Arrhythmias Flashcards
What sxs might be associated with a-fib?
-palpitations, SOB, dyspnea, dizziness, fatigue
What are the 3 goals in management of a-fib?
- control rate
- prevent thromboembolism
- 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?
- beta blockers
- 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?
- atenolol
- metoprolol
What must be monitored when using BB for a-fib rate control?
- BP for HoTN
- bradycardia
- 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
- serum level
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?
- procainamide, quinindine
- propafenon, flecanide
- amiodarone
- ibutilide, dofetilide, sotalol
MOA of Procainamide/Quinindine/Disopyramide
- inhibit fast sodium channels
- decreases conduction velocity
- increases refractory time
- decreases automaticity
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
- hepatic dysfunction
- skin discoloration
- ocular toxicities
What must be monitored short term with amiodarone?
- bradycardia
- heart block
- HoTN
- drug interactions w/ warfarin, digoxin, statins
- GI disturbances
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?
-with amiodarone
How is unstable v-tach (non-cardiac arrest) treated?
-with cardioversion
Besides amiodarone, what other drugs can be used for v-tach (non-cardiac arrest)?
- lidocaine
- procainamide
How is torsades de pointes with a prolonged QT interval corrected?
- correct electrolytes
- give magnesium
What are the various ventricular arrhythmias?
- v-fib
- v-tach
- asystole
- 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?
- amiodarone
- lidocaine
- procainamide
During asystole or PEA, what drugs can “fix” the rhythm?
-atropine possibly
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
- digoxin toxicity
MOA of Atropine
-anticholinergic effects –> increased SA node firing and AV node conduction
How much epi is given to a patient in cardiac arrest?
1 mg IV q3-5 minutes
