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Specialized excitatory and
conductive system of the heart
Automatic electrical rhythmicity of
sinus fibers
Mechanism of sinus nodal
rhythmicity
 iK: delayed rectifier current
 slow voltage-gated K+
channels (activated by
depolarization)
 if: funny current
 Voltage-gated Na+ channels
activated at
hyperpolarization beyond -50
mV
 iCa2+: L-type Ca2+ channel
 activated at Em higher than 55 mV
Transmission of cardiac impulse through
atria and internodal pathways
Ends of SA nodal fibers connect (gap junctions)
direclty with:

1.
Surrounding atrial muscle fibers (0.3 m/s)
2.
Conduction fibers (1 m/s):

Anterior interatrial band

Anterior, lateral and posterior internodal pathways
Atrioventricular node
 The only pathway of
cardiac impulse entry into
ventriculi.
 Delays the impuls
transmission – slow
conduction.
 transmission in only one
direction.
Transmission of cardiac impulse in
ventriculi
 Fast transmission through
Purkinje fibers (1.5-4 m/s).
 Subendocardial position of
left and right bundle branch.
 Penetration of their branches
to 1/3 thickness of LV.
 Then, connection with
cardiac muscle fibers and
slower conduction (0.3-0.5
m/s).
Sinus node- cardiac pacemaker
Discharge rates:

SA node: 70-80 /min

AV node: 40-60 /min

Purkinje fibers: 15-40 /min
Abnormal “ectopic” pacemakers

increased discharge rate most often in AV-node and
Purkinje fibers.
 Or,

blockage in A-V transmission.
Stokes-Adams syndrome
 sudden A-V bundle block
 synkope
Control of heart rhythmicity and impulse
conduction
 Regulation by autonomic nervous system:

Parasympathetic innervation

Sinus node, AV-node, lesser atria, ventriculi no

supresseion of sinus node rhythmicity

slows down conduction through AV-node (can cause complete
AV-block – ventricular escape)


mechanism: hyperpolarization (-65 to-75 mV)
Sympathetic innervation

whole heart (conduction and contractile fibers)

β1-receptors: increase permeability to Ca2+ and Na+
Modulation of pacemaker rhythmicity