BETA BLOKERS
Tintinalli's Emergency Medicine 2010
BY DR. TAYEBEH SALEHI
Epidemiology

common medications used in the treatment of various
cardiovascular, neurologic, endocrine, ophthalmologic,
and psychiatric disorders

accidental and intentional toxicity is common
`

The beta -blockers by decreasing calcium entry into the
cell modulate the activity of myocyte and vascular
smooth muscle contraction

excessive beta -blockade may lead to profound pump
failure, with bradycardia, decreased contractility, and
hypotension.

selectivity is often lost following large overdoses.

Sotalol is unique among beta-blockers in its ability to
block potassium channels

Sotalol is class III antiarrhythmic drugs.

Under normal conditions, the heart uses free fatty acids
as its primary energy source,

but during times of stress, it switches to using
carbohydrates to maintain metabolism

Inhibition of glycogenolysis and gluconeogenesis reduces the availability
of carbohydrates for use by cells

hypoglycemia occurs as a consequence of beta -blocker toxicity, it is
actually very rare. In the presence of adequate glucose stores,
euglycemia and hyperglycemia are more common than hypoglycemia.
Clinical Presentation

Absorption of regular-release beta -blockers occurs rapidly, often with peak
effects within 1 to 4 hours

sustained-release cardiac drugs, it is assumed that symptoms may be delayed
>6 hours after ingestion

Coingestants that alter gut function, such as opioids and anticholinergics, may
affect absorption of beta -blockers and subsequent onset of symptoms.

The primary organ system affected by beta-blocker toxicity is the
cardiovascular system, and the hallmark of severe toxicity is
bradycardia and shock.

The beta -blockers with sodium channel antagonism can cause a
wide-complex bradycardia, and may contribute to development
of seizures (especially when the QRS interval is >100 milliseconds).


sotalol ability to block potassium channels and prolong the QT interval
sotalol is more often associated with ventricular dysrhythmias, includin :
 premature

ventricular contractions
bigeminy
 ventricular
tachycardia

ventricular fibrillation

torsades de pointes

Neurologic manifestations include depressed mental status, coma,
and seizures.

More lipophilic beta-blockers, such as propranolol, cause greater
neurologic toxicity than the less lipophilic agents.

Seizures can occur but are generally brief, and status epilepticus is
rare.
Diagnosis

including patient history, physical examination findings, and results of
basic diagnostic testing.

exposures to other drugs and toxins can present with bradycardia and
hypotension

The 12-lead ECG and Bedside echocardiography are useful to
evaluate myocardial performance in cases of undifferentiated
shock.

Invasive monitoring with central venous or pulmonary artery
catheters may be necessary to help direct resuscitation.

renal function, glucose level, oxygenation, and acid-base status
Treatment

General Management

should be evaluated in a critical-care area of the ED with
appropriate monitoring

protect air way

GI Decontamination

ingestion
of a
significant
quantity
of beta
-blockers
decontamination should be considered.

Activated charcoal may be of benefit if it can be given
within 1 to 2 hours after ingestion. Multiple dose of activated
charcoal therapy following ingestion of sustained-release -

Use of ipecac syrup is not recommended

Gastric lavage is not routinely used, but may be considered
for life-threatening ingestions when the airway is adequately
protected from aspiration.

Whole-bowel irrigation may be beneficial after ingestion of a
sustained-release product, If whole-bowel irrigation is used,
adequate airway protection and normal GI function are
important.
Pharmacologic Treatment
Glucagon

Glucagon is a first-line agent in the treatment of acute beta –
blocker induced bradycardia and hypotension.

Effects from an IV bolus of glucagon are seen within 1 to 2 minutes,
reach a peak in 5 to 7 minutes
duration of action of 10 to 15 minutes.

Due to the short duration of effect, a continuous infusion is often
necessary after bolus administration.

The bolus dose of glucagon is
0.05 to 0.15 milligram/kg (3 to 10 milligrams for the average 70-kg (
and can be repeated as needed.

If a beneficial effect is seen from bolus, a continuous infusion
1 to 10 milligrams/h

the positive inotropic and chronotropic effects of glucagon may not be
maintained for a prolonged period due to possible tachyphylaxis.

side effects of high-dose glucagon therapy :
Nausea and vomiting
esophageal sphincter relaxation

Intubation prior to glucagon administration may be warranted in any
patient with altered mental status to limit the risk of aspiration.
Adrenergic Receptor Agonists

The beta -adrenergic receptor agonists—such as norepinephrine,
dopamine, epinephrine, and isoproterenol

The
most
effective
adrenergic
receptor
agonist
may
be
norepinephrine due to its ability to increase heart rate and blood
pressure.
Hyperinsulinemia-Euglycemia Therapy

insulin facilitates myocardial utilization of glucose, the desired substrate
during stress

This is in contrast to glucagon, epinephrine, and calcium, which promote
free fatty acid utilization

The initial dose is regular insulin
1 unit/kg IV bolus
followed by
0.5 to 1.0 unit/kg/h
continuous infusion.

adverse effects from hyperinsulinemia-euglycemia therapy are
hypoglycemia and hypokalemia

0.5 gram/kg bolus of glucose should accompany the initial insulin bolus in
a patient whose serum glucose level is <400 milligrams/dL.

Serum glucose levels should be monitored regularly: every 20 to 30
minutes until stable euglycemia is achieved, and then every 1 to 2 hours
thereafter.

Serum potassium levels may fall during hyperinsulinemia-euglycemia
therapy.

Serum potassium level should be monitored,

replacement is not required unless
it falls to <2.5 mEq/L (<2.5 mmol/L) or
the patient has other sources of true potassium loss
Atropine

a muscarinic blocker, is unlikely to be effective in the management
of beta blocker–induced bradycardia and hypotension,

although its use is unlikely to cause harm.
Calcium

calcium administration is not routinely recommended in beta -blocker
overdose, it may be worth considering in patients with refractory shock
unresponsive to other therapies.

Calcium for IV administration is available in two forms, gluconate and
chloride, both in a 10% solution. Calcium chloride solution contains three
times more elemental calcium than calcium gluconate solution

10% calcium gluconate 0.6 mL/kg given over 5 to 10 minutes
followed by a continuous infusion of 0.6 to 1.5 mL/kg/h

10% calcium chloride 0.2 mL/kg given via central line over 5 to 10 minutes
followed by a continuous infusion of 0.2 to 0.5 mL/kg/h.

Ionized calcium levels should be checked every 30 minutes initially and
then every 2 hours to achieve an ionized calcium level of twice the normal
value.
Phosphodiesterase Inhibitors

such as inamrinone (formerly known as amrinone), milrinone, and
enoximone

These agents inhibit the breakdown of cAMP thereby maintaining
intracellular calcium levels

In animal models, phosphodiesterase inhibitors produce positive
inotropic effects without increasing myocardial oxygen demand,
but have no appreciable effect on heart rate.

In the setting of a beta -blocker overdose, phosphodiesterase
inhibitors are administrated as a continuous IV infusion,
starting at 5 micrograms/kg/min for inamrinone
0.5 microgram/kg/min for milrinone
0.75 microgram/kg/min for enoximone
Sodium Bicarbonate

In a patient demonstrating a QRS interval longer than 120 to 140
milliseconds, it is reasonable to administer sodium bicarbonate

The suggested dose is a rapid bolus of 2 to 3 mEq/kg,
Thus, a 70-kg adult receives a bolus of 140 to 210 mEq of sodium
bicarbonate,
or three to four ampules (50 mL each) of 8.4% sodium
bicarbonate

Repeat boluses may be required to maintain the QRS interval at
<120 milliseconds.
Cardiac Pacing

Electrical capture and restoration of blood pressure is not always
successful

Cardiac pacing may be most beneficial in treating torsades de
pointes associated with sotalol toxaicity.
Extracorporeal Elimination
(Hemodialysis)

acebutolol

atenolol

nadolol

sotalol
their lower protein binding, water solubility, and lower volume of
distribution
Extracorporeal Circulation

extreme of resuscitation,
intra-aortic balloon pumps
have been successful when pharmacologic measures have failed
to reverse cardiogenic shock
Treatment of Sotalol Toxicity

Inhibition of K channel and prolang QT

magnesium supplementation

lidocaine

cardiac overdrive pacing

The goal of resuscitation is to improve hemodynamics and organ perfusion

cardiac ejection fraction of 50%,

reduction of the QRS interval to <120 milliseconds,

heart rate of >60 beats/min,



systolic blood pressure of >90 mm Hg in an adult
urine output of 1 to 2 mL/kg/h
improved mentation
Disposition and Follow-Up

Patients with altered mental status, bradycardia, conduction
delays, or hypotension are often managed in an intensive care
unit.

any patient who ingests a sustained-released beta -blocker
product warrants admission and monitoring for the development of
delayed toxicity

Patients ingesting an overdose of regular beta -blocker tablets who
remain
asymptomatic and have normal vital signs for 6 hours after
ingestion
safe for discharge
THANKS FOR YOUR
ATTENTION