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Konduksi Listrik Jantung
dan Gangguannya
Indry Putri Festari
Pendahuluan
• Fungsi jantung normal berjalan sesuai dengan impuls
elektrik yang bekerja di jantung secara terkoordinasi
• Jika terjadi abnormalitas ritme elektrik tersebut maka
terjadi aritmia atau disritmia
• Keadaan abnormal irama lambat disebut bradikardia
• Keadaan abnormal irama cepat disebut takikardia
Mekanisme Konduksi Listrik Jantung
SA node
AV node
Bundle His
LBB - fasikulus posterior
LBB - fasikulus anterior
RBB
Serabut Purkinye
ATRIUM
VENTRIKEL
3
• Potensial Aksi terdapat 2 jenis:
• Pada Sel Pacemaker
• Pada Sel Otot jantung
• Kedua potensial aksi ini memiliki potensial
membrane istirahat yang berbeda, dan memiliki
karakteristik lainnya
Potensial Aksi Sel Pacemaker
• Pacemaker cells : capable of self-initiated
depolarization in a rhythmic fashion
• Have automaticity, by which the cells undergo
spontaneous depolarization during phase 4.
When the threshold voltage is reached in such
cells, the action potential upstroke is triggered
• The maximum negative voltage of pacemaker
cells is approximately 60 mV, substantially less
negative than the resting potential of
ventricular muscle cells (90 mV). The
persistently less negative membrane voltage of
pacemaker cells causes the fast sodium
channels within these cells to remain
inactivated.
• Phase 4 is not flat but has an upward slope 
spontaneous gradual depolarization. This
spontaneous depolarization is the result of an
ionic flux known as the pacemaker current
(denoted by If)
SA Node
• Sinus node complex terletak di
subepicardial, pada pertemuan
RA tinggi dan SVC j
• Terletak pada superior dan
lateral RA, dan sedikit melebar
ke posteromedial basis
interatrial
• Lokasi secara umum di atap RA, disekitar pertemuan SVC, RA appendage, dan
sulkus terminalis
• Spindle-shaped complex of cells  lebih kurang 1 mm di bawah the epicardium,
panjangnya 10–20 mm & tebalnya sampai 5 mm
• Terdiri dari kolagen yang mengandung bervariasi
sel, terutama yang terbesar adalah sel P
(Pacemaker cell) yang diketahui menginisiasi
impuls; transisional sel, adalah struktur
intermediate antara sel P dan sel miokardium atrial.
• Nervus frenikus kanan berjalan mendekati Sinus
Node pada permukaan epikardial RA
• The sinus node dipersarafi oleh parasimpatis and
simpatis
Perdarahan
The sinus node diperdarahi
oleh cabang proximal (cabang
atrial) dari RCA apa 60%, dan
oleh LCX pada 40% pasien
Jalur Internodal
• Jalur internodal
• Anterior tract (Bachman’s
ke LA)
• Middle (weckenbach)
• Posterior
Nodus Atrioventrikular
• In general, the AV node is located
in the so-called floor of the right
atrium, over the muscular part of
the interventricular septum, and
inferior to the membranous
septum
• The compact or dense AV node is
present within atrial musculature
above the septal leaflet of the TV
• The AV node is a complex of cells,
which lies within the confines of
the triangle of Koch
• The triangle is bordered by the
coronary sinus, the tricuspid valve
annulus along the septal leaflet,
and the tendon of Todaro.
His-Purkinje System
• The proximal portion of the
His bundle begins on the
atrial aspect of the TV in the
membranous atrial septum.
The AV junction refers to the
combination of the AV node
and the proximal portion of
the His bundle
• The His bundle penetrates
the septum between the
CFB and the septal leaflet of
the TV and splits into the
left and right bundle branch
systems
 The left bundle branch begins in the
membranous septum directly below the
right and noncoronary aortic cusps. It is
composed of a posteromedial or left
posterior fascicle and the anterolateral or
anterior fascicle. There usually is a septal
branch of the left bundle
 The right bundle branch runs in the
septum as an insulated sheath until it
reaches the base of the right ventricular
papillary muscles. It then fans out into
the myocardium at the apex of the right
ventricle (RV)
 The His bundle has relatively sparse
autonomic innervation
 Blood supply emanating from both the
AV nodal artery and septal branches of
the left anterior descending artery
Rhythmical Excitation of the Heart
• The impulse normally arises in the sinus node, normal rate of the
sinus node of 60 to 100 times per minute
• The A-V nodal, when not stimulated from some outside source,
discharge at an intrinsic rhythmical rate of 40 to 60 times per
minute, and the Purkinje fibers discharge at a rate somewhere
between 15 and 40 times per minute
• The discharge rate of the SA is considerably faster than the
natural self-excitatory discharge rate of either the A-V node or the
Purkinje fibers. Each time the sinus node discharges, its impulse is
conducted into both the A-V node and the Purkinje fibers, also
discharging their excitable membranes.
• But the sinus node discharges again before either the A-V node
or the Purkinje fibers can reach their own thresholds for self-
excitation. Therefore, the new impulse from the sinus node
discharges both the A-V node and the Purkinje fibers before self-
excitation can occur in either of these
 Once the impulse leaves the SA it travels inferiorly toward the
atrioventricular (AV) node located in the low septal aspect of the RA.
Conduction to the left atrium occurs through activation of the
coronary sinus (CS) and through a series of fibers called the
Bachmann bundle
 The spread of depolarizations from nodal cells can go directly to
adjacent myocardial cells, and internodal pathways allow this
excitation to transverse the right atrium rapidly to both the left
atrium and the AV node
 The velocity of conduction in most atrial muscle is about 0.3 m/sec,
but conduction is more rapid, about 1 m/sec, internodal pathways
 Toward the end of atrial depolarization, the excitatory signal reaches
the AV node with the final excitation of the AV node generally
described as occurring via the slow or fast pathways
 The slow conduction in the transitional, nodal, and penetrating HIS
bundle fibers  by diminished numbers of gap junctions between
successive cells in the conducting pathways  great resistance to
conduction of excitatory ions from one conducting fiber to the next
 Purkinje fibers are very large fibers, even larger than
the normal ventricular muscle fibers, and they
transmit action potentials at a velocity of 1.5 to 4.0
m/sec, a velocity about 6 times that in the usual
ventricular muscle and 150 times that in some of the
A-V nodal fibers  allows almost instantaneous
transmission of the cardiac impulse throughout the
entire remainder of the ventricular muscle
 Caused by a very high level of permeability of the gap
junctions at the intercalated discs between the
successive cells that make up the Purkinje fibers
 Once the impulse reaches the ends of the Purkinje
fibers, it is transmitted through the ventricular muscle
mass by the ventricular muscle fibers themselves. The
velocity of transmission is now only 0.3 to 0.5 m/sec,
one sixth that in the Purkinje fibers.
Aritmia
• Mekanisme aritmia
• Gangguan otomatisitas
• Gangguan konduksi
• Gangguan keduanya
• Gangguan otomatisitas, dan konduksi dapat dinilai
pada EKG
• Gangguan otomatisitas;
• Sinus Bradikardia atau Takikardia
• SA arrest
• Gangguan konduksi;
• AV Blok
• WPW
Terimakasih

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Aritmia dan mekanismenya

  • 1. Konduksi Listrik Jantung dan Gangguannya Indry Putri Festari
  • 2. Pendahuluan • Fungsi jantung normal berjalan sesuai dengan impuls elektrik yang bekerja di jantung secara terkoordinasi • Jika terjadi abnormalitas ritme elektrik tersebut maka terjadi aritmia atau disritmia • Keadaan abnormal irama lambat disebut bradikardia • Keadaan abnormal irama cepat disebut takikardia
  • 3. Mekanisme Konduksi Listrik Jantung SA node AV node Bundle His LBB - fasikulus posterior LBB - fasikulus anterior RBB Serabut Purkinye ATRIUM VENTRIKEL 3
  • 4. • Potensial Aksi terdapat 2 jenis: • Pada Sel Pacemaker • Pada Sel Otot jantung • Kedua potensial aksi ini memiliki potensial membrane istirahat yang berbeda, dan memiliki karakteristik lainnya
  • 5. Potensial Aksi Sel Pacemaker
  • 6. • Pacemaker cells : capable of self-initiated depolarization in a rhythmic fashion • Have automaticity, by which the cells undergo spontaneous depolarization during phase 4. When the threshold voltage is reached in such cells, the action potential upstroke is triggered • The maximum negative voltage of pacemaker cells is approximately 60 mV, substantially less negative than the resting potential of ventricular muscle cells (90 mV). The persistently less negative membrane voltage of pacemaker cells causes the fast sodium channels within these cells to remain inactivated. • Phase 4 is not flat but has an upward slope  spontaneous gradual depolarization. This spontaneous depolarization is the result of an ionic flux known as the pacemaker current (denoted by If)
  • 7.
  • 8. SA Node • Sinus node complex terletak di subepicardial, pada pertemuan RA tinggi dan SVC j • Terletak pada superior dan lateral RA, dan sedikit melebar ke posteromedial basis interatrial • Lokasi secara umum di atap RA, disekitar pertemuan SVC, RA appendage, dan sulkus terminalis • Spindle-shaped complex of cells  lebih kurang 1 mm di bawah the epicardium, panjangnya 10–20 mm & tebalnya sampai 5 mm
  • 9. • Terdiri dari kolagen yang mengandung bervariasi sel, terutama yang terbesar adalah sel P (Pacemaker cell) yang diketahui menginisiasi impuls; transisional sel, adalah struktur intermediate antara sel P dan sel miokardium atrial. • Nervus frenikus kanan berjalan mendekati Sinus Node pada permukaan epikardial RA • The sinus node dipersarafi oleh parasimpatis and simpatis
  • 10. Perdarahan The sinus node diperdarahi oleh cabang proximal (cabang atrial) dari RCA apa 60%, dan oleh LCX pada 40% pasien
  • 11. Jalur Internodal • Jalur internodal • Anterior tract (Bachman’s ke LA) • Middle (weckenbach) • Posterior
  • 12. Nodus Atrioventrikular • In general, the AV node is located in the so-called floor of the right atrium, over the muscular part of the interventricular septum, and inferior to the membranous septum • The compact or dense AV node is present within atrial musculature above the septal leaflet of the TV • The AV node is a complex of cells, which lies within the confines of the triangle of Koch • The triangle is bordered by the coronary sinus, the tricuspid valve annulus along the septal leaflet, and the tendon of Todaro.
  • 13. His-Purkinje System • The proximal portion of the His bundle begins on the atrial aspect of the TV in the membranous atrial septum. The AV junction refers to the combination of the AV node and the proximal portion of the His bundle • The His bundle penetrates the septum between the CFB and the septal leaflet of the TV and splits into the left and right bundle branch systems
  • 14.  The left bundle branch begins in the membranous septum directly below the right and noncoronary aortic cusps. It is composed of a posteromedial or left posterior fascicle and the anterolateral or anterior fascicle. There usually is a septal branch of the left bundle  The right bundle branch runs in the septum as an insulated sheath until it reaches the base of the right ventricular papillary muscles. It then fans out into the myocardium at the apex of the right ventricle (RV)  The His bundle has relatively sparse autonomic innervation  Blood supply emanating from both the AV nodal artery and septal branches of the left anterior descending artery
  • 15. Rhythmical Excitation of the Heart • The impulse normally arises in the sinus node, normal rate of the sinus node of 60 to 100 times per minute • The A-V nodal, when not stimulated from some outside source, discharge at an intrinsic rhythmical rate of 40 to 60 times per minute, and the Purkinje fibers discharge at a rate somewhere between 15 and 40 times per minute • The discharge rate of the SA is considerably faster than the natural self-excitatory discharge rate of either the A-V node or the Purkinje fibers. Each time the sinus node discharges, its impulse is conducted into both the A-V node and the Purkinje fibers, also discharging their excitable membranes. • But the sinus node discharges again before either the A-V node or the Purkinje fibers can reach their own thresholds for self- excitation. Therefore, the new impulse from the sinus node discharges both the A-V node and the Purkinje fibers before self- excitation can occur in either of these
  • 16.  Once the impulse leaves the SA it travels inferiorly toward the atrioventricular (AV) node located in the low septal aspect of the RA. Conduction to the left atrium occurs through activation of the coronary sinus (CS) and through a series of fibers called the Bachmann bundle  The spread of depolarizations from nodal cells can go directly to adjacent myocardial cells, and internodal pathways allow this excitation to transverse the right atrium rapidly to both the left atrium and the AV node  The velocity of conduction in most atrial muscle is about 0.3 m/sec, but conduction is more rapid, about 1 m/sec, internodal pathways  Toward the end of atrial depolarization, the excitatory signal reaches the AV node with the final excitation of the AV node generally described as occurring via the slow or fast pathways
  • 17.  The slow conduction in the transitional, nodal, and penetrating HIS bundle fibers  by diminished numbers of gap junctions between successive cells in the conducting pathways  great resistance to conduction of excitatory ions from one conducting fiber to the next
  • 18.  Purkinje fibers are very large fibers, even larger than the normal ventricular muscle fibers, and they transmit action potentials at a velocity of 1.5 to 4.0 m/sec, a velocity about 6 times that in the usual ventricular muscle and 150 times that in some of the A-V nodal fibers  allows almost instantaneous transmission of the cardiac impulse throughout the entire remainder of the ventricular muscle  Caused by a very high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up the Purkinje fibers  Once the impulse reaches the ends of the Purkinje fibers, it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves. The velocity of transmission is now only 0.3 to 0.5 m/sec, one sixth that in the Purkinje fibers.
  • 19. Aritmia • Mekanisme aritmia • Gangguan otomatisitas • Gangguan konduksi • Gangguan keduanya
  • 20. • Gangguan otomatisitas, dan konduksi dapat dinilai pada EKG • Gangguan otomatisitas; • Sinus Bradikardia atau Takikardia • SA arrest • Gangguan konduksi; • AV Blok • WPW