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SURIYAWUT SURIYA/SHUTTERSTOCK SURIYAWUT Common used in the ICU

By Carrie L. Griffiths, PharmD, BCCCP, FCCM; Arzu Patel, BS; and Kristie A. Hertel, MSN, RN, CCRN, ACNP-BC

Abstract: When ingested, some common household products can be poisonous, and, when taken improperly, both prescription and over- the-counter can result in overdoses. This article describes several common encountered in the ICU and their respec- tive antidotes.

Keywords: acetaminophen, , , beta-blocker, , , , , , hyperinsulinemia-euglycemia therapy (HIET), , N-, , toxic

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According to the 2018 National for overdose include advanced sites. That is, digoxin immune Data System Annual age, metabolic disorders, and fab binds to digoxin, removing it Report, there were 2,099,751 interactions.4 Medications from its tissue binding sites, and human exposures to substances such as verapamil, atorvastatin, the bound drug is then pushed ranging from household cleaning omeprazole, potassium-depleting into the extracellular fluid. As products to prescription medica- , , erythromy- a result, it is unable to exert its tions.1 In the critical care setting, cin, and tetracycline may lead to effect on its target tissues, revers- patients present with a variety of increased serum concentrations ing adverse events associated conditions, including intentional of digoxin.6,7 with overdose.7 or unintentional or Mechanism of . Adverse reactions. There have overdoses. Antidotes are used to Digoxin’s mechanism of action been reported allergic reactions counteract the toxicity of . involves a blockade of sodium- to digoxin immune fab, includ- In the US, poison control centers potassium triphospha- ing urticaria, pruritus, erythema, are available 24/7 in every state tase, especially in myocardial tissue. angioedema, bronchospasm, and the District of Columbia to At therapeutic levels, this results in , and . In assist with any type of . increased contractility, shortened addition, infusion-related reactions Poison control centers are avail- atrial contraction, and a prolonged have been observed, and are relat- able in several countries globally.2 atrioventricular (AV) refractory ed directly to the rate of admin- This article discusses several period. However, at supratherapeu- istration. The infusion should be common household substances tic levels, overexcitation of cardiac, stopped if either reaction type and over-the-counter (OTC) and gastrointestinal (GI), and central occurs. Digoxin immune fab may prescription medications along nervous tissues can lead to a variety also cause worsening of conges- with the proper use of their of toxicity symptoms.4,7 tive , , respective antidotes. Please note Clinical . and phlebitis. Overcorrection of the that reversal agents Clinical signs of toxicity caused by digoxin tox- are not discussed, as they were include , loss of appe- icity may also lead to .7 covered in a previous issue of tite, and GI symptoms including Clinical pearls. Obtaining a this journal.3 nausea, , and diarrhea. serum digoxin level before treat- Patients may also experience ment is preferred, as this value Digoxin and digoxin immune vision disturbances, which are can be used to devise a dosing fab (Digibind, DigiFab) generally characterized by yellow- strategy for digoxin immune fab. Digoxin is a narrow therapeutic ing or blurry vision, light sensitiv- However, it is important to note index . Clinical ben- ity, or seeing “halos” or flashing that serum digoxin measurements efit is generally seen at serum lights.7 More severe symptoms of are nonessential for treatment concentrations ranging from overdose include cardiac arrhyth- monitoring. Serum concentrations 0.8 to 2 ng/mL; however, clini- mias, such as ventricular fibril- may appear to rise after digoxin cal benefit may be limited to a lation, , immune fab administration, but lower range of 0.5–0.9 ng/mL asystole, AV block (first-, second-, this can be misleading as this in patients with heart failure.4 and third-degree), ventricular value can be attributed to drug Due to the narrow therapeutic extrasystoles, ventricular ectopic already bound to digoxin immune index of digoxin, unintentional activity, and .4 fab and therefore unable to cause overdose or toxicity is possible. Treatment and monitoring. toxicity. Until the bound drug For example, in cases of severe Digoxin immune fab is an immu- is excreted in the urine, serum renal insufficiency, the half-life noglobulin fragment that possesses levels will not be truly indicative of digoxin can be increased from a highly specific affinity for digox- of unbound digoxin.6 In patients 36 to 48 hours up to 100 hours; in. It has been available for use with renal impairment, excre- as a result, these patients have in since 1986.4 tion can be delayed by a week an increased risk of accidental This affinity is greater than that or longer. Monitoring measures overdose.5 Other risk factors of digoxin for its tissue binding recommended are ECG changes,

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Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. temperature, BP, and electrolytes cemia, lactic acidosis, metabolic glucose should be checked every (in particular, potassium levels).7 acidosis, altered mental status, 20 minutes, then hourly for the dysrhythmias, and seizures.8 duration of the infusion. The Beta-blockers/calcium Treatment and monitoring. onset of action of is gener- channel blockers and Hyperinsulinemia-euglycemia ally 15 to 45 minutes; however, it hyperinsulinemia- therapy (HIET) can be used as can be delayed, even by several euglycemia therapy an antidote for beta-blocker and hours. HIET should be continued Two classes of widely used anti- calcium channel blocker over- until the patient’s is hypertensive medications, beta- dose, in addition to supportive greater than 50 beats/minute, and blockers and calcium channel care. Advantages of HIET include systolic BP remains greater than blockers, are associated with high its wide availability, relatively 100 mm Hg. A dextrose infusion mortality due to overdose and lower cost, and minimal adverse may be required for up to 24 resulting poison-induced cardiogenic events.9 There are no irreversible hours after discontinuation of the shock. In the US, beta-blockers adverse reactions associated with insulin infusion.8 are the fifth most-commonly HIET; it may cause prescribed class of medication.8 and hypokalemia, both of which Acetaminophen and Mortality associated with calcium can be resolved with relative N-acetylcysteine channel blockers is the highest ease.8 Insulin works to reverse Acetaminophen is one of the most among cardiovascular medications.9 the effects of beta-blockers and commonly used OTC medica- Mechanism of toxicity. calcium channel blockers via tions; its and antipyretic Overdose occurs either intention- several mechanisms; it increases properties lend itself to being ally or unintentionally due to low inotropy and intracellular glucose used in many combination prod- health literacy.9 Beta-blockers transport, and enhances micro- ucts. Because of its ubiquity, it is work by competitively inhibiting vascular perfusion. Overall, this often viewed as benign, and at beta-receptors, indirectly decreas- leads to increased cardiac output therapeutic concentrations, the ing the amount of cyclic adenos- and elevated BP.9 safety profile of acetaminophen ine monophosphate produced. Although there are no estab- is very good. In addition, acet- This reduces the amount of cal- lished guidelines for the use of aminophen is often included in cium entering calcium channels. insulin as an antidote, typical dos- OTC combination cough, cold, As a result, heart rate and con- ing includes an I.V. bolus dose, and pain medications, increas- tractility are decreased.10 followed by a continuous infu- ing the likelihood of accidental Calcium channel blockers also sion. It is recommended to titrate overdose. Accidental overdose is affect the entry of calcium by the dose based on the patient’s exceedingly prevalent and can directly blocking calcium chan- glycemic status. In addition, an lead to significant hepatotoxicity nels.11 This leads to relaxation of I.V. dextrose bolus, followed by that progresses rapidly.12,13 In the vascular smooth muscle and a continuous dextrose infusion, US, acetaminophen toxicity is the . Non-dihydropyridine may be given with the insulin most common cause of acute calcium channel blockers such bolus based on the patient’s failure and the primary reason for as diltiazem and verapamil also glucose. However, it is likely, emergent liver transplants.13 inhibit the sinoatrial and AV especially in cases of calcium Mechanism of toxicity. nodes. channel blocker overdose, that Acetaminophen is metabolized by Clinical signs and symp- the patient will be hyperglycemic, a variety of pathways in the liver, toms. Overdose can lead to even with insulin.8 the majority of which produce extreme vasodilation with Due to the risk of hypokale- nontoxic metabolites. However, decreased systemic vascular mia, serum electrolytes should be these pathways can be over- resistance, bradycardia, hypoten- closely monitored. In addition, whelmed by excessive intake, sion, and cardiogenic shock. In continuous cardiac monitoring is resulting in the production and addition, excessively limiting cal- recommended.9 During the first accumulation of the toxic metab- cium influx can cause hypergly- hour of insulin infusion, blood olite N-acetyl-p-benzoquinone www.nursingcriticalcare.com July l Nursing2020CriticalCare l 11

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imine (NAPQI), which causes tered within 8 hours of overdose. phen levels.12 NAC is available in severe hepatocyte damage and NAC prevents the accumulation oral and I.V. formulations. Oral eventual hepatic failure.13 (See of toxic NAPQI through the fol- NAC is often poorly tolerated Acetaminophen toxicity pathway.) lowing mechanisms: due to its unpleasant “rotten egg” Clinical signs and symp- • It converts existing NAPQI or sulfur smell. Oral NAC can be toms. Clinical signs of acetamin- back to acetaminophen or non- given with high-dose ophen overdose are nonspecific, toxic and mercaptate to prevent vomiting. In addition, and a detailed patient history is conjugates. the smell can be “disguised” by integral to diagnosis. Most com- • It acts as a precur- administering the oral formula- monly, patients will present with sor, increasing glutathione avail- tion in a covered cup and straw nausea, vomiting, decreased ability and allowing for safer or with a flavored beverage. The appetite, abdominal pain, confu- acetaminophen .13,14 drug should be readministered sion, and malaise.13 The necessity for treatment if vomiting occurs within 1 hour Treatment and monitoring. with NAC is determined by the of administration. If vomiting N-acetylcysteine (NAC) is the Rumack-Matthew nomogram, continues, the route of admin- treatment of choice for acetamin- which indicates the severity istration should be changed to ophen-induced hepatotoxicity of toxicity based on time after I.V.13,14 NAC is usually admin- and is effective when adminis- ingestion and serum acetamino- istered based on site-specific

Acetaminophen toxicity pathway

APAP

Sulfation Glucuronidation Cytochrome P450

NAC

Glutathione store saturated

Nontoxic Glutathione Toxic metabolites conjugation NAPQI accumulation

Abbreviations: APAP, acetaminophen; NAC, N-acetylcysteine

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Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. protocols. It should be continued For example, toxicity that are not meant for ingestion, until acetaminophen serum lev- may present symptoms for up to including , ethylene els are no longer measurable and 70 hours.17 glycol, and isopropyl .19 liver transaminases trend toward Clinical signs and symp- Toxicity caused by methanol and normal.12,14 toms. Generally, clinical presen- has been shown Adverse reactions. Adverse tation of benzodiazepine over- to cause significant morbidity and reactions of NAC include ana- dose is loss of consciousness, or mortality. Methanol is a typical phylaxis related to dose or rate difficulty waking accompanied ingredient found in antifreeze, of I.V. infusion. More commonly, by slow respirations.17 cleaning solutions, dyes, paint patients can experience pruritus, Treatment and monitoring. removers, and illegally produced rash, or hives, which respond well Flumazenil is often used as an anti- alcoholic beverages. Ethylene to and slowing dote in glycol can be found in antifreeze the infusion rate. Life-threatening and toxicity. It is a 1,4-benzodiaze- and deicing solutions.20 Exposure reactions are rare and are usually pine derivative. It works to reverse can occur accidentally, or inten- caused by too rapid administration the sedation associated with toxic- tionally, in the case of purposeful of the loading dose, accompanied ity by competing for binding of the inebriation, homicide, or . by risk factors such as underlying GABA receptor. Although effec- Additionally, people with altered airway disease. Recommended tive, it is not recommended for mental status may ingest sub- monitoring parameters include use empirically or in situations of stances containing toxic alcohols complete blood cell count, com- coingestion of other toxic substanc- unknowingly.19 After ingestion, prehensive metabolic panel, es and benzodiazepine withdrawal, toxic metabolites accumulate arterial blood gas, blood glucose, due to seizure risk.18 within the body, causing a cascade serum aminotransferases, and Serious, but uncommon, adverse of worsening symptoms. (See bilirubin. In addition, the patient reactions associated with fluma- Toxic alcohols pathway.) may require treatment for hypo- zenil include seizures, cardiac Mechanism of toxicity. glycemia, hypophosphatemia, and , unspecified tachycar- Generally clinical signs and symp- hypokalemia.14,15 dia, convulsions, and sudden drop toms of toxicity are nonspecific, in systolic BP; more commonly making diagnosis difficult. Toxic and seen symptoms include mild, tran- alcohol poisoning should be con- flumazenil (Romazicon) sient nausea and vomiting.16 It is sidered in the differential diag- Toxicity caused by benzodiaze- important to monitor a patient’s nosis if the patient exhibits any pines is frequently seen, either as , presence of seizure of the following criteria: history single or multiple drug overdoses. activity, and mental status while of alcohol use disorder/ Although often used for their administering flumazenil, as well use, reported ingestion of house- effects, benzodiazepines as 30 to 60 minutes before and 30 hold cleaners, history of suicidal can also cause respiratory depres- to 60 minutes after administration ideation, or presence of acidemia sion. Prognosis is worsened by of flumazenil.18 with altered mental status. It is concomitant intoxication with Given that the half-life of ben- possible that serum levels will not alcohol, medications such as anx- zodiazepines is longer than that be available or significant because iolytics, tricyclic , of flumazenil, repeat dosing of the process of alcohol metabolism opioids, or illicit .16 flumazenil may be warranted if occurs very quickly.19 Mechanism of toxicity. sedation recurs. Treatment and monitoring. Benzodiazepines act via high- Treatment of toxicity is warranted affinity binding to gamma- Toxic alcohols and if the patient has one of the following: aminobutyric acid (GABA) receptors fomepizole (Antizol) history of toxic ingestion, levels of in the central . In 2015, 12,000 cases of toxic alco- methanol or ethylene glycol greater Due to the long half-life of some hol poisoning were reported in the than or equal to 20 mg/dL, or sus- benzodiazepines, symptoms of US. Toxic alcohols are substances pected toxic ingestion with large overdose can last for several days. containing a hydroxyl group anion gap metabolic acidosis with www.nursingcriticalcare.com July l Nursing2020CriticalCare l 13

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an arterial pH of less than 7.3, malities are present. Fomepizole drug . Causes of serum bicarbonate of less than 20 is more expensive than , analgesic-related toxicity include mmol/L, or osmolal gap of greater an alternative treatment for ethyl- medication use errors, prescrib- than 10 mOsm/L. Fomepizole ene glycol/, but ing practices, and intentional combats methanol/ethylene glycol is associated with fewer adverse overdose. Approximately 130 poisoning by competitively inhib- reactions, including inebriation, individuals in the US suffer a iting both substances. Its affinity hypoglycemia, hyperosmolarity, fatal daily, and for is 500 vasodilation, and worsened acido- in 2018, nearly 70% of drug over- times that of ethanol, and 5,000 to sis. Fomepizole therapy should be dose deaths involved an opioid.21 10,000 times that of methanol and continued until plasma methanol Mechanism of toxicity. ethylene glycol. It is administered or ethylene glycol levels are less Opioids enact their effects on as an I.V. infusion. than 20 mg/dL.20 mu, delta, and kappa opioid is indicated if plasma levels of receptors, located in the central methanol or ethylene glycol are Opioids (prescription and and peripheral nervous system, greater than 50 mg/dL, vital signs illicit) and naloxone (Narcan) as well as peripheral tissues. are deteriorating despite support- Opioids include and Each receptor is coupled to mul- ive care, metabolic acidosis occurs medications derived from or tiple cellular mechanisms, which that is refractory to sodium bicar- structurally like morphine such in turn bring about physiologic bonate and supportive care, or renal as hydrocodone, , and changes throughout the body. failure or severe electrolyte abnor- fentanyl, as well as the illicit When receptors in the are acted on by opioid-containing medications, Toxic alcohols pathway they can produce profound analgesia, changes in mood, and tolerance. In addition, the release Methanol Ethylene glycol of caused by opioid use may create a “reward” effect, leading to and misuse. When acting upon areas of the peripheral nervous system, particularly in the GI tract, opioid medications can Alcohol Alcohol Fomepizole cause severe constipation.22 dehydrogenase dehydrogenase Clinical signs and symp- toms. In cases of opioid analgesic overdose, it is common for the patient to experience or loss of consciousness. Pupils may be extremely constricted, and the patient’s skin may be pale blue and cold to the touch. In addition, opioid overdose is characterized by profound respi- ratory , with respira- tory rate decreased to less than 23 Toxicity 12 breaths/minute. Treatment and monitoring. Naloxone has a strong affinity for opioid receptors in the body,

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Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. and acts as a potent antagonist, hypotension, an indicator of hypo- quickly reversing the effects of perfusion. For over- opioid-containing medications. dose, placement of a central line Naloxone is available in intrana- for hemodialysis may be required sal, I.M., and I.V. formulations. for drug removal. Knowing the Typically, intranasal and I.M. treatments for specific drug toxic- naloxone are prescribed in the ity and overdose will help a nurse outpatient setting; often, patients be prepared for the appropriate taking higher-strength opioid line placement. will be prescribed nal- Preparation for placement oxone in conjunction, and family of invasive monitoring devices members are often counseled must be completed for overdose on the importance of identifying patients. Digoxin toxicity along and treating accidental overdoses with beta-blocker and calcium quickly. I.V. naloxone is typically channel blocker overdose can lead used in hospital settings and is to significant bradycardia and/ very effective due to its rapid or arrhythmias that may require onset of action. Dosing of I.V. placement of a transvenous pac- naloxone is typically repeated ing wire. Nurses must be edu- every 2-3 minutes as needed for cated on transvenous pacing with reversal of respiratory depres- knowledge of ECG confirmation sion.23 Due to the short duration of capture as well as how to adjust of action of naloxone (half-life Knowing the treatments the milliamps to obtain capture 30-81 minutes), patients generally for specific drug toxicity when the wire has been floated. require hospital admission, and and overdose will help Cardiogenic shock can be a compli- additional I.V. naloxone doses or a nurse be prepared cation of overdose of these cardiac even a continuous I.V. infusion for the appropriate medications. There is a potential over the course of several hours or line placement. need for a pulmonary artery cath- days, with the goal of titrating the eter or noninvasive cardiac moni- naloxone to balance the risks of toring equipment to assess and life-threatening respiratory depres- manage cardiogenic shock.24 sion and extreme withdrawal.22,23 minimal parameters that should Gastric decompression via Opioid withdrawal syndrome is be assessed. Physical assessment nasogastric tube insertion may characterized by nausea, vomiting, should be focused on neurologic, be indicated for a patient who diarrhea, tachycardia (heart rate cardiac, respiratory, and renal is being treated for an overdose. greater than 100 beats/minute), systems. These patients need to be Gastric decompression decreases aggression, insomnia, hot and cold admitted/transferred to a CCU for the risk of aspiration in patients flashes, diaphoresis, and muscle close observation and monitoring. experiencing altered mental cramps. Generally, supportive care Critical care nurses should be status such as with opioid and is indicated in these instances.23 prepared to assist the medical benzodiazepine overdoses. Use team with placement of a central of a nasogastric tube may help Nursing considerations venous catheter and an arterial reduce and/or eliminate nausea Nursing care of a patient line. Antidote medications for and vomiting often associated from overdose or intoxication of reversal of overdose can be caustic with overdose or as an adverse any medication(s) must start with to peripheral veins necessitating reaction of the antidote. Critical a high suspicion of circulatory and a central line. Hemodynamic care nurses must be aware of respiratory collapse. Cardiac mon- monitoring with an arterial line proper placement techniques itoring along with noninvasive for continuous evaluation of BP and how to evaluate for appro- BP and pulse oximetry are the is useful for early recognition of priate placement. www.nursingcriticalcare.com July l Nursing2020CriticalCare l 15

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Patients who have overdosed ated with digoxin/beta-blocker/ 11. Calcium Channel Blockers. Clinical Pharma- on toxic alcohols, opioids, and calcium channel blocker toxicity.24 cology. Tampa, FL: Elsevier; 2020. www.clinical- .com. benzodiazepines have a high risk If these specialists are not available 12. Bateman DN. : beyond of related to at a particular institution, nurses the nomogram. Br J Clin Pharmacol. 2015;80(1): bradypnea from sedation as a should be prepared for transfer to 45-50. 13. Saccomano SJ. Acute acetaminophen toxicity result of the overdose. Intubation an appropriate tertiary facility. in adults. Nurse Pract. 2019;44(11):42-47. and mechanical ventilation for 14. Fixl AN, Woods RM, Dervay K. Intravenous N-acetylcysteine for acetaminophen toxicity. respiratory support is likely in Conclusion AACN Adv Crit Care. 2017;28(4):305-310. 25 these patients. Nurses should be When evaluating the toxicities 15. Koppen A, van Riel A, de Vries I, Meulen- prepared with appropriate medi- mentioned above, important belt J. Recommendations for the paracetamol treatment nomogram and side effects of N-acet- cations and equipment to proceed considerations include promptly ylcysteine. Neth J Med. 2014;72(5):251-257. with intubation. Placement of and accurately identifying which 16. Penninga EI, Graudal N, Ladekarl MB, Jür- gens G. Adverse events associated with flumaze- continuous pulse oximetry and an substances are causing toxicity and nil treatment for the management of suspected end-tidal carbon dioxide monitor rapid administration of treatment benzodiazepine intoxication--a systematic review with meta-analyses of randomised trials. Basic should be implemented for close or supportive care. Therefore, Clin Pharmacol Toxicol. 2016;118(1):37-44. respiratory status monitoring of obtaining a thorough patient histo- 17. Mora CT, Torjman M, White PF. Sedative patients who do not immediately ry is essential. In addition, consid- and ventilatory effects of infusion: effect of flumazenil reversal. Can J Anaesth. require intubation. ering medication-related toxicity in 1995;42(8):677-684. Neurologic deterioration is a the context of a patient exhibiting 18. Nguyen TT, Troendle M, Cumpston K, Rose SR, Wills BK. Lack of adverse effects from of overdose. Overdose nonspecific symptoms could lead flumazenil administration: an ED observational of opioids and benzodiazepines to a diagnosis and treatment plan study. Am J Emerg Med. 2015;33(11):1677-1679. as well as toxic alcohols will being formed more quickly, result- 19. Ng PCY, Long BJ, Davis WT, Sessions 25 ■ DJ, Koyfman A. Toxic alcohol diagnosis and result in altered mental status. ing in better patient outcomes. management: an review. Benzodiazepine, beta-blocker, and 2018;13(3):375-383. REFERENCES 20. Rietjens SJ, de Lange DW, Meulenbelt J. calcium channel blocker toxicity 1. Gummin DD, Mowry JB, Spyker DA, et al. Ethylene glycol or methanol intoxication: which can progress to seizures. Frequent 2018 Annual Report of the American Association antidote should be used, fomepizole or ethanol? neurologic assessments and knowl- of Poison Control Centers’ National Poison Data Neth J Med. 2014;72(2):73-79. System (NPDS): 36th Annual Report. Clin Toxicol 21. Centers for Disease Control and Prevention. edge of appropriate treatment of (Phila). 2019;57(12):1220-1413. Understanding the epidemic. 2020. www.cdc. seizures are nursing responsibili- 2. American Association of Poison Control Cen- gov/drugoverdose/epidemic/index.html. ties with this patient population. ters. 2020. www.aapcc.org. 22. Sivilotti MLA. Flumazenil, naloxone and 3. Griffiths CL, Vestal ML, Livengood SJ, Hicks the ‘ cocktail’. Br J Clin Pharmacol. If seizures occur, nurses must S. Reversal agents for oral . Nurse 2016;81(3):428-436. understand seizure precautions to Pract. 2017;42(11):8-14. 23. Wong F, Edwards CJ, Jarrell DH, Patanwala 4. Hauptman PJ, Blume SW, Lewis EF, Ward S. AE. Comparison of lower-dose versus higher- ensure patient safety. Continuous Digoxin toxicity and use of digoxin immune fab: dose intravenous naloxone on time to recurrence electroencephalogram monitoring insights from a national hospital database. JACC of opioid toxicity in the emergency department. may be required. Heart Fail. 2016;4(5):357-364. Clin Toxicol (Phila). 2019;57(1):19-24. 5. Chan BSH, Buckley NA. Digoxin-specific 24. Bartlett D. β-Blocker and calcium channel Some patients receiving treat- fragments in the treatment of digoxin blocker poisoning: high-dose insulin/glucose ment for an overdose or medication toxicity. Clin Toxicol (Phila). 2014;52(8):824-836. therapy. Crit Care Nurse. 2016;36(2):45-50. 6. Ledwitch KV, Barnes RW, Roberts AG. Un- 25. Clark A, Burnie J, Johann R, Baker R, Has- toxicity will need to be evaluated ravelling the complex drug-drug interactions of sert C. 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Calcium Kristie A. Hertel is an advanced practice provider, channel antagonist and beta-blocker overdose: Trauma and Surgical Critical Care, Vidant Medical for drug removal. A cardiologist antidotes and adjunct therapies. Br J Clin Center, Greenville, N.C., and a member of the Nursing2020 Critical Care Editorial Board. or cardiovascular specialist may Pharmacol. 2016;81(3):453-461. 10. Beta Blockers. Clinical Pharmacology. The authors have disclosed no financial relation- ships related to this article. be needed for arrhythmias or Tampa, FL: Elsevier; 2020. www.clinicalpharma- heart failure management associ- cology.com. DOI-10.1097/01.CCN.0000668560.03626.5c

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