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HIGH DOSE INSULIN IN BETA BLOCKER AND CALCIUM CHANNEL BLOCKER OVERDOSE TOM SCULLARD RN MSN CCRN CLINICAL CARE SUPERVISOR MEDICAL INTENSIVE CARE UNIT HENNEPIN COUNTY MEDICAL CENTER MINNEAPOLIS MINNESOTA OBJECTIVES 1. Identify the cardiovascular effects of beta blocker and calcium channel blocker overdoses 2. Describe the proposed mechanism of high dose insulin use in beta blocker and calcium channel blocker overdose 3. Describe the role of the nurse when caring for the patient receiving high dose insulin therapy. OVERDOSE • Intentional ingestion • Unintentional ingestion • Patient error • Medication interaction • Children BETA BLOCKER & CALCIUM CHANNEL BLOCKER OVERDOSE • Overdose is associated with a high incidence of morbidity and mortality due to cardiovascular toxicity including profound hypotension and conduction disturbances AMERICAN ASSOCIATION OF POISON CONTROL CENTERS’ NATIONAL POISON DATA SYSTEM • 2012 • 10691 beta blocker overdoses • 5076 calcium channel blocker overdoses • Fatalities • beta blocker 13 • calcium channel blocker 24 BETA BLOCKERS & CALCIUM CHANNEL BLOCKERS • Beta Blockers • 128 million prescriptions for β-blockers filled in 2009 • 5th most commonly prescribed medication class • Calcium channel blockers • 98 million prescriptions filled in 2010 BETA BLOCKER USES • Beta blockers are used for treating: Abnormal heart rhythm High blood pressure Heart failure Angina (heart pain) Tremor Pheochromocytoma Prevention of migraines CALCIUM CHANNEL BLOCKERS Amlodipine (Norvasc) Diltiazem (Cardizem LA, Tiazac) Felodipine (Plendil) Isradipine (Dynacirc) Nifedipine (Adalat, Procardia) Nicardipine (Cardene) Nimodipine (Nimotop) Nisoldipine (Sular) Verapamil (Covera-hs, Verelan PM, Calan) Diltiazem Nicardipine CALCIUM CHANNEL BLOCKER USES Calcium channel blockers are approved for treating: High blood pressure Angina Abnormal heart rhythms (for example, atrial fibrillation, paroxysmal supraventricular tachycardia) Subarachnoid hemorrhage Raynaud's phenomenon Cardiomyopathy Migraine headaches CARDIAC MYOCTES • Myocte: Type of cell found in muscle tissue • Cardiac myoctes responsible for: • Electrical impulses • Contractility • Exchange ions BETA AND CALCIUM CHANNEL RECEPTORS What do they do? BETA RECEPTORS • Beta 1 • Primarily regulate myocardial tissue and affect the rate of contraction via impulse conduction • Beta 2 • smooth muscle tone and influence vascular and bronchiolar relaxation • Beta 3 • thought to primarily affect lypolysis and may have effects on cardiac inotropy BETA RECEPTORS ACTION • Beta receptors coupled with Gs protiens • Activate adenylate cyclase • Form cAMP from ATP activates cAMP dependent protein kinase (PK-A) • Causes increase calcium into the cell • Leads to increased release calcium by sarcoplasmic reticulum in the heart • Increased contractility heart rate BETA- BLOCKERS • Beta-blockers selectively antagonize the effects of catecholamines at the beta-adrenergic receptor that are linked to G proteins BETA BLOCKERS • Beta-adrenergic antagonists competitively antagonize the effects of catecholamines at the beta-adrenergic receptor and blunt the chronotropic and inotropic response to catecholamines BETA BLOCKER OVERDOSE SYMPTOMS • • • • Hypotension Bradycardia Bronchospasms Cool extremities r/t vasoconstriction • Beta 2 blockade and alpha -1 activity • Low blood sugars ? • Inhibition of release of glucagon in the pancreas L-TYPE CALCIUM CHANNELS • Found on myocardial cells • contractility • Vascular smooth muscle cells • Contractility • Conducting cells • Pacemaker cells • β-islet cells of the pancreas CALCIUM CHANNELS • Calcium enters open voltage-sensitive calcium channels to promote the release of calcium from the sarcoplasmic reticulum. The released calcium combines with troponin to cause muscle contraction via actin and myosin fibers CALCIUM CHANNEL BLOCKER OVERDOSE • Calcium channel blockers prevent the opening of the voltage-gated calcium channels and reduce calcium entry into cells during phase 2 of an action potential. CALCIUM CHANNEL BLOCKERS • Dihydropyridines • Preferentially block L-type calcium channels in the vasculature (vasodilators) • Nondihydropyridines • Selectively block L-type calcium channels in the myocardium (depressive effect on conduction and contractility). CALCIUM CHANNEL BLOCKER OVERDOSE SYMPTOMS Hypotension Bradycardia Hyperglycemia Hypoinsulinemia Warm extremities (vasodilation) Conduction delays Metabolic Acidosis (poor perfusion) BETA BLOCKER/ CALCIUM CHANNEL BLOCKER DRUG INDUCED SHOCK • Heart preferred energy source • Free Fatty Acids • Stress • Carbohydrate • Increased glucose (glycogenolysis) • Decreased insulin (pancreatic b-islet cell blockage) • Lack of fuel for energy production • Aerobic Anaerobic metabolism BETA BLOCKER AND CALCIUM CHANNEL OVERDOSE • In overdose, β-blockers and CCBs often have similar presentation and there is much overlap in treatment. • Cardiotoxicity characterized by hypotension and bradycardia is the common clinical feature TREATMENT • • • • Airway Breathing Circulation Decontamination (Gastrointestinal) • Gastric lavage • Activated charcoal • Whole bowel irrigation TREATMENT • • • • • • Fluids Atropine Calcium Glucagon Pacing Adrenergic drugs • dopamine, norepinephrine, epinephrine • Insulin INSULIN • Case series • Animal models INSULIN • When to use • Conventional therapies fail • • • • • • Fluids Atropine Calcium Glucagon Pacing Adrenergic drugs • dopamine, norepinephrine, epinephrine INSULIN • Strong positive inotropic effect • Increases uptake of carbohydrates • The preferred fuel substrate of the heart under stressed conditions • Inhibits free fatty acid metabolism • Vasodilation • Improves local microcirculation • Accelerates oxidation of myocardial lactate and reversal of metabolic acidosis INSULIN DOSING • 1 unit/kg bolus dose ( regular insulin) • 10 units/kg/ bolus • continuous infusion 0.5-1 unit/kg /hr • 10 - 20 units/kg/hr • Titrate to response (20-30 minutes) • Heart rate 50 • Systolic blood Pressure 100 INSULIN DOSING • Onset of action = 15-45 minutes ? 2 hours • Continue until hemodynamically stable • Duration – hemodynamic status • 9-72 hours DEXTROSE • Dextrose bolus 0.5g/kg with initial insulin bolus if blood sugar < 400 mg/dl • Infusion 125-250 ml/Hr of 10% solution • Goal glucose- 100-200 mg/dl COMPLICATIONS OF HIGH DOSE INSULIN • Hypoglycemia • Supplemental glucose • Hypokalemia • • • • Extracellular intracellular shift Monitor every hour while insulin titration Every 6 hours once stable Target 2.8-3.2 NURSING CARE • General nursing care • Frequent glucose monitoring • 20-30 minutes for the 1st hour then hourly • Insulin/dextrose titration • Frequent labs WEANING INSULIN • Slow taper • Do not stop abruptly • Continue to monitor blood glucose for 24 hour after insulin discontinued CASE STUDY ED • • • • • • BP 88/54 Pulse 57 Temp(Src) 37 °C 98.6 °F Resp 15 Wt 47.9 kg MEDICATIONS MEDICATIONS ED • ED • Hypotensive and Bradycardic • HR 55, BP 60/30 • • • • • Norepinephrine drip started .01 50 Units Regular insulin IV Central line D50 drip Calcium ED • Insulin drip started at 1 unit/kg/hr • Norepinephrine weaned off • Transferred to MICU CASE STUDY • Transferred to MICU • Hypotensive SBP ( 60-70s) • Insulin 2 units/kg/hr 8 units kg/hr - MAP of 65 • q15 minute glucose checks with D50 infusion • Norepinephrine up to 0.4 mcg/kg/min • Start dopamine as needed with goal MAP of 65 • Hourly potassium checks with replacement as needed • Calcium and ionized calcium ARRIVAL TO MICU 1600 6/23 6/23 • D5 @ 75 • D50 @ 80 6/23 6/23 6/24 • D5 @ 75 • D50 @80 • MAP-68-72 6/24 • D50 = 60 • D5 =100 • D50 = 40 cc/hr • D5 = 100 cc/hr • Levophed 0.17 mcg/kg/min CALCIUM QUESTIONS • [email protected] REFERENCES • Doepker, B., Healy, W., Cortez, E., & Adkins, E. J. (2014). High-dose insulin and intravenous lipid emulsion therapy for cardiogenic shock induced by intentional calcium-channel blocker and beta-blocker overdose: A case series. The Journal of Emergency Medicine, 46(4), 486–490. doi: http://dx.doi.org/10.1016/j.jemermed.2013.08.135 • Engebretsen, K. M., Kaczmarek, K. M., Morgan, J., & Holger, J. S. (2011). High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning . Clinical Toxicology, 49, 277-283. doi: 10.3109/15563650.2011.582471 • Kerns, W. (2007). Management of b-adrenergic blocker and calcium channel antagonist toxicity. Emergency Medicine Clinics of North America, 25, 309-339. doi: 10.1016/j.emc.2007.02.001 • Lheureux, P., Zahir, S., Gris, M., Derrey, N., & Penaloza, A. (2006). Bench-to-bedside review: Hyperinsulinaemia/euglycaemia. Critical Care, 10(3). Retrieved March 4, 2014, from http://ccforum.com/content/10/3/212 • Lyden AE, Cooper C, Park E (2014) Beta-Blocker Overdose Treated with Extended Duration High Dose Insulin Therapy. J Pharmacol Clin Toxicol 2(1):1015. • Mowry, J., Spyker, D., Cantilena, L., Bailey, E., Ford, M., (2013). 2012 annual report of the american association of poisoncontrol centers ’ national poison data system (npds): 30th annual report . Clinical Toxicology, doi: 10.3109/15563650.2013.863906 • Shepard, G. (2006). Treatment of poisoning caused by β-adrenergic. American Journal of Health-System Pharmacy , 63, 1828-35. doi: 10.2146/ajhp060041 REFERENCES • Woodward, C., Pourmand, A., & Mazer-Amirshahi, M. (2014). High dose insulin therapy, an evidence based approach to beta blocker/calcium channel blocker toxicity . DARU Journal of Pharmaceutical Sciences , 22, 36. doi: 10.1186/2008-2231-22-36