Gangguan penghantaran impuls

Departemen Fisiologi

Fakultas Kedokteran

Universitas Sumatera Utara

Arrhythmias

At rest, the heart is normally activated at a rate of 50–100 beats/min.

Abnormal rhythms of the heart (arrhythmias) can be classified as either too slow (bradycardias) or too fast (tachycardias).

Bradycardia

Bradycardia can arise from two basic mechanisms;

(1) reduced automaticity of the sinus node can result in slow heart rates or pauses.

Reduced sinus node automaticity can occur during: increased vagal tone (sleep,

carotid sinus massage, "common faint"),

with increasing age and secondary to drugs (beta-blockers, calcium channel blockers).

(2) slow heart rates can occur if the cardiac impulse is prevented from activating the ventricles normally, because of blocked conduction.

AV node and His bundle form the only electrically active connection between atria and ventricles.

vulnerable sites for blocked conduction between the atria and ventricles

Bila gangguan hantaran pada satu cabang berkas His menimbulkan blok cabang berkas kanan atau kiri

Impuls akan menjalar menuruni berkas pada sisi yang utuh lalu menjalar balik melalui otot untuk mengaktifkan ventrikel pada sisi yang mengalami blok

First degree atrioventricular block; when there is an abnormally long atrioventricular conduction time (PR interval > 0.22 s) but activation of the atria and ventricles still demonstrates 1:1 association.

Penyebab: blok nodus AV; 45 x/menit (infark miokard

septum) blok infranodus; 35 x/menit bahkan

sampai 15 x/menit (kerusakan bundle of His akibat pembedahan)

Terdapat periode asistol selama semenit atau lebih

Sindrom Stokes-Adams; iskemi serebrum yg timbul menyebabkan pusing dan pingsan.

Second-degree atrioventricular block, some but not all atrial impulses are conducted to the ventricles.

Third-degree block, there is no association between atrial and ventricular activity.

Implantasi pacemaker

Indikasi : Sick sinus syndrome (blok jantung

derajat tiga) Disfungsi nodus sinus, blok AV, blok

bifasikular atau trifasikular Pasien sinkop neurogenik parah;

adanya periode jeda > 3 detik antar denyut jantung akibat stimulasi sinus karotikus

Tachycardia

Tachycardias can arise from three basic cellular mechanisms;

(1)increased automaticity from more rapid phase 4 depolarization

(2) spontaneous depolarizations during phase 3 (early afterdepolarizations; EAD) or phase 4 (late afterdepolarizations; DAD) can repetitively reach threshold and cause tachycardia.

.

This appears to be the mechanism of the polymorphic ventricular tachycardia (torsades de pointes) observed in some patients taking procainamide or quinidine and the arrhythmias associated with digoxin toxicity.

These depolarizations are called triggered activity because they are dependent on the existence of a preceding action potential

Third, the most common mechanism for tachyarrhythmia is reentry.

In reentry, two parallel pathways with different conduction properties exist (perhaps at the border zone of a myocardial infarction or a region of myocardial ischemia).

The electrical impulse normally travels down the fast pathway and the slow pathway (shaded region), but at the point where the two pathways converge the impulse traveling down the slow pathway is blocked since the tissue is refractory from the recent depolarization via the fast pathway (a).

However, when a premature beat reaches the circuit, block can occur in the fast pathway, and the impulse will travel down the slow pathway (shaded region) (b). After traveling through the slow pathway the impulse can then enter the fast pathway in retrograde fashion (which because of the delay has recovered excitability), and then reenter the slow pathway to start a continuous loop of activation, or reentrant circuit (c).

After traveling through the slow pathway the impulse can then enter the fast pathway in retrograde fashion (which because of the delay has recovered excitability), and then reenter the slow pathway to start a continuous loop of activation, or reentrant circuit (c).

Implantasi pacemaker

Indikasi : Sick sinus syndrome (blok jantung

derajat tiga) Disfungsi nodus sinus, blok AV, blok

bifasikular atau trifasikular Pasien sinkop neurogenik parah;

adanya periode jeda > 3 detik antar denyut jantung akibat stimulasi sinus karotikus

Fokus Eksitasi Ektopik

Serabut His-Purkinje atau serabut miokardium (fokus ektopik) melepaskan impuls secara spontan, menimbulkan adanya denyut muncul sebelum denyut normal (ekstrasistol) dan bila berulang kali dengan frekuensi lebih tinggi dari nodus SA menimbulkan takikardi cepat dan teratur (takikardia paroksismal)

Let it beat!