Ads 468x60px



Wednesday, August 26, 2009

Calcium Channel Blocker, Poisoning

Calcium Channel Blocker, Poisoning
Three Classes of Calcium Channel Blockers
• Phenylalkylamines (verapamil):
o Vasodilation resulting in a decrease in blood pressure (BP)
o Negative chronotropic and inotropic effects: reflex tachycardia not seen with a drop in BP.
• Dihydropyridine (nifedipine):
o Decreased vascular resistance resulting in a drop in BP
o Little negative inotropic effect: reflex tachycardia occurs.
• Benzodiazepine (diltiazem):
o Decreased peripheral vascular resistance leading to a decrease in BP
o Heart rate (HR) and cardiac output initially increased
o Direct negative chronotropic effect, which leads to a fall in HR
Effects of Calcium Channel Blockade
• Calcium plays key role in cardiac and smooth muscle contractility.
• Calcium channel blockers (CCBs) prevent:
o The entry of calcium, resulting in a lack of muscle contraction
o The normal release of insulin from pancreatic islet cells, resulting in hyperglycemia
Signs and Symptoms
• Cardiovascular:
o Hypotension
o Bradycardia
o Reflex tachycardia (dihydropyridine)
o Conduction abnormalities/heart blocks
• Neurologic:
o CNS depression
o Coma
o Seizures
• Metabolic:
o Hyperglycemia
Essential Workup
• Bradycardia (tachycardia with nifedipine)
• Conduction delays: QRS-complex prolongation
• Heart blocks
• Ionized calcium level when administering calcium
• Digoxin level if patient taking digoxin (dictate safety of calcium administration)
• Electrolytes, BUN, creatinine, glucose:
o Hyperglycemia/metabolic acidosis may occur.
• Toxicology screen if coingestants suspected
Differential Diagnosis
• β-Blocker toxicity
• Clonidine toxicity
• Digitalis toxicity
• Acute myocardial infarction with heart block
Pre Hospital
• Transport pill/pill bottles to ED.
• Calcium for bradycardic/unstable patient with confirmed CCB overdose
Initial Stabilization
Airway, breathing, circulation (ABCs):
• Airway protection as indicated
• Supplemental oxygen as needed
• 0.9% normal saline (NS) IV access
• Hemodynamic monitoring
ED Treatment
• Heart rate >60 beats/minute
• Systolic BP >90 mm Hg
• Adequate urine output
• Improving level of consciousness
GI Decontamination
• Syrup of ipecac: contraindicated in the ED
• Activated charcoal:
o May be helpful, especially in the presence of coingestants
• Whole bowel irrigation:
o Beneficial with ingestion of sustained-release preparations
o Contraindicated in hemodynamically unstable patients
• First-line agent for CCB toxicity
• Calcium chloride (10%):
o Contains 1.36 mEq Ca2+/mL (three times more calcium than calcium gluconate)
o Can cause tissue necrosis and sloughing with extravasation
o Very irritating to veins
• Calcium gluconate (10%):
o Contains 0.45 mEq Ca2+/mL
o Does not cause tissue necrosis as calcium chloride does
o Calcium gluconate: preferred agent in an acidemic patient
• Follow serum calcium levels if repeated doses of calcium administered.
• Contraindicated in digoxin toxicity because calcium can produce serious adverse effects in digoxin toxicity
• IV fluids:
o Administer cautiously in the hypotensive patient.
o Swan-Ganz catheter or central venous pressure (CVP) monitoring to help follow volume status
• Atropine usually ineffective
• Pressor agents:
o No clear evidence that one agent is more effective than another
o Institute invasive monitoring to help guide treatment.
o Dopamine:
 β1-Receptor agonist at low doses, which causes a positive inotropic effect on the myocardium
 α-Receptor agonist at higher doses, which leads to vasoconstriction
o Epinephrine:
 Potent α- and β-receptor agonist
• Glucagon:
o Promotes cAMP production through a receptor site other than the β-receptor
o May cause nausea and vomiting
o Mix with NS or 5% dextrose in water.
• Amrinone:
o Selective phosphodiesterase III inhibitor
o Indirectly increases cAMP
• Electrical pacing: when other treatment options have failed
• Insulin:
o Promotes more efficient myocardial metabolism
• Hypertonic sodium bicarbonate:
o Potential treatment in the future
Medication (Drugs)
• Amrinone: loading dose 0.75 mg/kg; maintenance drip 2-20 µg/kg/min; titrate for effect
• Atropine: 0.5 mg (peds: 0.02 mg/kg) IV; repeat 0.5-1.0 mg IV (peds: 0.04 mg/kg)
• Calcium chloride: 10 mL of 10% solution slow IVP (peds: 0.2-0.25 mL/kg; repeat in 10 minutes if necessary) followed by infusion 20-50 mg/kg/h
• Calcium gluconate: 10 mL of 10% solution slow IVP (peds: 1 mL/kg; may repeat in 10 minutes if necessary)
• Dopamine: 2-20 µg/kg/min; titrate to effect
• Epinephrine: 2 µg/min (peds: 0.1 µg/kg/min); titrate to effect
• Glucagon: 3.5-5 mg (peds: 0.03-0.1 mg/kg) IV bolus followed by 70 µg/kg/h infusion
• GoLYTELY WBI: 2 L/h PO or by nasogastric tube (NGT) for 4-6 hours or until rectal effluent is clear (peds: 40 mL/kg/h)
• Insulin: 1 IU/kg bolus IV followed by 0.5-1.0 IU/kg/h titrated to clinical response

Admission Criteria
• Admit symptomatic patients to a monitored bed for hemodynamic monitoring.
• Admit all patients who ingested sustained-release CCBs for 24 hours of observation and monitoring owing to the potential delay in symptoms.
Discharge Criteria
Discharge asymptomatic patients 8 hours after ingestion of immediate-release preparation.

1. Boyer EW, Shannon MW. Treatment of calcium channel blocker intoxication with insulin infusion. New Engl J Med. 2001;344:1721-1722.
2. Kalman S, Berg S, Lisander B. Combined overdose with verapamil and atenolol: treatment with high doses of adrenergic agonists. Acta Anaesthesiol Scand. 1998;45:379-382.
3. Salhanick SD, Shannon MW. Management of calcium channel antagonist overdose. Drug Safety. 2003;26:65-79.
4. Tanen DA, Ruha AM, Curry SC, et al. Hypertonic sodium bicarbonate is effective in the acute management of verapamil toxicity in swine model. Ann Emerg Med. 2000;36:547-553.

No comments: