anti-arrhythmic Flashcards
Amiodarone
Class III anti-arrhythmic
K channel blocker; inhibits repolarization
Uses;
- Atrial and Ventricular dysrhythmias
- recurrent VF, unstable VT, A-fib and SVT
- Prophylaxis for Afib r/t cardiac surgery
MOA;
- K channel blocker; inhibits repolarization, prolongs AP plateau, decreasing depolarization and re-entry
- prolongs refractory period in cardiac tissue
- Class I; Na channel blocker; decreases rate of firing
- Class II; Alpha and Beta Blocker
- Class IV; CCB; decreases SA node function (HR) and AV node conduction
- Coronary Artery vasodilation; decreases workload of heart (decreases demand)
Dose; 150 - 300 mg over 2 -5 min –> 1mg/min x 6hs –> 0.5mg/min x 18 hrs
Pharmacokinetics;
- crosses placenta
- onset; rapid (IV)
- E1/2t; 10 - 100 days
- Vd; 66 L/kg
- Pb;96%
- metabolized by the liver into N-desethylamiodarone (long E1/2t)
- <1% excreted unchanged in urine
Side Effects;
- PROLONGED QT
- hypotension
- bradycardia
- AV block
- pulmonary fibrosis
- ARDS/ pulmonary edema
- hyper/hypothyroid
- blue/gray skin color
- CYP450 inhibitor
Contraindicated;
- hypersensitivity
- iodine sensitivity
- bradycardia
- heart block
- pregnancy
Caution;
- increases blood level of warfarin, digoxin, phenytoin
- increases effects of benzo and CCB
- BB and CCB –> excessive AV block
- VA–> myocardial depression
Digoxin
Cardiac Glycoside
Inotrope
Class V anti-arrythmic
Uses;
- Rate and rhythm control for Afib/ Aflutter ad AVT
- HF (increase contractility)
MOA; blocks the Na/K ATPase; causing more Na in the cells and a less exchange of Ca out of the cell via the Na/Ca pump; ↑ Ca available for subsequent contractions
- ↑ Ca released from SR ↑ force of contraction = ↑ contractility (+ inotrope)
- ↓ sympathetic tone and ↑ vagal tone; ↓ SA node activity ↓ AV node conduction
- can lead to AV block and atrial arrhythmias*
Dose; 0.5 - 1 mg IV
Pharmacokinetics;
onset; 30 - 60 min
E1/2t; 36 hrs
Pb; 25%
Vd; 640 L
** narrow therapeutic index 0.5 - 1.2 ng/ml
metabolized b the liver and excreted 90% unchanged by the kidneys
(clearance directly proportional to creating clearance)
Side Effects;
- Prolonged PR interval
- ST depression
- T wave changes
- dysrhythmias
- Heart block
- blurred vision
- N/V
- Diarrhea
- headache
- fatigue
Contraindicated;
- V-fib and V-tach
- Hypertrophic sub aortic stenosis
*narrow TI; toxicity potentiated with ↓ K+, ↓Mg and ↑ Ca
- caution with K wasting diuretics
- verapamil and amiodarone ↑ plasma concentration
- BB and CCB antagonize the inotropic effect
- BB, CCB and digoxin cause AV heart block
Tx toxicity with digibind
Tx arrhythmia with phenytoin
Give atropine to offset vagal affect
Adenosine
endogenous nucleoside present in every cell of the body (regulates CV function; HR, contractility, coronary blood flow)
Class V anti-arrhythmic
Uses;
- acute treatment only
- SVT (can be used in WPW)
- diagnosis of tachycardia arrhythmias
- stress test to dilate coronaries
MOA;
binds to G protein coupled adenosine receptors (CV electrophysiologic effects via A1)
-naturally tissue hypoxia stimulates release of adenosine which blocks release of NE ↓ SNS ↓ work on heart and dilates coronaries
-when give as IV bolus for SVT adenosine binds to A1 receptors linked to acetylcholine activated G-protein K channels and temporarily hyper-polarizes the cardiac conduction tissue; ↓ SA node and ↓ AV node conduction
-Ca dependent AP also blocked by blocking catecholamine release that stimulates cAMP; stop AV boded re-entry pathways
Dose; 6 mg IV push; PRN 6 - 12 mg
Pharmacokinetics;
onset; rapid
E1/2t; 30 seconds
-eliminated by carrier mediated uptake (occurs in most cell types)
-intra-cellular adenosine is phosphorylated
Side Effects;
- excessive SA and AV node inhibition
- chest pain/ tightness
- SOB
- bronchospasm
- N/V
- headache
- dizzy
- facial flushing
- palpitations
- hypotension
Contraindicated
- asthmatic
- heart block
