drugs affecting dysrth

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Anonymous
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241250
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drugs affecting dysrth
Updated:
2013-10-17 16:51:36
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dysrth
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  1. Drugs Affecting Hemodynamic Status
    • Antidysrhythmics
    • Angina
    • Anticoagulation
  2. Etiology of Dysrhythmias
    •  Disturbances of impulse formation (automaticity)
    • SA or AV nodes & His-Purkinje fibers
    • Injury or ANS stimulation can cause abnormal spontaneous depolarization
    • Aberrant beat (abarrency)
    • Disturbances of conduction
    • AV block
    • Reentry (re-circulating activation)
  3. Classification of Antidysrhythmics
    • Based on site of action potential disruption
    • Vaughan Williams classification
    • Class I       blocks sodium channels
    • Class II      beta blockers
    • Class III     potassium channel blockers
    • Class IV    calcium channel blockers
    • Other         digoxin, adenosine
  4. Non-pharmacologic Therapy
    • All can cause or worsen dyshythmias AICD Automatic implanted                               cardiac  defibrillators
    • Ablation
    • Radio waves to destroy  abnormal foci
  5. Class I-Sodium Channel blockers  1a   
    Delay repolarizing 

    • Class 1A-Quinidine (bark of the cinchona tree)
    • Slows conduction
    • atria, ventricles, His, Purkinje
    • Widens qrs, Prolongs qt
    • Broad spectrum dysrhythmias suppression
    • Cardiotoxicity-
    • slows conduction causing more arrhythmias Gi-severe diarrhea, vasodilation & hypotension, Cinchonism-tinnitus, N/V, blurred vision
    • Procainamide/Pronestyl
    • SLE-like syndrome, blood dyscrasias
  6. Class I-Sodium Channel blockers 1b
    •  Class 1B
    • Slows conduction
    • Decreases automaticity
    • Accelerates repolarization
    • Does not change ECG
    • Lidocaine/Xylocaine
    • Short Term Ventricular arrhythmias
    • Toxicity
    • confusion, parasthesias, seizures, arrest
    • First pass inactivation, so given IV
    • Mexiletine/Mexitil-oral
  7. Class I-Sodium Channel blockers  1c
    Decrease conduction velocity

    • Class 1C-prodysrhythmic action
    • Used for life threatening ventricular dysrhythmias
    • Can exacerbate dysrhythmias and cause new Wide qrs, long qt
    • Not widely used-only for refractory arrhythmias
    • Flecainide/Tambocor
    • Propafenone/Rythmol
  8. Class II Beta Blockers
    • Tachydysrhythmias and PVC’s
    • Propranolol-non-selective B1 & B2
    • Slows heart rate, bronchoconstriction
    • Suppresses all conduction
    • Intensifies AV conduction problems
    • Exacerbation of asthma, hypotension r/t reduced CO
    • Metroprolol/Lopressor
    • Esmolol/brevibloc
  9. Class III Potassium Channel Blockers 
    • Delay repolarization  (Prolong QT interval )Bretylium Only short term severe V dysrhythmias
    • Profound hypotension
  10. Class III K+ Blockers
    • Amiodarone/Cardarone
    • A & V dysrhythmias
    • K+, NA+, Ca+ channels blocked to produce overall reduction in conduction
    • Wide qrs and long pr & qt
    • Highly lipid soluble, accumulates, long ½ life
    • Pulmonary toxicity-
    • pneumonitits, pulmonary fibrosis
    • Liver failure
  11. Class III K+ Blockers
    • Amiodarone/Cardarone
    • SA/AV block or heart failure
    • Corneal micro-deposits-blurred vision
    • Blue-gray skin discoloration, GI problems, ataxia
    • Iodine base-thyroid dysfunction
    • IV administration
    • Hypotension, brady-dysrhythmias, AV block
  12. Class III K+ Blockers
    refractory dysrhythmias

    • Sotalol/Betapace
    • Has both K+ and beta blocking effects
    • Atrial fib/flutter
    • Torsades de pointes-5% of users
    • Dofetilide/Tikosyn
    • Atrial fib/flutter
    • Torsades de pointes
    • reserved for symptomatic a fib
    • Some drugs interfere with excretion

    • Ibutilide/Corvert 
    • Terminates a fib, a flutter of recent onset
    • Prolongs QT interval
    • 1 mg infused over 10 minutes
    • Can convert up to 90 mins post infusion
    • 1 mg dose can be repeated within 10 mins of first infusion
  13. Class IV-calcium channel blockers
    • Verapamil/Calan Diltiazem/cardizem
    • 1
    • 2
    • 3
    • Terminate SVT caused by reentrant circuit
    • Slow ventricular rate in atrial fibrillation
  14. Digoxin/Lanoxin
    •  Supraventricular dysrythmias
    • Dec conduction in AV node
    • Dec automaticity in SA node
    • Parasympathetic (Vagal) cardiac effect
    • Positive inotrope-inc force of contraction
    • Adverse effect: dysrhythmias with toxicity
    • Worse with hypokalemia
    • Requires therapeutic range (0.5-2.0)
    • Many drug interactions so not used as much
    • Drug levels
  15. Adenosine/Adenocard
    • Naturally occurring nucleotide
    • Terminates paroxysmal SVT
    • Dec automaticity in SA
    • Dec conduction in AV
    • Active only for SVT
    • Bolus IV only-needs NaCl flush
    • 6 mgs, 12 mgs, 12mgs

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