Delve into the fascinating world of cardiac electrophysiology with our comprehensive guide. From the automatic generation of action potentials in the sinoatrial node to the intricate conduction pathways of the atria and ventricles, this resource provides a detailed exploration of the electrical act...
Electrical Activity of the Heart
The mechanical activity of the heart is produced by
rhythmic contraction of the ventricular myocardium, which
is preceded by the contraction of the atrial myocardium to
fill the ventricle completely. Contraction of the heart is a
coordinated activity that follows this sequence of events:
a) Automatic, rhythmic generation of action potentials
(AP) in the sinoatrial node (SAN)
b) AP of the SAN propagates across the atrium
c) AP is then blocked by the fibrous atrioventricular
septum
d) In the meantime, it reaches the atrioventricular
node (AVN) in which they propagate slowly, so that
e) AP(s) invade the His bundle with an adequate delay,
time needed for the atrium to actively fill the ventricle
before its contraction
f) AP(s) propagate in the (right + left) Tawara branches (located in the interventricular septum)
g) AP(s) reach the myocardium throughout Purkinje fibers that lie on the endocardial surface of the
ventricles (Purkinje fibers are fast conducting but have little contractile material)
h) AP(s) finally invade of the whole myocardium
Automaticity is a property of the cells of the SAN and, to a minor extent, of the AVN; these cells have
mostly an electrical function; they are thin and contain little contractile material.
Purkinje fibers also have a slight automaticity, but they fire when invaded by the AP.
Slow cells – Nodes’ cells
Sinus node’s cells - SAN
Small, flattened and ellipsoid-shaped cells of the sinus are located in the superior posterolateral wall of
the right atrium, they have almost no contractile fibers and are very thin (small in diameter, 3 to 5 micro-
m). However, these sinoatrial node’s cells connect directly to the atrial muscle fibers, therefore every
AP that starts in the node then spreads immediately to the atrial muscle cells.
As already mentioned, the sinus node has the capability of self-excitation and causing contraction; it
ordinarily controls the beat rate of the entire heart.
Some very important differences between the sinus node fibers and the fibers of the ventricular muscles
need to be noted:
- first of all we need to remember that membrane potential and AP in the contractile cells of
the heart are generally regulated by 3 types of channels – the fast sodium channels, low
voltage calcium channels and potassium channels – ;
o fast sodium channels let sodium in and are responsible for the rapid upstroke spike of
the AP observed into the ventricular muscles (a fast depolarization, entering of Na+),
o the plateau (0.3 s) is caused by the slow calcium channels,
o finally opening of outward rectifier potassium channels makes the membrane potential
return to its rest state.
- Another element to be noted is the resting membrane potential of the ventricular myocytes
which is -90 mV, while the sinus node’s ones is at -55 mV, at which sodium channels are
normally already blocked.
Therefore, to sum up some crucial characteristics of the nodes’ cells:
- They lack of Na channels: their action potential is sustained only by T-type Ca channels, which
can produce positive feedback and an all or none response because they open upon depolarization
and cause further depolarization, but they have much lower kinetics than Na channels3. Their
resting state is found at -55 mV, at which sodium channels are already inactivated.
3 Na is faster because is very easy to go down concentration while for Ca is a little bit harder because the
concentration are different but not so different.
62 Body At Work II
, Enrico Tiepolo
- Depolarization is slower because Ca channels let much smaller current in (the speed of
depolarization depends on how fast entering charges accumulate on the membrane capacitor) à
therefore are called “slow cells”
o Smaller current = slower depolarization + smaller region of the membrane is depolarized.
o Smaller region depolarized à AP only regenerates at shorter distance à AP
propagation is slowed down.
- Conduction velocity is also low, this is due to the fact that these cells are thin. à “slow cells”
AVN’s low conduction velocity is important to create a delay between atrial and ventricular
activation.
- Prolonged action potential and following refractory period: this limits the frequency of
impulses that they can conduct; this constitutes a protective mechanism for the ventricle, in that an
excessive ventricular frequency becomes ineffective because the ventricle does not have the time to
be effectively filled. à “slow cells”
E.g. if in a pathological condition the atrium were to fire more than 200 beats per minute, only some
of these impulses would propagate to the ventricle.
- They possess T-type Ca2+ channels. (Tiny/transient). Once the threshold has been overcome,
then these channels let some current in that rushes the depolarization causing the opening of HVA
L-type channels.
- L-type Ca2+ channels let a significant amount of Ca in and do not inactivate due to the
depolarization, but they tend to close when intracellular Ca rises.
- In the meantime, voltage dependent K channels have started to open; when the resulting
repolarizing current begins to predominate on Ca2+ current, the cell starts to repolarize; this
activates inward rectifier K channels (that were turned off by the AP) and a rapid phase of
repolarization ensues, that concludes the AP.
- Funny (inward) currents describe the movement of sodium ions inside the cell, a “leakage”
caused by high concentration of sodium extracellularly and the fact that a moderate number of
sodium channels are already opened. Therefore, between heartbeats, the influx of positively charged
sodium ions causes a slow rise in the resting potential up to -55 mVthat corresponds to the threshold
for L-type Ca channels, really creating an AP.
63 Body At Work II
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