Emergency Strategy - How to treat calcium channel blocker poisoning
Emergency Strategy - How to treat calcium channel blocker poisoning
Initial treatment include assessment of the airway, breathing and circulation. Airway need to be protected . Oxygen supplement is given and 0.9% of normal saline solution is given. It is important to keep the vital signs within the normal range with the systolic blood pressure more than 90 mmHg and heart rate more than 60 beats per minutes as well as respiratory rates around 16 - 20 beats per minutes. Urine output also should be adequate . Continuous monitoring of hemodynamic status is vital.
Gastric bowel irrigation is performed in case of overdose of sustained release calcium channel blocker. Bowel irrigation is avoided in case of unstable hemodynamic status. Activated charcoal is also considered as well as syrup of ipecac.
The bottle of calcium channel blocker is sent along with the patient to the emergency department . Calcium such as calcium gluconate and calcium chloride are given to correct the calcium level after confirming calcium channel blocker poisoning. However, we need to make sure that the patient also does not suffer from digoxin toxicity due to adverse effect of calcium on digoxin toxicity. Calcium chloride is irritative to the veins. Extravasation and tissue necrosis with sloughing are common. Calcium gluconate is preferred as it does not cause necrosis and sloughing of the tissue and is useful in acidemia patient.
Patient with calcium channel blocker overdose may also suffer from hypotension and bradycardia. IV fluids need to be carefully administered and volume level and status are monitored using central venous pressure or Swan - Ganz catheter. Pressor agent such as epinephrine ( alpha and beat receptor agonist ) is given as well as dopamine ( alpha receptor agonist - when the doses is higher and lead to vasoconstriction and beta 1 receptor agonist - when the doses is lower and acts as positive inotropic agent on myocardium). Amrinone may incrase cAMP indirectly due to its effects as selective phosphodiesterase type III inhibitor. Glucagon may also cause an increase in the production of the cAMP when glucagon is mixed with 5% dextrose or normal saline.
High doses of insulin ( 15000 units) with dextrose and potassium are administrated as insulin will facilitate efficient metabolism of the carbohydrates of the myocardium. Dextrose is considered when blood glucose is less than 200 mg/dl. If serum potassium is less than 2.5 mEq/l , potassium is considered. This treatments are considered due to failure in fluid resuscitation. Electrical pacing is consider when other treatments are failed.
Alternative treatments include hypertonic sodium bicarbonate and 20% intralipid IV fat emulsion.
Symptomatic patient with evidence of calcium channel blocker poisoning as well as patient who ingested sustained release preparation of calcium channel blocker should be admitted for assessment and monitoring due to delay presentation of symptoms and signs. Psychiatric evaluation is required , after the patient has been discharge. Patient may be discharge after 8 hours of immediate release preparation ingestion with a condition that he /she remain asymptomatic.
It is vital for the physician to focus on any suicidal intention or any risk of error in taking medication while assessing the patient. The patient may present with seizures, agitation, coma, confusion, depression, bradycardia, reflex tachycardia ( due to dihydropyridine) , hypotension, hyperglycemia or conduction abnormalities or heart block. The skin of the patient also may appear warm.
Common disorders that may mimic calcium channel blocker poisoning are heart block with acute myocardial infarction, digitalis toxicity, clonidine toxicity and beta blocker toxicity.
The investigations require are full blood count, urea and electrolytes, arterial blood gases, glucose, creatinine , blood urea nitrogen, toxicology screen, calcium level and digoxin level. Glucose test may reveal hyperglycemia while arterial blood gases may reveal metabolic acidosis.
How does calcium channel blocker works? Calcium channel blocker will block the calcium channel. Calcium channel blocker will prevent the entry of calcium which lead to lack of contraction of smooth muscle and cardiac muscle contractibility. Calcium channel blockers may also prevent the release of insulin from the pancreatic islet cell which later lead to hyperglycemia.
There are three different form of calcium channel blocker. This includes diltiazem which has a direct negative chronotropic effect and lead to decreased in peripheral vascular resistance which later causes a decrease in blood pressure and heart rate. However, initially there is an increase in cardiac output and heart rate.
Nifedipine ( dihydropyridine ) has a mild negative inotropic effect. Nifedipine may cause drop in blood pressure due to decrease in peripheral vascular resistance. Reflex tachycardia may also occur.
Verapamil ( phenylakylamines) is a negative chronotropic and negative ionotropic agent which cause a drop in blood pressure due to vasolidation.
References
1.DeWitt, Dr Christopher R., and Javier C. Waksman. “Pharmacology, Pathophysiology and Management of Calcium Channel Blocker and β-Blocker Toxicity.” Toxicological Reviews 23, no. 4 (December 1, 2004): 223–238. doi:10.2165/00139709-200423040-00003.
2.Ramoska, Edward A, Henry A Spiller, and Amy Myers. “Calcium Channel Blocker Toxicity.” Annals of Emergency Medicine 19, no. 6 (June 1990): 649–653. doi:10.1016/S0196-0644(05)82469-2.
3.Anderson, Angela C. “Calcium-Channel Blocker Overdose.” Clinical Pediatric Emergency Medicine 6, no. 2 (June 2005): 109–115. doi:10.1016/j.cpem.2005.04.007.
4.Costello, Merilee, and Rebecca S. Syring. “Calcium Channel Blocker Toxicity.” Journal of Veterinary Emergency and Critical Care 18, no. 1 (2008): 54–60. doi:10.1111/j.1476-4431.2007.00270.x.
Initial treatment include assessment of the airway, breathing and circulation. Airway need to be protected . Oxygen supplement is given and 0.9% of normal saline solution is given. It is important to keep the vital signs within the normal range with the systolic blood pressure more than 90 mmHg and heart rate more than 60 beats per minutes as well as respiratory rates around 16 - 20 beats per minutes. Urine output also should be adequate . Continuous monitoring of hemodynamic status is vital.
Gastric bowel irrigation is performed in case of overdose of sustained release calcium channel blocker. Bowel irrigation is avoided in case of unstable hemodynamic status. Activated charcoal is also considered as well as syrup of ipecac.
The bottle of calcium channel blocker is sent along with the patient to the emergency department . Calcium such as calcium gluconate and calcium chloride are given to correct the calcium level after confirming calcium channel blocker poisoning. However, we need to make sure that the patient also does not suffer from digoxin toxicity due to adverse effect of calcium on digoxin toxicity. Calcium chloride is irritative to the veins. Extravasation and tissue necrosis with sloughing are common. Calcium gluconate is preferred as it does not cause necrosis and sloughing of the tissue and is useful in acidemia patient.
Patient with calcium channel blocker overdose may also suffer from hypotension and bradycardia. IV fluids need to be carefully administered and volume level and status are monitored using central venous pressure or Swan - Ganz catheter. Pressor agent such as epinephrine ( alpha and beat receptor agonist ) is given as well as dopamine ( alpha receptor agonist - when the doses is higher and lead to vasoconstriction and beta 1 receptor agonist - when the doses is lower and acts as positive inotropic agent on myocardium). Amrinone may incrase cAMP indirectly due to its effects as selective phosphodiesterase type III inhibitor. Glucagon may also cause an increase in the production of the cAMP when glucagon is mixed with 5% dextrose or normal saline.
High doses of insulin ( 15000 units) with dextrose and potassium are administrated as insulin will facilitate efficient metabolism of the carbohydrates of the myocardium. Dextrose is considered when blood glucose is less than 200 mg/dl. If serum potassium is less than 2.5 mEq/l , potassium is considered. This treatments are considered due to failure in fluid resuscitation. Electrical pacing is consider when other treatments are failed.
Alternative treatments include hypertonic sodium bicarbonate and 20% intralipid IV fat emulsion.
Symptomatic patient with evidence of calcium channel blocker poisoning as well as patient who ingested sustained release preparation of calcium channel blocker should be admitted for assessment and monitoring due to delay presentation of symptoms and signs. Psychiatric evaluation is required , after the patient has been discharge. Patient may be discharge after 8 hours of immediate release preparation ingestion with a condition that he /she remain asymptomatic.
It is vital for the physician to focus on any suicidal intention or any risk of error in taking medication while assessing the patient. The patient may present with seizures, agitation, coma, confusion, depression, bradycardia, reflex tachycardia ( due to dihydropyridine) , hypotension, hyperglycemia or conduction abnormalities or heart block. The skin of the patient also may appear warm.
Common disorders that may mimic calcium channel blocker poisoning are heart block with acute myocardial infarction, digitalis toxicity, clonidine toxicity and beta blocker toxicity.
The investigations require are full blood count, urea and electrolytes, arterial blood gases, glucose, creatinine , blood urea nitrogen, toxicology screen, calcium level and digoxin level. Glucose test may reveal hyperglycemia while arterial blood gases may reveal metabolic acidosis.
How does calcium channel blocker works? Calcium channel blocker will block the calcium channel. Calcium channel blocker will prevent the entry of calcium which lead to lack of contraction of smooth muscle and cardiac muscle contractibility. Calcium channel blockers may also prevent the release of insulin from the pancreatic islet cell which later lead to hyperglycemia.
There are three different form of calcium channel blocker. This includes diltiazem which has a direct negative chronotropic effect and lead to decreased in peripheral vascular resistance which later causes a decrease in blood pressure and heart rate. However, initially there is an increase in cardiac output and heart rate.
Nifedipine ( dihydropyridine ) has a mild negative inotropic effect. Nifedipine may cause drop in blood pressure due to decrease in peripheral vascular resistance. Reflex tachycardia may also occur.
Verapamil ( phenylakylamines) is a negative chronotropic and negative ionotropic agent which cause a drop in blood pressure due to vasolidation.
References
1.DeWitt, Dr Christopher R., and Javier C. Waksman. “Pharmacology, Pathophysiology and Management of Calcium Channel Blocker and β-Blocker Toxicity.” Toxicological Reviews 23, no. 4 (December 1, 2004): 223–238. doi:10.2165/00139709-200423040-00003.
2.Ramoska, Edward A, Henry A Spiller, and Amy Myers. “Calcium Channel Blocker Toxicity.” Annals of Emergency Medicine 19, no. 6 (June 1990): 649–653. doi:10.1016/S0196-0644(05)82469-2.
3.Anderson, Angela C. “Calcium-Channel Blocker Overdose.” Clinical Pediatric Emergency Medicine 6, no. 2 (June 2005): 109–115. doi:10.1016/j.cpem.2005.04.007.
4.Costello, Merilee, and Rebecca S. Syring. “Calcium Channel Blocker Toxicity.” Journal of Veterinary Emergency and Critical Care 18, no. 1 (2008): 54–60. doi:10.1111/j.1476-4431.2007.00270.x.
