Page 198 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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temporarily stop (Adams–Stokes attack), but atrial myocardium. Similar AP changes also oc-
ventricular (tertiary) pacemakers then take cur if, for example, an ectopic stimulus or elec-
over excitation of the ventricles (ventricular tric shock falls into the relative refractory peri-
bradycardia with normal atrial rate). Partial or od of the preceding AP (→ E). This phase of
complete temporal independence of the QRS myocardial excitation is also called the vulner-
complexes from the P waves is the result able period. It is synchronous with the rising
(→ B5). The heart (i.e., ventricular) rate will limb of the T wave in the ECG.
fall to 40–60 per minute if the AV node takes Causes of ESs (→ H4) include:
over as pacemaker (→ B), or to 20–40 per min- – A less negative diastolic membrane potential
ute when a tertiary pacemaker (in the ventri- (see above) in the cells of the conduction
cle) initiates ventricular depolarization. This system or myocardium. This is because de-
could be an indication for employing, if neces- polarization also results in the potential los-
sary implanting, an artificial (electronic) pace- – Depolarizing after-potentials (DAPs). In this
ing its stability and depolarizing sponta-
neously (→ H1);
maker. Complete bundle branch block (left or
Heart and Circulation in the ECG, because the affected part of the Early DAPs occur when the AP duration is
right bundle) causes marked QRS deformation
case an ES is triggered. DAPs can occur dur-
ing repolarization (“early”) or after its end
myocardium will have an abnormal pattern of
(“late”).
depolarization via pathways from the healthy
side.
Changes in cell potential. Important prereq-
markedly prolonged (→ H2), which registers
syndrome). Causes of early DAPs are bradycar-
ventricular myocardium are: 1) a normal and
dia (e.g., in hypothyroidism, 18 and 28 AV
stable level of the resting potential (– 80 to
7 uisites for normal excitation of both atrial and in the ECG as a prolonged QT interval (long QT
– 90 mV); 2) a steep upstroke (dV/dt = 200– block), hypokalemia, hypomagnesemia (loop
1000 V/s); and 3) an adequately long duration diuretics), and certain drugs such as the Na +
of the AP. channel blockers quinidine, procainamide,
These three properties are partly indepen- and disopyramide, as well as the Ca 2+ channel
dent of one another. Thus the “rapid” Na + blockers verapamil and diltiazem. Certain ge-
+
channels (→ p.180) cannot be activated if the netic defects in the Na channels or in one of
+
+
resting potential is less negative than about the K channels (HERG, KV LQT1 or min K chan-
– 55 mV (→ H9). This is caused mainly by a nel) lead to early DAPs due to a lengthening of
raised or markedly lowered extracellular con- the QT interval. If such early DAPs occur in the
+
centration of K (→ H8), hypoxia, acidosis, or Purkinje cells, they trigger ventricular ES in the
drugs such as digitalis. If there is no rapid Na + more distal myocardium (the myocardium has
current, the deplorization is dependent on the a shorter AP than the Purkinje fibers and is
slow Ca 2+ influx (L type Ca 2+ channel; block- therefore already repolarized when the DAP
able by verapamil, diltiazem or nifedipine). reaches it). This may be followed by burst-like
The Ca 2+ influx has an activation threshold of repetitions of the DAP with tachycardia (see
– 30 to – 40 mV, and it now generates an AP of above). If, thereby, the amplitude of the (wid-
its own, whose shape resembles the pacemak- ened) QRS complex regularly increases and de-
er potential of the sinus node. Its rising gradi- creases, a spindle-like ECG tracing results (tor-
ent dV/dt is only 1–10 V/s, the amplitude is sades de pointes).
lower, and the plateau has largely disappeared The late DAPs are usually preceded by post-
(→ H1). (In addition, spontaneous depolariza- hyperpolarization that changes into postdepo-
tion may occur in certain conditions, i.e., it be- larization. If the amplitude of the latter
comes a source of extrasystoles; see below). reaches the threshold potential, a new AP is
Those APs that are produced by an influx of triggered. (→ H3). Such large late DAPs occur
Ca 2+ are amplified by norepinephrine and cell mainly at high heart rate, digitalis intoxication,
stretching. They occur predominantly in dam- and increased extracellular Ca 2+ concentra-
aged myocardium, in whose environment the tion. Oscillations of the cytosolic Ca 2+ concen-
188 concentrations of both norepinephrine and ex- tration seem to play a causative role in this.
+
tracellular K are raised, and also in dilated
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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