Download - Beta Blocker
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