cardiac abnormalities cvs-k15

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    CardiacAbnormalities

    Departemen Fisiologi

    Fakultas Kedokteran

    Universitas Sumatera Utara

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    Arrhythmias At rest, the heart is normally

    activated at a rate of 60100

    beats/min. Abnormal rhythms of the heart

    (arrhythmias) can be classified as

    either too slow (bradycardias) or toofast (tachycardias).

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    Bradycardia Bradycardia can arise from two basic

    mechanisms;

    (1) reduced automaticity of the sinus

    node can result in slow heart rates orpauses.

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    Reduced sinus node automaticitycan occur during:

    increased vagal tone (sleep,

    carotid sinus massage, "commonfaint"),

    with increasing age and secondary

    to drugs (beta-blockers, calciumchannel blockers).

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    (2) slow heart rates can occur if the

    cardiac impulse is prevented fromactivating the ventricles normally,because of blocked conduction.

    AV node and His bundle form theonly electrically active connectionbetween atria and ventricles.

    vulnerable sites for blockedconduction between the atria andventricles

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    Bila gangguan hantaran pada satucabang berkas His menimbulkanblok cabang berkas kanan

    atau kiri Impuls akan menjalar menuruni

    berkas pada sisi yang utuh lalumenjalar balik melalui otot untukmengaktifkan ventrikel pada sisiyang mengalami blok

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    First degree atrioventricular block; whenthere is an abnormally long

    atrioventricular conduction time (PRinterval > 0.22 s) but activation of theatria and ventricles still demonstrates1:1 association.

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    Penyebab:

    blok nodus AV; 45 x/menit (infarkmiokard septum)

    blok infranodus; 35 x/menit bahkansampai 15 x/menit (kerusakan bundle

    of His akibat pembedahan)Terdapat periode asistol selama

    semenit atau lebih Sindrom Stokes-Adams; iskemi

    serebrum yg timbul menyebabkanpusing dan pingsan.

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    Second-degree atrioventricularblock, some but not all atrial

    impulses are conducted to theventricles.

    Third-degree block, there is no

    association between atrial andventricular activit .

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    Implantasi pacemakerIndikasi :

    Sick sinus syndrome (blok jantungderajat tiga)

    Disfungsi nodus sinus, blok AV,

    Pasien sinkop neurogenik parah;adanya periode jeda > 3 detik antar

    denyut jantung akibat stimulasi sinuskarotikus

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    Tachycardia Tachycardias can arise from three

    basic cellular mechanisms;

    (1)increased automaticity from morerapid phase 4 depolarization

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    (2) spontaneous depolarizations duringphase 3 (early afterdepolarizations; EAD)

    or phase 4 (late afterdepolarizations;DAD) can repetitively reach threshold andcause tachycardia.

    .

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    This appears to be the mechanism of thepolymorphic ventricular tachycardia(torsades de pointes) observed in somepatients taking procainamide orquinidine and the arrhythmiasassociated with digoxin toxicity.

    These depolarizations are called triggered activity

    because they are dependent on the existence of a

    preceding action potential

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    Third, the most common mechanism fortachyarrhythmia is reentry.

    In reentry, two parallel pathways withdifferent conduction properties exist(perhaps at the border zone of a

    myocardial infarction or a region ofm ocardial ischemia .

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    The electrical impulse normally travelsdown the fast pathway and the slow

    pathway (shaded region), but at the pointwhere the two pathways converge theimpulse traveling down the slow pathway isblocked since the tissue is refractory from

    the recent depolarization via the fast

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    However, when a premature beat reaches thecircuit, block can occur in the fast pathway,

    and the impulse will travel down the slowpathway (shaded region) (b). After travelingthrough the slow pathway the impulse canthen enter the fast pathway in retrogradefashion (which because of the delay has

    recovered excitability), and then reenter the

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    After traveling through the slowpathway the impulse can then enter the

    fast pathway in retrograde fashion(which because of the delay hasrecovered excitability), and then reenterthe slow pathway to start a continuous

    loop of activation, or reentrant circuit

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    Fokus Eksitasi Ektopik Serabut His-Purkinje atau serabut

    miokardium (fokus ektopik)

    melepaskan impuls secara spontan,menimbulkan adanya denyutmuncul sebelum denyut normal(ekstrasistol) dan bila berulang kalidengan frekuensi lebih tinggi darinodus SA menimbulkan takikardicepat dan teratur (takikardia

    paroksismal)

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    Let it

    beat!