Flashcards in Arrhythmias: Treatment Deck (19):
1. What are relevant treatment for reentry currents?
reentry: anti arrhythmic drugs, catheter ablation, overdrive pacing and defibrillation (prolongation of refractoriness, reduce conduction)
1. What are relevant treatments for abnormal automaticity
abnormal automaticity (remove reversible causes, anti arrhythmic drugs, ablation, decrease rate of spontaneous depolarization or increase threshold for AP generation in automatic tissue)
1. What are relevant treatment for triggered activity?
triggered activity (EAD- shorten AP depolarization, DAD-eliminate Ca overload)
What are the 3 main goals of arrhythmia treatment.
improve symptoms and qua lit of life
rapid cardioversion/defibrillation to restore sinus rhythm in hemodynamically unstable arrhythmias
improve mortality rates with reduction in risk of sudden cardiac death
2. Contrast the preferred drug treatment for short excitable gap and long excitable gap reentrant arrhythmias
long excitable gap, use drugs to depress conduction to stop rhythm (Na channel block via lidocaine, Ca channel block via verapamin)
in short excitable gap prolong refractoriness (K channel block by procainamide or sotalol or dofetilide)
3. List anti arrhythmic drugs for each Vaughn Williams classification
Class I Na channel blocker (reduce phase 0)
Class II B blockers
Class III K+ channel blockers (APD prolongation)
Class IV: Ca++ channel blockers
Class V: other (digoxin, adenosine)
What is the action of Ia drugs and give examples.
IA block Na channels intermediate kinetics of recovery and increase refractory period by prolonging phase 3
procainamide, disopyramide, quinidine
prolong QT, QRS widening
What is the action of IB drugs, give examples.
IB block Na channel rapid recovery
lidocaine, mexilitine, phenytoin
shortens AP duration
What is the action of IC drugs, give examples.
IC block Na channels with slow recovery
Describe the PVC hypothesis hypothesis of class IC agents.
although this class decreases PVCs that are associated sudden cardiac death, there is actually an increased mortality associated with class IC agents and these drug should not be used in post MI patients or in patients with LV dysfunction
What is the mechanism of action for B blockers?
decrease phase 4 depolarization in nodal cells resulting in reduced heart rate
reduction of sympathetic stimulation to AV node and prolonging AV conduction
results in slowing of the sinus rate and an increase in the PR interval
Give examples of selective and non-selective B-blockers
nonselective: propranolol (more non-cardiac effects)
B1 selective: metoprolol, atenolol
What is the action of class III drugs, give examples.
increase AP depolarization and end depolarization period throughout the myocardium primarily by blocking voltage-dependent K channels during phase 3
includes dofetilide, amiodarone, stall and dronederone
Why is amiodarone particularly special?
blocks sodium, potassium, calcium, noncompetitive beta and alpha
has a really long half life of 60 days
is most effective but severe toxicity with deposits in thyroid, liver, lungs, skin, eye and nerves (avoid in younger patients particularly)
Name two class V drugs.
digoxin: binds Na/KATPase to increase Na/K gradient driving the Ca/Na exchanger, increasing intracellular Ca
adenosine (opposite of amioderone) acts only at a1 receptor via G1, reducing L-type Ca++currents and activates GIRK
reduces phase 4 depolarization in SA nodal cels, inhibits conduction through AV node and prolongs AV refractory period (half life 10s)
Give indications for use of a pacemaker
slow rhythms: sinus arrest, symptomatic sinus bradycardia, heart block and AF with slow ventricular response
heart failure: bi ventricular pacing
What is defibrillation?
does not jumpstart the heart, but instead of sudden voltage to generate direct current to stop the rhythm and organized rhythm hopefully resumes after this resetting
What is the mechanism of class IV drugs?
Ca channel blockers (non-dihydropyridine) slow the rate of phase 4 depolarization in SA nodal cells and inhibiting conduction through AV node
examples are nifedipine and amodipine
on EKG- increase in PR interval and slower sinus rate