mL (Mirpuri 2008). Using a milk concentration of 0.71 mcg/mL, the estimated daily infant dose via breast milk is 0.1065 mg/kg/day providing a relative infant dose (RID) of 3.6% compared to an infant therapeutic dose of 3 mg/kg/day. In general, breastfeeding is considered acceptable when the RID is <10% (Anderson 2016; Ito 2000).
Breast milk concentrations have not been found to correspond to maternal serum concentrations (Lunell 1985; Michael 1979). Peak breast milk concentrations are noted to occur 1 to 3 hours after the maternal dose (Lunell 1985).
Asymptomatic bradycardia was observed in a preterm infant exclusively breastfed following maternal use of labetalol (Mirpuri 2008). Nipple pain and Raynaud phenomenon of the nipple has been associated with labetalol in case reports (Rolfes 2014).
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother. Labetalol is considered compatible for use in patients who are breastfeeding (ACOG 2019; ESC [Cífková 2020]; SOGC [Magee 2022]).
BP (especially with initial dosing and dosing increases), heart rate, continuous cardiac monitoring recommended for IV administration (consult individual institutional policies and procedures); periodic LFTs if clinically indicated; mental alertness; signs and symptoms of bronchospasm in patients with existing bronchospastic disease; serum glucose (in patients with diabetes).
Hypertension, acute in pregnancy (hypertensive emergency/urgency): Once target BP is achieved, monitor every 10 minutes for the first hour, then every 15 minutes for 1 hour, then every 30 minutes for 1 hour, then every hour for 4 hours (ACOG 2020b).
BP goal: May vary depending on clinical conditions, different clinical practice guidelines, and expert opinion. Refer to "Clinical Practice Guidelines" for specific treatment goals.
Blocks alpha1-, beta1-, and beta2-adrenergic receptor sites; elevated renins are reduced. The ratios of alpha- to beta-blockade differ depending on the route of administration estimated to be 1:3 (oral) and 1:7 (IV) (Goa 1989).
Onset of action: Oral: 20 minutes to 2 hours (McNeil 1984); IV: Within 5 minutes (Goa 1989)
Peak effect: Oral: 2 to 4 hours; IV: 5 to 15 minutes (Goa 1989)
Duration: Blood pressure response:
Oral: 8 to 12 hours (dose dependent)
IV: Average: 16 to 18 hours (dose dependent)
Absorption: Complete
Distribution: Apparent Vd: Adults: 2.5 to 15.7 L/kg (Goa 1989)
Protein binding: ~50%
Metabolism: Hepatic, primarily via glucuronide conjugation; extensive first-pass effect
Bioavailability: Oral: 25%; increased with liver disease, elderly, and concurrent cimetidine
Half-life elimination: Oral: 6 to 8 hours; IV: ~5.5 hours
Time to peak, plasma: Oral: 1 to 2 hours
Excretion: Urine (55% to 60% as glucuronide conjugates, <5% as unchanged drug [Goa 1989]); feces (12% to 27% as metabolites) (Goa 1989)
Older adult: Elimination is reduced in elderly patients.
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