Download high dose insulin in beta blocker and calcium

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