Adv EP Lesson 3 - Tachycardia Mechanisms

cardiac muscle cell fast action potential

membrane potential reaches a threshold

sodium and calcium channels open and enter cell

potassium channel open and they shift outward causing repolarization

why are pacemaker cells depolarized slower

presence of calcium channels and absence of sodium

cardiac cell action potential

phase 4 resting phase - potassium channels open > spontaneous depolarization

phase 0 depolarization - influx of sodium and calcium ions

phase 1 to 3 repolarization - 1: sodium channels close and potassium open causing outward flow of K+

2: plateau; inward of Ca++ and calcium induced Ca++ release occurs from the sarcoplasmis reticulum causing cellular contraction

3: potassium channels open and repolarization is triggered > closes sodium and calcium channels

pacemaker cell action potential

ERP

occurs in phases 0-3

depolarization cannot be initiated no matter how strong the impulse, because it follows the initial depolarization too closely

RRP

following the ERP; cardiac cell can be stimulated to depolarize, but only by a stimulus or impulse that is stronger than what is normally required for depolarization

late phase 3

mechanisms of tachycardia

abnormal automaticity

triggered activity

reentry

focal tachycardias

abnormal automaticity or triggered activity

reentrant tachycardias

reentry

abnormal automaticity

development of spontaneous phase 4 depolarization in cardiac muscle cells from accelerated phase 4 sodium leakage into cardiac cells

reentry

trigger activity

A second action potential arising during repolarization is called an early after-depolarization (EAD), while one arising after repolarization is called delayed after-depolarization (DAD)

triggered activity cause

electrical instability in the myocardial cell membrane during bradycardia, hypokalemia, hypoxia, or drug effects

EADs are integral to initiation of

torsades de pointes and atrial fibrillation and long QT syndrome

reasons for abnormal automaticity

ischemia stretch, electrolyte imbalance, high sympathetic tone

EADs can initiate and maintain atrial fibrillation T/F

F because a reentrant circuit must be present to maintain the tachycardia

range of resting potentials for spontaneous activity

-70to -30 mV

DAD cause and example

digoxin toxicity

RVOT ventricular tachycardia

examples of arrhythmias caused by abnormal automaticity

inappropriate atrial tachy cardia, multifocal atrial tachycardia, premature atrial contractions

torsades de pointes

prolonged QT interval

fast heart rhythm starting in the heart's lower chambers that can lead to sudden cardiac arrest

multifocal atrial tachycardia

RVOT Ventricular tachycardia

where fast electrical signals begin in the RVOT near the pulmonary valve.

reentry

continuous propagation of a wavefront that perpetually re-excites the tissue. 

requirements for reentry

two pathways that form a circuit (fast and slow)

two pathways with differing refractory pathways (slow and fast)

unidirectional block in one of the pathways because of a premature beat often initiates reentry

examples of reentrant atrial tachycardia

atrioventricular reentrant tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT),  atrial flutter,atrial tachycardia

AVNRT

pwave hidden in QRS in V1

AH jump >50ms which indicates conduction changes from fast to slow

Atrial flutter

reg conduction of the fast path and the isthmus between tricuspid valve and inferior vena cava called the CTI cavo tricuspid isthmus

travels CC around tricuspid annulus

sawtooth pattern 2:1, 3:1, or 4:1

atypical flutter: conducts Clockwise or in the LA

AVRT

accessory pathway present on the left around mitral valve or on the right side around the tricuspid valve

accessory pathway conducts antegrade > delta wave > WPW (antidromic/overt)

accessory pathway conducts retrograde > RP interval is shorter than the PR interval > P wave hidden in T or within ST >