Calcium channel blocker: Difference between revisions

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[[File:LipidEmulsion.JPG|thumb|[[Lipid emulsion]] as used in CCB toxicity]]
[[File:LipidEmulsion.JPG|thumb|[[Lipid emulsion]] as used in CCB toxicity]]


Mild CCB [[toxicity]] is treated with supportive care. Nondihydropyridine CCBs may produce profound toxicity, and early [[decontamination]], especially for slow-release agents, is essential. For severe [[overdoses]], treatment usually includes close monitoring of vital signs and the addition of vasopressive agents and intravenous fluids for blood pressure support. Intravenous [[calcium gluconate]] (or [[calcium chloride]] if a central line is available) and atropine are first-line therapies. If the time of the overdose is known and presentation is within two hours of [[ingestion]], [[activated carbon|activated charcoal]], [[gastric lavage]], and [[polyethylene glycol]] may be used to decontaminate the gut. Efforts for gut decontamination may be extended to within 8 hours of ingestion with extended-release preparations.{{cn|date=July 2022}}
Mild CCB [[toxicity]] is treated with supportive care. Nondihydropyridine CCBs may produce profound toxicity, and early [[decontamination]], especially for slow-release agents, is essential. For severe [[overdoses]], treatment usually includes close monitoring of vital signs and the addition of vasopressive agents and intravenous fluids for blood pressure support. Intravenous [[calcium gluconate]] (or [[calcium chloride]] if a central line is available) and atropine are first-line therapies. If the time of the overdose is known and presentation is within two hours of [[ingestion]], [[activated carbon|activated charcoal]], [[gastric lavage]], and [[polyethylene glycol]] may be used to decontaminate the gut. Efforts for gut decontamination may be extended to within 8 hours of ingestion with extended-release preparations.


Hyperinsulinemia-euglycemia therapy has emerged as a viable form of treatment.<ref>{{Cite journal|last1=Engebretsen|first1=Kristin M.|last2=Kaczmarek|first2=Kathleen M.|last3=Morgan|first3=Jenifer|last4=Holger|first4=Joel S.|date=2011|title=High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning|journal=Clinical Toxicology|volume=49|issue=4|pages=277–283|doi=10.3109/15563650.2011.582471|issn=1556-9519|pmid=21563902|s2cid=32138463}}</ref> Although the mechanism is unclear, increased insulin may mobilize glucose from peripheral tissues to serve as an alternative fuel source for the heart (the heart mainly relies on oxidation of fatty acids). Theoretical treatment with lipid emulsion therapy has been considered in severe cases, but is not yet standard of care.
Hyperinsulinemia-euglycemia therapy has emerged as a viable form of treatment.<ref>{{Cite journal|last1=Engebretsen|first1=Kristin M.|last2=Kaczmarek|first2=Kathleen M.|last3=Morgan|first3=Jenifer|last4=Holger|first4=Joel S.|date=2011|title=High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning|journal=Clinical Toxicology|volume=49|issue=4|pages=277–283|doi=10.3109/15563650.2011.582471|issn=1556-9519|pmid=21563902|s2cid=32138463}}</ref> Although the mechanism is unclear, increased insulin may mobilize glucose from peripheral tissues to serve as an alternative fuel source for the heart (the heart mainly relies on oxidation of fatty acids). Theoretical treatment with lipid emulsion therapy has been considered in severe cases, but is not yet standard of care.