Flashcards in Arrhythmias Deck (47):
What sxs might be associated with a-fib?
-palpitations, SOB, dyspnea, dizziness, fatigue
What are the 3 goals in management of a-fib?
1. control rate
2. prevent thromboembolism
3. correct to normal sinus rhythm, maintain
What is the goal of pharm therapy to control the ventricular rate in a-fib?
-slow the conduction velocity
-increase refractory period at AV node
What drugs can be used to control ventricular rate in a-fib?
-non-dihydropyridine calcium channel blockers
-digoxin and amiodarone are alternative choices
MOA of Non-Dihydropyridines in A-fib Rate Control
-work at AV node to decrease conduction velocity and increase refractory period
-slows down the ventricular rate
What CCB are used for a-fib rate control?
-non-dihydropyridines: diltiazem and verapamil
What must be monitored when using CCB for a-fib rate control?
-BP because diltiazem and verapamil are vasodilators
-signs of CHF due to negative inotropic effect
MOA of Beta Blockers in A-fib Rate Control
-block beta adrenergic receptors in heart
-decreased conduction at AV node and increased refractory period
What oral BBs are commonly used in a-fib rate control?
What must be monitored when using BB for a-fib rate control?
-BP for HoTN
-exacerbation of CHF
Adverse Effects of BBs in A-fib Rate Control
-CNS: fatigue, lethargy, depression, sexual dysfunction
MOA of Digoxin in A-fib Rate Control
-increases vagal tone to slow conduction at AV node
It is advantageous to use digoxin in 2 circumstances for a-fib control. What are they?
-pt HoTN: other agents reduce BP, dig has no effect on BP
-advantage in CHF exacerbation: other agents may decrease heart's contractility
What must be monitored when using digoxin in a-fib rate control?
-HR, BP, electrolytes (for hypokalemia/magnesemia)
-rhythm for any new arrhythmias
-signs of toxicity: hallucinations, N/V, AV block
MOA of Amiodarone in A-Fib Rate Control
-beta blocker and CCB to slow down heart rate
-also has anti-arrhythmic actions to convert a-fib
When is anticoagulation needed when converting a-fib to NSR?
-if a-fib 48 hours or unknown, anticoag is needed: 3 weeks of warfarin before cardioversion
What are some of the agents that can be used to convert a-fib to NSR?
-ibutilide, dofetilide, sotalol
MOA of Procainamide/Quinindine/Disopyramide
-inhibit fast sodium channels
-decreases conduction velocity
-increases refractory time
In what patients do propafenone and flecanide need to be avoided?
-pt with with structural heart dz like CAD or CHF
MOA of Amiodarone
-provides rate control
-may convert to NSR and maintain NSR once converted
What are some downsides of amiodarone use?
-potentially serious long term risk of pulmonary fibrosis
-hypo or hyperthyroidism
What must be monitored short term with amiodarone?
-drug interactions w/ warfarin, digoxin, statins
What must be monitored long term with amiodarone?
-PFT and CXR at baseline then annual CXR
-LFTs at baseline and q6 months
-thyroid function test at baseline and 2-3x/yr thereafter
How is ibutilide used?
-one time IV dose to convert to NSR
What are some problems associated with ibutilide/dofetilide use?
-can cause QT prolongation, proarrhythmias, torsades de pointes
What is important to remember about dofetilide dosing?
-adjust for renal function (lower doses for poorer CrCl)
What is sotalol indicated for?
-BB with additional anti-arrhythmic properties
-indicated for maintaining NSR once converted
What must happen with paroxysmal supraventricular tachycardia in order to convert to NSR?
-must break the re-entry pathway in the AV node
How is PSVT treated and what is the DOC?
-initially, carotid sinus massage
-use drugs to slow AV nodal conduction
-adenosine is DOC, but verapamil, diltiazem and BBs also work
MOA of Adenosine
-briefly interrupts conduction at AV node to break re-entry
What must be monitored with adenosine use?
-peripheral vasodilation: HoTN, flushing, SOB, chest tightness, apprehension
When is adenosine contraindicated?
-in heart transplant patients
What is primary prevention of ventricular arrhythmias?
-at elevated risk of ventricular arrhythmias, but have never experienced an episode
What is secondary prevention of ventricular arrhythmias?
-have survived or experienced v-tach w/o a precipitating cause or experience syncope thought to be caused by tachyarryhthmias
How is stable v-tach (non-cardiac arrest) treated?
How is unstable v-tach (non-cardiac arrest) treated?
Besides amiodarone, what other drugs can be used for v-tach (non-cardiac arrest)?
How is torsades de pointes with a prolonged QT interval corrected?
What are the various ventricular arrhythmias?
-pulseless electrical activity (PEA)
During v-fib/v-tach, asystole or PEA, what drugs can improve perfusion?
-epinephrine or vasopressin
During v-fib/v-tach, what drugs can "fix" the rhythm?
During asystole or PEA, what drugs can "fix" the rhythm?
MOA of Epinephrine
-improves perfusion to heart and brain during CPR
-peripheral vasoconstriction = increased cardiac conduction and improved cardiac contractility
MOA of Vasopressin
-improves perfusion to heart and brain during CPR
-alternative to epi
-increase coronary perfusion pressure, vital organ blood flow, cerebral blood flow
Indications for Mag Sulfate
-torsades de pointes
-suspected hypomagnesemic state
-refractory ventricular arrhythmias
MOA of Atropine
-anticholinergic effects --> increased SA node firing and AV node conduction