Arrhythmia Flashcards
what is “inappropriate automaticity”?
impulse initiated at areas of heart other than sinus node
Describe 1st degree, 2nd degree (types I and II) and 3rd degree heart block. What is general treatment for each?
1st degree - PR interval >200ms (medication)
2nd degree
Type 1 - gradual increase of PR interval until
beat is not conducted (medication)
Type II - constant PR with intermittent loss of
QRS (pacemaker)
3rd degree - loss of atrial/ventricle conduction (pacemaker)
What are the 3 mechanisms of tachyarrhythmia?
- increased automaticity
- triggered automaticity
- reentry circuit
what is the most common cause of supraventricular arrhythmia?
AV Nodal Reentry Tachycardia (AVNRT)
what is junctional tachycardia?
abnormal impulse coming from AV junction
what is triggered automaticity?
abnormal impulses arising either at phase 3 of phase 4 of a normally evoked AP (rare)
- Early Afterdepolarization (EAD) interrupt phase 3
- Delayed Afterdepolarization (DAD) interrupt phase 4
What are 3 components that need to be present for AVNRT to occur?
- fast and slow parallel conduction pathway at AV node (normally found in population)
- unidirectional block (usually fast pathway due to repolarization phase)
- final common pathway
What is a typical result of AVNRT?
atrial and ventricle contraction at the same time
What is Wolff Parkinson White syndrome?
cells with conduction properties (accessory pathway) remains around mitral and tricuspid valves during embryologic development –> faster pathway that can bypass AV node and will not “screen” incoming impulses (like in A. flutter) so can get ventricular beats >150
-can be an example of AVRT
What does a PR interval <120ms mean?
impulse conduction other than AV node (i.e. wolff parkinsons)
What is 1st line treatment for AVNRT? Mechanism?
ablation --> disable tissue (slow pathway) with radio-frequency energy
What is “use-dependent” versus “reverse use dependent” mean when talking about antiarrhythmics?
- Use-dependent: works on activated channels –> works better with high HR
- Reverse use-dependent: works on resting membrane potential –> more effective at slow HR
What are 3 class I A antiarrhythmics? Mechanism of action?
Quinidine
Procainamide
Disopyramide
–> block Na+ channels at high concentrations in pts w/ fast HR [prolong phase 0];
–> block Ikr (K+) at normal concentrations in pts w/ slow HR
What is the mechanism of action and use of Quinidine?
(Class IA)
Mainly blocks fast Na+ channels but has some K+ channel blocking effects as well as alpha-blocking effects
–> used in Atrial fibrillation (Brugada’s, short QT syndrome)
What are the 2 main adverse effects of quinidine?
diarrhea (1/3)
proarrhythmia
Which anti-arrhythmic agent induces SLE in 1/3 of patients? What are 2 other side effects? What is unique about its metabolite?
Procainamide
- also can get hypotension (ganglionic blocking properties); proarryhthmia
- NAPA is active metabolite (liver) and is a class III antiarrhythmic
What are the differences between the class I antiarrhythmics?
Class IA - prolongs phase 0 (prolonged AP)
Class IB - shortens phase 2 (shortened AP)
Class IC - no effect on AP duration
Which class IA antiarrhythmic is used for vagally-mediated atrial fibrillation?
Disopyramide
What are 2 class IB antiarrhythmics? How are they related and what are they exclusively used to treat?
Lidocaine Mexiletine (oral form of lidocaine) --> used exclusively for ischemic ventricular tachycardia (do not work in atrial tissue)
What is the order of potency of the class I antiarrhythmics?
IC = most potent > IA > IB = least potent
What are the adverse effects for each Class IB antiarrhyhmic?
- Lidocaine: Neurologic (after 3 days continuous infusion), including tremor, slurred speech, convulsion, seizure
- Mexiletine: GI disturbance [reduced by taking w/ meal]
What are the 2 class IC antiarrhythmics? What is their therapeutic use? Due to their adverse effects, in what patients are they contraindicated?
Flecainide; Propafenone
- used to treat patients w/PVC; atrial fibrillation
- negative ionotropes and depress LV function so contraindicated in patients with CAD, active ischemia, QRS >120ms
What are the 5 class III antiarrhythmics? How do they work? Do they work better in a fast or slow heart?
Amiodarone Dronedarone Sotalol Ibutilide Dofetilide -delayed repolarization by K+-channel blockade (prolong phase 3) -work best in slow heart
Which class III drug is iodine based? What are the consequences? Which drug was made in an attempt to bypass these?
Amiodarone –>
multiple end organ toxicities (pulmonary fibrosis, blue discoloration, thyroid dysfunction, photophobia, etc) so only used acutely
-Dronedarone made to be “softer” amiodarone w/o iodine (less SE but less potent)
Which class III drug is very efficacious but must be monitored in the hospital for 5 days due to 1% development of Torsades de Pointes? Mechanism of action?
Dofetilide
–>highly selective IKr blocker (prolong phase 3)
What is adenosine primarily used to treat? Mechanism of action? Half life? Main side effect?
- supraventricular tachycardia
- -> works primarily at the AV node to increase K+ current, inhibit Ca++ current and prolong hyperpolarization (t1/2 <10s)
- SE: dyspnea/ chest tightness
