beta blokers tintinalli's emergency medicine 2010 by dr. tayebeh salehi
TRANSCRIPT
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BETA BLOKERSTintinalli's Emergency Medicine 2010BY DR. TAYEBEH SALEHI
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Epidemiology
common medications used in the treatment of
various cardiovascular, neurologic, endocrine,
ophthalmologic, and psychiatric disorders
accidental and intentional toxicity is common
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`
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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.
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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.
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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
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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.
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Clinical Presentation
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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.
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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).
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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
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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.
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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
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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
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Treatment
General Management
should be evaluated in a critical-care area of the ED with
appropriate monitoring
protect air way
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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 -blockers
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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.
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Pharmacologic Treatment
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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.
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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
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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.
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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.
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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
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The initial dose is regular insulin
1 unit/kg IV bolus
followed by
0.5 to 1.0 unit/kg/h
continuous infusion.
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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.
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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
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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.
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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
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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.
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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.
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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
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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.
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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.
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Extracorporeal Elimination (Hemodialysis)
acebutolol
atenolol
nadolol
sotalol
their lower protein binding, water solubility, and lower volume
of distribution
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Extracorporeal Circulation
extreme of resuscitation,
intra-aortic balloon pumps
have been successful when pharmacologic measures have
failed to reverse cardiogenic shock
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Treatment of Sotalol Toxicity
Inhibition of K channel and prolang QT
magnesium supplementation
lidocaine
cardiac overdrive pacing
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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
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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
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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
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THANKS FOR YOUR ATTENTION