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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