β-Adrenergic Receptor Antagonist Intoxication
Agents
Non-Selective Beta Blockers
Carteolol
Nadolol (Corgard, Anabet, Solgol, Corzide, Alti-Nadolol, Apo-Nadol, Novo-Nadolol) (see Nadolol )
Penbutolol
Pindolol (Visken, Betapindol, Blockin L, Blocklin L, Calvisken, Cardilate, Decreten, Durapindol, Glauco-Visken, Pectobloc, Pinbetol, Prindolol, Pynastin)
Propafenone (Rhythmol) (see Propafenone ): with additional Class 1C antiarrhythmic properties (inhibits sodium channels)
Propanolol (Inderal) (see Propanolol )
Sotalol (Betapace, Betapace AF, Sotalex, Sotacor) (see Sotalol ): with additional Class III antiarrhythmic properties (inhibits potassium channels)
Timolol (Blocadren, Timoptic) (see Timolol )
Cardioselective (β1-Selective) Beta Blockers
Acebutolol (Sectral, Prent) (see Acebutolol )
Atenolol (Tenormin) (see Atenolol )
Betaxalol (Betoptic, Lokren, Kerlone) (see Betaxalol )
Bisoprolol (Concor, Zebeta) (see Bisoprolol )
Esmolol (Brevibloc) (see Esmolol )
Metoprolol (Lopressor) (see Metoprolol )
Nebivolol (Bystolic) (see Nebivolol )
Practolol : although structurally similar to propanolol, it is no longer used in humans (due to adverse effect of oculomucocutaneous syndrome)
Beta Blockers with Intrinsic Sympathomimetic Activity (β-Adrenergic Receptor Antagonism + Low Level β-Adrenergic Receptor Agonism)
Acebutolol (see Acebutolol )
Carteolol
Celiprolol
Mepindolol
Oxprenolol
Penbutolol
Pindolol (Visken, Betapindol, Blockin L, Blocklin L, Calvisken, Cardilate, Decreten, Durapindol, Glauco-Visken, Pectobloc, Pinbetol, Prindolol, Pynastin)
Beta Blockers with Alpha Blocking Activity
Pharmacology
Bronchial Smooth Muscle β2-Adrenergic Receptors
Gastrointestinal β2-Adrenergic Receptors
Mediate Slowing of Peristalsis
Mediate Slowing of Secretions
Hepatic β2-Adrenergic Receptors
Mediate Gluconeogenesis
Mediate Glycogenolysis
Mediate Lipolysis
Ocular Ciliary Muscle β2-Adrenergic Receptors
Mediate Flow of Aqueous Humor
Mediate Accommodation
Urinary Bladder Detrusor Muscle β2-Adrenergic Receptors
Mediate Detrusor Muscle Relaxation
Uterine Muscle β2-Adrenergic Receptors
Mediate Uterine Relaxation (Tocolysis)
Vascular Smooth Muscle β2-Adrenergic Receptors
Clinical Manifestations
Cardiovascular Manifestations
Bradycardia (see xxxx )
Congestive Heart Failure (CHF) (see Congestive Heart Failure ): due to negative inotropy
Hypotension (see xxxx )
Pulmonary Manifestations
Other Manifestations
Treatment
Glucagon
Dose: 3-10 mg IV, then 2-5 mg/hr drip
Enhances myocardial contractility and AV conduction
Increases heart rate
Nasogastric Lavage : indicated if performed within 1-2 hrs of ingestion
Charcoal
Hemodialysis
Cardiac Pacing
IV Fluid Resuscitation
Hyperinsulinemia-Euglycemia Therapy for Calcium Channel Blocker Intoxication (see Calcium Channel Blockers )
Rationale
Hyperinsulinemia-Euglycemia Therapy Results in Positive Inotropic Effects in the Treatment of Calcium Channel Blocker Intoxication (J Pharmacol Exp Ther, 1993) [MEDLINE ] (NEJM, 2001) [MEDLINE ] (Intensive Care Med, 2007) [MEDLINE ] (Am J Crit Care, 2007) [MEDLINE ]
Administration
Correct Hypoglycemia and Hypokalemis Prior to Starting Hyperinsulinemia-Euglycemia Therapy
Titrate Up to Max of 10 U/kg/hr
Then Titrate D50W Drip to Maintain Glucose >200 mg/dL
Adverse Effects
Hypotension (see Hypotension )
Especially in the Setting of Amlodipine Overdose
Dihydropyridine (Amlodipine, Nifedipine) Intoxication Generally Causes Arterial Vasodilation and Reflex Tachycardia
Diltiazem/Verapamil Intoxication Generally Cause Peripheral Vasodilation, Negative Cardiac Inotropy, and Bradycardia
However, as the Dose is Increased, This Selectivity of These Agents is Lost, Resulting in Negative Cardiac Inotropy and Bradycardia in the Setting of Dihydropyridine Overdose
Clinical Efficacy
References
General
Treatment
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