Page 200 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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Consequences of an ES. When the mem- If, for example, because of hypoxia or scarring
brane potential of the Purkinje fibers is normal (possibly made worse by an increased vagal
(frequency filter; see above), there will be only tone with its negative dromotropic effect), the
the one ES, or a burst of ESs with tachycardia already relatively slow conduction in the AV
follows (→ H6,7). If, however, the Purkinje fi- node decreases even further (→ Table, p.183),
bers are depolarized (anoxia, hypokalemia, hy- the orthograde conduction may come to a
perkalemia, digitalis; → H8), the rapid Na + standstill in one of the parallel pathways (→ F,
channel cannot be activated (→ H9) and as a block). Reentry can only occur if excitation
consequence dV/dt of the upstroke and there- (also slowed) along another pathway can cir-
fore the conduction velocity decreases sharply cumvent the block by retrograde transmission
(→ H10) and ventricular fibrillation sets in as a so that excitation can reenter proximal to the
result of reentry (→ H11). block (→ F, reentry). There are two therapeutic
Reentry in the myocardium. A decrease in ways of interrupting the tachycardia: 1) by fur-
dV/dt leads to slow propagation of excitation
ther lowering the conduction velocity ϑ so that
Heart and Circulation refractory period (t R ). Both are important by increasing ϑ to a level where the orthograde
retrograde excitation cannot take place; or 2)
(ϑ), and a shortening of the AP means a shorter
conduction block is overcome (→ Fa and b, re-
causes of reentry, i.e., of circular excitation.
spectively).
When the action potential spreads from the
In Wolff–Parkinson–White syndrome (→ G)
Purkinje fibers to the myocardium, excitation
the circle of excitation has an anatomic basis,
normally does not meet any myocardial or Pur-
conducting pathway (in addition to the nor-
they are still refractory. This means that the
mal, slower conducting pathway of AV node
product of ϑ · t R is normally always greater
7 kinje fibers that can be reactivated, because namely the existence of an accessory, rapidly
than the length s of the largest excitation loop and His bundle) between right atrium and
(→ D1). However, reentry can occur as a result right ventricle. In normal sinus rhythm the ex-
if citation will reach parts of the right ventricular
– the maximal length of the loop s has in- wall prematurely via the accessory pathway,
creased, for example, in ventricular hyper- shortening the PR interval and deforming the
trophy, early part of the QRS complex (δ wave; → G1).
– the refractory time t R has shortened, and/or Should an atrial extrasystole occur in such a
– the velocity of the spread of excitation ϑ is case, (→ G2; negative P wave), excitation will
diminished (→ D2). first reach the right ventricle via the accessory
A strong electrical stimulus (electric shock), pathway so early that parts of the myocardium
for example, or an ectopic ES (→ B3) that falls are still refractory from the preceding normal
into the vulnerable period can trigger APs with action potential. Most parts of the ventricles
decreased upstroke slope (dV/dt) and duration will be depolarized via the AV node and the
(→ E), thus leading to circles of excitation and, bundle of this so that the QRS complex for the
in certain circumstances, to ventricular fibril- most part looks normal (→ G2,3). Should,
lation (→ B4, H11). If diagnosed in time, the however, the normal spread of excitation (via
latter can often be terminated by a very short AV node) reach those parts of the ventricle
high-voltage current (defibrillator). The entire that have previously been refractory after early
myocardium is completely depolarized by this depolarization via the accessory pathway, they
countershock so that the sinus node can again may in the meantime have regained their ex-
take over as pacemaker. citability. The result is that excitation is now
Reentry in the AV node. While complete AV conducted retrogradely via the accessory
block causes a bradycardia (see above), partial pathway to the atria, starting a circle of excita-
conduction abnormality in the AV node can tion that leads to the sudden onset of (parox-
lead to a tachycardia. Transmission of conduc- ysmal) tachycardia, caused by excitation reen-
tion within the AV node normally takes place try from ventricle to atrium (→ G3).
along parallel pathways of relatively loose
190 cells of the AV node that are connected with
one another through only a few gap junctions.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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