Tox i c o l o g y 18 3SPECIFIC POISONSCalcium-channel blocking drugs
DIAGNOSIS
1 Toxicity is related to underlying cardiac disease, co-ingestants, delay to
treatment, increased age, and the specific calcium-channel blocker (CCB)
ingested.
(i) Sustained-release (SR) verapamil or diltiazem are associated with
the majority of significant poisonings.
2 Clinical signs of toxicity usually present within 2 h, but may be delayed up to
8 h with sustained-release preparations. Features include:
(i) Gastrointestinal: nausea and vomiting.
(ii) Cardiovascular: hypotension, sinus bradycardia and complex
cardiac arrhythmias.
(iii) CNS: lethargy, slurred speech, confusion, coma and convulsions.
3 Gain i.v. access and send blood for U&Es, LFTs and a blood sugar level. Take
an arteria l or venous blood gas.
(i) Hyperglycaemia and metabolic acidosis are common with
significant toxicity.
4 Perform an ECG. Look for toxic conduction defects such as high-grade
AV block, complete heart block, and accelerated atrioventricular nodal
rhythms.
MANAGEMENT
1 Ensure the airway is secure and administer high-f low oxygen. Commence
i.v. f luid administration.
2 Administer oral activated charcoal to all patients as soon as possible. More
aggressive decontamination, such as whole bowel irrigation, may be required
with large ingestions of SR tablets.
3 Give 10% calcium chloride 10 mL i.v. bolus, and repeat up to 30 mL i.v.
followed by an infusion. Calcium increases cardiac output and restores
perfusion to vital organs.
4 If hypotension and reduced myocardial contractility persist:
(i) Commence an adrenaline (epinephrine) infusion at up to
0.5–1.0 g/kg per min, titrated to maintain organ perfusion.
(ii) High-dose insulin therapy (0.5–1.0 IU/kg/h), in combination
with 50% dextrose infusion to maintain euglycaemia, is effective
treatment for severe CCB poisoning.
(iii) Discuss management early with a poisons centre clinical
toxicologist.
5 Admit the patient to ICU for cardiorespiratory monitoring.