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automaticity
ability of a cardiac cell to automatically fire; depolarization occurs in phase 0
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mechanisms of arrhythmias
- problems with impulse formation (sinus tachy/bradycardia or abnormal pace maker)
- problems with conduction (AV node block, re-entry phenomenon)
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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)
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ventricular arrhythmias
- premature ventricular contractions
- ventricular tachycardia (DCC, defib, lidocaine, procainamide, amiodarone to treat)
- ventricular fibrillation (defib)
- torsades de pointes (magnesium sulfate to treat)
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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)
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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)
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NAVEL
- drugs that can be given endotracheally (double dose for all excep vasopressin)
- narcan, atropine, vasopressine, epinephrine, lidocaine
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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)
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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
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amiodarone
- class III
- increases refractory period without altering conduction time
- very long half life (20-50 days)
- ANTIARRYTHMIC OF CHOICE
- toxicity: hyper/hypothyroidism, photosensitivity, pulmonary fibrosis, optic neuritis wiht long term therapy
- increases DIGOXIN and WARFARIN levels
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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
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atropine
- blocks muscarinic receptors
- increases HR and improves conduction
- paradoxical bradycardia if dose is too small
- used for heart block, bradycardia, asystole
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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
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magnesium sulfate
drug of choice for torsades de pointes
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