Biomedical Engineering Reference
In-Depth Information
4.1.4.7 Bundle Branch Blocks
Bundle branch blocks are the most frequent type of conduc-
tion disorders. They are caused by impaired conduction at
the level of the right or left bundle branch and are present in
approximately 0.6 % of the population, with a higher occur-
rence in the elderly. In bundle branch block, there is delayed
activation of the myocardium of the corresponding ventricle.
This delay leads to subsequent characteristic morphological
changes in the QRS complex. Right bundle branch block
(RBBB) commonly occurs in right ventricular disease and
left bundle branch block in left ventricular dilation and
hypertrophy.
4.2.1
Classi fi cation of Antiarrhythmic Drugs
Antiarrhythmic drugs affect certain ion channels responsible
for the membrane potential of a cell. A change in the mem-
brane potential affects depolarization and repolarization of
the cell membrane and may thus affect the basic mechanisms
of origin and maintenance of tachycardia. The slowing of
depolarization avoids spontaneous depolarization, and slow-
ing the rate of depolarization and repolarization avoids the
maintenance of tachycardia in a reentry circuit. The Vaughan-
Williams classification (Table
4.1
) divides antiarrhythmic
drugs into four classes based on their effect on a specific ion
channel [ 23 ] .
A limitation of this classification of antiarrhythmic drugs
is that it does not include some drugs (digoxin, adenosine,
magnesium sulfate). A more recent classification, called the
“Sicilian gambit” [ 23 ] , divides all known antiarrhythmic
drugs according to the site where their effect is exerted
(membrane channels, receptors, and pumps).
In practice, it is suitable to classify antiarrhythmic drugs
according to the cardiac structure that is to be affected.
Antiarrhythmic drugs are divided into two groups consisting
of four drugs. The first includes AV nodal blockers that slow
impulse conduction in the AV node. The second includes sta-
bilizers that stabilize electrical processes in the atria and the
ventricles (Table
4.2
).
4.1.4.8 Fascicular Blocks
Impulse conduction in the left ventricular myocardium
occurs via two fascicles, anterior and posterior, that are con-
tinuations of the left bundle branch. The right bundle branch
in the right ventricle is the third fascicle. Left anterior and
left posterior fascicular blocks are distinguished. Bifascicular
blocks are caused by a RBBB with concomitant left anterior
or left posterior fascicular block. Trifascicular block is a
combination of a RBBB and a block of the two fascicles of
the left bundle branch.
4.2
Pharmacological Treatment
of Arrhythmias
4.2.2
Pharmacological Treatment
Despite the advent of nonpharmacological treatment that
involves pacemaker implantation in bradycardia (e.g., radiof-
requency catheter ablation in supraventricular tachycardia)
and ICD implantation in ventricular arrhythmias [ 26, 27 ] ,
pharmacotherapy still has a firm place in the long-term man-
agement of arrhythmias. However, the primary indications for
pharmacotherapy are acute management of tachycardia and
prevention of tachycardia in patients in whom ablation has
failed, followed by atrial fibrillation and VT, for which phar-
macotherapy is a complementary treatment to reduce the ICD
shock rate. In practice, it is necessary to keep in mind some
proarrhythmogenic effects of certain antiarrhythmic drugs.
Permanent treatment of bradycardias mainly involves non-
pharmacological treatment using permanent pacing. To
ascertain the method of treatment, it is necessary to deter-
mine the degree of symptomaticity and severity of bradycar-
dia. Treatment is indicated only in symptomatic bradycardias
[ 29 ] . The following conditions are considered symptomatic:
those leading to cardiac arrest, syncopes with underlying SA
or AV blocks, presyncopes, or collapses. The treatment of
acute bradycardias involves administration of atropine or
isoprenaline, application of temporary pacing, or both.
Table 4.1
The Vaughan-Williams classi fi cation of antiarrhythmic drugs [ 23, 28 ]
Class
Blocks
Effect on depolarization
Effect on repolarization
Drugs
Ia
Na
+
channel
Moderate prolonged
Prolonged
Quinidine, disopyramide, procainamide
Ib
Na
+
channel
Weak
Shortened
Mexiletine, lidocaine
Na
+
channel
Strong prolonged
Weak
Propafenone, fl ecainide
Ic
Weak
Weak
Metoprolol, atenolol
II
b
receptors
K
+
channel
Weak
Amiodarone, bretylium, sotalol
III
IV
Ca
2+
channel
Weak
Weak
Diltiazem, verapamil
