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    CardiacArrhythmiasPathophysiology PDF

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    Neelam Raj Thakur
    This document summarizes various types of brady-arrhythmias and tachy-arrhythmias. Brady-arrhythmias include sinus bradycardia due to decreased sinus node automaticity from increased parasympathetic or decreased sympathetic stimulation. They can also involve conduction blocks that delay cardiac impulse propagation. Tachy-arrhythmias are caused by altered impulse formation, conduction, or re-entry mechanisms. Re-entry involves an impulse traveling in a continuous loop within the myocardium, continuously depolarizing cardiac tissue.

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    CardiacArrhythmiasPathophysiology PDF

    Uploaded by

    Neelam Raj Thakur
    369 views1 page
    This document summarizes various types of brady-arrhythmias and tachy-arrhythmias. Brady-arrhythmias include sinus bradycardia due to decreased sinus node automaticity from increased parasympathetic or decreased sympathetic stimulation. They can also involve conduction blocks that delay cardiac impulse propagation. Tachy-arrhythmias are caused by altered impulse formation, conduction, or re-entry mechanisms. Re-entry involves an impulse traveling in a continuous loop within the myocardium, continuously depolarizing cardiac tissue.

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    This document summarizes various types of brady-arrhythmias and tachy-arrhythmias. Brady-arrhythmias include sinus bradycardia due to decreased sinus node automaticity from increased parasympathetic or decreased sympathetic stimulation. They can also involve conduction blocks that delay cardiac impulse propagation. Tachy-arrhythmias are caused by altered impulse formation, conduction, or re-entry mechanisms. Re-entry involves an impulse traveling in a continuous loop within the myocardium, continuously depolarizing cardiac tissue.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    369 views1 page

    CardiacArrhythmiasPathophysiology PDF

    Uploaded by

    Neelam Raj Thakur
    This document summarizes various types of brady-arrhythmias and tachy-arrhythmias. Brady-arrhythmias include sinus bradycardia due to decreased sinus node automaticity from increased parasympathetic or decreased sympathetic stimulation. They can also involve conduction blocks that delay cardiac impulse propagation. Tachy-arrhythmias are caused by altered impulse formation, conduction, or re-entry mechanisms. Re-entry involves an impulse traveling in a continuous loop within the myocardium, continuously depolarizing cardiac tissue.

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    Yan Yu, 2012 (www.yanyu.

    ca)
    Brady-arrhythmias

    ↓ SA node automaticity (i.e. sinus bradycardia) Conduction Block


    (↑ parasympathetic, ↓ sympathetic stimulation) (i.e. AV block, BB block)
    If SA node rate ↓ enough, AV node & perkinje Delayed propagation of impulse due to
    fibers initiate impulses called “espcape beats”. electrically unexcitable tissue (from
    A series of escape beats = “escape rhythm” Pathophysiology ischemia, fibrosis, inflammation, drugs)

    of Cardiac
    Altered Impuse Altered Impulse
    Formation Arrhythmias Conduction

    Re-entry loops
    ↑ automaticity An impulse travels continuously around a
    circular (re-entrant )path in the myocardium,
    continuously depolarizing that cardiac region.
    ↑ SA node ↑ automaticity of latent Abnormal automaticity Triggered activity Re-entry loops occur in branched,
    automaticity pacemakers (ectopic pacemakers in atrial (“R on T phenomenon”) dysfunctional/fibrotic myocardium w/:
    (↑ sympathetic If the AV node and purkinje &/or ventricular myoctes) ”after-depolarizations” cause 1) Unidirectional block: when impulses can’t
    stimulation of β1- fibers intrinsically depolarize If normally non-conducting extra ventricular contractions conduct forwards, but can be conducted
    adrenergic faster than SA node (produce heart cells depolarize faster during their repolarization. backwards, in the piece of myocardium
    receptors) “ectopic beats”), they’ll control than SA node, they’ll produce Early after-depol’s in Long QT 2) Slowed retrograde conduction velocity:
    impulse formation (produce an an abnormal ectopic rhythm pts  torsades de pointes backward impulse conduction speed is slow,
    Usually due to myocyte injury Delayed after-depol’s in high- allows normal myocardium to repolarize so
    “ectopic rhythm”) – I.e. AV
    Ca2+-pts  idiopathic V-tach that the impulse propagates in a loop
    Junctional Tachychardia

    Tachy-arrhythmias
    More on Re-entry loops:
    Rate of re-entrant circuits is only limited by the refractory period of
    the tissues involved. Thus, re-entry can ↑ contractions >300bpm!
    Re-entry loops around distinct anatomical pathways  Ex. VT due to ventricular scar, A-flutter,
    monophorphic tacychardia on ECG (each QRS looks the same) AVNRT, AVRT (WPW)
    Re-entry loops that are disorganized and constantly changing 
    Polymorphic tachycardia on ECG (no distinct QRS complexes visible) Ex. Polymorphic VT, V-fib, A-fib

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