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drugs share the ability to cause arteriolar vasodilation and depression of cardiac contractility, especially after acute overdose Patients may present with bradycardia, atrioventricular (AV) nodal block, hypotension, or a combination of these effects With severe poisoning, cardiac arrest may occur

There are a wide variety of -adrenergic blocking drugs, with varying pharmacologic and pharmacokinetic properties (see Table 11 7) The most toxic -blocker is propranolol Propranolol competitively blocks 1 and 2 adrenoceptors and also has direct membrane-depressant and central nervous system effects

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Maintain a patent airway and assist ventilation, if necessary Treat coma, hypotension, and seizures as described at the beginning of this chapter Treat bradycardia with atropine (05 2 mg intravenously), isoproterenol (2 20 mcg/min by intravenous infusion), or a transcutaneous or internal cardiac pacemaker For ingested drugs, administer activated charcoal (see p 1362) In addition, whole bowel irrigation should be initiated as soon as possible if the patient has ingested a sustainedrelease product

The most common findings with mild or moderate intoxication are hypotension and bradycardia Cardiac depression from more severe poisoning is often unresponsive to conventional therapy with -adrenergic stimulants such as dopamine and norepinephrine In addition, with propranolol and other lipid-soluble drugs, seizures and coma may occur The diagnosis is based on typical clinical findings Routine toxicology screening does not usually include -blockers

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Initially, treat bradycardia or heart block with atropine (05 2 mg intravenously), isoproterenol (2 20 mcg/min by intravenous infusion, titrated to the desired heart rate), or an external transcutaneous cardiac pacemaker However, these measures are often ineffective, and specific antidotal treatment may be necessary (see below) For ingested drugs, administer activated charcoal (see p 1362)

Define Reasons for Blocking in Shipping | Deliveries: Blocking Reasons/Criteria As you can see in Figure 10-22, we have created a delivery block called ZV

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If bradycardia and hypotension are not reversed with these measures, administer calcium chloride intravenously Start with calcium chloride 10%, 10 mL, or calcium gluconate 10%, 20 mL Repeat the dose every 3 5 minutes The optimum (or maximum) dose has not been established, but there are reports of success after as much as 10 12 g of calcium chloride Calcium is most useful in reversing negative inotropic effects and is less effective for AV nodal blockade and bradycardia Epinephrine infusion (1 4 mcg/min initially) and glucagon (5 10 mg intravenously) have also been recommended In addition, high doses of insulin (05 1 U/kg intravenous bolus followed by 05 1 U/kg/h infusion) along with sufficient dextrose to maintain euglycemia have been reported to be beneficial but there are no controlled studies

DeWitt CR et al Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity Toxicol Rev 2004;23(4):223 38 [PMID: 15898828] Shepherd G et al High-dose insulin therapy for calcium-channel blocker overdose Ann Pharmacother 2005 May;39(5): 923 30 [PMID: 15811898]

If the above measures are not successful in reversing bradycardia and hypotension, give glucagon, 5 10 mg intravenously, followed by an infusion of 1 5 mg/h Glucagon is an inotropic agent that acts at a different receptor site and is therefore not affected by -blockade

Shepherd G Treatment of poisoning caused by beta-adrenergic and calcium-channel blockers Am J Health Syst Pharm 2006 Oct 1;63(19):1828 35 [PMID: 16990629]

Calcium channel blockers used in the United States include verapamil, diltiazem, nifedipine, nicardipine, amlodipine, felodipine, isradipine, nisoldipine, and nimodipine These

Carbon monoxide is a colorless, odorless gas produced by the combustion of carbon-containing materials Poisoning may

Contents Amyl nitrite, 03 mL aspirol for inhalation; sodium nitrite 300 mg in a 10-mL vial; sodium thiosulfate 125 g in a 50-mL vial Hydroxocobalamin 5 g in two 25-g vials

Action Nitrites induce methemoglobinemia, which binds CN; thiosulfate hastens CN conversion to less toxic thiocyanate Converts CN to cyanocobalamin (vitamin B12)

FIGURE 10-22

occur as a result of suicidal or accidental exposure to automobile exhaust, smoke inhalation in a fire, or accidental exposure to an improperly vented gas heater or other appliance Carbon monoxide avidly binds to hemoglobin, with an affinity approximately 250 times that of oxygen This results in reduced oxygen-carrying capacity and altered delivery of oxygen to cells (see also Smoke Inhalation in 9)

Juurlink DN et al Hyperbaric oxygen for carbon monoxide poisoning Cochrane Database Syst Rev 2005 Jan 25;(1):CD002041 [PMID: 15674890]

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