AKTIVITAS ELEKTRIK

JANTUNG

Rahmatina B. Herman
Bagian Fisiologi
Fakultas Kedokteran - Unand
 Anatomy - Physiology of Heart
Two separate parts: left and right
Respectively:
- left atrium and ventricle
- right atrium and ventricle
Atrial function: primary pumps for ventricular
Ventricular function: pumping blood to all parts of
body and to the lungs
Ventricles pump more powerful than the atria
Atria contract prior to ventricles
Structure of the heart, and course of blood flow through the heart
chambers and heart valves.
Anatomy – Physiology of Cardiac Muscles

Myocardium:
- Atrial muscles
- Ventricular muscles
- Specialized excitatory and conductive system
of the heart
Involuntary muscles
Similar manner to skeletal muscle contraction
Syncytium
Specialized excitatory and conductive system of the heart
Structure of Cardiac Muscle Fibers
Sarcolemma
Myofibril
Filaments: - Actin
- Myosin
Sarcoplasma
Sarcoplasmic reticulum
Structure of Cardiac Muscle Fibers…..
Structure of Cardiac Muscle Fibers…..

Intercalate Disc

“Syncytial,” interconnecting nature of cardiac muscle fibers

Structure of Cardiac Muscle Fibers…..
Electrical Activity of Cardiac Muscle Fibers

Polarization
Depolarization: - Plateau
- Rhythmicity
Repolarization
Conductivity
Refractory period
Electrical Activity of Cardiac Muscle Fibers…..
Electrical Activity of Cardiac Muscle Fibers…..
Electrical Activity of Cardiac Muscle Fibers…..
Electrical Activity of Cardiac Muscle Fibers…..
 Causes of Plateau
1. Action potential in cardiac muscle is caused by
opening of two types of channels:
- fast sodium channels as those in skeletal muscle
- calcium-sodium channels
slower to open remain open for several tenths of a
second → quantity of both Ca++ and Na+ flows into
cardiac muscle fiber → prolonged period of
depolarization → plateau in action potential
Ca++ that enter during plateau phase activate the
muscle contractile process, derived from the
intracellular sarcoplasmic reticulum
 Causes of Plateau…..
2. Decreased of permeability of cardiac muscle membrane
for K+ ± 5 times, that does not occur in skeletal muscle
- May result from the excess Ca++ influx
- Decreased K+ permeability → greatly decreases the
outflux of K+ during action potential plateau →
prevents early return to resting level
When slow Ca – Na channels close at the end of 0.2 to
0.3 second and the influx of Ca++ and Na+ ceases,
membrane permeability for K+ also increases rapidly →
rapid loss of K+ from the fiber → immediately returns the
membrane potential to its resting level → ending action
potential
Rhythmicity of Cardiac Action Potential
Specialized excitatory and conductive system of heart have
capability of self-excitation
Basically, due to inherent leakiness of sinus nodal fibers to
Na+ and Ca++
Why does this leakiness not cause sinus nodal fibers to
remain depolarized all the time?
1. Na-Ca channels become inactivated within ± 100 to 150
msec after opening → influx of Na+ and Ca++ ceases
2. At about the same time, greatly increased numbers of K
channels open →i large quantities of K+ diffuse out
Both of these → reduce intracellular potential back to its
resting level → terminate the action potential
Rhythmicity of Cardiac Action Potential…..

K channels remain open for another few tenths of a second

→ continuing movement of positive charges out of cell →
excess negativity inside fiber, called hyperpolarization →
“resting” membrane potential down to more negative
Why hyperpolarization is not maintained forever
During next few tenths of a second after action potential is
over, K channels close progressively → inward-leaking Na+
and Ca++ overbalance the outward flux of K+ → “resting”
potential to drift upward once more, finally reaching
threshold level for discharge at a potential of ± -40 mV
Then the entire process begins again
This process continues indefinitely throughout a person’s
life
Rhythmicity of Cardiac Action Potential…..
Rhythmicity of Cardiac Action Potential…..
Refractory Period of Cardiac Muscle
Cardiac muscle, like all excitable tissue, is refractory to
restimulation during the action potential (absolute)
Normal refractory period of ventricle is 0.25 to 0.30
second, duration of prolonged plateau action potential
There is an additional relative refractory period of ±
0.05 second → more difficult than normal to excite,
but can be excited by a very strong excitatory signal, as
demonstrated by early “premature” contraction
Refractory period atrial muscle is much shorter than
that for ventricles (± 0.15 second for atria, and 0.25 to
0.30 second for the ventricles
Force of ventricular heart muscle contraction, showing also duration of refractory period
and relative refractory period, plus effect of premature contraction.
Note: premature contractions do not cause wave summation, as occurs in skeletal muscle
Conductivity Of Cardiac Action Potential
Conduction velocity in atrial and ventricular muscle
fibers:
 0,3 – 0,5 m/second
 = 1/250 conduction velocity of action
potential in large nerve fibers
 = 1/10 conduction velocity of action potential in
skeletal muscle fibers
Conduction velocity in Purkinye system
 0,02 – 4 m/second depend on location
 Mechanism of Contraction
The term “excitation-contraction coupling” refers to
mechanism by which the action potential causes
myofibrils of muscle to contract
When an action potential passes over cardiac muscle
membrane → spreads to the interior of cardiac muscle
fiber along the membranes of the transverse (T)
tubules → act on membranes of longitudinal
sarcoplasmic tubules → release of Ca++ into muscle
sarcoplasm from sarcoplasmic reticulum → Ca++ diffuse
into myofibrils → catalyze chemical reactions that
promote sliding of the actin and myosin filaments
along one another → muscle contraction
Mechanism of Contraction
 Duration of Contraction
Duration of contraction = duration of action potential:
- In atrial: 0,2 second
- In ventricular 0.3 second

Greatly influenced by frequency of heart rate (HR)

- The faster the frequency of HR, the shorter the
duration of contraction, especially diastolic period
- HR 72x/sec  syst period : diast period = 40:60
- HR increased 3x  syst period : diast period = 65:35
 Conductive System of Heart
SA Node (sinoatrial node)/ sinus node :
- located in the superior lateral wall of right atrium,
immediately below and slightly lateral to the
opening of the superior vena cava
Internodal pathways:
- conductive system from SA node to AV node
AV node (atrioventricular node):
- located in the posterior septal wall of right atrium,
immediately behind tricuspid valve and adjacent to
the opening of coronary sinus
AV bundle/ His bundle
Purkinje System
Conductive System of Heart…..
Organization of AV node
Transmission of Cardiac Impulse
TABLE. Conduction speeds in cardiac tissue
Conducting system of the heart.
Left: Anatomical depiction of human heart with focus on areas of the conduction system.
Right: Typical transmembrane action potentials for the SA and AV nodes, other parts of
conduction system, and atrial and ventricular muscles, along electrocardiogram (ECG)
LAF, left anterior fascicle
Effect of sympathetic (noradrenergic) and vagal (cholinergic) stimulation on membrane
potential of SA node.
Note: the reduced slope of the prepotential after vagal stimulation and the increased
spontaneous discharge after sympathetic stimulation.