Mechanisms of Tachyarrhythmias I and II Flashcards
3 mechanisms of tachycardias
reentry, automaticity, triggered activity
How does reentry happen?
there are two pathways in 1/3 of people’s AV node:
- slow = slow conduction, fast recovery
- fast = fast conduction, slow recovery
after a regular beat wherein the fast pathway dominates conduction and also cancels out the slow beat, the slow pathway recovers quickly. a premature beat that occurs after recovery of the slow pathway but before recovery of the fast pathway will choose to go down the slow path and consequently backwards up the fast pathway leading to a reentry cycle –> rapid circuit on the order of 150-200 bpm
How many people have a slow pathway in their AV node?
1/3 of people
What are the EKG findings in reentry tachycardia (generally)
inverted p wave in inferior leads, rapid rate
At what point in an EKG reading is the wave front passing through the AV node?
the isolectric PR segment
What is the nature of AVRT: Wolff-Parkinson-White/ventricular preexcitation and what are the EKG findings associated with the condition?
in addition to the normal connection in the heart, there is an accessory pathway (fast conduction, slow recovery)
- b/c accessory pathway is faster than regular pathway, it reaches ventricle first (during normal AV delay) –> no isoelectric PR interval/PR<120
- b/c initial ventricular depolarization is cell-cell, there is a wide QRS with an early delta wave before the regular signal arrives and leads to the activation of the his purkinje system
What is the mechanism of a supraventricular rentry tachycardia?
this occurs with a premature beat in a heart w/an accessory pathway
since the accessory pathway recovers slower than the AV nodal pathway, a premature beat will block in the accessory pathway but get through the AV nodal pathway. it will conduct retrograde in the accessory pathway and come back up through the atrium
What are EKG findings in supraventricular reentry tachycardia?
initial wide QRS with delta wave (regular preexcitation) followed by a PAC followed by a series/cycle of narrow QRS followed by inverted p waves
What is the mechanism of ventricular tachycardia?
pockets of healthy muscle (e.g. in a scar from an MI) serve as the slow pathway in the ventricle –> reentry circuit w/in ventricle
What are the EKG findings in ventricular tachycardia?
tachycardia (<3 big boxes) and wide QRS complexes (b/c using cell-cell in parts of the ventricle due to reentry circuit AND this happens before the activation of his-purkinje/sharp peak)
What is the mechanism of atrial flutter?
reentry circuit occurs around tricuspid valve leading to separate cyclical depolarization of one atrium while rest of heart remains normal
What are the EKG findings of atrial flutter?
saw tooth pattern in leads II, III, aVF
2 mechanisms of antiarrhythmic druggs
- class iii K channel blockers increase time for repolarization of tail of reentry circuit –> head runs into tail and extinguishes reentry circuit
- clas i Na channel blockers decrease conduction velocity/wavelength of head of reentry circuit –> slows down reentry to make less symptomatic
What intervention can be used to treat an accessory pathway?
catheter ablation
How do subsidiary pacers in the heart take over automaticity and override the SA node?
phase 4 of AP is reduced and therefore reaches threshold faster allowing for a second pacer –> random extra beats or complete override of SA node
What are the EKG features of atrial tachycardia?
normal p wave (but often inverted in I and/or aVF) and normal PR interval (just a different pacer in the atrium than the SA node) w/ tachycardia
What are the EKG features of sinus tachycardia?
upright p waves in leads 1, aVF, biphasic p wave in V1
What are the mechanisms for triggered activity?
intracellular calcium overload leads to afterdepolarizations –> either from digitalis toxicity or from a ryanodine receptor mutation/catecholaminergic polymorphism VT that causes leaky SR
What is the difference between early and delayed afterdepolarization?
early = occurs during AP plateau (e.g. in long QT) delayed = occurs after AP (and can reach threshold)
What is the mechanism of torsade de points and its EKG features?
triggered beats occur –> EKG has QRS of varying heights, tachycardia
How is atrial fibrillation initiated and maintained?
initiated by automaticity and maintained by multiple wavelet reentry (lots of reentry circuits get mashed up together and go nuts)
What are the EKG features of afib?
no p wave/undulating baseline b/c everything is crazy in the atria, normal QRS complexes; however, QRS comes irregularly because not all the atrial depolarizations get through the AV node
What are the EKG (and clinical) features of vfib?
qrs complexes replaced by disorganized chaotic low amplitude activity –> loss of pulsatile CO and loss of consciousness –> death
EKG difference expected between supraventricular and ventricular tachycardias
supraventricular: narrow QRS b/c functioning his-purkinje
ventricular: wide QRS b/c cell-cell conduction
Is it possible to have a supraventricular tachycardia with a wide QRS?
yes–> if you also have bundle branch block or an accessory pathway
3 ways to get monomorphic wide complex QRS tachycardias
- ventricular tachycardia
- SVT w/bb block
- SVT w/preexcitation/accessory pathway
2 ways to get a polymorphic wide complex QRS tachycardia
- vfib
2. torsades de pointes
1 way to get an irregularly irregular ventricular rate w/narrow complex tachycardia
afib
5 ways to get regular ventricular rate narrow complex tachycardia
- AVNRT: negative p wave in inferior leads
- AVRT w/WPW
- atrial tachycardia
- sinus tachycardia: positive p wave in inferior leads
- atrial flutter: saw tooth
