Page 190 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Origin and Spread of Excitation in the Heart
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The heart contains muscle cells (fibers) that ward K flux I K , the pacemaker cell is again re-
produce and distribute excitation impulses polarized to the MDP.
(conducting system), as well as working myo- Each AP in the sinus node normally results
cardium, which responds to the excitation by in a heart beat, i.e., the impulse frequency of
contracting. Contrary to the situation in skele- the pacemaker determines the rate of the
tal muscle, excitation originates within the or- heart beat. The rate is lower if
gan (autorhythmicity or autonomy of the – the rise of the slow depolarization becomes
heart). Atrial and ventricular myocardium less steep (→ B3a),
each consists functionally of a syncytium, i.e., – the TP becomes less negative (→ B3b),
the cells are not insulated from one another – the MDP becomes more negative so that
but connected through gap junctions. A stimu- – repolarization in an AP starts later or is
spontaneous depolarization begins at a
lower level (→ B3 c), or
lus that originates somewhere within the atria
Heart and Circulation contraction of both atria or of both ventricles, What the first three processes have in common
or ventricles thus always leads to complete
slower.
respectively (all-or-nothing contraction).
is that the threshold is reached later than be-
Normal excitation of the heart originates
within the sinus node, the heart’s pacemaker.
fore.
All parts of the excitation/conduction sys-
Excitation (→ A) spreads from there through
ization, but the sinus node plays the leading
node) and from there, via the His bundle and
role in normal cardiac excitation (sinus
its two (Tawara) branches, reaches the Pur-
7 both atria to the atrioventricular node (AV tem have the capacity of spontaneous depolar-
kinje fibers, which transmit the excitation to rhythm is ca. 70–80 beats per minute). The
the ventricular myocardium. Within the myo- reason for this is that the other parts of the
cardium the excitation spreads from inside to conduction system have a lower intrinsic fre-
outside (endocardium toward epicardium) quency than the sinus node (→ Table in C;
and from apex toward the base, a process that causes are that slow depolarization and repo-
can be followed—even in the intact organism— larization are flatter; see above). Excitation
by means of the ECG (→ p.184; → C). starting from the sinus node will thus arrive
The potential in the cells of the sinus node is at more distal parts of the conducting system,
a pacemaker potential (→ B1, bottom). It has before their spontaneous depolarization has
no constant resting potential, but rises after reached the TP. However, if conduction of the
each repolarization. The most negative value sinus impulse is interrupted (→ p.186ff.), the
of the latter is called maximal diastolic poten- intrinsic frequency of more distal parts of the
tial ([MDP] ca. – 70 mV). It rises steadily until conduction system take over and the heart
the threshold potential ([TP] ca. – 40 mV) is then beats in AV rhythm (40–60 beats per
reached once more and an action potential minute) or, in certain circumstances, at the
(AP) is again triggered. even lower rate of the so-called tertiary
The following changes in ionic conductance (ventricular) pacemakers (20–40 beats per
(g) of the plasma membrane and thus of ionic minute).
currents (I) cause these potentials (→ B1, top): In contrast to the sinus and AV nodes with
Beginning with the MDP, nonselective conduc- their relatively slowly rising AP, due largely to
tance is increased and influx (I f ; f = funny) of an influx of Ca 2+ (→ A), there are in the work-
cations into the cell leads to slow depolariza- ing myocardium so-called rapid, voltage-gated
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tion (prepotential = PP). Once the TP has been Na channels that at the beginning of the AP
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reached, g Ca now rises relatively rapidly, the briefly cause a high Na influx and therefore,
potential rising more steeply so that an in- compared with the pacemaker potential, a re-
creased influx of Ca 2+ (I Ca ) produces the up- latively rapid rise in the upstroke of the AP
stroke of the AP. While the potential over- (→ A). The relatively long duration (compared
180 shoots to positive values, leading to an out- with skeletal muscle) of myocardial AP, giving
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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