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Calcium channel blockers. Professor Ian Whyte Hunter Area Toxicology Service. Calcium channel blockers. Phenylalkylamines verapamil Benzothiazepines diltiazem Dihydropyridines nifedipine, felodipine, nimodipine, nicardipine, amlodipine, lercanidipine . Calcium channel blockers.

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calcium channel blockers

Calcium channel blockers

Professor Ian Whyte

Hunter Area Toxicology Service

calcium channel blockers2
Calcium channel blockers
  • Phenylalkylamines
    • verapamil
  • Benzothiazepines
    • diltiazem
  • Dihydropyridines
    • nifedipine, felodipine, nimodipine, nicardipine, amlodipine, lercanidipine
calcium channel blockers3
Calcium channel blockers
  • Block calcium channels (L-type) in heart and blood vessels
    • prolong depolarisation
      • ↑QRS width
    • block SA and AV node conduction
      • heart block
      • asystole
    • vasodilators
    • cerebral protection
calcium channel blockers4
Calcium channel blockers
  • Hypotension
    • peripheral vasodilatation and myocardial depression
  • Bradycardia
    • AV and SA node block
  • Correction of acidosis
  • Calcium loading
  • Glucagon
  • Insulin-dextrose euglycaemia
  • Atropine
  • Inotropic agents
  • Cardiac pacing
  • Bay K 8644 (calcium channel agonist)
correction of acidosis
Correction of acidosis
  • Correct acidosis to a pH within the normal range
    • L calcium channel function is impaired when the pH falls outside the physiological range
    • acidosis enhances the effect of verapamil and decreases the effect of calcium
    • sodium bicarbonate significantly improved myocardial contractility and cardiac output in a swine model of verapamil poisoning
calcium loading
Calcium loading
  • Calcium loading is the most logical and appears to be the most effective agent to use in calcium channel blocker poisoning
  • It is primarily indicated in patients with heart block (who have usually taken verapamil or diltiazem)
  • Glucagon is a well-accepted antidote for beta-blocker poisoning
  • The rationale for its use in CCB poisoning is that it activates myosin kinase independent of calcium flux
  • Clinical experience suggests it is less effective in this setting than in beta-blocker poisoning
insulin dextrose euglycaemia
Insulin-dextrose euglycaemia
  • Insulin infusions should be used to treat hyperglycaemia or hyperkalaemia
  • Insulin-dextrose euglycaemia is more effective in animal models than calcium, adrenaline or glucagon
  • Effective in a case series of clinically serious poisonings
  • Hypotension that is refractory to volume loading, correction of acidosis and calcium salts
insulin euglycaemia
  • Insulin as an inotrope
    • myocardial ischaemia/infarction
    • endotoxic shock
    • cardiogenic shock post cardiopulmonary bypass
    • CCB and –blocker induced myocardial depression
          • Yuan TH, Kerns WP, Tomaszewski CA,Ford MD, Kline JA. Insulin-glucose as adjunctive therapy for severe calcium channel antagonist poisoning. J Tox Clin Tox 1999; 37(4): 463–474
insulin euglycaemia11
  • Rationale
    • In unstressed, aerobic state the myocardium relies primarily on free fatty acids (FFAs) for mechanical energy
    • During shock, substrate preference shifts from FFAs to carbohydrate oxidation
insulin euglycaemia12
  • In the presence of
    • inhibition of insulin release
    • insulin resistance
    • poor tissue perfusion
      • impaired glycolysis and carbohydrate delivery
  • Systemic hyperglycaemia and inefficient myocardial energy transfer
    • myocardial depression
insulin euglycaemia13
  • Hypokalaemia
    • Shift of extracellular K+ to intracellular via Na+/K+ pump
    • Na+ shift means resting membrane potential becomes more negative (hyperpolarisation)
      • decrease arrhythmias
    • Prolongs plateau phase of action potential
      • increases calcium entry
    • Aim for K+ 2.8–3.2
      • Replace if K+ < 2.5
  • Vagal tone is increase by vomiting and gastrointestinal decontamination
  • Atropine should be given to all patients who are vomiting or having GI decontamination
  • Atropine should be given to all patients with bradycardia
  • A response may only occur after calcium loading
inotropic agents
Inotropic agents
  • Dopamine is the initial pressor agent of choice (75% response) for diltiazem overdose
  • Isoprenaline produces a therapeutic response in 50% of patients
  • Action is predominantly through increasing the frequency of impulses originating in the SA node
  • These agents are often ineffective as chronotropic agents when there is a high degree of conduction block
cardiac pacing
Cardiac pacing
  • Ventricular rather than atrial pacing
  • In severe poisoning the heart may fail to capture and pharmacological therapy will still be required
calcium channel agonists
Calcium channel agonists
  • Calcium channel agonists (eg. Bay K 8644) would appear to be a logical antidote
  • Animal studies using these compounds have not been very promising