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140 Calcium Channel Blocker Drug Toxicosis

care management and surgeons skilled in Prevention • Rotate the patient and location of the
surgical burn management, including skin • Use circulating warm water/air blankets for warming device frequently.
grafting.
VetBooks.ir • Severe eschars causing constriction of ventila- or hot water bottles, especially during SUGGESTED READING
patient warmth, not electric heating blankets
diagnostic imaging with MRI.
tory muscles or limb ischemia require early
Vaughn L, et al: Severe burn injury, burn shock, and
debridement and primary wound closure or
grafting to limit wound infection and reduce • Duration of time in contact with the smoke inhalation in small animals. Part 2. Diag-
warming device influences the extent of
nosis, therapy, complications and prognosis. J Vet
the risk of compartmentalization. injury; therefore, the patient or warming Emerg Crit Care 22(2):187-200, 2012.
• Respiratory distress in a patient with evidence device should be repositioned frequently. AUTHOR: Kristin Welch, DVM, DACVECC
of smoke inhalation (e.g., burned whiskers) EDITOR: Benjamin M. Brainard, VMD, DACVAA,
may be due to pharyngeal or laryngeal edema Technician Tips DACVECC
and warrants intubation to obtain and • Always place a towel or blanket between a
maintain airway patency. patient and a warming device.

Calcium Channel Blocker Drug Toxicosis Client Education
Sheet

BASIC INFORMATION cardiac glycoside–containing plants, Bufo
Etiology and Pathophysiology toad), antidepressant, organophosphate,
Definition Source: and carbamate insecticides toxicoses
Calcium channel blocker (CCB) drugs are com- • Prescription medication (human or Spontaneous, non-toxicologic:
monly used for the treatment of hypertension veterinary) • Primary cardiac disease, systemic illness
and tachyarrhythmias in human and veterinary • Dihydropyridine-type CCBs (e.g., amlo- causing hypotension
medicine. Adverse effects at therapeutic dose dipine, nifedipine): effects are confined to
or with overdose result in hypotension and vascular smooth muscle. They are used for Initial Database
bradycardia or tachycardia, weakness, ataxia, treating hypertension. • Arterial blood pressure (BP): hypotension
and inappetence within 30 minutes to 12 hours • Nondihydropyridine-type CCBs (e.g., (p. 1065)
after ingestion. diltiazem, verapamil) have greater potency • Electrocardiogram (ECG) (p. 1096)
in cardiac muscle and cardiac nodal tissues ○ Sinus bradycardia, AV block with vera-
Epidemiology than in the vasculature. They are used for pamil or diltiazem
SPECIES, AGE, SEX treating arrhythmias and hypertrophic heart ○ Sinus tachycardia with dihydropyridines
All animals are susceptible. Exposure is more diseases. • Serum chemistry profile: hyperglycemia,
common in dogs. Mechanism of toxicosis: hypokalemia, hypophosphatemia, hypo-
• CCBs close L-type calcium channels by magnesemia possible
RISK FACTORS binding to their alpha-1c subunits. Decreased • Acid-base status: lactic acidosis possible
• Pre-existing renal or cardiovascular disease calcium influx results in vasodilation (dihy-
may predispose to signs. dropyridine type) or a decrease in myocardial Advanced or Confirmatory Testing
• Hepatic disease may reduce metabolism and contractility and electrical impulse conduc- Plasma CCB levels may be measured at a
elimination of CCBs. tion at the sinoatrial (SA) and atrioventricular human hospital for confirmation of exposure.
(AV) nodes (nondihydropyridine type). Therapeutic monitoring to assess response to
Clinical Presentation • CCBs decrease pancreatic insulin secretion, treatment is not useful for animals.
DISEASE FORMS/SUBTYPES resulting in hyperglycemia.
Sustained/controlled/extended/delayed-release • CCBs may cause noncardiogenic pulmonary TREATMENT
preparations may delay onset of signs (6-12 edema (mechanism unknown).
hours), whereas immediate-release preparations Treatment Overview
can cause signs within 30 minutes. DIAGNOSIS Treatment consists of decontamination (emesis
and charcoal administration), stabilizing
HISTORY, CHIEF COMPLAINT Diagnostic Overview the cardiovascular system, and maintaining
• History of suspected or observed exposure The diagnosis is suspected based on observation tissue perfusion by maintaining adequate BP.
• Weakness, depression, ataxia, vomiting or evidence of ingestion (chewed container) Continuous monitoring in a veterinary facility
possible along with physical exam findings of hypoten- for 12-24 hours or longer after ingestion is
sion and/or bradycardia. Confirmation with recommended because signs can be delayed,
PHYSICAL EXAM FINDINGS plasma drug levels is uncommonly performed, especially with extended-release formulations.
• Hypotension and bradycardia are common; and treatment generally should be initiated
reflex tachycardia possible if hypotension without such results. Acute General Treatment
predominates (dihydropyridine CCBs) Decontamination (p. 1087):
• Pale mucous membranes Differential Diagnosis • Emesis for a recent ingestion or an animal
• Hypothermia possible (due to hypotension) Toxicologic: showing no overt signs of toxicosis (p. 1188)
• Depression, ataxia, seizures, or coma • Beta-adrenergic receptor antagonists overdose • Activated charcoal 1-2 g/kg (or labeled
possible (propranolol, metoprolol), alpha-adrenergic dosage) with a cathartic PO; repeat one-half
• Respiratory distress possible (pulmonary receptor agonists (imidazoline-type decon- of the original dose q 6h for large ingestions
edema) gestants), cardiac glycosides (e.g., digoxin, or extended-release preparations

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