《心肺复苏指南》参考资料（英文版）Part 10-2 Toxicology in ECC

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Part 10.2: Toxicology in ECC ients, but it is a leading cause of cardiac arrest Opiate poisoning causes respiratory depression victims <40 years of age. I-4 When a patient with poisoning followed by respiratory ins cy or arrest. Heroin over is in cardiac st, immediate support of dose may cause respiratory depression, and it frequently irway, breathing, and circulation is essential. Urgent consul- causes pulmonary edema. The respiratory effects of opioids ation with a medical toxicologist or certified regional poison are rapidly reversed by the opiate antagonist naloxone center is recommended,6 because standard guidelines for In the hospital setting the administration of naloxone for emergency cardiovascular care may not be optimal in the acute opioid exposure has been successful without prior anagement of acute poisoning and overdose ventilation(LOE: 414 5: 516, 17; 718) if the airway was main This section presents recommendations for the care of the tained and high-flow oxygen administered and the patient patient with a toxicologic problem. Some recommendations was otherwise healthy with no chronic opioid addiction and are evidence-based, but most toxicology research in this area no cardiovascular disease. In the out-of-hospital setting consists primarily of small case series(LOE 5), case reports, however, the evidence indicates fewer adverse events when and animal studies(LOE 6). Hence many of these recom- emergency medical services(EMS)system personnel provide mendations are based on expert consensus, and further ventilation(ie, provide positive-pressure ventilation with bag research is needed to validate them and mask) before administration of naloxone to all patients Clinicians may see a patient with a history of ingestion of an with opioid-induced respiratory depression (LOE 59-2 in unknown substance. In such cases the clinician must be familiar adults, extrapolated from pediatric cases[LOE 722.23:LOE with common toxidrome and their therapies. To assist during 81). 24 The adverse effects seen in patients receiving naloxone sts drug-induced cardiovascular prior to ventilation may be due to the underlying cardiovas- emergencies or altered vital signs, potential therapies to con- cular disorders or chronic epileptic conditions, and thus the sider. and interventions that should be used with caution. hazards of naloxone might be overstated in some cases. Clinician history of As a general practice for the treatment of suspected opiate known ingestion. Then the clinician must anticipate the overdose, providers should try to support ventilation before complications from that substance and be prepared to treat administration of naloxone. Naloxone may be administered them. Table 2 lists potentially cardiotoxic drugs, signs of before intubation(ie, with bag and mask ). however, because toxicity, and therapy to consider. significant complications after administration of naloxone are uncommon and effective reversal of opiate-induced respira Drug-Induced Emergencies: Prearrest tory depression may make intubation unnecessary Naloxone Airway and Respiratory Management can be administered by the intravenous(IV), intramuscular Poisoned patients may deteriorate rapidly. Providers must (M), intranasal, or subcutaneous (SC)routes. IV is preferred ssess and frequently reassess airway, breathing, and circu- If the patient is already intubated and vascular access is not lation and support them as needed. Although consultation available, naloxone may be administered by the endotracheal with a poison control center or toxicologist may be needed to oute, although a slightly higher dose may be needed than that identify a particular toxin or antidote, the first priority of care administered by other routes. There is only anecdotal(case is support of airway, breathing, and circulation. In patients report) support for endotracheal administration of naloxone who are obtunded or comatose, perform rapid sequence for opioid overdose; intravenous and other routes (SC, IM) intubation before gastric lavage crease the risk of are preferred to the endotracheal route aspiration. Gastric lavage is recommended only for patients The duration of action of naloxone is approxin who have ingested a potentially lethal amount of a drug 70 minutes, but respiratory depression may persist for 4 to 5 toxin and present within I hour of ingestion. 7 hours with opiate ingestion or overdose. Thus, the clinical Reversal of benzodiazepine intoxication with flumazenil is effects of naloxone may not last as long as those of a associated with significant toxicity in patients with benzodi- significant opioid overdose, and repeat doses of naloxone azepine dependence8-12 or congestion of proconvulsant med- may be needed. The end points of opiate reversal are adequate ications such as tricyclic antidepressants. But it may be useful airway reflexes and ventilation, not complete arousal to reverse excessive sedation when benzodiazepines are used Acute withdrawal from opiates produces a state of sympa- for procedural sedation. 3 Thus, the routine use of flumazenil thetic excess and severe agitation. Pulmonary edema and in"coma cocktail protocols is not recommended ventricular arrhythmias are less common complications. Nal- oxone reversal of opiate intoxication should be used with (Circulation. 2005: 112: IV-126-1V-132) o 2005 American Heart Association caution in patients who are suspected of being opiate dependent, especially if they have cardiovascular disease This special supplement to Circulation is freely available at http://www.circulationaha.org In the emergency setting the recommended adult do range is 0.4 mg to 2 mg IV or 0. 4 mg to 0. 8 mg IM or SC, DOI: 10.1161/CIRCULATIONAHA. 105.166564 repeated as needed. Some opiate overdoses may require IV-126

Part 10.2: Toxicology in ECC Poisoning is an infrequent cause of cardiac arrest in older patients, but it is a leading cause of cardiac arrest in victims 40 years of age.1– 4 When a patient with poisoning is in cardiac arrest or near-arrest, immediate support of airway, breathing, and circulation is essential. Urgent consultation with a medical toxicologist or certified regional poison center is recommended5,6 because standard guidelines for emergency cardiovascular care may not be optimal in the management of acute poisoning and overdose. This section presents recommendations for the care of the patient with a toxicologic problem. Some recommendations are evidence-based, but most toxicology research in this area consists primarily of small case series (LOE 5), case reports, and animal studies (LOE 6). Hence many of these recommendations are based on expert consensus, and further research is needed to validate them. Clinicians may see a patient with a history of ingestion of an unknown substance. In such cases the clinician must be familiar with common toxidromes and their therapies. To assist during such encounters, Table 1 lists drug-induced cardiovascular emergencies or altered vital signs, potential therapies to consider, and interventions that should be used with caution. Clinicians may also encounter patients with a history of known ingestion. Then the clinician must anticipate the complications from that substance and be prepared to treat them. Table 2 lists potentially cardiotoxic drugs, signs of toxicity, and therapy to consider. Drug-Induced Emergencies: Prearrest Airway and Respiratory Management Poisoned patients may deteriorate rapidly. Providers must assess and frequently reassess airway, breathing, and circulation and support them as needed. Although consultation with a poison control center or toxicologist may be needed to identify a particular toxin or antidote, the first priority of care is support of airway, breathing, and circulation. In patients who are obtunded or comatose, perform rapid sequence intubation before gastric lavage to decrease the risk of aspiration. Gastric lavage is recommended only for patients who have ingested a potentially lethal amount of a drug or toxin and present within 1 hour of ingestion.7 Reversal of benzodiazepine intoxication with flumazenil is associated with significant toxicity in patients with benzodiazepine dependence8 –12 or coingestion of proconvulsant medications such as tricyclic antidepressants. But it may be useful to reverse excessive sedation when benzodiazepines are used for procedural sedation.13 Thus, the routine use of flumazenil in “coma cocktail” protocols is not recommended. Opiate Poisoning Opiate poisoning commonly causes respiratory depression followed by respiratory insufficiency or arrest. Heroin overdose may cause respiratory depression, and it frequently causes pulmonary edema. The respiratory effects of opioids are rapidly reversed by the opiate antagonist naloxone. In the hospital setting the administration of naloxone for acute opioid exposure has been successful without prior ventilation (LOE: 414,15; 516,17; 718) if the airway was maintained and high-flow oxygen administered and the patient was otherwise healthy with no chronic opioid addiction and no cardiovascular disease. In the out-of-hospital setting, however, the evidence indicates fewer adverse events when emergency medical services (EMS) system personnel provide ventilation (ie, provide positive-pressure ventilation with bag and mask) before administration of naloxone to all patients with opioid-induced respiratory depression (LOE 519 –21 in adults, extrapolated from pediatric cases [LOE 722,23; LOE 8]).24 The adverse effects seen in patients receiving naloxone prior to ventilation may be due to the underlying cardiovascular disorders or chronic epileptic conditions, and thus the hazards of naloxone might be overstated in some cases. As a general practice for the treatment of suspected opiate overdose, providers should try to support ventilation before administration of naloxone. Naloxone may be administered before intubation (ie, with bag and mask), however, because significant complications after administration of naloxone are uncommon and effective reversal of opiate-induced respiratory depression may make intubation unnecessary. Naloxone can be administered by the intravenous (IV), intramuscular (IM), intranasal, or subcutaneous (SC) routes. IV is preferred. If the patient is already intubated and vascular access is not available, naloxone may be administered by the endotracheal route, although a slightly higher dose may be needed than that administered by other routes. There is only anecdotal (case report) support for endotracheal administration of naloxone for opioid overdose; intravenous and other routes (SC, IM) are preferred to the endotracheal route. The duration of action of naloxone is approximately 45 to 70 minutes, but respiratory depression may persist for 4 to 5 hours with opiate ingestion or overdose. Thus, the clinical effects of naloxone may not last as long as those of a significant opioid overdose, and repeat doses of naloxone may be needed. The end points of opiate reversal are adequate airway reflexes and ventilation, not complete arousal. Acute withdrawal from opiates produces a state of sympathetic excess and severe agitation. Pulmonary edema and ventricular arrhythmias are less common complications. Naloxone reversal of opiate intoxication should be used with caution in patients who are suspected of being opiatedependent, especially if they have cardiovascular disease. In the emergency setting the recommended adult dose range is 0.4 mg to 2 mg IV or 0.4 mg to 0.8 mg IM or SC, repeated as needed. Some opiate overdoses may require (Circulation. 2005;112:IV-126-IV-132.) © 2005 American Heart Association. This special supplement to Circulation is freely available at http://www.circulationaha.org DOI: 10.1161/CIRCULATIONAHA.105.166564 IV-126

Part 10.2: Toxicology in ECC IV-127 TABLE 1. Drug-Induced Cardiovascular Emergencies or Altered Vital Signs*: Therapies to Considert and Contraindicated interventions Drug-Induced Cardiovascular Emergency or Contraindicated Interventions Altered Vital Signs* Therapies to Consider Bradycardia Pacemaker(transcutaneous or transvenous Atropine(seldom helpful except for cholinesterase Toxic drug-calcium channel blocker: inhibitor poisonings) epinephrine, calcium salt? glucose/insulin? Isoproterenol if hypotensive glucagon? NS (if hypotensive Toxic drug-B-blocker: NS, epinephrine, calcium salt? glucose/insulin? glucagon? Tachycardia Toxic drug-sympathomimetics: benzodiazepines, B-Blockers (not generally useful in drug-induced nitroprusside, labetalol Do not use propranolol for cocaine intoxication Toxic drug-tricyclic antidepressants: sodium Cardioversion(rarely indicated) bicarbonate, hyperventilation, NS, magnesium Adenosine(rarely indicated) Calcium channel blockers(rarely indicated) Toxic drug-anticholinergics: physostigmine Impaired conduction/ventricular arrhythmias Sodium bicarbonate If TCA overdose: amiodarone or type bow antiarrhythmics(eg, procainamide Hypertensive emergencies Toxic drugsympathomimetics: benzodiazepines, B-Blockers lidocaine, sodium bicarbonate, nitroglycerin Base reperfusion strategy on cardiac Shock Toxic drug-calcium channel blocker epinephrine, norepinephrine, dopamine, calcium . Avoid calcium salts if digoxin toxicity is suspecter If refractory to maximal medical therapy consider circulatory assist devices Pralidoxime/obidoxime Acute anticholinergic syndrome Physostigmine(not for TCA overdose) Opioid poisoning Assisted ventilation Do not use naloxone for meperidine-induced Tracheal intubation Unless stated otherwise, listed alterations of vital signs(bradycardia, tachycardia, tachypnea) are " hemodynamically significant tHerapies to consider should be based on specific indications Therapies followed by"? are Class Indeterminate. NS indicates normal saline; TCa, tricyclic antidepressant, and w, Vaughan Williams. titration to a total naloxone dose of 6 to 10 mg over a short Drug-Induced Hemodynamically period. For the patient with chronic opioid addiction, use Significant Bradycardia smaller dose and titrate slowly to minimize adverse cardio- Hemodynamically significant bradycardia from poisoning or vascular effects and withdrawal symptoms. There is no good drug overdose may be refractory to standard aCls protocols evidence to suggest that naloxone improves outcome in the because some toxins bind receptors or produce direct cellular patient with an opioid-induced cardiac arrest. Thus, once toxicity In these cases specific antidote therapy may be needed. rest has occurred, normal guidelines for advanced cardio- Administration of atropine may be lifesaving in organo- vascular life support(ACLS)should be followed, with airway phosphate, carbamate, or nerve agent poisoning(LOE 4).25 control coming before use of naloxone(Class [Ia). 19-21 Atropine may be administered in an initial dose of 2 to 4 mg

titration to a total naloxone dose of 6 to 10 mg over a short period. For the patient with chronic opioid addiction, use smaller dose and titrate slowly to minimize adverse cardiovascular effects and withdrawal symptoms. There is no good evidence to suggest that naloxone improves outcome in the patient with an opioid-induced cardiac arrest. Thus, once arrest has occurred, normal guidelines for advanced cardiovascular life support (ACLS) should be followed, with airway control coming before use of naloxone (Class IIa).19 –21 Drug-Induced Hemodynamically Significant Bradycardia Hemodynamically significant bradycardia from poisoning or drug overdose may be refractory to standard ACLS protocols because some toxins bind receptors or produce direct cellular toxicity. In these cases specific antidote therapy may be needed. Administration of atropine may be lifesaving in organophosphate, carbamate, or nerve agent poisoning (LOE 4).25 Atropine may be administered in an initial dose of 2 to 4 mg TABLE 1. Drug-Induced Cardiovascular Emergencies or Altered Vital Signs*: Therapies to Consider† and Contraindicated Interventions Drug-Induced Cardiovascular Emergency or Altered Vital Signs* Therapies to Consider† Contraindicated Interventions (or Use With Caution) Bradycardia • Pacemaker (transcutaneous or transvenous) • Toxic drug—calcium channel blocker: epinephrine, calcium salt? glucose/insulin? glucagon? NS (if hypotensive) • Toxic drug—-blocker: NS, epinephrine, calcium salt? glucose/insulin? glucagon? • Atropine (seldom helpful except for cholinesterase inhibitor poisonings) • Isoproterenol if hypotensive • Prophylactic transvenous pacing Tachycardia • Toxic drug—sympathomimetics: benzodiazepines, lidocaine, sodium bicarbonate, nitroglycerin, nitroprusside, labetalol • Toxic drug—tricyclic antidepressants: sodium bicarbonate, hyperventilation, NS, magnesium sulfate, lidocaine • Toxic drug—anticholinergics: physostigmine • -Blockers (not generally useful in drug-induced tachycardia) • Do not use propranolol for cocaine intoxication • Cardioversion (rarely indicated) • Adenosine (rarely indicated) • Calcium channel blockers (rarely indicated) • Physostigmine for TCA overdose Impaired conduction/ventricular arrhythmias • Sodium bicarbonate • Lidocaine • If TCA overdose: amiodarone or type IVW antiarrhythmics (eg, procainamide) Hypertensive emergencies • Toxic drug—sympathomimetics: benzodiazepines, lidocaine, sodium bicarbonate, nitroglycerin, nitroprusside, phentolamine • -Blockers Acute coronary syndrome • Benzodiazepines • Lidocaine • Sodium bicarbonate • Nitroglycerin • Aspirin, heparin • Base reperfusion strategy on cardiac catheterization data • -Blockers Shock • Toxic drug—calcium channel blocker: NS, epinephrine, norepinephrine, dopamine, calcium salt? glucose/insulin? glucagon? • Toxic drug—-blocker: NS, epinephrine, norepinephrine, dopamine, calcium salt? glucose/insulin? glucagon? • If refractory to maximal medical therapy: consider circulatory assist devices • Isoproterenol • Avoid calcium salts if digoxin toxicity is suspected Acute cholinergic syndrome • Atropine • Pralidoxime/obidoxime • Succinylcholine Acute anticholinergic syndrome • Benzodiazepine • Physostigmine (not for TCA overdose) • Antipsychotics • Other anticholinergic agents Opioid poisoning • Assisted ventilation • Naloxone • Tracheal intubation • Do not use naloxone for meperidine-induced seizures *Unless stated otherwise, listed alterations of vital signs (bradycardia, tachycardia, tachypnea) are “hemodynamically significant.” †Therapies to consider should be based on specific indications. Therapies followed by “?” are Class Indeterminate. NS indicates normal saline; TCA, tricyclic antidepressant; and VW, Vaughan Williams. Part 10.2: Toxicology in ECC IV-127

IV-128 Circulation December 13. 2005 2. Potentially Cardiotoxic Drugs: Cardiopulmonary Signs* of Toxicity and therapy to consider Toxic Drugs: by Type of Agent monary Signs* of Toxicity herapy to Consider · Tachycardia Benzodiazepines · Amphetamines Supraventricular arrhythmias Lidocaine · Methamphetamines · Ventricular arrhythmias Sodium bicarbonate (for cocaine-related ventricular arrhythmias Cocaine · Impaired conduction · Nitroglycerin · Phencyclidine(PCP · Hypertensive crises Acute coronary syndromes Reperfusion strategy based on cardiac catheterization data Phentolamine (ar-adrenergic blocke Cardiac arrest B-Blockers relatively contraindicated (do not use propranolol for cocaine intoxicaton Calcium channel blockers · Bradycardia NS boluses(0.5 to 1 L) · Impaired conduction Epinephrine IV; or other a/B-agonists Nifedipine(and other dihydropyridines Diltiazem Cardiac arrest Circulatory assist devices? Calcium infusions B-Adrenergic receptor antagonists · Bradycardia · NS boluses0.5to1u Propranolol · Impaired conduction Epinephrine IV; or other a/B-agonists Atenolol Shock Pacemakers Sotalol Cardiac arrest Circulatory assist devices? Metropolol Tricyclic antidepressant · Tachycardia Sodium bicarbonate · Amitriptyline · Bradycardia Hyperventilate De · Ventricular arrhythmias NS boluses (0.5 to 1 L) · Nortriptyline · mpaired conduction Magnesium sulfate Lidocaine Cardiac arrest Epinephrine IV; or other a/B-agonists Cardiac glycosides · Bradycardia Restore total body K- Supraventricular arrhythmias store intravascular volum · Ventricular arrhythmias Digoxin-specific antibodies(Fab fragments: Digibind or DigiFab · Impaired conduction Pacemakers (use caution and monitor for ventricular arrhythmias Cardiac arrest Anticholinergic Physostigmine Diphenhydramine Supraventricular arrhythmias Doxylamine Ventricular arrhythmias · Impaired conduction · Shock, cardiac arrest · Bradycardia Carbamates Decontamination Nerve agents Impaired conduction, shock Pralidoxime Organophosphates · Pulmonary edema Opioids Hypoventilation(slow and shallow Assisted ventilation Heroi respirations, apnea Naloxone · Bradycardia Tracheal intubation Methadone potension · Morphine · Miosis (pupil constriction Lactic acidosis with/without seizures Pyridoxine (vitamin Bahlarge doses may be needed (ie, 1 g Tachycardia or bradycardia pyridoxine/g of ingested · Shock, cardiac arrest Sodium channel blockers(Class lyw Sodium bicarbonate antiarrhythmics Procainamide · Impaired conduction aeand B-agonist sopyramide Seizures Lidocaine(not for lidocaine overdose) Lidocaine · Shock, cardiac arrest Hypertonic saline Propafenone Unless stated otherwise, listed alterations of vital signs(bradycardia, tachycardia, tachypnea) are " hemodynamically signific specific therapy to consider should be based on specific indications. Therapies followed by"? are Class Indeterminate

TABLE 2. Potentially Cardiotoxic Drugs: Cardiopulmonary Signs* of Toxicity and Therapy to Consider† Potentially Toxic Drugs: by Type of Agent Cardiopulmonary Signs* of Toxicity Therapy to Consider† Stimulants (sympathomimetics) • Amphetamines • Methamphetamines • Cocaine • Phencyclidine (PCP) • Ephedrine • Tachycardia • Supraventricular arrhythmias • Ventricular arrhythmias • Impaired conduction • Hypertensive crises • Acute coronary syndromes • Shock • Cardiac arrest • Benzodiazepines • Lidocaine • Sodium bicarbonate (for cocaine-related ventricular arrhythmias) • Nitroglycerin • Nitroprusside • Reperfusion strategy based on cardiac catheterization data • Phentolamine (1-adrenergic blocker) • -Blockers relatively contraindicated (do not use propranolol for cocaine intoxication) Calcium channel blockers • Verapamil • Nifedipine (and other dihydropyridines) • Diltiazem • Bradycardia • Impaired conduction • Shock • Cardiac arrest • NS boluses (0.5 to 1 L) • Epinephrine IV; or other /-agonists • Pacemakers • Circulatory assist devices? • Calcium infusions • Glucose/insulin infusion? • Glucagon -Adrenergic receptor antagonists • Propranolol • Atenolol • Sotalol • Metropolol • Bradycardia • Impaired conduction • Shock • Cardiac arrest • NS boluses (0.5 to 1 L) • Epinephrine IV; or other /-agonists • Pacemakers • Circulatory assist devices? • Calcium infusions? • Glucose/insulin infusion? • Glucagon Tricyclic antidepressants • Amitriptyline • Desipramine • Nortriptyline • Imipramine • Tachycardia • Bradycardia • Ventricular arrhythmias • Impaired conduction • Shock • Cardiac arrest • Sodium bicarbonate • Hyperventilation • NS boluses (0.5 to 1 L) • Magnesium sulfate • Lidocaine • Epinephrine IV; or other /-agonists Cardiac glycosides • Digoxin • Digitoxin • Foxglove • Oleander • Bradycardia • Supraventricular arrhythmias • Ventricular arrhythmias • Impaired conduction • Shock • Cardiac arrest • Restore total body K, Mg • Restore intravascular volume • Digoxin-specific antibodies (Fab fragments: Digibind or DigiFab) • Atropine • Pacemakers (use caution and monitor for ventricular arrhythmias) • Lidocaine • Phenytoin? Anticholinergics • Diphenhydramine • Doxylamine • Tachycardia • Supraventricular arrhythmias • Ventricular arrhythmias • Impaired conduction • Shock, cardiac arrest • Physostigmine Cholinergics • Carbamates • Nerve agents • Organophosphates • Bradycardia • Ventricular arrhythmias • Impaired conduction, shock • Pulmonary edema • Bronchospasm • Cardiac arrest • Atropine • Decontamination • Pralidoxime • Obidoxime Opioids • Heroin • Fentanyl • Methadone • Morphine • Hypoventilation (slow and shallow respirations, apnea) • Bradycardia • Hypotension • Miosis (pupil constriction) • Assisted ventilation • Naloxone • Tracheal intubation • Nalmefene Isoniazid • Lactic acidosis with/without seizures • Tachycardia or bradycardia • Shock, cardiac arrest • Pyridoxine (vitamin B6)—large doses may be needed (ie, 1 g pyridoxine/g of ingested isoniazid) Sodium channel blockers (Class IVW antiarrhythmics) • Procainamide • Disopyramide • Lidocaine • Propafenone • Flecainide • Bradycardia • Ventricular arrhythmias • Impaired conduction • Seizures • Shock, cardiac arrest • Sodium bicarbonate • Pacemakers • - and -agonist • Lidocaine (not for lidocaine overdose) • Hypertonic saline *Unless stated otherwise, listed alterations of vital signs (bradycardia, tachycardia, tachypnea) are “hemodynamically significant.” †Specific therapy to consider should be based on specific indications. Therapies followed by “?” are Class Indeterminate. IV-128 Circulation December 13, 2005

Part 10.2: Toxicology in ECC IV-129 for bradycardia resulting from acetylcholinesterase-inhibiting blood pressure may not be warranted. Thus, short-acting gents, and large total doses may be required. Providers antihypertensive agents, such as nitroprusside, are preferred should notify the pharmacy to obtain a large amount(eg, 20 in patients who are refractory to benzodiazepine therapy to 40 mg or higher) of atropine for use if needed. Nonselective B-antagonist receptor blocking agents, such as Isoproterenol is contraindicated in acetylcholinesteras propranolol, are contraindicated in poisoning by sympath- nduced bradycardias, although it may be useful at high doses mimetic agents. Blockade of B-receptors with unopposed in refractory bradycardia induced by B-antagonist receptor a-receptor stimulation may worsen hypertension. 31 Labetalol, blockade. Heart block and ventricular arrhythmias associated a mixed a-and B-receptor antagonist, may be used with with digoxin or digitalis glycoside poisoning may be effec- caution as thir apy(LOE 5). 6 Antibody-specific therapy may also be effec- tive in poisoning caused by plants and Chinese herbal Drug-Induced Acute Coronary Syndromes medications containing digitalis glycosides (LOE 2,827.28, Acute coronary syndromes(ACS) can develop in patients LOE 526). Transcutaneous pacing may be effective in mild to with cocaine overdose. ACS results from coronary artery moderate hemodynamically significant bradycardia associ- vasoconstriction with resultant coronary ischemia that is ated with poisoning and overdose exacerbated by tachycardia and hypertension associated with excess sympathetic nervous system stimulation Drug-Induced Hemodynamically Significant Tachycardia Fibrinolytics are thought to have a higher risk-to-benefit ratio when used in the context of drug-induced ACS, partic- Drug-induced hemodynamically significant tachycardia may ularly in the presence of severe hypertension, so they should cause myocardial ischemia, myocardial infarction, or ventric- ular arrhythmias and may lead to high-output heart failure be used with caution if at all. 32 Intracoronary administration and shock. Adenosine and synchronized cardioversion are of fibrinolytics or coronary vasodilators is preferred to unlikely to be of benefit in this context given the ongoing peripheral administration Cardiac catheterization studies in cocaine overdose have presence of a toxin. Some drug-induced tachyarrhythmias however, may be successfully treated with adenosine (LOe shown that nitroglycerin and phentolamine reverse cocaine- 5).29 In patients with borderline hypotension, diltiazem and induced vasoconstriction. Labetalol has no significant effect. verapamil are contraindicated because they may further lower and propranolol worsens it.33-36 Therefore, nitroglycerin and blood pressure benzodiazepines are first-line agents, phentolamine Benzodiazepines such as diazepam or lorazepam are safe second-line agent, and propranolol is contraindicated for and effective in patients with drug-induced hemodynamically cocaine-induced ACS. Although labetalol has been reported significant tachycardia resulting from sympathomimetic to be effective in isolated cases of cocaine toxicity, 37, 38 use of this agent is controversial because it blocks the peripheral agents. When large quantities of benzodiazepines are used to signs of drug-induced sym treat poisoning or overdose, providers must closely monitor the patients level of consciousness, ventilatory effort, and central nervous system effects such as seizures. Esmolol and respiratory function because the sedative effects of the metoprolol may induce hypotension. 39 enzodiazepines may produce respiratory depression and loss of protective airway reflexes Drug-Induced Ventricular Tachycardia and hysostigmine is a specific antidote that may be preferable Ventricular fibrillation for drug-induced hemodynamically significant tachycardia When a patient develops sudden conversion to a wide- and central anticholinergic syndrome caused by pure anticho- complex rhythm with hypotension, drug-induced ventricular linergic poisoning 30 Physostigmine must be used with cau tachycardia (VT) is likely and cardioversion is indicated. If tion because it can produce symptoms of cholinergic crisis the patient is unstable and polymorphic VT is present, such as copious tracheobronchial secretions(frequent high-energy unsynchronized shocks(defibrillation doses) tioning will be required), seizures, bradycardia, and even Use of antiarrhythmics is indicated in cases of hemod asystole if given in excessive doses or given too rapidly. namically stable drug-induced VT. Lidocaine is the antar- rhythmic of choice in most cases of drug-induced monomor aged with benzodiazepines alone, but at least one clinical phic VT. Types IA and Ic and other antiarrhythmics that block study suggested that physostigmine used appropriately may the fast sodium channel (eg, sotalol) are contraindicated in offer superior results (LOE 4). 30 Physostigmine should not be cases of poisoning with tricyclic antidepressants or other fast administered for anticholinergic symptoms associated with sodium channel blockers because of the risk of synergistic tricyclic antidepressant overdose. Consultation with a medi toxicity. The efficacy and safety of phenytoin for tricyclic cal toxicologist or regional poison center is recommended antidepressant poisoning has been questioned and is no longer recommended. 40 41 Magnesium has beneficial effects Drug-Induced Hypertensive Emergencies in certain cases of drug-induced VT(LOE 542), but it may Benzodiazepines are the drug class of choice for treatment of also aggravate drug-induced hypotension. 43.44 drug-induced hypertension because they decrease the effects Torsades de pointes can occur with either therapeutic or of endogenous catecholamine release. Hypotension may fol- toxic exposure to many drugs. Administration of magnesium low drug-induced hypertension, and aggressive control of is recommended for patients with torsades de pointes even

for bradycardia resulting from acetylcholinesterase-inhibiting agents, and large total doses may be required. Providers should notify the pharmacy to obtain a large amount (eg, 20 to 40 mg or higher) of atropine for use if needed. Isoproterenol is contraindicated in acetylcholinesteraseinduced bradycardias, although it may be useful at high doses in refractory bradycardia induced by -antagonist receptor blockade. Heart block and ventricular arrhythmias associated with digoxin or digitalis glycoside poisoning may be effectively treated with digoxin-specific antibody fragment therapy (LOE 5).26 Antibody-specific therapy may also be effective in poisoning caused by plants and Chinese herbal medications containing digitalis glycosides (LOE 2, 827,28; LOE 526). Transcutaneous pacing may be effective in mild to moderate hemodynamically significant bradycardia associated with poisoning and overdose. Drug-Induced Hemodynamically Significant Tachycardia Drug-induced hemodynamically significant tachycardia may cause myocardial ischemia, myocardial infarction, or ventricular arrhythmias and may lead to high-output heart failure and shock. Adenosine and synchronized cardioversion are unlikely to be of benefit in this context given the ongoing presence of a toxin. Some drug-induced tachyarrhythmias, however, may be successfully treated with adenosine (LOE 5).29 In patients with borderline hypotension, diltiazem and verapamil are contraindicated because they may further lower blood pressure. Benzodiazepines such as diazepam or lorazepam are safe and effective in patients with drug-induced hemodynamically significant tachycardia resulting from sympathomimetic agents. When large quantities of benzodiazepines are used to treat poisoning or overdose, providers must closely monitor the patient’s level of consciousness, ventilatory effort, and respiratory function because the sedative effects of the benzodiazepines may produce respiratory depression and loss of protective airway reflexes. Physostigmine is a specific antidote that may be preferable for drug-induced hemodynamically significant tachycardia and central anticholinergic syndrome caused by pure anticholinergic poisoning.30 Physostigmine must be used with caution because it can produce symptoms of cholinergic crisis such as copious tracheobronchial secretions (frequent suctioning will be required), seizures, bradycardia, and even asystole if given in excessive doses or given too rapidly. Often patients with anticholinergic intoxication can be managed with benzodiazepines alone, but at least one clinical study suggested that physostigmine used appropriately may offer superior results (LOE 4).30 Physostigmine should not be administered for anticholinergic symptoms associated with tricyclic antidepressant overdose. Consultation with a medical toxicologist or regional poison center is recommended. Drug-Induced Hypertensive Emergencies Benzodiazepines are the drug class of choice for treatment of drug-induced hypertension because they decrease the effects of endogenous catecholamine release. Hypotension may follow drug-induced hypertension, and aggressive control of blood pressure may not be warranted. Thus, short-acting antihypertensive agents, such as nitroprusside, are preferred in patients who are refractory to benzodiazepine therapy. Nonselective -antagonist receptor blocking agents, such as propranolol, are contraindicated in poisoning by sympathomimetic agents. Blockade of -receptors with unopposed -receptor stimulation may worsen hypertension.31 Labetalol, a mixed - and -receptor antagonist, may be used with caution as third-line therapy in patients with refractory drug-induced hypertension. Drug-Induced Acute Coronary Syndromes Acute coronary syndromes (ACS) can develop in patients with cocaine overdose. ACS results from coronary artery vasoconstriction with resultant coronary ischemia that is exacerbated by tachycardia and hypertension associated with excess sympathetic nervous system stimulation. Fibrinolytics are thought to have a higher risk-to-benefit ratio when used in the context of drug-induced ACS, particularly in the presence of severe hypertension, so they should be used with caution if at all.32 Intracoronary administration of fibrinolytics or coronary vasodilators is preferred to peripheral administration. Cardiac catheterization studies in cocaine overdose have shown that nitroglycerin and phentolamine reverse cocaineinduced vasoconstriction. Labetalol has no significant effect, and propranolol worsens it.33–36 Therefore, nitroglycerin and benzodiazepines are first-line agents, phentolamine is a second-line agent, and propranolol is contraindicated for cocaine-induced ACS. Although labetalol has been reported to be effective in isolated cases of cocaine toxicity,37,38 use of this agent is controversial because it blocks the peripheral signs of drug-induced sympathetic excess without affecting central nervous system effects such as seizures. Esmolol and metoprolol may induce hypotension.39 Drug-Induced Ventricular Tachycardia and Ventricular Fibrillation When a patient develops sudden conversion to a widecomplex rhythm with hypotension, drug-induced ventricular tachycardia (VT) is likely and cardioversion is indicated. If the patient is unstable and polymorphic VT is present, use high-energy unsynchronized shocks (defibrillation doses). Use of antiarrhythmics is indicated in cases of hemodynamically stable drug-induced VT. Lidocaine is the antiarrhythmic of choice in most cases of drug-induced monomorphic VT. Types IA and IC and other antiarrhythmics that block the fast sodium channel (eg, sotalol) are contraindicated in cases of poisoning with tricyclic antidepressants or other fast sodium channel blockers because of the risk of synergistic toxicity. The efficacy and safety of phenytoin for tricyclic antidepressant poisoning has been questioned and is no longer recommended.40,41 Magnesium has beneficial effects in certain cases of drug-induced VT (LOE 542), but it may also aggravate drug-induced hypotension.43,44 Torsades de pointes can occur with either therapeutic or toxic exposure to many drugs. Administration of magnesium is recommended for patients with torsades de pointes even Part 10.2: Toxicology in ECC IV-129

lV-130 Circulation December 13. 2005 when the serum magnesium concentration is normal (Class ever, typically includes cardiovascular dysfunction with de IIa) Summary of therapy creased myocardial contractility and low SvR that requires a combination of volume therapy and myocardial support. Correction of hypoxia, hypokalemia, and hypomagnesemia is critical Initial treatment will require a fluid challenge to correct The effectiveness of lidocaine in treatment of torsades de relative hypovolemia and optimize preload. In cardiotoxic poisoning congestive heart failure may limit tolerance of, and Electrical overdrive pacing at rates of 100 to 120 beats per response to, fluid administration. Central hemodynamic mon- minute may terminate torsades de pointes. titrate therap Pharmacologic overdrive pacing with isoproterenol may be effective (loe 8).45 Patients unresponsive to fluid loading may require inotrope or vasopressor support, or both. Dopamine is often the Some toxicologists recommend potassium supplementation recommended initial agent. However, drug-induced shock even when the serum potassium is normal. following overdose of some drugs (eg, calcium channel High level studies have not established the safety and blockers)will require administration and titration of a variety efficacy of any of these recommended therapies for drug of cardiovascular medication duced polymorphic VT( Class Indeterminate Drug-Induced Distributive Shock Distributive shock is associated with normal or even high Drug-Induced Impaired Conduction cardiac output and low SVR. Treatment with a-adrenergic Hypertonic saline and systemic alkalinization may prevent or drugs such as norepinephrine or phenylephrine may be terminate VT secondary to poisoning from sodium channel needed. Case reports suggest that vasopressin may also be blocking agents(eg, procainamide, flecainide)and tricyclic useful. 51 More powerful vasoconstrictors such as endothelin antidepressants (LOE 5). 0.47 Sodium bicarbonate provides are not yet available in the United States and have not been hypertonic saline and induces systemic alkalinization; hyper well studied. Watch for the development of ventricular nic saline alone may be effective in treating the impaired arrhythmias with the use of these agents. Caution: Avoid conduction associated with these agents 4s when sodium dobutamine and isoproterenol, which may worsen hypoten bicarbonate is used to treat arrhythmias and hypotension, the sion by further decreasing SVR. goal of alkalinization is to maintain an arterial pH of 7.45 to 7.55 with repeated boluses of I to 2 mEq/kg of sodium Drug-Induced Cardiogenic Shock bicarbonate.Although no study has investigated the optimal Drug-induced cardiogenic shock is associated with low car- target pH with bicarbonate therapy, this pH range has been diac output and high SVR. Cardiac ischemia may also be commonly accepted and seems reasonable. A maintenance present in these patients. In addition to volume titration and infusion of 150 mEq/L of sodium bicarbonate plus 30 mEq use of sympathomimetic drugs such as dobutamine, inotropic KCI/L in D5 W is recommended(Class IIa). Boluses of support may be provided by agents such as inamrinone sodium bicarbonate are used without prior determination of calcium, glucagon, insulin, or even isoproterenol, dependir serum pH for acute decompensation if the QRS duration is on the toxic agent(s) identified 52.53 Concurrent vasopressor >100 milliseconds or if hypotensi therapy is often required. 54 There is insufficient evidence to recommend for or against the use of sodium bicarbonate in adults with calcium channel Drug-Induced Cardiac Arrest blocker overdose (Class Indeterminate). Calcium channe Cardioversion/defibrillation antagonist and B-adrenergic antagonist overdose may lead to Electric defibrillation is appropriate for pulseless patient seriously impaired conduction. These patients may require with drug-induced VT or ventricular fibrillation (VF) and chronotropic adrenergic agents such as epinephrine, use also for unstable patients with polymorphic VT. In cases of glucagon in high doses(although the data to support this is sympathomimetic poisoning with refractory VE, increase the inadequate and primarily limited to animal studies ), 49 or interval between doses of epinephrine and use only standard possibly pacing. 50 dosing. Propranolol is contraindicated in cocaine overdose. It was thought to be contraindicated in sympathomimetic poi- Drug-Induced Shock soning, but there are some case reports suggesting that it may Drug-induced shock may produce a decrease in intravascular be useful in the treatment of ephedrine and pseudoephedrine volume, a decrease in systemic vascular resistance (SVR), overdose. 55 these factors. In addition, drugs can disable normal compen- Prolonged CPR and Resuscitantotation may be warranted in vascular dysfunction that render drug-induced shock refrac- patients with poisoning or overdose, especially those with tory to many standard therapies. calcium channel blocker poi LOE 5).56 In cases of severe poisoning, recovery with good neurologic outcomes Drug-Induced Hypovolemic Shock has been reported in patients who received prolonged CPR Overdose of some drugs or chemicals(eg, zinc salts)can (eg, 3 to 5 hours). 52,53 Cardiopulmonary bypass (extracorpo- cause excessive fluid loss through the gastrointestinal tract, real membrane oxygenation) has been used successfully resulting in pure hypovolemia. Drug-induced shock, how- resuscitation of patients with severe poisoning. 57

when the serum magnesium concentration is normal (Class IIa). Summary of therapy: ● Correction of hypoxia, hypokalemia, and hypomagnesemia is critical. ● The effectiveness of lidocaine in treatment of torsades de pointes has not been demonstrated. ● Electrical overdrive pacing at rates of 100 to 120 beats per minute may terminate torsades de pointes. ● Pharmacologic overdrive pacing with isoproterenol may be effective (LOE 8).45 ● Some toxicologists recommend potassium supplementation even when the serum potassium is normal. High level studies have not established the safety and efficacy of any of these recommended therapies for druginduced polymorphic VT (Class Indeterminate). Drug-Induced Impaired Conduction Hypertonic saline and systemic alkalinization may prevent or terminate VT secondary to poisoning from sodium channel blocking agents (eg, procainamide, flecainide) and tricyclic antidepressants (LOE 5).46,47 Sodium bicarbonate provides hypertonic saline and induces systemic alkalinization; hypertonic saline alone may be effective in treating the impaired conduction associated with these agents.48 When sodium bicarbonate is used to treat arrhythmias and hypotension, the goal of alkalinization is to maintain an arterial pH of 7.45 to 7.55 with repeated boluses of 1 to 2 mEq/kg of sodium bicarbonate. Although no study has investigated the optimal target pH with bicarbonate therapy, this pH range has been commonly accepted and seems reasonable. A maintenance infusion of 150 mEq/L of sodium bicarbonate plus 30 mEq KCl/L in D5W is recommended (Class IIa). Boluses of sodium bicarbonate are used without prior determination of serum pH for acute decompensation if the QRS duration is 100 milliseconds or if hypotension develops. There is insufficient evidence to recommend for or against the use of sodium bicarbonate in adults with calcium channel blocker overdose (Class Indeterminate). Calcium channel antagonist and -adrenergic antagonist overdose may lead to seriously impaired conduction. These patients may require chronotropic adrenergic agents such as epinephrine, use of glucagon in high doses (although the data to support this is inadequate and primarily limited to animal studies),49 or possibly pacing.50 Drug-Induced Shock Drug-induced shock may produce a decrease in intravascular volume, a decrease in systemic vascular resistance (SVR), diminished myocardial contractility, or a combination of these factors. In addition, drugs can disable normal compensatory mechanisms. It is these combined aspects of cardiovascular dysfunction that render drug-induced shock refractory to many standard therapies. Drug-Induced Hypovolemic Shock Overdose of some drugs or chemicals (eg, zinc salts) can cause excessive fluid loss through the gastrointestinal tract, resulting in pure hypovolemia. Drug-induced shock, however, typically includes cardiovascular dysfunction with decreased myocardial contractility and low SVR that requires a combination of volume therapy and myocardial support. Initial treatment will require a fluid challenge to correct relative hypovolemia and optimize preload. In cardiotoxic poisoning congestive heart failure may limit tolerance of, and response to, fluid administration. Central hemodynamic monitoring with a pulmonary artery catheter may be required to titrate therapy. Patients unresponsive to fluid loading may require inotrope or vasopressor support, or both. Dopamine is often the recommended initial agent. However, drug-induced shock following overdose of some drugs (eg, calcium channel blockers) will require administration and titration of a variety of cardiovascular medications. Drug-Induced Distributive Shock Distributive shock is associated with normal or even high cardiac output and low SVR. Treatment with -adrenergic drugs such as norepinephrine or phenylephrine may be needed. Case reports suggest that vasopressin may also be useful.51 More powerful vasoconstrictors such as endothelin are not yet available in the United States and have not been well studied. Watch for the development of ventricular arrhythmias with the use of these agents. Caution: Avoid dobutamine and isoproterenol, which may worsen hypotension by further decreasing SVR. Drug-Induced Cardiogenic Shock Drug-induced cardiogenic shock is associated with low cardiac output and high SVR. Cardiac ischemia may also be present in these patients. In addition to volume titration and use of sympathomimetic drugs such as dobutamine, inotropic support may be provided by agents such as inamrinone, calcium, glucagon, insulin, or even isoproterenol, depending on the toxic agent(s) identified.52,53 Concurrent vasopressor therapy is often required.54 Drug-Induced Cardiac Arrest Cardioversion/Defibrillation Electric defibrillation is appropriate for pulseless patients with drug-induced VT or ventricular fibrillation (VF) and also for unstable patients with polymorphic VT. In cases of sympathomimetic poisoning with refractory VF, increase the interval between doses of epinephrine and use only standard dosing. Propranolol is contraindicated in cocaine overdose. It was thought to be contraindicated in sympathomimetic poisoning, but there are some case reports suggesting that it may be useful in the treatment of ephedrine and pseudoephedrine overdose.55 Prolonged CPR and Resuscitation More prolonged CPR and resuscitation may be warranted in patients with poisoning or overdose, especially those with calcium channel blocker poisoning (LOE 5).56 In cases of severe poisoning, recovery with good neurologic outcomes has been reported in patients who received prolonged CPR (eg, 3 to 5 hours).52,53 Cardiopulmonary bypass (extracorporeal membrane oxygenation) has been used successfully in resuscitation of patients with severe poisoning.57 IV-130 Circulation December 13, 2005

Part 10.2: Toxicology in ECC IV-131 Summary 19. Osterwalder J. Naloxone for intoxications with intravenous heroin and Use of standard ACLs protocols for all patients who are Toxicol Clin Toxicol 1996 3 critically poisoned may not result in an optimal outcome. 20. Sporer KA, Firestone I, Isaacs SM. Out-of-hospital treatment of opioid Care of patients with severe poisonin be enhanced by verdoses in an urban setting. Acad Emerg Med. 1996: 3: 660-667 consultation with a medical toxicologist or regional poison 21. Wanger K, Brough L, Macmillan I, Goulding J, MacPhail I, Christenson JM. center. Alternative approaches that fective in Intravenous vs subcutaneous naloxone for out-of-hospital management of presumed opioid overdose. Acad Emerg Med. 1998: 5: 293-299 22. Hasan RA, Benko AS, Nolan BM. Campe J, Duff J, Zureikat GY Higher doses of medication than those in standard 23. Sporer KA. Acute heroin overdose. Ann Intern Med. 1999: 130: 584-590 Nonstandard drug therapies, including inamrinone, calcium 24. Schneir AB, Vadeboncoeur TF, Offerman SR, Barry JD, Ly BT, williams SR, Clark RF. Massive OxyContin ingestion refractory to naloxone chloride, glucagon, insulin, labetalol, phenylephrine, phy- therapy. Ann Emerg Med. 2002: 40: 425-428 sostigmine, and sodium bicarbonate 25. Sungur M, Guven M. Intensive care management of organophosphate Use of specific antagonists or antidotes insecticide poisoning. Crit Care. 2001: 5: 211-215 26. Bosse GM, Pope TM. Recurrent digoxin Heroic measures, such as prolonged CPR and possible use digoxin-specific Fab antibody fragments. J Emerg Med. 1994: 12: 179-18 of circulatory assist devices such as extracorporeal mem- 27. Eddleston M, Rajapakse S, Rajakanthan, Jayalath S, Sjostrom L, San brane oxyger tharaj w, Thenabadu PN, Sheriff MH, Warrell DA. Anti-digoxin Fab ragments in cardiotoxicity induced by ingestion of yellow oleander: randomised controlled trial. Lancet. 2000: 355: 967-972 References 28. Dasgupta A, Szelei-Stevens KA. Neutralization of free digoxin-like 1. Litovitz TL, Felberg L, white S, Klein-Schwartz w.1995 annual report immunoreactive components of oriental medicines Dan Shen and of the American Association of Poison Control Centers Toxic Exposure Lu-Shen-Wan by the Fab fragment of antidigoxin antibody(Digibind) Surveillance System. Am J Emerg Med. 1996: 14: 487-537 Am J Clin Pathol. 2004: 121: 276-28I 2. McCaig LF, Burt Cw. Poisoning-related visits to emergency departments 29. Tracey JA, Cassidy N, Casey PB, Ali I Bupropion(Zyban) toxicity. Ir in the United States. 1993-1996.J Toxicol Clin Toxicol. 1999: 37. MedJ.2002;95:23-24 30. Burns M. Linden Ch Graudins A. Brown RM. Fletcher KE. A con 3. Fingerhut LA, Cox CS. Poisoning mortality, 1985-1995. Public Health parison of physostigmine and benzodiazepines for the treatment of anti- Rep.1998:113:218-233. cholinergic poisoning. Ann Energ Med. 2000: 35: 374-381 4. Watson WA, Litovitz TL, Klein-Schwartz w, Rodgers GC Jr, Youniss J, 31.Ramoska E, Sacchetti AD Propranolol-induced hypertension in treatment Reid n, Rouse wG, Rembert Rs, Borys D. 2003 annual report of the of cocaine intoxication. Ann Emerg Med. 1985: 14: 1112-1113 American Association of Poison Control Centers Toxic Exposure Sur- 32. Hollander JE, Wilson LD, Shih LP. Complications from the use of veillance System. Am J Emerg Med. 2004: 22: 335-40 thrombolytic agents in patients with cocaine associated chest pain. 5. Facility assessment guidelines for regional toxicology treatment centers. J Emerg Med.1996:14:731-736 American Academy of Clinical Toxicology. J Taxico! Clin Toxicol. 33. Brogan wCl. Lange ra. Kim AS Moliterno DJ. Hillis LD. Alleviation 993:31:211-217 of cocaine-induced coronary vasoconstriction by nitroglycerin. J Am Coll 6. Poison information and treatment systems. American College of Cardiol.1991;18:58l-586 mergency Physicians. Ann Emerg Med. 1996: 28: 384 34. Lange RA, Cigarroa RG, Yancy CW Jr, willard JE, Popma JJ, Sills MN, 7. Chyka PA. Seger D, Krenzelok EP. Vale JA Position paper: single-dose McBride w,Kim AS, Hillis LD Cocaine-induced coronary-artery vaso- activated charcoal. Clin Taxico!(Phila). 2005: 43: 61-87. constriction. N Engl J Med. 1989 321: 1557-1562. 8. Amrein R, Hetzel w, Hartmann D, Lorscheid T. Clinical pharmacology 35. Lange RA, Cigarroa RG, Flores ED, McBride w, Kim As, Wells PJ, of flumazenil. Eur J Anaesth. 1988: 2: 65-80. Bedotto JB. Danziger RS. Hillis LD. Potentiation of cocaine-induced 9. Amrein R, Leishman B, Bentzinger C. et al. Flumazenil in benzodi- oronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990:112897-903 thesiology. Med Toxicol. 1987; 2: 411-429 36. Boehrer JD, Moliterno DJ. willard JE, Hillis LD. Lange RA. Influence of 10. Fluckiger A, Hartmann D, Leishman B, et al. Lack of effect of the labetalol on cocaine-induced coronary vasoconstriction in humans benzodiazepine antagonist flumazenil(Ro 15-1788)on the performanc of healthy subjects during experimentally induced ethanol intoxication. 57. Gay GR, Loper KA. The use of labetalol in the management of cocaine Eur J Clin Pharmacol. 1988: 34: 273-276 17:282-283. 11. Lukes SE, Griffiths RR. Precipitated withdrawal by a benzodiazepine 38. Dusenberry SJ, Hicks MI, Mariani PJ. Labetalol treatment of cocaine receptor antagonist(Ro-15-1788)after 7 days of diazepam. Science. Ann Emerg Med. 1987; 16: 235 982;217:l161-116 39. Sand IC, Brody SL, Wrenn KD Slovis CM. Experience with esmolol for 12. Martens F, Koppel C, Ibe K, et al. Clinical experience with the benzo- the treatment of cocaine-associated cardiovascular complications AIm J Emerg Med. 1991: 9: 161-163. ist flumazenil in suspected benzodiazepine or ethanol 40. Mayron R. Ruiz E. Phenytoin: does it reverse tricyclic-ant poisoning. J Taricol Clin Toxicol. 1990: 28: 341-356 ant-induced 13. Pitetti RD. Singh S, Pierce MC. Safe and efficacious use of procedural rdiac conduction abnormalities? Ann Emerg Med. 1986, 15: 876-880 41. Callaham M, Schumaker H, Pentel P. Phenytoin prophy laxis of cardio- department. Arch Pediatr Adolesc Med. 2003: 157: 1090-1096. in experimental amitriptyline poisoning. J Pharmacol Erp Ther 14. Gill AM, Cousins A, Nunn AJ, Choonara JA Opiate-induced respiratory 42. Citak A, Soysal DD, Ucsel R, Karabocuoglu M, Uzel N. Efficacy of long depression in pediatric patients. Ann Pharmacother. 1996: 30: 125-12 15. Herschel M. Kloshnood B. Lass NA. Role of naloxone in newbom isoning. Eur J Emerg Med. 2002: 9: 63-66 resuscitation. Pediatrics. 2000: 106: 831-834 43. Knudsen K, Abrahamsson J. Effects of magnesium sulfate and lidocaine 16. Lewis JM. Klein-Schwartz w. Benson BE, Oderda GM. Takai S. Con- n the treatment of ventricular arm in experimental amitriptyline naloxone infusion in pediatric narcotic overdose. Am J/ Dis Child poisoning in the rat. Crit Care Med. 1994: 22: 494-40 44. Kline JA. DeStefano AA, Schroeder JD. Raymond RM. Magnesium 17. Romac DR. Safety of prolonged, high-dose infusion of naloxone hydro- potentiates imipramine toxicity in the isolated rat heart. Ann Emerg Med. chloride for severe methadone overdose. Clin Phar. 1986: 5: 251-254 1994:24:224-232 18. Singhal N, McMillan DD, Yee WH, Akierman AR. Yee YJ. Evaluation 45. Gowda RM. Khan IA. Punukollu g. vasavada BC. Sacchi T]. Wilbur SL. of the effectiveness of the standardized neonatal resuscitation program. Female preponderance in ibutilide-induced torsade de pointes. Int Perinatol.2001:21:388-392 Cardio.200495:219-222

Summary Use of standard ACLS protocols for all patients who are critically poisoned may not result in an optimal outcome. Care of patients with severe poisoning can be enhanced by consultation with a medical toxicologist or regional poison center. Alternative approaches that may be effective in severely poisoned patients include ● Higher doses of medication than those in standard protocols ● Nonstandard drug therapies, including inamrinone, calcium chloride, glucagon, insulin, labetalol, phenylephrine, physostigmine, and sodium bicarbonate ● Use of specific antagonists or antidotes ● Heroic measures, such as prolonged CPR and possible use of circulatory assist devices such as extracorporeal membrane oxygenation References 1. Litovitz TL, Felberg L, White S, Klein-Schwartz W. 1995 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 1996;14:487–537. 2. McCaig LF, Burt CW. Poisoning-related visits to emergency departments in the United States, 1993–1996. J Toxicol Clin Toxicol. 1999;37: 817– 826. 3. Fingerhut LA, Cox CS. Poisoning mortality, 1985–1995. Public Health Rep. 1998;113:218 –233. 4. Watson WA, Litovitz TL, Klein-Schwartz W, Rodgers GC Jr, Youniss J, Reid N, Rouse WG, Rembert RS, Borys D. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2004;22:335– 404. 5. Facility assessment guidelines for regional toxicology treatment centers. American Academy of Clinical Toxicology. J Toxicol Clin Toxicol. 1993;31:211–217. 6. Poison information and treatment systems. American College of Emergency Physicians. Ann Emerg Med. 1996;28:384. 7. Chyka PA, Seger D, Krenzelok EP, Vale JA. Position paper: single-dose activated charcoal. Clin Toxicol (Phila). 2005;43:61– 87. 8. Amrein R, Hetzel W, Hartmann D, Lorscheid T. Clinical pharmacology of flumazenil. Eur J Anaesth. 1988;2:65– 80. 9. Amrein R, Leishman B, Bentzinger C, et al. Flumazenil in benzodiazepine antagonism: actions and clinical use in intoxications and anaesthesiology. Med Toxicol. 1987;2:411– 429. 10. Flückiger A, Hartmann D, Leishman B, et al. Lack of effect of the benzodiazepine antagonist flumazenil (Ro 15-1788) on the performance of healthy subjects during experimentally induced ethanol intoxication. Eur J Clin Pharmacol. 1988;34:273–276. 11. Lukes SE, Griffiths RR. Precipitated withdrawal by a benzodiazepine receptor antagonist (Ro-15-1788) after 7 days of diazepam. Science. 1982;217:1161–1163. 12. Martens F, Köppel C, Ibe K, et al. Clinical experience with the benzodiazepine antagonist flumazenil in suspected benzodiazepine or ethanol poisoning. J Toxicol Clin Toxicol. 1990;28:341–356. 13. Pitetti RD, Singh S, Pierce MC. Safe and efficacious use of procedural sedation and analgesia by nonanesthesiologists in a pediatric emergency department. Arch Pediatr Adolesc Med. 2003;157:1090 –1096. 14. Gill AM, Cousins A, Nunn AJ, Choonara JA. Opiate-induced respiratory depression in pediatric patients. Ann Pharmacother. 1996;30:125–129. 15. Herschel M, Kloshnood B, Lass NA. Role of naloxone in newborn resuscitation. Pediatrics. 2000;106:831– 834. 16. Lewis JM, Klein-Schwartz W, Benson BE, Oderda GM, Takai S. Continuous naloxone infusion in pediatric narcotic overdose. Am J Dis Child. 1984;138:944 –946. 17. Romac DR. Safety of prolonged, high-dose infusion of naloxone hydrochloride for severe methadone overdose. Clin Pharm. 1986;5:251–254. 18. Singhal N, McMillan DD, Yee WH, Akierman AR, Yee YJ. Evaluation of the effectiveness of the standardized neonatal resuscitation program. J Perinatol. 2001;21:388 –392. 19. Osterwalder JJ. Naloxone—for intoxications with intravenous heroin and heroin mixtures— harmless or hazardous? A prospective clinical study. J Toxicol Clin Toxicol. 1996;34:409 – 416. 20. Sporer KA, Firestone J, Isaacs SM. Out-of-hospital treatment of opioid overdoses in an urban setting. Acad Emerg Med. 1996;3:660 – 667. 21. Wanger K, Brough L, Macmillan I, Goulding J, MacPhail I, Christenson JM. Intravenous vs subcutaneous naloxone for out-of-hospital management of presumed opioid overdose. Acad Emerg Med. 1998;5:293–299. 22. Hasan RA, Benko AS, Nolan BM, Campe J, Duff J, Zureikat GY. Cardiorespiratory effects of naloxone in children. Ann Pharmacother. 2003;37:1587–1592. 23. Sporer KA. Acute heroin overdose. Ann Intern Med. 1999;130:584 –590. 24. Schneir AB, Vadeboncoeur TF, Offerman SR, Barry JD, Ly BT, Williams SR, Clark RF. Massive OxyContin ingestion refractory to naloxone therapy. Ann Emerg Med. 2002;40:425– 428. 25. Sungur M, Guven M. Intensive care management of organophosphate insecticide poisoning. Crit Care. 2001;5:211–215. 26. Bosse GM, Pope TM. Recurrent digoxin overdose and treatment with digoxin-specific Fab antibody fragments. J Emerg Med. 1994;12:179 –185. 27. Eddleston M, Rajapakse S, Rajakanthan, Jayalath S, Sjostrom L, Santharaj W, Thenabadu PN, Sheriff MH, Warrell DA. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial. Lancet. 2000;355:967–972. 28. Dasgupta A, Szelei-Stevens KA. Neutralization of free digoxin-like immunoreactive components of oriental medicines Dan Shen and Lu-Shen-Wan by the Fab fragment of antidigoxin antibody (Digibind). Am J Clin Pathol. 2004;121:276 –281. 29. Tracey JA, Cassidy N, Casey PB, Ali I. Bupropion (Zyban) toxicity. Ir Med J. 2002;95:23–24. 30. Burns MJ, Linden CH, Graudins A, Brown RM, Fletcher KE. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med. 2000;35:374 –381. 31. Ramoska E, Sacchetti AD. Propranolol-induced hypertension in treatment of cocaine intoxication. Ann Emerg Med. 1985;14:1112–1113. 32. Hollander JE, Wilson LD, Shih LP. Complications from the use of thrombolytic agents in patients with cocaine associated chest pain. J Emerg Med. 1996;14:731–736. 33. Brogan WCI, Lange RA, Kim AS, Moliterno DJ, Hillis LD. Alleviation of cocaine-induced coronary vasoconstriction by nitroglycerin. J Am Coll Cardiol. 1991;18:581–586. 34. Lange RA, Cigarroa RG, Yancy CW Jr, Willard JE, Popma JJ, Sills MN, McBride W, Kim AS, Hillis LD. Cocaine-induced coronary-artery vasoconstriction. N Engl J Med. 1989;321:1557–1562. 35. Lange RA, Cigarroa RG, Flores ED, McBride W, Kim AS, Wells PJ, Bedotto JB, Danziger RS, Hillis LD. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990;112:897–903. 36. Boehrer JD, Moliterno DJ, Willard JE, Hillis LD, Lange RA. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993;94:608 – 610. 37. Gay GR, Loper KA. The use of labetalol in the management of cocaine crisis. Ann Emerg Med. 1988;17:282–283. 38. Dusenberry SJ, Hicks MJ, Mariani PJ. Labetalol treatment of cocaine toxicity. Ann Emerg Med. 1987;16:235. 39. Sand IC, Brody SL, Wrenn KD, Slovis CM. Experience with esmolol for the treatment of cocaine-associated cardiovascular complications. Am J Emerg Med. 1991;9:161–163. 40. Mayron R, Ruiz E. Phenytoin: does it reverse tricyclic-antidepressant-induced cardiac conduction abnormalities? Ann Emerg Med. 1986;15:876–880. 41. Callaham M, Schumaker H, Pentel P. Phenytoin prophylaxis of cardiotoxicity in experimental amitriptyline poisoning. J Pharmacol Exp Ther. 1988;245:216 –220. 42. Citak A, Soysal DD, Ucsel R, Karabocuoglu M, Uzel N. Efficacy of long duration resuscitation and magnesium sulphate treatment in amitriptyline poisoning. Eur J Emerg Med. 2002;9:63– 66. 43. Knudsen K, Abrahamsson J. Effects of magnesium sulfate and lidocaine in the treatment of ventricular arrhythmias in experimental amitriptyline poisoning in the rat. Crit Care Med. 1994;22:494 – 498. 44. Kline JA, DeStefano AA, Schroeder JD, Raymond RM. Magnesium potentiates imipramine toxicity in the isolated rat heart. Ann Emerg Med. 1994;24:224 –232. 45. Gowda RM, Khan IA, Punukollu G, Vasavada BC, Sacchi TJ, Wilbur SL. Female preponderance in ibutilide-induced torsade de pointes. Int J Cardiol. 2004;95:219 –222. Part 10.2: Toxicology in ECC IV-131

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