Beta-blocker Tintinalli chpter 188

:2011.12.20 EM 2

Epidemiology common medications used in the treatment

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Cardiovascular Neurologic Endocrine Ophthalmologic Psychiatric disorders

In 2008, the American Association of Poison Control Centers received reports of 21,282 exposures to beta-blockers with six associated 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 ingestion 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
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bradycardia shock

The beta-blockers with sodium channel antagonism

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2.

cause a wide-complex bradycardia 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
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premature ventricular contractions ventricular tachycardia ventricular fibrillation torsades de pointes

 Neurologic manifestations
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depressed mental status coma seizures

These symptoms most likely occur as a result of a combination of

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3.

hypoxia due to poor perfusion sodium channel antagonism direct neuronal toxicity

 More lipophilic -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
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patient history physical examination findings results of basic diagnostic testing

Although exposures to other drugs and toxins can present with bradycardia and hypotension, 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 fashion to affect acute management

Treatment 1. critical monitoring these patients may experience abrupt cardiovascular collapse or neurologic depression 2.Activated charcoal May be bebenifit if it can be given within 1 to 2 hours after ingestion 3.ipecac syrup is not recommended due to the risk of coma and seizures

4.Gastric lavage not routinely used, but may be considered for life-threatening ingestions 5.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 Duration
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Effects from an IV bolus of glucagon are seen within 1 to 2 minutes reach a peak in 5 to 7 minutes have a duration of action of 10 to 15 minutes

 Due to the short duration of effect, a continuous infusion is often necessary after bolus administration. Dose
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2.

The bolus dose of glucagon is 0.05 to 0.15 milligram/kg (3 to 10 milligrams for the average 70-kg adult) and can be repeated as needed. 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 isoproterenolare used routinely to treat beta-blocker toxicity. Results have been variable The most effective adrenergic receptor agonist is norepinephrine

Hyperinsulinemia-euglycemia therapy Insulin facilitates myocardial utilization of glucose. In animal models, hyperinsulinemiaeuglycemia 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 infusion of 35 to 70 units/h

Adverse effect 1.Hypoglycemia

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B.

Glucose supplementation is used to maintain euglycemia and prevent hypoglycemia. An initial 0.5 gram/kg bolus of glucose should accompany the initial insulin bolus Serum potassium level does not indicate global depletion Replacement is not required unless it falls to <2.5 mEq/L (<2.5 mmol/L)

2.Hypokalemia
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B.

Atropine Is unlikely to be effective in the management of beta-blockerinduced bradycardia and hypotension

Calcium calcium administration is not routinely recommended in Beta-blocker overdose but, it may be worth considering in patients with refractory shock unresponsive to other therapies. Calcium for IV two form
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Calcium gluconate 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 provides 13 mEq of calcium versus 4.5 mEq provided

 Side effect 1. Hypercalcemia 2. conduction blocks 3. worsening bradycardia Severe soft tissue injury associated with inadvertent IV infiltration of the chloride formulation is the most concerning adverse event. Thus, calcium chloride is ideally given via a central line.

 The recommended dosage

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10% calcium gluconate is 0.6 mL/kg given over 5 to 10 minutes 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 blockade QRS interval longer than 120 to 140 milliseconds Suggested dose is a rapid bolus of 2 to 3 mEq/kg Repeat boluses may be required to maintain the QRS interval at <120 milliseconds.

Aggressive resuscitation measure 1. Cardiac Pacing

2. Extracorporeal Elimination (Hemodialysis)

3. Extracorporeal Circulation

Goal of treatment 1. 2. 3. 4. 5. 6. Cardiac ejection fraction of 50% QRS interval to <120 milliseconds Heart rate of >60 beats/min Systolic blood pressure of >90 mm Hg Urine output of 1 to 2 mL/kg/h Improved mentation