Labetalol
- Dosage must be individualized.
- The recommended initial dosage is 100 mg twice daily whether used alone or added to a diuretic regimen. After 2 or 3 days, using standing blood pressure as an indicator, dosage may be titrated in increments of 100 mg b.i.d. every 2 or 3 days. The usual maintenance dosage of labetalol HCl is between 200 and 400 mg twice daily.
- Since the full antihypertensive effect of labetalol HCl is usually seen within the first 1 to 3 hours of the initial dose or dose increment, the assurance of a lack of an exaggerated hypotensive response can be clinically established in the office setting. The antihypertensive effects of continued dosing can be measured at subsequent visits, approximately 12 hours after a dose, to determine whether further titration is necessary.
- Patients with severe hypertension may require from 1,200 to 2,400 mg per day, with or without thiazide diuretics. - Should side effects (principally nausea or dizziness) occur with these doses administered twice daily, the same total daily dose administered three times daily may improve tolerability and facilitate further titration. Titration increments should not exceed 200 mg twice daily.
- When a diuretic is added, an additive antihypertensive effect can be expected. In some cases this may necessitate a labetalol HCl dosage adjustment. As with most antihypertensive drugs, optimal dosages of labetalol hydrochloride tablets are usually lower in patients also receiving a diuretic.
- When transferring patients from other antihypertensive drugs, labetalol hydrochloride tablets should be introduced as recommended and the dosage of the existing therapy progressively decreased.
As in the general patient population, labetalol therapy may be initiated at 100 mg twice daily and titrated upwards in increments of 100 mg b.i.d. as required for control of blood pressure. Since some elderly patients eliminate labetalol more slowly, however, adequate control of blood pressure may be achieved at a lower maintenance dosage compared to the general population. The majority of elderly patients will require between 100 and 200 mg b.i.d.
Labetalol hydrochloride injection is intended for intravenous use in hospitalized patients. Dosage must be individualized depending upon the severity of hypertension and the response of the patient during dosing.
Patients should always be kept in a supine position during the period of intravenous drug administration. A substantial fall in blood pressure on standing should be expected in these patients. The patients ability to tolerate an upright position should be established before permitting any ambulation, such as using toilet facilities.
Either of two methods of administration of labetalol hydrochloride injection may be used:
- Repeated intravenous injections.
- Slow continuous infusion.
Initially, labetalol hydrochloride injection should be given in a dose of 20 mg labetalol HCl (which corresponds to 0.25 mg/kg for an 80 kg patient) by slow intravenous injection over a 2-minute period.
Immediately before the injection and at 5 and 10 minutes after injection, supine blood pressure should be measured to evaluate response. Additional injections of 40 mg or 80 mg can be given at 10 minute intervals until a desired supine blood pressure is achieved or a total of 300 mg labetalol HCl has been injected. The maximum effect usually occurs within 5 minutes of each injection.
Labetalol hydrochloride injection is prepared for continuous intravenous infusion by diluting the contents with commonly used intravenous fluids (see below). Examples of methods of preparing the infusion solution are:
The contents of either two 20 mL vials (40 mL), or one 40 mL vial, are added to 160 mL of a commonly used intravenous fluid such that the resultant 200 mL of solution contains 200 mg of labetalol hydrochloride, 1 mg/mL. The diluted solution should be administered at a rate of 2 mL/min to deliver 2 mg/min.
Alternatively, the contents of either two 20 mL vials (40 mL), or one 40 mL vial, of labetalol hydrochloride injection are added to 250 mL of a commonly used intravenous fluid. The resultant solution will contain 200 mg of labetalol hydrochloride, approximately 2 mg/3 mL. The diluted solution should be administered at a rate of 3 mL/min to deliver approximately 2 mg/min.
The rate of infusion of the diluted solution may be adjusted according to the blood pressure response, at the discretion of the physician. To facilitate a desired rate of infusion, the diluted solution can be infused using a controlled administration mechanism, e.g., graduated burette or mechanically driven infusion pump.
Since the half-life of labetalol is 5 to 8 hours, steady-state blood levels (in the face of a constant rate of infusion) would not be reached during the usual infusion time period. The infusion should be continued until a satisfactory response is obtained and should then be stopped and oral labetalol hydrochloride started. The effective intravenous dose is usually in the range of 50 to 200 mg. A total dose of up to 300 mg may be required in some patients.
Subsequent oral dosing with labetalol hydrochloride tablets should begin when it has been established that the supine diastolic blood pressure has begun to rise. The recommended initial dose is 200 mg, followed in 6 to 12 hours by an additional dose of 200 or 400 mg, depending on the blood pressure response. Thereafter, inpatient titration with labetalol hydrochloride tablets may proceed as follows:
While in the hospital, the dosage of labetalol hydrochloride tablets may be increased at 1 day intervals to achieve the desired blood pressure reduction.
- Developed by: ACC/AHA
- Class of Recommendation: Class IIb
- Strength of Evidence: Level of Evidence C
- Dosing Information/Recommendation
- 200 to 600 mg bid for the treatment of cocaine induced ACS.
- Dosing Information
- 100 mg bid.
- Dosing Information
- Oral: 800 mg/day (hypertension + premature ventricular beats)
- IV: 1 mg/min (sinus rhythm restoration in patients resenting: sinus tachycardia,  paroxysmal SVT, paroxysmal AFib, chronic AFib or VT
- Dosing Information
- 5 mg/mL (treatment of hypertension and arrhythmias).
- Dosing Information
- Initial dose of 10 mg IV over 2 minutes, 10 to 20 mg  doses every 10 minutes to a maximum of 300 mg/day may be administered if required.
- Dosing Information
- 200 mg PO.
- Dosing Information
- 1 to 2 mg/kg IV bolus.
- Dosing Information
- Initial dose of 0.3 mg/kg IV, then 0.05 to 0.07 mg/kg administered every 30 minutes.
- Dosing Information
- Continuous infusion 0.05 to 0.75 mg/kg/hour or 10 to 20 mg IV boluses with 60 to 120 minute intervals.
- Dosing Information
- 75 mg PO q12h.
- Dosing Information
- (Dosage)
- Dosing Information
- (Dosage)
- Overt cardiac failure
- Second degree heart block
- Third degree heart block
- Cardiogenic shock
- Severe bradycardia
- Hypotension
- Hypersensitivity
Beta-blockers, even those with apparent cardioselectivity, should not be used in patients with a history of obstructive airway disease, including asthma.
Severe hepatocellular injury, confirmed by rechallenge in at least one case, occurs rarely with labetalol therapy. 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. Similar hepatic events have been reported with a related compound, dilevalol HCl, including two deaths. Dilevalol HCl is one of the four isomers of labetalol. Thus, for patients taking labetalol, periodic determination of suitable hepatic laboratory tests would be appropriate. Laboratory testing should also be done at the very first symptom or sign of liver dysfunction (e.g., pruritus, dark urine, persistent anorexia, jaundice, right upper quadrant tenderness, or unexplained flu-like symptoms). If the patient has jaundice or laboratory evidence of liver injury, labetalol should be stopped and not restarted.
Sympathetic stimulation is a vital component supporting circulatory function in congestive heart failure. Beta-blockade carries a potential hazard of further depressing myocardial contractility and precipitating more severe failure. Although beta-blockers should be avoided in overt congestive heart failure, if necessary, labetalol can be used with caution in patients with a history of heart failure, who are well compensated. Congestive heart failure has been observed in patients receiving labetalol. Labetalol does not abolish the inotropic action of digitalis on heart muscle.
In patients with latent cardiac insufficiency, continued depression of the myocardium with beta-blocking agents over a period of time can lead, in some cases, to cardiac failure. At the first sign or symptom of impending cardiac failure, patients should be fully digitalized and/or be given a diuretic, and the response observed closely. If cardiac failure continues, despite adequate digitalization and diuretic, labetalol therapy should be withdrawn (gradually if possible).
Angina pectoris has not been reported upon labetalol discontinuation. However, following abrupt cessation of therapy with some beta-blocking agents in patients with coronary artery disease, exacerbations of angina pectoris and, in some cases, myocardial infarction have been reported. Therefore, such patients should be cautioned against interruption of therapy without the physicians advice. Even in the absence of overt angina pectoris, when discontinuation of labetalol is planned, the patient should be carefully observed and should be advised to limit physical activity. If angina markedly worsens or acute coronary insufficiency develops, labetalol administration should be reinstituted promptly, at least temporarily, and other measures appropriate for the management of unstable angina should be taken.
Since labetalol injection at the usual intravenous therapeutic doses has not been studied in patients with nonallergic bronchospastic disease, it should not be used in such patients.
Intravenous labetalol has been shown to be effective in lowering the blood pressure and relieving symptoms in patients with pheochromocytoma; higher than usual doses may be required. However, paradoxical hypertensive responses have been reported in a few patients with this tumor; therefore, use caution when administering labetalol to patients with pheochromocytoma.
Beta-adrenergic blockade may prevent the appearance of premonitory signs and symptoms (e.g., tachycardia) of acute hypoglycemia. This is especially important with labile diabetics. Beta-blockade also reduces the release of insulin in response to hyperglycemia; it may therefore be necessary to adjust the dose of antidiabetic drugs.
Do not routinely withdraw chronic beta-blocker therapy prior to surgery. The effect of labetalols alpha adrenergic activity has not been evaluated in this setting.
Several deaths have occurred when labetalol injection was used during surgery (including when used in cases to control bleeding).
A synergism between labetalol and halothane anesthesia has been shown.
Caution must be observed when reducing severely elevated blood pressure. A number of adverse reactions, including cerebral infarction, optic nerve infarction, angina, and ischemic changes in the electrocardiogram, have been reported with other agents when severely elevated blood pressure was reduced over time courses of several hours to as long as 1 or 2 days. The desired blood pressure lowering should therefore be achieved over as long a period of time as is compatible with the patient's status.
While taking beta-blockers, patients with a history of severe anaphylactic reaction to a variety of allergens may be more reactive to repeated challenge, either accidental, diagnostic, or therapeutic. Such patients may be unresponsive to the usual doses of epinephrineused to treat allergic reaction.
due to one or more adverse effects was required in 7% of all patients. In these same trials, other agents with solely beta-blocking activity used in the control groups led to discontinuation in 8% to 10% of patients, and a centrally acting alpha-agonist led to discontinuation in 30% of patients.
The incidence rates of adverse reactions listed in the following table were derived from multicenter, controlled clinical trials comparing labetalol HCl, placebo, metoprolol, and propranolol over treatment periods of 3 and 4 months. Where the frequency of adverse effects for labetalol HCl and placebo is similar, causal relationship is uncertain. The rates are based on adverse reactions considered probably drug related by the investigator. If all reports are considered, the rates are somewhat higher (e.g., dizziness, 20%; nausea, 14%; fatigue, 11%), but the overall conclusions are unchanged.
The adverse effects were reported spontaneously and are representative of the incidence of adverse effects that may be observed in a properly selected hypertensive patient population, i.e., a group excluding patients with bronchospastic disease, overt congestive heart failure, or other contraindications to beta-blocker therapy.
Clinical trials also included studies utilizing daily doses up to 2,400 mg in more severely hypertensive patients. Certain of the side effects increased with increasing dose, as shown in the following table that depicts the entire U.S. therapeutic trials data base for adverse reactions that are clearly or possibly dose related.
In addition, a number of other less common adverse events have been reported:
- Body as a Whole: Fever.
- Cardiovascular: Hypotension, and rarely, syncope, bradycardia, heart block.
- Central and Peripheral Nervous Systems: Paresthesia, most frequently described as scalp tingling. In most cases, it was mild and transient and usually occurred at the beginning of treatment.
- Collagen Disorders: Systemic lupus erythematosus, positive antinuclear factor.
- Eyes: Dry eyes.
- Immunological System: Antimitochondrial antibodies.
- Liver and Biliary System: Hepatic necrosis, hepatitis, cholestatic jaundice, elevated liver function tests.
- Musculoskeletal System: Muscle cramps, toxic myopathy.
- Respiratory System: Bronchospasm.
- Skin and Appendages: Rashes of various types, such as generalized maculopapular, lichenoid, urticarial, bullous lichen planus, psoriaform, and facial erythema; Peyronie's disease; reversible alopecia.
- Urinary System: Difficulty in micturition, including acute urinary bladder retention.
- Hypersensitivity: Rare reports of hypersensitivity (e.g., rash, urticaria, pruritus, angioedema, dyspnea andanaphylactoidreactions.
- Following approval for marketing in the United Kingdom, a monitored release survey involving approximately 6,900 patients was conducted for further safety and efficacy evaluation of this product. Results of this survey indicate that the type, severity, and incidence of adverse effects were comparable to those cited above.
- Potential Adverse Effects: In addition, other adverse effects not listed above have been reported with other beta-adrenergic blocking agents.
- Central Nervous System: Reversible mental depression progressing to catatonia, an acute reversible syndrome characterized by disorientationfor time and place, short-term memory loss, emotional lability, slightly clouded sensorium, and decreased performance on psychometrics.
- Cardiovascular: Intensification of A-V block (see CONTRAINDICATIONS).
- Allergic: Fever combined with aching and sore throat, laryngospasm, respiratory distress.
- Hematologic: Agranulocytosis, thrombocytopenic or nonthrombocytopenic purpura.
- Gastrointestinal: Mesenteric artery thrombosis, ischemic colitis.
- The oculomucocutaneous syndrome associated with the beta-blocker practolol has not been reported with labetalol HCl.
- Clinical Laboratory Tests: There have been reversible increases of serum transaminases in 4% of patients treated with labetalol HCl and tested and, more rarely, reversible increases in blood urea.
- Beta-Blockers: Drugs possessing beta-blocking properties can blunt the bronchodilator effect of beta-receptor agonist drugs in patients with bronchospasm; therefore, doses greater than the normal antiasthmatic dose of beta-agonist bronchodilator drugs may be required.
- Cimetidine: Has been shown to increase the bioavailability of labetalol HCl. Since this could be explained either by enhanced absorption or by an alteration of hepatic metabolism of labetalol HCl, special care should be used in establishing the dose required for blood pressure control in such patients.
- Halothane: Synergism has been shown between halothane anesthesia and intravenously administered labetalol HCl. During controlled hypotensive anesthesia using labetalol HCl in association with halothane, high concentrations (3% or above) of halothane should not be used because the degree of hypotension will be increased and because of the possibility of a large reduction in cardiac output and an increase in central venous pressure. The anesthesiologist should be informed when a patient is receiving labetalol HCl.
- Nitroglycerin: Labetalol HCl blunts the reflex tachycardia produced by nitroglycerin without preventing its hypotensive effect. If labetalol HCl is used with nitroglycerin in patients with angina pectoris, additional antihypertensive effects may occur.
- Calcium channel blockers: Care should be taken if labetalol is used concomitantly with calcium channel blockers of the verapamil type.
- Digitalis glycosides: Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia.

# Drug & OR Laboratory Test Interactions
The presence of labetalol metabolites in the urine may result in falsely elevated levels of urinary catecholamines, metanephrine, normetanephrine, and vanillylmandelic acid when measured by fluorimetric or photometric methods. In screening patients suspected of having a pheochromocytoma and being treated with labetalol HCl, a specific method, such as a high performance liquid chromatographic assay with solid phase extraction (e.g., J Chromatogr 385:241,1987) should be employed in determining levels of catecholamines.
Labetalol HCl has also been reported to produce a false-positive test for amphetamine when screening urine for the presence of drugs using the commercially available assay methods Toxi-Lab A(thin-layer chromatographic assay) and Emit-d.a.u (radioenzymatic assay). When patients being treated with labetalol have a positive urine test for amphetamine using these techniques, confirmation should be made by using more specific methods, such as a gas chromatographic-mass spectrometer technique.
Teratogenic studies were performed with labetalol in rats and rabbits at oral doses up to approximately six and four times the maximum recommended human dose (MRHD), respectively. No reproducible evidence of fetal malformations was observed. Increased fetal resorptions were seen in both species at doses approximating the MRHD. A teratology study performed with labetalol in rabbits at IV doses up to 1.7 times the MRHD revealed no evidence of drug related harm to the fetus. There are no adequate and well-controlled studies in pregnant women. Labetalol should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Hypotension, bradycardia, hypoglycemia, and respiratory depression have been reported in infants of mothers who were treated with labetalol HCl for hypertension during pregnancy. Oral administration of labetalol to rats during late gestation through weaning at doses of two to four times the MRHD caused a decrease in neonatal survival.
The blood pressure should be monitored during and after completion of the infusion or intravenous injections. Rapid or excessive falls in either systolic blood pressure or diastolic blood pressure during intravenous treatment should be avoided. In patients with excessive systolic hypertension, the decrease in systolic pressure should be used as indicator of effectiveness in addition to the response of the diastolic pressure.
- Ringer's Injection, USP
- Lactated Ringer's Injection, USP
- 5% Dextrose and Ringer's Injection
- 5% Lactated Ringer's and 5% Dextrose Injection
- 5% Dextrose Injection, USP
- 0.9% Sodium Chloride Injection, USP
- 5% Dextrose and 0.2% Sodium Chloride Injection, USP
- 2.5% Dextrose and 0.45% Sodium Chloride Injection, USP
- 5% Dextrose and 0.9% Sodium Chloride Injection, USP
- 5% Dextrose and 0.33% Sodium Chloride Injection, USP.
- Labetalol hydrochloride injection was NOT compatible with 5% sodium bicarbonate injection, USP.
Care should be taken when administering alkaline drugs, including furosemide, in combination with labetalol. Compatibility should be assured prior to administering these drugs together.
- Excessive ]administer atropine or epinephrine.
- Cardiac failureadminister a digitalis glycoside and a diuretic.
- Dopamine or dobutamine may also be useful.hypotensionadminister vasopressors, e.g., norepinephrine. There is pharmacologic evidence that norepinephrine may be the drug of choice.
- Bronchospasmadminister epinephrine and/or an aerosolized beta2-agonist.
- Seizuresadminister diazepam.
In severe beta-blocker overdose resulting in hypotension and/or bradycardia, glucagon has been shown to be effective when administered in large doses (5 to 10 mg rapidly over 30 seconds, followed by continuous infusion of 5 mg per hour that can be reduced as the patient improves).
Neither hemodialysis nor peritoneal dialysis removes a significant amount of labetalol HCl from the general circulation (<1%).
The oral LD50 value of labetalol HCl in the mouse is approximately 600 mg/kg and in the rat is >2 g/kg. The IV LD50 in these species is 50 to 60 mg/kg.
Labetalol hydrochloride (HCl) is a racemate chemically designated as 2-hydroxy-5- ethyl] benzamide monohydrochloride, and it has the following structure:
Labetalol HCl has the molecular formula C19H24N2O3HCl and a molecular weight of 364.9. It has two asymmetric centers and therefore exists as a molecular complex of two diastereoisomeric pairs. Dilevalol, the R, R stereoisomer, makes up 25% of racemic labetalol.
Labetalol HCl is a white or off-white crystalline powder, soluble in water.
Labetalol hydrochloride tablets contain 100, 200, or 300 mg of labetalol HCl and are taken orally. The tablets also contain the inactive ingredients lactose monohydrate, corn starch, crospovidone, colloidal silicon dioxide, magnesium stearate, polyvinyl alcohol, polyethylene glycol, titanium dioxide and talc.
Single oral doses of Labetalol  administered to patients with coronary artery disease had no significant effect on sinus rate, intraventricular conduction, or QRS duration. The atrioventricular (A-V) conduction time was modestly prolonged in two of seven patients. In another study, IV Labetalol  slightly prolonged A-V nodal conduction time and atrial effective refractory period with only small changes in heart rate. The effects on A-V nodal refractoriness were inconsistent.
Labetalol  produces dose-related falls in blood pressure without reflex tachycardia and without significant reduction in heart rate, presumably through a mixture of its alpha- and beta-blocking effects. Hemodynamic effects are variable, with small, nonsignificant changes in cardiac output seen in some studies but not others, and small decreases in total peripheral resistance. Elevated plasma renins are reduced.
Doses of Labetalol  that controlled hypertension did not affect renal function in mildly to severely hypertensive patients with normal renal function.
Due to the alpha1-receptor blocking activity of Labetalol , blood pressure is lowered more in the standing than in the supine position, and symptoms of postural hypotension (2%), including rare instances of syncope, can occur. Following oral administration, when postural hypotension has occurred, it has been transient and is uncommon when the recommended starting dose and titration increments are closely followed. Symptomatic postural hypotension is most likely to occur 2 to 4 hours after a dose, especially following the use of large initial doses or upon large changes in dose.
The peak effects of single oral doses of Labetalol  occur within 2 to 4 hours. The duration of effect depends upon dose, lasting at least 8 hours following single oral doses of 100 mg and more than 12 hours following single oral doses of 300 mg. The maximum, steady-state blood pressure response upon oral, twice-a-day dosing occurs within 24 to 72 hours.
The antihypertensive effect of labetalol has a linear correlation with the logarithm of labetalol plasma concentration, and there is also a linear correlation between the reduction in exercise-induced tachycardia occurring at 2 hours after oral administration of Labetalol  and the logarithm of the plasma concentration.
About 70% of the maximum beta-blocking effect is present for 5 hours after the administration of a single oral dose of 400 mg with suggestion that about 40% remains at 8 hours.
The antianginal efficacy of Labetalol  has not been studied. In 37 patients with hypertension and coronary artery disease, Labetalol  did not increase the incidence or severity of angina attacks.
Exacerbation of angina and, in some cases, myocardial infarction and ventricular dysrhythmias have been reported after abrupt discontinuation of therapy with beta-adrenergic blocking agents in patients with coronary artery disease. Abrupt withdrawal of these agents in patients without coronary artery disease has resulted in transient symptoms, including tremulousness, sweating, palpitation, headache, and malaise. Several mechanisms have been proposed to explain these phenomena, among them increased sensitivity to catecholamines because of increased numbers of beta receptors.
Although beta-adrenergic receptor blockade is useful in the treatment of angina and hypertension, there are also situations in which sympathetic stimulation is vital. For example, in patients with severely damaged hearts, adequate ventricular function may depend on sympathetic drive. Beta-adrenergic blockade may worsen A-V block by preventing the necessary facilitating effects of sympathetic activity on conduction. Beta2-adrenergic blockade results in passive bronchial constriction by interfering with endogenous adrenergic bronchodilator activity in patients subject to bronchospasm, and it may also interfere with exogenous bronchodilators in such patients.
The plasma half-life of labetalol following oral administration is about 6 to 8 hours. Steady-state plasma levels of labetalol during repetitive dosing are reached by about the third day of dosing. In patients with decreased hepatic or renal function, the elimination half-life of labetalol is not altered; however, the relative bioavailability in hepatically impaired patients is increased due to decreased "first-pass" metabolism.
The metabolism of labetalol is mainly through conjugation to glucuronide metabolites. These metabolites are present in plasma and are excreted in the urine and, via the bile, into the feces. Approximately 55% to 60% of a dose appears in the urine as conjugates or unchanged labetalol within the first 24 hours of dosing.
Labetalol has been shown to cross the placental barrier in humans. Only negligible amounts of the drug crossed the blood-brain barrier in animal studies. Labetalol is approximately 50% protein bound. Neither hemodialysis nor peritoneal dialysis removes a significant amount of Labetalol  from the general circulation (<1%).
Some pharmacokinetic studies indicate that the elimination of labetalol is reduced in elderly patients. Therefore, although elderly patients may initiate therapy at the currently recommended dosage of 100 mg b.i.d., elderly patients will generally require lower maintenance dosages than nonelderly patients.
- Labetalol hydrochloride tablets, USP 100 mg, white, round, film-coated tablets with bisect, debossed N on top and T on bottom of the bisect on one side and "041" on the other side of the tablet, bottles of 100 (NDC 49884-122-01), 500 (NDC 49884-122-05) and 1000(NDC 49884-122-10).
- Labetalol hydrochloride tablets, USP 200 mg, white, round, film-coated tablets with bisect, debossed N on top and T on bottom of the bisect on one side and "042" on the other side of the tablet, bottles of 100 (NDC 49884-123-01), 500 (NDC 49884-123-05), and 1000(NDC 49884-123-10).
- Labetalol hydrochloride tablets, USP 300 mg, white, round, film-coated tablets with bisect, debossed N on top and T on bottom of the bisect on one side and "043" on the other side of the tablet, bottles of 100 (NDC 49884-124-01), 500 (NDC 49884-124-05), and 1000(NDC 49884-124-10).
NDC	Labetalol Hydrochloride Injection, USP (5 mg per mL):
- 100 mg per 20 mL Multi-Dose Vial (25021-300-20)
- 200 mg per 40 mL Multi-Dose Vial (25021-300-40)
- Labetalol hydrochloride tablets, USP should be stored at 20 to 25C (68 to 77F).
- Store at 20 to 25C (68 to 77F).
- Do not freeze.
- Protect from light. Retain in carton until time of use.
- Trandate
-  Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE;  et al. (2007). "ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction): developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons: endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". Circulation. 116 (7): e148304. doi:10.1161/CIRCULATIONAHA.107.181940. PMID 17679616.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link) .mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
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-  Stoudemire A, Knos G, Gladson M, Markwalter H, Sung YF, Morris R;  et al. (1990). "Labetalol in the control of cardiovascular responses to electroconvulsive therapy in high-risk depressed medical patients". J Clin Psychiatry. 51 (12): 50812. PMID 2258364.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
-  Orlowski JP, Vidt DG, Walker S, Haluska JF (1989). "The hemodynamic effects of intravenous labetalol for postoperative hypertension". Cleve Clin J Med. 56 (1): 2934. PMID 2731325.CS1 maint: Multiple names: authors list (link)
-  Davies AB, Bala Subramanian V, Gould B, Raftery EB (1982). "Rapid reduction of blood pressure with acute oral labetalol". Br J Clin Pharmacol. 13 (5): 70510. PMC 1402081. PMID 7082539.CS1 maint: Multiple names: authors list (link) CS1 maint: PMC format (link)
-  Smith WB, Clifton GG, O'Neill WM, Wallin JD (1983). "Antihypertensive effectiveness of intravenous labetalol in accelerated hypertension". Hypertension. 5 (4): 57983. PMID 6862581.CS1 maint: Multiple names: authors list (link)
-  Saarnivaara L, Klemola UM, Lindgren L (1987). "Labetalol as a hypotensive agent for middle ear microsurgery". Acta Anaesthesiol Scand. 31 (3): 196201. PMID 3577641.CS1 maint: Multiple names: authors list (link)
-  Orlowski JP, Shiesley D, Vidt DG, Barnett GH, Little JR (1988). "Labetalol to control blood pressure after cerebrovascular surgery". Crit Care Med. 16 (8): 7658. PMID 3396371.CS1 maint: Multiple names: authors list (link)
-  Grubb BP (1991). "The use of oral labetalol in the treatment of arrhythmias associated with the long QT syndrome". Chest. 100 (6): 17245. PMID 1959422.