Beta Blocker Poisoning

18/5/2021 Beta blocker poisoning - UpToDate
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Beta blocker poisoning

Author: Fermin Barrueto, Jr, MD, FACEP, FAAEM, FACMT
Section Editor: Stephen J Traub, MD
Deputy Editor: Jonathan Grayzel, MD, FAAEM
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2021. | This topic last updated: Nov 04, 2020.
INTRODUCTION
Beta adrenergic antagonists (beta blockers) have been in clinical use for more than 30 years, and are
employed in the management of a range of disorders, including hypertension, ischemic heart disease,
heart failure, arrhythmias, migraine headache, tremor, portal hypertension, and aortic dissection.
Although safe for most patients when taken as prescribed, beta blocker toxicity is associated with
significant morbidity and mortality [1]. A 10-year review (2006 to 2015) of "double-dose" ingestions from
the California Poison Control System revealed that antihypertensives like beta-blockers and calcium
channel blockers caused moderate to severe effects in 37 percent of cases. For comparison, the second
drug class with moderate to severe effects were stimulants at 17 percent [2].
Complications following beta blocker overdose are related to excessive beta adrenergic blockade, and
occasionally the proarrhythmic (membrane-stabilizing) activity of these agents on cardiac conduction [3].
Ingestion of other cardioactive agents in association with beta blockers increases mortality following
overdose [3,4]. Common and potentially dangerous coingestions include calcium channel blockers, cyclic
antidepressants, and neuroleptics [3].
An overview of beta blocker intoxication will be presented here. A summary table to facilitate emergency
management is provided ( table 1). A general approach to an adult patient with possible drug
intoxication, and an overview of adverse effects of beta blockade, are discussed separately. (See "General
approach to drug poisoning in adults" and "Major side effects of beta blockers".)
PHARMACOLOGY
Receptor types and general mechanism — There are at least three distinct types of beta receptors:
● Beta 1, which are found primarily in heart muscle. Activation of these receptors results in an increase
in heart rate, contractility, atrioventricular (AV) conduction, and a decrease in AV node refractoriness.
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● Beta 2, which are present in heart muscle but are more prominent in bronchial and peripheral
vascular smooth muscle. Activation of these receptors results in vasodilation and bronchodilation.
● Beta 3, which are found in adipose tissue and the heart. Activation of these receptors may mediate
catecholamine-induced thermogenesis and may reduce cardiac contractility.
Competitive antagonism of the beta receptor decreases cellular levels of cyclic adenosine
monophosphate (cAMP). Beta-1 selective blockade results in depressed myocardial contractility,
decreased automaticity in pacemaker cells, and decreased conduction velocity through the
atrioventricular node [4]. The lungs, peripheral blood vessels, glucose metabolism, and central nervous
system are all affected by beta blockade. Nonselective beta blockade results in systemic effects including
bronchoconstriction, impaired gluconeogenesis, and decreased insulin release. (See "Major side effects
of beta blockers".)
CELLULAR TOXICOLOGY
There are many beta blockers available for clinical use, and although they all inhibit the beta-
adrenoreceptor, there are several characteristics that differ among these agents. Following overdose,
manifestations of toxicity are observed in varying degrees, depending on the specific agent and dose
involved [4,5]. In addition to beta-adrenoreceptor blockade, three properties that affect toxicity include
the membrane stabilizing activity (MSA), lipophilicity, and intrinsic sympathomimetic activity (ISA) of the
ingested agent ( table 2).
● Membrane stabilizing activity (MSA) – Membrane stabilizing agents (eg, propranolol, acebutolol)
inhibit myocardial fast sodium channels, which can result in a widened QRS interval and may
potentiate other dysrhythmias.
● Lipophilicity – Beta blockers with high lipid solubility (eg, propranolol) rapidly cross the blood brain
barrier into the central nervous system, predisposing to neurologic sequelae such as seizures and
delirium. Beta Blockers with this characteristic are more amenable to treatment with 20 percent lipid
emulsion therapy in the setting of a clinically significant overdose [6].
● Intrinsic sympathomimetic activity (ISA) – Many agents demonstrate a partial agonist effect at the
beta receptor site, resulting in less bradycardia and hypotension in therapeutic and supratherapeutic
doses. Bronchoconstriction is also less likely to occur with compounds that possess intrinsic
sympathomimetic activity (ISA), or beta-1 selectivity. However, the protective effects of ISA do not
completely prevent cardiovascular toxicity following intentional or accidental overdose.
TOXICITY OF SPECIFIC AGENTS
Of all the variables contributing to toxicity, membrane stabilizing activity (MSA) appears to have the
greatest influence on adverse cardiovascular effects ( table 2). Agents with significant MSA include

propranolol, acebutolol, betaxolol, and oxprenolol. The effect of MSA is thought to be negligible at
therapeutic doses, but in overdose can cause significant cardiovascular morbidity. In one retrospective
study, 94 percent (15 out of 16) of patients with cardiovascular toxicity had a history of ingesting beta
blockers with MSA [3].
Acebutolol, a cardioselective agent with partial agonist activity and significant MSA, is one of the most
toxic beta blockers in overdose [7]. Acebutolol toxicity may predispose the patient to ventricular
repolarization resulting in arrhythmias [7].
Sotalol combines class III antidysrhythmic properties with beta adrenergic antagonism. Sotalol prolongs
the action potential duration and increases the refractory period by blocking delayed potassium
channels. This leads to prolongation of the QTc interval, and can contribute to the development of
Torsades de Pointes [8]. (See "Clinical uses of sotalol" and "Acquired long QT syndrome: Definitions,
causes, and pathophysiology", section on 'Medications'.)
Carvedilol has been associated with toxic epidermal necrolysis at therapeutic levels [9].
PHARMACOKINETICS
In therapeutic use, most beta blockers have half-lives ranging from two to eight hours, but kinetics can
change in overdose ( table 2). Ingestion of sustained release preparations can delay the onset of
symptoms and substantially prolong the duration of toxicity.
Many beta blockers are metabolized via the liver. Esmolol is metabolized by erythrocyte esterases.
Atenolol, bisoprolol, labetalol, and sotalol are eliminated by the kidney.
CLINICAL FEATURES OF OVERDOSE
Diagnosis of beta blocker intoxication is made on the basis of history and clinical presentation.
History — Data obtained should include the specific agent, amount ingested, time of ingestion, and any
coingestions. Historical features that suggest increased risk for severe toxicity include:
● Coingestion of other cardioactive agents

● Underlying cardiac disease (eg, heart failure)
● Ingestion of sotalol or another agent with membrane-stabilizing activity (eg, propranolol or
acebutolol) (see 'Toxicity of specific agents' above)
Any possible witnesses and emergency medical services (EMS) personnel who may have recovered pill
bottles at the scene should be contacted. The patient's pharmacy may provide valuable information
regarding prescribed medications, the date of the most recent refill, and the total number of pills
dispensed.

Physical findings — Most patients who overdose on beta blockers become symptomatic within two
hours following ingestion, and nearly all develop symptoms within six hours [3,10]. Exceptions to this
general rule include ingestions of sustained release medications and sotalol [11]. In these cases, delayed
toxicity up to 24 hours after ingestion can occur.
Bradycardia and hypotension are the most common effects, and in severe overdoses can result in
profound myocardial depression and cardiogenic shock. Ventricular dysrhythmias are seen more
frequently following propranolol and acebutolol exposures, probably because of the increased
membrane-stabilizing activity (MSA) of these agents ( table 2) [3,12]. Other potential effects of severe
toxicity include mental status change, seizure, hypoglycemia, and bronchospasm.
Mental status changes, including delirium, coma, and seizures, occur most frequently in patients with
severe hypotension, but can occur in those with normal blood pressure [13]. Similarly, respiratory
depression usually occurs in hypotensive, comatose patients, but has been reported in awake patients.
Specific agents, particularly propranolol, are associated with neurologic effects in the absence of cerebral
hypoperfusion. This was demonstrated in a report comparing the clinical course of patients following
overdose with either propranolol or other beta blockers [10]. Although the minimum pulse and systolic
and diastolic ranges were not significantly different between groups, 29 percent of the propranolol group
experienced seizures versus none in the non-propranolol group. This difference is probably due to the
increased lipophilicity of propranolol, allowing rapid diffusion into the central nervous system.
In addition to the cardiovascular and neurologic manifestations, bronchospasm and hypoglycemia can
complicate acute beta blocker intoxication. Early recognition and prompt treatment of hypoglycemia is
critical. (See 'Management' below.)
LABORATORY EVALUATION
Laboratory studies — Although serum concentrations of most beta blockers can be measured, they
cannot be obtained in time to be clinically useful and are generally performed only for academic or
forensic purposes.
In patients with beta blocker overdose, we generally obtain the following studies: an electrocardiogram
(ECG), a fingerstick glucose, serum electrolytes including calcium, and blood urea nitrogen and creatinine
levels. If calcium is administered repeatedly, levels should be measured every four to six hours. If an
insulin/glucose treatment regimen is used, glucose and potassium levels must be measured every 30 to
60 minutes. (See 'Insulin and glucose' below and 'Calcium' below.)
Routine laboratory evaluation of any poisoned patient should include acetaminophen and salicylate
levels, to rule out these common coingestions, and a pregnancy test in women of childbearing age.
A serum lactate concentration above 3 mmol/L is used to predict life-threatening overdose of some
medications. However, this may be an insensitive finding with beta blocker overdose. In one

retrospective study, four of nine deaths associated with beta blocker poisoning were associated with
serum lactate concentrations below 3 mmol/L [14].
Additional tests are obtained based upon clinical findings. As an example, a plain chest radiograph is
obtained in patients with signs of pulmonary edema.
Electrocardiogram — Beta blockers decrease conduction velocity across the atrioventricular (AV) node,
resulting in PR prolongation ( waveform 1) and possibly AV block ( waveform 2); they also slow
automaticity within the sinoatrial (SA) node, causing bradycardia ( waveform 3) [15].
QRS prolongation occurs more commonly when beta blockers with membrane stabilizing activity (MSA)
are ingested. Significant QTc prolongation can develop following sotalol overdose as a result of its
independent Class III antiarrhythmic activity. In severe poisoning, the electrocardiogram (ECG) can show
ANY bradydysrhythmia, and can progress to asystole. (See "Advanced cardiac life support (ACLS) in
adults", section on 'Asystole and pulseless electrical activity'.)
A Brugada-like ECG pattern ( waveform 4) has been reported in the setting of propranolol poisoning,
suggesting that other beta blockers that are lipophilic or possess membrane stabilizing activity might
have similar effects [16].
DIAGNOSIS
The diagnosis of beta blocker poisoning is made clinically on the basis of the history and clinical
presentation. Typically there is a history of overdose combined with findings of bradycardia and
hypotension, which can be profound in severe overdose, resulting in cardiogenic shock. Other findings
can include ventricular dysrhythmia, altered mental status, seizure, hypoglycemia, and bronchospasm.
Although serum concentrations of most beta blockers can be measured, such measurements cannot be
obtained in time to be clinically useful.
DIFFERENTIAL DIAGNOSIS
Many drugs can cause profound hypotension or bradydysrhythmia in overdose. Calcium channel
blockers, digoxin, clonidine, and cholinergic agents must be considered when evaluating
bradydysrhythmia potentially caused by a toxic ingestion.
● Calcium channel blocker poisoning ‒ Calcium channel blockers are less likely than beta blockers to
produce alterations in mental status, and frequently do not do so unless the patient is in profound
shock. Hyperglycemia occurs more often with calcium channel blocker toxicity, while beta blockers
are associated with hypoglycemia. (See "Calcium channel blocker poisoning".)
● Digoxin poisoning ‒ Nausea and vomiting occur more often with digoxin toxicity than beta blocker
toxicity. Digoxin may cause characteristic changes in an electrocardiogram, such as scooped ST

segment depressions ( waveform 5). Digoxin is more likely to produce rhythms of increased
automaticity, such as atrial tachycardia with atrioventricular block, premature ventricular
contractions, or ventricular arrhythmias. (See "Digitalis (cardiac glycoside) poisoning".)
● Clonidine poisoning ‒ Clonidine produces a constellation of signs that can resemble opioid
overdose, including somnolence and miosis, but are accompanied by hypotension and bradycardia.
● Cholinergic drug poisoning ‒ Overdose of a cholinergic agent can present with bradycardia but
also includes other characteristic features (salivation, lacrimation, urination, defecation, GI upset,
and muscle excitability).
MANAGEMENT
Acute stabilization and overview of therapy
Airway, breathing, circulation — Management begins with assessment of the patient’s airway,

breathing, and circulation. The airway is secured as necessary and adequate oxygenation ensure.
Advanced cardiac life support is provided as necessary. A table summarizing emergency interventions is
provided ( table 1). Atropine should be given early in bradycardic patients and whenever possible as a
pretreatment agent when rapid sequence intubation is required [17]. Intravenous access should be
obtained and continuous cardiac monitoring performed. (See "Rapid sequence intubation for adults
outside the operating room" and "Advanced cardiac life support (ACLS) in adults".)
Hypotension is treated initially with intravenous (IV) boluses of isotonic fluid; symptomatic bradycardia is
treated with atropine. Atropine is given in a dose of 0.5 to 1 mg every three to five minutes up to a total
of 0.03 to 0.04 mg/kg. Sodium bicarbonate and magnesium may be needed to treat QRS prolongation
and ventricular arrhythmia (torsade de pointe), respectively. (See 'Other therapies' below.)
Hypoglycemia and seizures — Symptomatic hypoglycemia is treated with IV dextrose. For adults,

administer boluses of 50 percent dextrose in water (D50W); for children administer an appropriate IV
bolus of dextrose (0.25 g/kg body weight). In infants and young children this is usually given as 2.5 mL/kg
of 10 percent dextrose solution. Multiple doses of dextrose may be necessary. Treatment of
hypoglycemia in children is discussed in detail separately. (See "Diagnostic approach to hypoglycemia in
infants and children".)
Treat seizures with benzodiazepines (eg, lorazepam). (See "Convulsive status epilepticus in adults:
Classification, clinical features, and diagnosis".)
Additional treatments — IV fluid and atropine often do not completely reverse the cardiotoxic effects
of beta blocker overdose. In such cases, additional treatments are given based upon the severity of the
presentation. These treatments may include:
● IV glucagon

● IV calcium salts
● Vasopressor
● High dose insulin and glucose infusions
● Lipid emulsion therapy
These therapeutic options are discussed below. (See 'Approach to the selection of specific therapies'
below.)
Hemodialysis may be needed in specific circumstances (eg, severely ill patient with ingestion of
medication amenable to hemodialysis and not responding to medical therapy), although this is
uncommon. In such cases a nephrologist should be contacted early in the patient’s course. (See 'Other
therapies' below.)
Many patients with isolated beta blocker overdose remain asymptomatic and can be discharged after a
period of observation. (See 'Disposition' below.)
Approach to the selection of specific therapies — Although it is ideal to institute treatments

individually to assess their success or failure, this is often not possible in patients who are severely ill
from a beta blocker poisoning. Our suggested approaches to therapy based upon the severity of the
clinical presentation are described here; a summary table to facilitate emergency management is
provided ( table 1).
Severely symptomatic patients — Our suggested approach to patients manifesting signs of severe

beta blocker poisoning (profound hypotension and/or severe bradycardia, depressed mental status)
consists of multiple simultaneous interventions, including all of the following treatments [18-20]:
● Stabilization of the airway as necessary (avoid induction agents that exacerbate hypotension)
● Additional IV boluses of isotonic crystalloid
● IV glucagon
● IV vasopressor (eg, epinephrine)
● IV high-dose insulin and glucose
● IV lipid emulsion therapy
Vasopressor therapy is typically administered via a central venous catheter. Although high-dose insulin
and glucose may be administered peripherally, they would likely be given through the central venous
catheter if one is placed. Dosing for each of these therapies is provided below. (See 'Specific therapies'
below.)
Mildly symptomatic patients — Our suggested approach to patients with mild hypotension or

bradycardia begins with IV boluses of isotonic crystalloid and atropine respectively. However, these
therapies often do not completely reverse the cardiotoxic effects of beta blocker poisoning. In such
cases, we add the following treatments in succession based upon patient response [20]. As an example,
we begin treatment with glucagon if IV crystalloid does not adequately improve the patient’s blood
pressure, but if hypotension resolves following treatment with glucagon, we do not proceed to IV
calcium salts or any other treatment specifically for the overdose.
● IV glucagon
● IV vasopressor (eg, epinephrine)
● IV high-dose insulin and glucose
● IV lipid emulsion therapy
A period of 15 minutes is reasonable to determine the effectiveness of a specific therapy before

proceeding to the next treatment. Dosing for each of these therapies is provided below and in the
following table ( table 1). (See 'Specific therapies' below.)
Asymptomatic patients — Many patients with an isolated beta blocker overdose remain

asymptomatic and may be discharged after a period of observation, unless the overdose was intentional,
involved a sustained release formulation, or there are additional clinical concerns. (See 'Disposition'
below.)
Specific therapies — Evidence supporting specific treatment interventions for beta blocker overdose is
largely limited to observational studies of limited quality. A systematic review of this evidence concluded
that catecholamines, high-dose insulin, and venoarterial extracorporeal membrane oxygenation were
associated with reduced mortality but noted that multiple treatments were often given simultaneously,
limiting the capacity to draw clear conclusions [20].
Glucagon — Despite limited data, glucagon is administered for beta blocker overdose [21,22].
Glucagon may be effective initially for a brief period, but prolonged treatment may become ineffective
due to tachyphylaxis. Intravenous (IV) glucagon is given as a slow bolus dose followed by continuous
infusion. An initial bolus of 5 mg intravenously is administered over one minute; if there is no increase in
pulse or blood pressure after 10 to 15 minutes, a second bolus should be administered. The initial
pediatric dose is 50 mcg/kg. An effect should be observed within one to three minutes, with a peak
response at five to seven minutes. If there is no observed effect after 10 minutes following a second
dose, it is unlikely an infusion will provide benefit.
If there is an increase in pulse or blood pressure, an infusion is started at a rate of 2 to 5 mg/hour

(pediatric dose 70 mcg/kg/hour). The goal is to maintain a mean arterial pressure of 60 mmHg. If this
cannot be achieved, additional therapies are implemented in a sequential manner, beginning with
calcium salts. When used as a sole agent in humans, glucagon has been associated with treatment
failures.
Vomiting is common following administration of glucagon. We suggest prophylactic or concurrent

administration of a serotonin antagonist antiemetic (eg, ondansetron). (See "Characteristics of antiemetic
drugs".)

Glucagon activates adenylate cyclase at a site independent from beta-adrenergic agents, causing an
increase in adenosine 3'-5'-cyclic monophosphate (cAMP). Elevations in cAMP increase the intracellular
pool of calcium available for release during depolarization, augmenting contractility. The successful use
of glucagon to manage beta blocker toxicity has been documented in many case reports, but no
controlled trials involving humans have been conducted [23]. One review of the available controlled trials
in animal models found that glucagon increased heart rate (HR), at least transiently, but had minimal
effect on mean arterial pressure (MAP) [21].
In 2006, a trial comparing vasopressin with glucagon in a swine model of propranolol overdose found no
difference in survival at four hours [24]. No difference was detected in HR, MAP, systolic BP, or cardiac
output, except in the first hour, when vasopressin caused a marked increase in MAP and systolic BP.
Notably, cardiac output did not improve following glucagon administration.
Calcium — A number of case reports demonstrate the efficacy of IV calcium salts in treating beta
blocker toxicity [23,24]. Either calcium chloride or calcium gluconate may be given.
Calcium chloride, 1 g of a 10 percent solution (10 mL), is given as a slow push, and should be
administered via a central venous catheter. The dose may be repeated up to a total of 3 g. The pediatric
dose is 20 mg/kg (maximum dose is 1 g); up to 60 mg/kg may be given.
Calcium gluconate should be given if only peripheral IV access is available. The percentage of elemental
calcium in calcium gluconate is one-third that of the calcium chloride salt, so 30 mL of a 10 percent
solution should be administered as an initial dose. In children, give 60 mg/kg per dose (maximum dose is
3 g).
Clinicians must monitor serum calcium concentrations if treatment with an IV calcium salt is given. Lethal
iatrogenic overdose has been reported [25].
IV calcium salts may improve hemodynamic parameters by increasing inotropy. Animal models suggest
that calcium salts increase blood pressure and cardiac output, but do not increase heart rate, following
combined calcium channel blocker and beta blocker overdose [26].
Vasopressor (catecholamine) — In animal models and human case reports, treatment of beta
blocker overdose with catecholamine infusion alone has resulted in poor outcomes [25-27].
Catecholamine infusions may be added if the combination of atropine, IV fluids, glucagon, and IV calcium
salts are unsuccessful in improving cardiovascular performance, or as a temporizing measure until high
dose insulin therapy starts to take effect. The vasopressor can then be titrated downward as tolerated.
(See "Use of vasopressors and inotropes".)
An infusion of epinephrine at 1 mcg/minute can be started and titrated upwards to maintain a MAP of 60
mmHg. Pediatric dosing starts at 0.1 mcg/kg/minute and is titrated upwards based upon the patient's
MAP. High infusion rates may be necessary to overcome competitive inhibition. An arterial line may be
needed to monitor blood pressure.

Catecholamines exert positive inotropic and chronotropic activity on the myocardium by stimulating
adrenergic receptors and increasing the concentration of cAMP. One possible explanation for the lack of
effectiveness of catecholamines in beta blocker overdose is that high doses are often required to achieve
a therapeutic effect, and such doses may increase the risk of arrhythmia. In addition, some speculate
that unopposed alpha constriction increases the cardiac workload, diminishing stroke volume and
cardiac output.
Insulin and glucose — High-dose insulin is being used with greater frequency to treat beta-blocker
overdose [28,29]. In patients who manifest hemodynamic instability refractory to the other therapies
described above, we suggest that a trial of high-dose insulin and glucose be administered, possibly in
combination with other agents depending on the clinical scenario, and titrated upward until blood
pressure stabilizes. (See 'Approach to the selection of specific therapies' above.)
The dosing regimen for high-dose insulin is described in detail separately and provided in the following
table ( table 1). (See "Calcium channel blocker poisoning", section on 'Insulin and glucose'.)
Of note, hypoglycemia is a possible complication of this treatment, as the dose of insulin is much higher
(approximately 10-fold) than that typically given for diabetic ketoacidosis. When necessary, euglycemia
can be maintained by means of a continuous IV infusion of 5 to 10 percent dextrose (a higher
concentration can be used if necessary to reduce fluid load). A hemodynamic response to high-dose
insulin therapy is delayed for 30 to 60 minutes, therefore simultaneous implementation of other
therapies to support the patient's pulse and blood pressure are generally required. Repletion of
potassium and magnesium may be needed. Serum glucose, serum potassium, and fluid intake and
output should all be closely monitored for the duration of treatment with high-dose insulin. We suggest
measuring glucose (eg, fingerstick) every 15 to 30 minutes while titrating the insulin infusion rate, and
approximately every one to two hours once a steady rate is determined and glucose measurements are
stable.
Animal studies and case reports of both isolated beta blocker overdose and combined calcium channel
blocker and beta blocker overdose suggest that treatment with high dose insulin and glucose is effective
[30-32]. However, the role for this therapy in pure beta blocker overdose remains unsettled, despite an
increasing number of case reports describing successful treatment of patients with severe beta-blocker
and mixed beta-blocker overdoses [33]. Often, such cases involve patients treated with multiple therapies
(eg, calcium, atropine, glucagon, vasopressors) before treatment with high dose insulin, making it
difficult to determine which therapy was most effective. High dose insulin has been well tolerated in
patients, and has been administered for prolonged periods, up to 116 hours in one case [33].
One animal study of insulin therapy in propranolol toxicity was terminated early when every pig in the
insulin and glucose treatment group achieved the study goal of four hour survival, while those treated
with vasopressin and epinephrine died within 90 minutes [25]. Cardiac output (CO) in animals treated
with insulin and glucose increased steadily and consistently, while CO in animals treated with vasopressin
and epinephrine decreased until death.
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It appears that insulin exhibits a steady dose response curve, and may be titrated upwards until blood
pressure improves. One study using a pig model of propranolol overdose, compared treatments with
placebo and insulin at doses of 1 unit/kg per hour, 5 units/kg per hour, and 10 units/kg per hour [34]. For
each one unit/kg per hour increase of insulin, there was a statistically significant increase in cardiac
output, and no ceiling effect was noted.
The pathophysiology of beta blocker intoxication is similar in many respects to that of calcium channel
blocker (CCB) intoxication, for which high dose insulin and glucose therapy has been more extensively
studied. Although the mechanism is not completely understood, both CCB and beta blocker poisoning
appear to interfere with myocyte metabolism. In addition, beta blockers inhibit pancreatic insulin release
further reducing available glucose and diminishing CO. Insulin appears to improve inotropy by providing
substrate for aerobic metabolism within the myocyte. (See "Calcium channel blocker poisoning", section
on 'Pathophysiology'.)
Lipid emulsion therapy — Lipid emulsions are the fats used in total parenteral nutrition (TPN).
Initially used to treat overdoses of local anesthetics such as bupivacaine, intravenous lipid emulsion (ILE)
has been used to treat poisonings involving a number of other lipophilic medications. A more complete
discussion of ILE, including suggested dosing, is found separately; we suggest consultation with a
medical toxicologist or poison control center to determine whether ILE therapy is appropriate [6]. (See
"Calcium channel blocker poisoning", section on 'Lipid emulsion therapy'.)
Studies of ILE therapy are preliminary and limited. ILE may have a useful role in the treatment of patients
who are hemodynamically unstable from particular poisonings, including beta blockers, after more
traditional therapies (eg, in the case of beta blocker poisoning: IV fluids, atropine, glucagon, high dose
insulin and glucose, and vasopressors) have failed to restore hemodynamic stability. ILE has been used
successfully in documented cases of severe beta blocker overdose [35,36]. Several case reports describe
patients treated with both high dose insulin and ILE with good results [37]. ILE may be used early in the
treatment of an overdose of a highly lipophilic agent (eg, propranolol), or as an adjunct to other
treatments as described above. (See 'Approach to the selection of specific therapies' above.)
Gastrointestinal (GI) decontamination — GI decontamination may involve activated charcoal (AC),

whole bowel irrigation, or gastric lavage; therapy is based upon clinical circumstance. (See
"Gastrointestinal decontamination of the poisoned patient".)
We suggest treatment with activated charcoal (AC), 1 g/kg by mouth or nasogastric tube, in all patients
who present within one to two hours of a known or suspected beta blocker ingestion, unless there are
contraindications to its administration. Charcoal should be withheld in patients who are sedated and may
not be able to protect their airway, unless endotracheal intubation is performed first. However,
endotracheal intubation should not be performed solely for the purpose of giving charcoal.
Asymptomatic patients who present more than two hours after a reported ingestion are unlikely to
benefit from AC, and we do not recommend routine treatment in these patients.

The role of activated charcoal in symptomatic patients who present several hours after ingestion is more
controversial. We suggest the administration of AC (1 g/kg by mouth or nasogastric tube) if there are no
contraindications to charcoal administration. Although there are no data to suggest improved outcomes
with AC in such patients, we believe that AC is a relatively safe intervention whose potential benefits in
this situation outweigh its risks.
Gastric lavage should not be routinely performed, but may be considered for patients who present within
one hour following ingestion of a large quantity of medication. Large sustained or controlled release
tablets may not pass through the oral gastric tube.
Whole bowel irrigation is reserved for patients who have ingested sustained release or enteric coated
preparations, or have suspected drug concretions (pharmacobezoars) in the GI tract.
Other therapies
● Sodium bicarbonate – Sodium bicarbonate has been used successfully in the treatment of beta
blocker induced arrhythmia [38,39]. Because it is a relatively safe intervention, we suggest giving it
as an adjunct for patients with QRS widening.
The dose of sodium bicarbonate is 1 to 2 mEq/kg given as an IV push, which may be repeated. If
treatment is effective, an infusion can be started. We mix 132 mEq of sodium bicarbonate in 1 L of
D5W and infuse at 250 mL/hour in adults, and at twice the maintenance fluid rate in children. The
infusion is tapered once the arrhythmia resolves. (See "Tricyclic antidepressant poisoning".)
● Magnesium – Magnesium may be administered when ventricular arrhythmias are present or

hypomagnesemia is suspected. Sotalol has a high propensity to induce ventricular arrhythmias and
will often require magnesium, administered as a 2 g IV bolus or as a continuous infusion.
● IV pacing – Ventricular pacing may be effective in patients with profound bradycardia, or in patients
with combined beta blocker and calcium channel blocker intoxication [40]. However, ventricular
pacing frequently fails to capture, or increases the heart rate without a corresponding increase in
perfusion [41]. IV pacing can be implemented if there is no response to pharmacologic therapies,
and the patient remains bradycardic and hypotensive. Some authors note a decrease in blood
pressure with pacing [5]. (See "Temporary cardiac pacing".)
● Intraaortic balloon pump – The intraaortic balloon pump has been used successfully after failure of
pharmacologic management in severe cases of propranolol and atenolol overdose [42,43] and in
combined verapamil-SR (sustained release) and atenolol overdose [44]. (See "Intraaortic balloon
pump counterpulsation".)
● Hemodialysis – Hemodialysis has a minimal role in the treatment of beta blocker overdose and is
effective only with hydrophilic, minimally protein-bound beta blockers such as atenolol [45]. Nadolol,
sotalol, acebutolol, and atenolol are reportedly removed by hemodialysis, but metoprolol,
propranolol, and timolol are not.

Hemodialysis is reserved for patients who have not improved despite aggressive medical
intervention, have ingested a significant amount of a beta blocker that can be removed using dialysis
(eg, acebutolol), or have ingested other cardioactive medications that may exacerbate toxicity. In
such cases, the emergency clinician should contact a nephrologist early in the patient's course to
avoid delays in preparing for hemodialysis.
● Extracorporeal membrane oxygenation – Extracorporeal membrane oxygenation has been used in

severe life-threatening ingestions with some reports of successful recovery [46]. This intervention
should be reserved for patients with severe ingestions who do not respond to standard therapy.
Continuous venovenous hemodialysis (VVHD) can be used if the patient is not able to tolerate traditional
hemodialysis due to pronounced hypotension. The decision to initiate hemodialysis and the selection of
the appropriate type is made in consultation with the nephrologist. (See "Enhanced elimination of
poisons".)
Pediatric considerations — Although hypoglycemia is seen more often in pediatric patients than adults,
overall management does not differ significantly in children. Children may be more susceptible to direct
central nervous system toxicity.
We recommend 24 hours of observation in a monitored setting for any initially asymptomatic child who
has ingested an extended release preparation, sotalol, or multiple cardioactive agents. Outside of such
cases, the great majority of isolated ingestions by young children are uneventful and they can be
discharged after a six hour period of observation [47,48].
Children may be observed safely at home after the witnessed ingestion of a single beta blocker tablet
and Poison Control Centers typically manage these exposures via telephone follow-up [49,50]. Should the
patient's family call the Emergency Department (ED) for advice, it is prudent to advise them to bring the
child to the ED for evaluation since follow-up can be problematic.
Disposition — Patients who have ingested a beta blocker and who manifest hemodynamic instability or
an altered mental status should be admitted to a critical care unit for cardiac monitoring and further
management.
Sotalol has a long half-life and toxicity may result in ventricular dysrhythmias. Thus, patients require 24
hours of inpatient cardiac monitoring following sotalol overdose, even if they are asymptomatic.
Any person who has taken an overdose of a beta blocker with membrane stabilizing activity ( table 2)
or multiple cardioactive medications is at increased risk of severe toxicity and should be observed in the
emergency department for six hours. Patients who remain asymptomatic without need of intervention
can be safely discharged. Patients who are asymptomatic at presentation after ingestion of a sustained
release beta blocker should be observed for at least six hours to insure that symptoms do not develop
[3].

Asymptomatic adults who have inadvertently ingested an amount of beta blocking agent no greater than
their total daily dose (excluding sotalol) may be observed safely at home [3].
ADDITIONAL RESOURCES
Regional poison control centers in the United States are available at all times for consultation on patients
who are critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In
addition, some hospitals have clinical and/or medical toxicologists available for bedside consultation
and/or inpatient care. Whenever available, these are invaluable resources to help in the diagnosis and
management of ingestions or overdoses. Contact information for poison centers around the world is
available at the website in the following reference [51].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the
world are provided separately. (See "Society guideline links: General measures for acute poisoning
treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other
than drugs of abuse".)
SUMMARY AND RECOMMENDATIONS
● Although beta blocker overdose generally follows a benign clinical course, patients with significant
toxicity require aggressive medical management. A summary table to facilitate emergency
management is provided ( table 1).
● Toxicity increases greatly when an agent has membrane stabilizing activity (MSA) ( table 2) or when
other cardioactive agents are ingested concomitantly. Lipophilic agents cross the blood brain barrier
and can cause neurologic dysfunction even in the absence of systemic hypotension ( table 2). (See
'Cellular toxicology' above and 'Toxicity of specific agents' above.)
● Sotalol is a unique agent with an extended half-life that can cause QTc interval prolongation and
severe ventricular arrhythmias in overdose. Propranolol and acebutolol possess properties that
increase their potential toxicity. (See 'Toxicity of specific agents' above and 'History' above.)
● Most patients who develop toxicity from beta blocker overdose do so within two hours of ingestion,
and virtually all do so within six hours. Bradycardia and hypotension are the most common effects.
Cardiogenic shock and ventricular dysrhythmias can occur with severe overdose. Other potential
effects of severe toxicity include mental status change, seizure, hypoglycemia, and bronchospasm.
Hypoglycemia is seen more often in children. (See 'Physical findings' above and 'Pediatric
considerations' above.)

● Obtain the following studies in patients with beta blocker poisoning: an electrocardiogram (ECG), a
fingerstick glucose, serum electrolytes including calcium, and blood urea nitrogen and creatinine
levels. Cardiac conduction delays can occur, most often a prolonged PR interval. In severe poisoning,
any bradydysrhythmia can develop, and may progress to asystole. (See 'Laboratory studies' above
and 'Electrocardiogram' above.)
● For patients with severely symptomatic beta blocker poisoning (eg, profound persistent hypotension
or bradycardia), we suggest simultaneous treatment with all of the following therapies (Grade 2C).
Dosing is provided in the text and the rapid overview table ( table 1). Severe beta blocker
poisoning can be difficult to manage and consultation with a medical toxicologist or regional poison
control center is highly encouraged (see 'Acute stabilization and overview of therapy' above and
'Severely symptomatic patients' above):
• Stabilization of the airway as necessary (avoid induction agents that exacerbate hypotension)
• Additional intravenous (IV) boluses of isotonic crystalloid
• IV glucagon
• IV calcium salts
• Vasopressor (eg, epinephrine)
• IV high-dose insulin and glucose
• IV lipid emulsion therapy
● For patients who are mildly symptomatic from beta blocker poisoning, and in whom IV fluids,
atropine, and glucagon prove ineffective at reversing signs of cardiotoxicity, we suggest a stepwise
treatment approach (Grade 2C). Give the following treatments, in succession, based upon patient
response: IV calcium salts, lipid emulsion therapy, vasopressors, and high-dose insulin and glucose.
The implementation of each therapeutic option is discussed in the text. (See 'Acute stabilization and
overview of therapy' above and 'Specific therapies' above.)
● Sodium bicarbonate and magnesium may be needed to treat some arrhythmias. Hemodialysis may
rarely be needed, in which case a nephrologist should be contacted early. (See 'Other therapies'
above.)
● The length of observation following inadvertent overdose varies according to the type and number
of medications ingested. (See 'Disposition' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Ellen Lemkin, MD, PharmD, who contributed to
an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.

Topic 330 Version 27.0

GRAPHICS
Beta blocker poisoning: Rapid overview of emergency management
To obtain emergency consultation with a medical toxicologist, call the United States Poison Control Network at 1-800-222-1222, or access the
World Health Organization's list of international poison centers (www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html).
Clinical and laboratory features
Hypotension and bradycardia are often prominent with significant ingestions
Electrocardiogram can show PR prolongation or any bradydysrhythmia
Ingestion of beta-blockers with membrane-stabilizing activity (eg, propranolol, carvedilol) may cause QRS prolongation and seizures
Laboratory findings may include hyperkalemia and hypoglycemia
Patients with beta blocker poisoning can deteriorate rapidly
Diagnostic evaluation
Assays for beta-blockers are not routinely available and do not aid management
Diagnosis is made on the basis of the history and clinical findings
Differential diagnosis for unexplained bradycardia also includes poisoning with calcium channel blockers, digoxin, clonidine, and
cholinergic agents
Structural heart disease and myocardial ischemia may cause similar findings and must be excluded
Treatment
Stabilize airway, breathing, and circulation:
Administer IV bolus crystalloid for hypotension (500 to 1000 mL isotonic saline)
Administer atropine 1 mg IV for bradycardia and hypotension; may repeat up to 3 total doses
For severe poisoning (eg, profound hypotension refractory to crystalloid boluses and atropine), give ALL of the following
treatments:
IV glucagon, IV calcium salt, vasopressor, IV high dose insulin and dextrose, and IV lipid emulsion therapy
For patients with milder symptoms, give the following treatments in succession, but proceed to the next treatment only if the prior
treatment or combination of treatments is ineffective:
IV crystalloid (for hypotension, as above), IV atropine (for bradycardia and hypotension, as above), IV glucagon, IV calcium salt,
vasopressor, IV high dose insulin and dextrose, and IV lipid emulsion therapy
Gastrointestinal decontamination:
Give a single dose of activated charcoal (1 g/kg, up to 50 g maximum) to all patients who present within 2 hours of ingestion, unless
contraindicated (eg, depressed mental status and not intubated)
Give whole bowel irrigation (2 L/hour by mouth until clear rectal effluent) for potentially life-threatening ingestion of extended-release
preparation
Dosing regimens:
Intravenous calcium (hypotension and/or bradycardia)
Bolus therapy (select one):
Calcium chloride – 10 to 20 mL of 10% solution (via central venous access if possible), or
Calcium gluconate – 30 to 60 mL of 10% solution
Continuous infusion:
0.5 meq calcium/kg per hour
Monitor serum calcium and ECG for evidence of hypercalcemia
Glucagon (bradycardia)
Bolus therapy:

1 to 5 mg IV push, may repeat up to 15 mg total
Continuous infusion:
Determine bolus amount needed to obtain response; give this "response dose" every hour as continuous infusion
Vasopressor (hypotension)
Norepinephrine – begin 2 mcg/minute IV, titrate rapidly to systolic blood pressure 100 mmHg
High dose insulin with dextrose (hypotension)
Bolus therapy:
Regular insulin – 1 Unit/kg IV
Dextrose – 25 to 50 grams IV; repeat for hypoglycemia; hold if serum glucose >300 mg/dL [16.7 mmol/L]; give potassium for
hypokalemia (hypomagnesemia often associated with hypokalemia)
Maintenance infusions:
Regular insulin – start infusion at 0.5 Units/kg per hour IV; titrate upwards until hypotension corrected or maximum dose of 10
Units/kg per hour reached
Dextrose – 0.5 grams/kg per hour; titrate to euglycemia; Measure blood glucose (eg, fingerstick) every 15 to 30 minutes until
infusion rate is steady and glucose measurements are stable; thereafter, measure glucose and potassium every 1 to 2 hours while
infusion continues
Intravenous lipid emulsion (20% solution)
Bolus therapy:
1.5 mL/kg over 2 minutes
Infusion:
1.5 mL/kg over 60 minutes
Additional interventions:
The following therapies may be necessary if the patient fails to improve with the interventions above or specific complications arise:
Sodium bicarbonate for QRS prolongation
Magnesium for ventricular arrhythmia
Transvenous cardiac pacing for profound bradycardia
Intraaortic balloon pump for refractory hypotension
IV: intravenous, ECG: electrocardiogram.
Graphic 82572 Version 17.0

Beta blocker properties
Alpha Beta-1 Usual Half life,

Drug ISA MSA Lipophilicity Elimination
blockade selectivity dose* hours ¶
Acebutolol No Yes Yes Yes Low 100 to 400 mg 3 to 4 Hepatic

twice per day (primary)
Renal
(secondary)
Atenolol No Yes No No Low 50 to 200 mg 6 to 9 Renal

once daily
Betaxolol No Yes No Yes Low 10 to 20 mg 14 to 22 Hepatic

once daily (primary)
Renal
(secondary)
Bisoprolol No Yes No No Moderate 2.5 to 20 mg 9 to 12 Renal and

once daily hepatic
Carteolol No No Yes No Low 2.5 to 5 mg 6 Renal

once daily
Carvedilol Yes No No Yes High 3.125 to 25 mg 7 to 10 Biliary

Hepatic
(secondary)
Esmolol No Yes No No Low IV only 250 to 9 minutes Blood

500 esterases
micrograms/kg
over one
minute then 25
to 50
micrograms/kg
per minute as
IV infusion;
titrate
incrementally
up to
maximum of
300
microgram/kg
per minute Δ
Labetalol Yes No Yes Low Moderate IV 20 mg Δ 3 to 4 Hepatic

(Beta 2 ) Orally 100-400
mg two or
three times per
day
Metoprolol No Yes No Low Moderate IV 1.25 to 5 3 to 4 Hepatic via

tartrate mg Δ (7 to 9 hours CYP2D6
Orally 25 to in poor (polymorphic)
100 mg two metabolizers)
times per day
Metoprolol No Yes No Low Moderate Orally 50 to Apparent Hepatic via

succinate 400 mg once half-life CYP2D6
(extended daily prolonged by (polymorphic)
release) continuous
osmotic
release over
~20 hours
Nadolol No No No No Low 40 to 160 mg 20 to 24 Renal

once daily
Nebivolol No Yes No No High 5 to 40 mg 10 to 12 Hepatic

once daily (19 to 32
poor
metabolizers)
Oxprenolol ◊ No No Yes Yes Moderate 40 to 80 mg 1.5 Hepatic

three times per
day
Penbutolol No No Yes No High 10 to 40 mg 5 Hepatic

once daily
Pindolol No No Yes Low Moderate 5 to 30 mg 3 to 4 Hepatic

Renal
(secondary)
Propranolol No No No Yes High IV 1 to 5 mg Δ 3 to 4 Hepatic

Orally 10 to 80
mg two to four
times daily
Sotalol § No No No No Low 80 to 160 mg 12 Renal

twice per day
Timolol No No No No Moderate 10 to 30 mg 4 to 5 Hepatic

Renal
(secondary)
ISA: intrinsic sympathomimetic activity; MSA: membrane stabilizing activity; IV: intravenous.
* Range of usual, oral, anti-hypertensive dose, unless "IV" noted.
¶ Duration of hypotensive effect, in general, is longer than may be predicted by serum half-life.
Δ Usual initial IV dose. Subsequent dosing generally needed. See drug monograph for detail.
◊ Not available in US.
§ Sotalol has independent class III antiarrhythmic activity.
Prepared with data from:

1. Frishman WH, Alwarshetty M. β-Adrenergic blockers in systemic hypertension pharmacokinetic considerations related to current guidelines. Clin
Pharmacokinet 2002; 41:505.
2. Brubacher JR. β-Adrenergic Antagonists. In: Goldfrank's Toxicologic Emergencies, 9th ed, Nelson LS (Ed), McGraw-Hill, New York 2010.

Single-lead electrocardiogram (ECG) showing first degree

atrioventricular (AV) block I
Electrocardiogram of lead II showing normal sinus rhythm, first degree atrioventricular

block with a prolonged PR interval of 0.30 seconds, and a QRS complex of normal
duration. The tall P waves and P wave duration of approximately 0.12 seconds suggest
concurrent right atrial enlargement.
Courtesy of Morton Arnsdorf, MD.
Normal rhythm strip
Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is
0.08 sec. Both the P and T waves are upright.
Courtesy of Morton F Arnsdorf, MD.

Junctional escape rhythm
Escape junctional beat or rhythm occurs when there is failure of impulse generation from the
sinus node or atrial myocardium. The 4th and 5th beats of this tracing are junctional beats that
are not preceeded by a P wave and occur after a pause that is longer than the underlying sinus
cycle length.
Sinus rhythm
The normal P wave in sinus rhythm is slightly notched since activation of the right
atrium precedes that of the left atrium. The P wave is upright in a positive direction
in leads I and II. A P wave with a uniform morphology precedes each QRS complex.
The rate is between 60 and 100 beats per minute and the cycle length is uniform
between sequential P waves and QRS complexes. In addition, the P wave
morphology and PR intervals are identical from beat to beat.

Single lead electrocardiogram (ECG) showing sinus bradycardia
Marked sinus bradycardia at a rate of 25 to 30 beats/min. The normal P waves (upright in lead II) and
PR interval are consistent with a sinus mechanism with normal atrioventricular (AV) conduction.
Courtesy of Ary Goldberger, MD.
Normal rhythm strip
Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is
0.08 sec. Both the P and T waves are upright.
Courtesy of Morton F Arnsdorf, MD.

12-lead electrocardiogram Brugada pattern
Patient with Brugada pattern ECG. Note the presence of pseudo-right bundle branch block and persistent ST segment elevation in leads V1 to V2.
ECG: electrocardiogram
Courtesy of Ann C Garlitski, MD, FACC, FHRS.

Digitalis effect
The ST segment is depressed and concave upward.


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18/5/2021 Beta blocker poisoning - UpToDate

Official reprint from UpToDate®

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TOXICITY OF SPECIFIC AGENTS

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CLINICAL FEATURES OF OVERDOSE

● Coingestion of other cardioactive agents

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Acute stabilization and overview of therapy

Airway, breathing, circulation — Management begins with assessment of the patient’s airway,

Hypoglycemia and seizures — Symptomatic hypoglycemia is treated with IV dextrose. For adults,

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Approach to the selection of specific therapies — Although it is ideal to institute treatments

Severely symptomatic patients — Our suggested approach to patients manifesting signs of severe

Mildly symptomatic patients — Our suggested approach to patients with mild hypotension or

A period of 15 minutes is reasonable to determine the effectiveness of a specific therapy before

Asymptomatic patients — Many patients with an isolated beta blocker overdose remain

If there is an increase in pulse or blood pressure, an infusion is started at a rate of 2 to 5 mg/hour

Vomiting is common following administration of glucagon. We suggest prophylactic or concurrent

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Gastrointestinal (GI) decontamination — GI decontamination may involve activated charcoal (AC),

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● Magnesium – Magnesium may be administered when ventricular arrhythmias are present or

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● Extracorporeal membrane oxygenation – Extracorporeal membrane oxygenation has been used in

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SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

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Beta blocker poisoning: Rapid overview of emergency management

Clinical and laboratory features

Hypotension and bradycardia are often prominent with significant ingestions

Electrocardiogram can show PR prolongation or any bradydysrhythmia

Laboratory findings may include hyperkalemia and hypoglycemia

Patients with beta blocker poisoning can deteriorate rapidly

Diagnosis is made on the basis of the history and clinical findings

Administer IV bolus crystalloid for hypotension (500 to 1000 mL isotonic saline)

Intravenous calcium (hypotension and/or bradycardia)

Bolus therapy (select one):

Calcium chloride – 10 to 20 mL of 10% solution (via central venous access if possible), or

Calcium gluconate – 30 to 60 mL of 10% solution

0.5 meq calcium/kg per hour

Monitor serum calcium and ECG for evidence of hypercalcemia

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High dose insulin with dextrose (hypotension)

Regular insulin – 1 Unit/kg IV

Intravenous lipid emulsion (20% solution)

1.5 mL/kg over 2 minutes

1.5 mL/kg over 60 minutes

Sodium bicarbonate for QRS prolongation

Magnesium for ventricular arrhythmia

Transvenous cardiac pacing for profound bradycardia

Intraaortic balloon pump for refractory hypotension

IV: intravenous, ECG: electrocardiogram.

Graphic 82572 Version 17.0