1. automaticity
    ability of a cardiac cell to automatically fire; depolarization occurs in phase 0
  2. mechanisms of arrhythmias
    • problems with impulse formation (sinus tachy/bradycardia or abnormal pace maker)
    • problems with conduction (AV node block, re-entry phenomenon)
  3. supraventricular arrhythmias
    • sinus bradycardia (treat with atropine)
    • AV node blockade (treat wiht atropine)
    • atrial fibrillation (treat with antocoagulation therapy, direct cardioversion (unstable), CCB/BB/dig/amiodarone (stable))
    • paroxysmal supraventricular tachycardia (treat with adenosine)
  4. ventricular arrhythmias
    • premature ventricular contractions
    • ventricular tachycardia (DCC, defib, lidocaine, procainamide, amiodarone to treat)
    • ventricular fibrillation (defib)
    • torsades de pointes (magnesium sulfate to treat)
  5. Procainamide
    • Class 1a
    • direct effects on heart (slows conduction, prolongs refractory period, reduces automaticity)
    • indirect effects on heart (vagolytic effect - blocks vagus nerve)
    • not often used, may increase mortatlity; may use if amiodarone has failed
    • toxicity: N/V/D, anticholinergic effects, torsades de pointes, way worsen systolic HF (negative inotropic effect)
    • pt related variables: systolic HF, AV block
    • drug interactions: DIGOXIN and WARFARIN (quinidine)
  6. Lidocaine
    • Class 1b
    • used for ventricular arrhythmias
    • IV (give bolus during an arrest)
    • toxicity: neuro (parathesias, agitation, slurred speech, confusion)
    • pt related variables: AV block, HF (reduce dose), cirrhosis (reduce dose)
    • drug interactions: CIMETIDINE (decreases metabolism of lidocaine)
  7. NAVEL
    • drugs that can be given endotracheally (double dose for all excep vasopressin)
    • narcan, atropine, vasopressine, epinephrine, lidocaine
  8. flecainide, moricizine, propafenone
    • class 1c
    • very effective for suppressing ventricular ectopy
    • used ONLY in pts w/o evidence of structural heart dz or left vent dysfuntion
    • interactions: CIMETIDINE
    • toxicity: blurred vision, dizziness, SLE like symptoms (for flecainide)
  9. propanolol, metoprolol
    • class II, beta blockers
    • decreases the effects of catacholamines (Epi, norepi) on heart
    • slows firing of SA node, slows conduction through AV node
    • used to control ventricular rate with a fib/a flutter, supraventricular tachycardia
    • very high first pass effect
  10. amiodarone
    • class III
    • increases refractory period without altering conduction time
    • very long half life (20-50 days)
    • toxicity: hyper/hypothyroidism, photosensitivity, pulmonary fibrosis, optic neuritis wiht long term therapy
    • increases DIGOXIN and WARFARIN levels
  11. verapamil, diltiazem
    • class IV, ca channel blockers (not nifedipine)
    • decreases flow of Ca into cells, slowing SA node and conduction through AV node
    • negative inotropic effect
    • causes arteriolar vasodilation, decreasign PR, may cause reflex tachycardia
    • high first pass effect
    • used to control vent rate in a fib/a flutter, PSVT
    • do not use for vent tachycarida
    • toxicities: bradycardia, HF, hypotension, constipation
    • increases concentrations of DIGOXIN
  12. atropine
    • blocks muscarinic receptors
    • increases HR and improves conduction
    • paradoxical bradycardia if dose is too small
    • used for heart block, bradycardia, asystole
  13. adenosine
    • slows conduction through AV node and reduces automaticity
    • used for PSVT (drug of choide), helps distiguish between PSVT (narrow QRS) and ventricular (wide QRS)
    • give IV bolus fast
    • toxicity: hypotension, facial flushing, SOB, HA
    • drug interactions: THEOPHYLLINE
  14. magnesium sulfate
    drug of choice for torsades de pointes
Card Set
Pharm exam 2