CHAPTER 2 • ELECTRICAL ACTIVITY OF THE HEART
29
the ventricular rate is irregular and usually
rapid. Atrial fibrillation and flutter illustrate
an important function of the AV node; it lim-
its the frequency of impulses that it conducts,
thereby limiting ventricular rate. This feature
is important because when ventricular rates
become very high (e.g., >200 beats/min), car-
diac output falls owing to inadequate time for
ventricular filling between contractions.
Atrial
rate
is
greater
than ventricular
rate in some forms of AV block (see Fig.
2.14). This is an example of an arrhythmia
caused by abnormal
(depressed)
impulse
conduction. With AV block, atrial rate is nor-
mal, but every atrial depolarization may not
be followed by a ventricular depolarization.
A second-degree AV block may have two or
three P waves preceding each QRS complex
because the AV node does not successfully
conduct every impulse. In a less severe form
of AV block, the conduction through the AV
node is delayed, but the impulse is still able
to pass through the AV node and excite the
ventricles. With this condition, termed first-
degree AV block, a consistent one-to-one cor-
respondence remains between the P waves
and QRS complexes; however, the PR interval
is found to be >0.2 seconds. In an extreme
form of AV nodal blockade, third-degree AV
block, no atrial depolarizations are conducted
through the AV node into the ventricles, and
P waves and QRS complexes are completely
dissociated. The ventricles still undergo depo-
larization because of the expression of a sec-
ondary, latent pacemaker site (e.g., within the
AV junction or from some ectopic foci within
the ventricles); however, the ventricular rate
is generally slow (<40 beats/min). Ventricu-
lar bradycardia occurs because the intrinsic
firing rate of secondary, latent pacemakers is
much slower than in the SA node. For exam-
ple, pacemaker cells within the AV node and
bundle of His have rates of 50 to 60 beats/min,
whereas those in the Purkinje system have
rates of only 30 to 40 beats/min. If the ectopic
foci are located within the ventricles, the QRS
complex will have an abnormal shape and
be wider than normal because depolariza-
tion does not follow the normal conduction
pathways.
CASE 2-2
A patient is being treated for
hypertension with a (3-blocker (a drug
that blocks p-adrenoceptors in the
heart) in addition to a diuretic. A routine
ECG reveals that the patient’s PR
interval is 0.24 seconds (first-degree AV
nodal block). Explain how removal of
the p-blocker might improve AV nodal
conduction.
A condition can arise in which ventricular
rate is greater than atrial rate; that is, the fre-
quency of QRS complexes is greater than the
frequency of P waves (see Fig. 2.14). This con-
dition is termed ventricular tachycardia (100
to 200 beats/min) or ventricular flutter (>200
beats/min). The most common causes of ven-
tricular tachycardias are reentry circuits caused
by abnormal impulse conduction within the
ventricles or rapidly firing ectopic pacemaker
sites within the ventricles (which may be
caused by afterdepolarizations). With ven-
tricular tachycardias, there is a complete dis-
sociation between atrial and ventricular rates
because ventricular depolarizations are not
being triggered by atrial sites. Both ventricular
tachycardia and ventricular flutter are serious
clinical conditions because they impair ventric-
ular filling, reduce stroke volume, and can lead
to ventricular fibrillation (see Fig. 2.14). This
latter condition is seen in the ECG as rapid,
low-voltage,
uncoordinated
depolarizations
(having no discernable QRS complexes), which
results in cardiac output going to zero. This
lethal condition can sometimes be reverted to a
sinus rhythm by applying strong but brief elec-
trical currents to the heart by placing electrodes
on the chest (electrical defibrillation).
The
ECG
can
reveal
another
type
of
arrhythmia, premature depolarizations (see
Fig. 2.14). These depolarizations can occur
within either the atria (premature atrial com-
plex) or the ventricles (premature ventricular
complex). They are usually caused by ectopic
pacemaker sites within these cardiac regions
and appear as extra (and early) P waves or QRS
complexes. These premature depolarizations
are often abnormally shaped, particularly in
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