Beta-blockerTintinalli chpter 188

발표일 :2011.12.20EM 2 년 조영관

Epidemiology

common medications used in the treatment1. Cardiovascular2. Neurologic3. Endocrine4. Ophthalmologic5. Psychiatric disorders

In 2008, the American Association of Poison Control Centers received reports of 21,282 exposures to beta-blockers with six associ-ated deaths.

Pharmacology

Clinical presentation

Toxicity due to beta-blockers can manifest as a spectrum of clinical symptoms

peak effects within 1 to 4 hours.4 However, delays of up to 6 hours following acute in-gestion have occurred.

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

the hallmark of severe toxicity 1. bradycardia 2. shock

The beta-blockers with sodium channel an-tagonism1. cause a wide-complex bradycardia2. development of seizures

The cardiotoxic profile of sotalol is different from that of other beta-blockers

block potassium channels and prolong the QT interval.

Ventricular dysrhythmias 1. premature ventricular contractions2. ventricular tachycardia3. ventricular fibrillation4. torsades de pointes

Neurologic manifestations 1. depressed mental status2. coma3. seizures

These symptoms most likely occur as a re-sult of a combination of 1. hypoxia due to poor perfusion2. sodium channel antagonism3. direct neuronal toxicity

More lipophilic -blockers, such as propra-nolol, cause greater neurologic toxicity than the less lipophilic agents.

Seizures can occur but are generally brief, and status epilepticus is rare.

Diagnosis

1. patient history2. physical examination findings3. results of basic diagnostic testing

Although exposures to other drugs and tox-ins can present with bradycardia and hy-potension, there are useful features that differentiate toxicity from these agents from that due to beta-blockers

1. The 12-lead ECG provides cardiac electrical function. 2.Cardiac US and formal echocardiography

evaluate myocardial performance 3.Central venous or pulmonary artery

catheters help direct resuscitation. 4.Laboratory testing monitoring provide renal function, glucose level,

oxygenation, and acid-base status..

5. specific -blocker drug levels later confirmation of an ingestion these levels are not helpful initially 1.

they do not correlate with the degree of toxicity

2. generally not available in a timely fash-ion to affect acute management

Treatment

1. critical monitoring these patients may experience abrupt

cardiovascular collapse or neurologic de-pression

2.Activated charcoal May be bebenifit if it can be given within

1 to 2 hours after ingestion3.ipecac syrup is not recommended due to the risk of coma and seizures

4.Gastric lavage not routinely used, but may be consid-

ered for life-threatening ingestions5.Whole-bowel irrigation may be beneficial

Glucagon

first-line agent in the treatment of acute bradycardia and hypotension

produced in the pancreatic cells from proglucagon

Duration1. Effects from an IV bolus of glucagon are seen

within 1 to 2 minutes2. reach a peak in 5 to 7 minutes3. have a duration of action of 10 to 15 minutes

Due to the short duration of effect, a con-tinuous infusion is often necessary after bo-lus administration.

Dose1. The bolus dose of glucagon is 0.05 to 0.15 mil-

ligram/kg (3 to 10 milligrams for the average 70-kg adult) and can be repeated as needed.

2. Continuous infusion of 1 to 10 milligrams/h There is no defined maximum therapeutic

dose or duration of treatment.

Adrenergic receptor agonist

Norepinephrine, dopamine, epinephrine, and isoproterenol—are used routinely to treat beta-blocker toxicity.

Results have been variable The most effective adrenergic receptor ag-

onist is norepinephrine

Hyperinsulinemia-euglycemia therapy

Insulin facilitates myocardial utilization of glucose.

In animal models, hyperinsulinemia-eug-lycemia therapy improved survival

The initial dose is regular insulin, 1 unit/kg IV bolus, followed by 0.5 to 1.0 unit/kg/h continuous infusion

For example, a 70-kg person is 70 units of regular insulin followed by constant infu-sion of 35 to 70 units/h

Adverse effect

1.HypoglycemiaA. Glucose supplementation is used to maintain

euglycemia and prevent hypoglycemia. B. An initial 0.5 gram/kg bolus of glucose should

accompany the initial insulin bolus 2.Hypokalemia

C. Serum potassium level does not indicate global depletion

D. Replacement is not required unless it falls to <2.5 mEq/L (<2.5 mmol/L)

Atropine

Is unlikely to be effective in the manage-ment of beta-blocker–induced bradycardia and hypotension

Calcium

calcium administration is not routinely rec-ommended in Beta-blocker overdose

but, it may be worth considering in patients with refractory shock unresponsive to other therapies.

Calcium for IV two form1. Calcium gluconate2. Calcium chloride, both in a 10% solution.

Calcium chloride solution contains three times more elemental calcium than calcium gluconate solution.

A 10-mL vial of 10% calcium chloride pro-vides 13 mEq of calcium versus 4.5 mEq provided

Side effect1. Hypercalcemia2. conduction blocks3. worsening bradycardiaSevere soft tissue injury associated with in-

advertent IV infiltration of the chloride for-mulation is the most concerning adverse event.

Thus, calcium chloride is ideally given via a central line.

The recommended dosage 1. 10% calcium gluconate is 0.6 mL/kg given over

5 to 10 minutes2. followed by a continuous infusion of 0.6 to 1.5

mL/kg/h.

Sodium bicarbonate

1. Treat severe acidosis 2. Wide-QRS-interval dysrhythmias due to

sodium channel blockadeQRS interval longer than 120 to 140 mil-

lisecondsSuggested dose is a rapid bolus of 2 to 3

mEq/kgRepeat boluses may be required to main-

tain the QRS interval at <120 milliseconds.

Aggressive resuscitation measure

1. Cardiac Pacing

2. Extracorporeal Elimination (Hemodialysis)

3. Extracorporeal Circulation

Goal of treatment

1. Cardiac ejection fraction of 50%2. QRS interval to <120 milliseconds3. Heart rate of >60 beats/min4. Systolic blood pressure of >90 mm Hg 5. Urine output of 1 to 2 mL/kg/h6. Improved mentation