Biomedical Engineering Reference
In-Depth Information
underlying heart disease, left ventricular function, and the
condition of the coronary bed always play an important role.
For sustained ventricular tachycardia to occur, an initial
abnormal stimulus and maintenance of the initiated arrhyth-
mia are required. The most common mechanism of main-
taining arrhythmia is reentry. Less frequently, it involves
repeated initiation by automaticity or triggering.
as a late complication of acute myocardial infarction and
coronary artery disease or as a response to overdose with
certain medications. Polymorphic VT with underlying con-
genital or acquired ion channel disorders is a distinct group.
4.1.3.5 Torsades De Pointes
The shape of this polymorphic VT on the ECG is character-
istic and resembles the resultant modulated signal of the
amplitude modulation, which is due to a periodic change in
the QRS vector around the isoelectric line in the frontal
plane. The rate is 200 beats/min or more. Early after-depo-
larization is the likely arrhythmogenic mechanism. Torsades
de pointes occurs in relation to a prolonged QT interval.
4.1.3.1 Ventricular Asystole
The ventricular myocardium is not electrically activated.
Only P waves or the isoelectric line are seen on the ECG.
Transient arrests are characteristic of sick sinus syndrome.
4.1.3.2 Idioventricular Rhythm
Heart action is activated only by tertiary impulse generation
from the ventricles. Heart rate decreases to 30-40 beats/min.
4.1.3.6 Ventricular Fibrillation
In ventricular fibrillation (VF), circulatory arrest occurs
because the ventricular myocardium does not contract effec-
tively. Uncoordinated electrical activity only results in hemo-
dynamically ineffective contractions. VF results from an
underlying heart muscle disorder with regions of inhomoge-
neous refractoriness. On the ECG, the individual waves are
not discernible, except for the fibrillation waves, frequently
with decaying amplitude.
4.1.3.3 Ventricular Extrasystoles
Ventricular extrasystoles (premature ventricular contraction)
arise in ectopic ventricular foci, most commonly in the ven-
tricular musculature or Purkinje fibers. They are more seri-
ous than supraventricular extrasystoles but can occur in
people with no organic heart disease. The incidence increases
with age. Depending on the frequency of their occurrence,
extrasystoles are categorized as single, multiple, and cou-
pling. According to the number of ectopic foci, they are
classified as unifocal (from one focus, a constantly identical
shape on the ECG) and multifocal (from several foci, a var-
ied shape). The QRS complex of ventricular extrasystoles is
always widened, whereas in supraventricular extrasystoles it
is mostly narrow. A ventricular extrasystole usually does not
propagate back to the atria and propagation of sinus impulses
is not impaired. A ventricular extrasystole is followed by a
full compensatory pause. This is because the ventricles are
still in the refractory period when the subsequent sinus
impulse is propagated after an extrasystole and therefore
only contract with the next sinus impulse. The sum of inter-
vals before and after the extrasystole is equal to two normal
cardiac cycles. Ventricular extrasystoles are most typically
manifested by palpitations. The most severe form of ven-
tricular extrasystoles is the so-called R-on-T phenomenon, in
which an extrasystole in the vulnerable period can trigger
ventricular fi brillation.
4.1.4
Disorders of Impulse Conduction
Disorders of impulse conduction (Fig.
4.5
) can occur at all
levels of the conduction system [ 25 ] . Thus, sinoatrial, AV,
bundle branch, and fascicular blocks are distinguished.
Impulse conduction can also be interrupted at several levels.
Typical ECG waveforms presented for the respective cardiac
rhythm and conduction disorders will be of particular use in
more complex applications of dual-chamber pacing.
4.1.4.1 Sinoatrial Block
In sinoatrial (SA) block, impulse conduction from the sinus
node to the atria is impaired (slowed or blocked). As in the
case of AV block (described below), there are three degrees of
SA block. Because the sinus node signal is not apparent on a
surface ECG, it is possible to diagnose only second-degree
block when there is progressive shortening of the PP interval
until one interval is lengthened and the QRS complex is
dropped. Of more importance is third-degree block, when no
impulse is conducted from the sinus node to the atria and only
the isoelectric line is visible on the ECG, and, subsequently,
junctional rhythm develops. SA block occurs in organic heart
disease; some medications may have an adverse effect.
4.1.3.4 Ventricular Tachycardia
Ventricular tachycardia (VT) refers to a sequence of three to
fi ve or more successive ventricular extrasystoles. Pathological
impulses activate the ventricles at a rate of 140-220/min.
According to the morphology of the QRS complex on the
ECG, VT is classified as monomorphic (identical QRS com-
plexes) or polymorphic (varying QRS morphology). The
width of the QRS complex is more than 0.12 s. Sustained
(more than 30 s) and unsustained (three to ten cardiac inter-
vals) VTs are distinguished according to duration. VT occurs
4.1.4.2 Atrioventricular Block
The region of the AV junction comprises the AV node (the
proximal portion), the bundle of His, and the beginning of
both bundle branches (the distal portion). Thus, in AV block,
impulse conduction from the atria to the ventricles is impaired
