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4 Antiaritmic
4 Antiaritmic
Antiarrhythmics are used to treat heart rhythm disorders, called arrhythmias, and to
lessen the symptoms associated with them. Some of the common symptoms of arrhythmias
include heart palpitations, irregular heartbeats, fast heartbeats, lightheadedness, fainting, chest
pain, and shortness of breath.
Arrhythmias may be caused by myocardial infarction, cardiosclerosis, valvularopathy,
some infections, endocrine dysfunctions, acute intoxications, ionic deregulations, overdosage of
glycosides; in children- by hypoxia, hypo and hyperpotasemia, hypoglycemia
Arrhythmias can be divided in:
tachyarrhythmia,
Sinus tachycardia (resting rate >100 beats/min). b-Blockers eliminate
sympathoexcitation and decrease cardiac rate.
Atrial flutter or fibrillation. An excessive ventricular rate can be decreased by
verapamil or cardiacglycosides. These drugs inhibit impulse propagation through the AV node,
so that fewer impulses reach the ventricles.
Ventricular fibrillation. This occurs when the ventricles beat in a very chaotic and
loosely organized fashion. Ventricular fibrillation is a serious, life-threatening condition that
must be corrected immediately or death will likely result. Antiarrhythmic medications are
sometimes prescribed to prevent ventricular fibrillation. In recent years, implantable cardioverter
defibrillators (ICDs) have become common in the prevention and immediate treatment of
ventricular fibrillation. These devices are implanted inside the chest. They monitor the heart
rhythm, and in the event of ventricular fibrillation, they administer an electric shock to jolt the
heart back into a normal rhythm. The device is similar to the defibrillators carried by emergency
paramedic crews. ICDs and antiarrhythmic medications are often used in the same patient. ICDs
are also frequently implanted in patients who are at risk of ventricle tachycardia.
ventricular tachycardia This is a rapid heart rhythm that occurs in the lower chambers of the
heart (ventricles). Ventricular tachycardia can be very dangerous if it progresses to ventricular
fibrillation .
bradyarrhythmia
Sinus bradycardia. An abnormally low sinoatrial impulse rate (<60/min) can be raised
by parasympatholytics. The quaternary ipratropium is preferable to atropine, because it lacks
CNS penetrability . Sympathomimetics also exert a positive chronotropic action; they have the
disadvantage of increasing myocardial excitability (and automaticity) and, thus, promoting
ectopic impulse generation (tendency to extrasystolic beats). In cardiac arrest epinephrine can
be used to reinitiate heart beat. and ectopic pacemaker activity.
Class IA antiarrhythmics have been used for many years, typically for supraventricular
tachycardia (SVT), abnormal heart rhythms that arise in parts of the heart above the ventricles
(lower chambers) or less often in the ventricles themselves. These are called supraventricular
arrhythmias. These drugs have only a moderate effect on sodium channels and usually prolong
the duration of repolarization - the time it takes to "recharge" the heart after every beat. Some of
these drugs, such as quinidine, also reduce the force of heart muscle contractions. They may not
be suitable for patients with heart failure and other conditions that weaken the pumping ability of
the heart
Class I - membrane stabilizers
- depress depolarization of cardiac cell membrane by restricting entry of fast sodium current resulting in
reduction in the maximum rate of rise of phase 0 of the action potential. This leads to slower rate of
conduction, increased threshold for excitation and prolongation of the effective refractory period.
- also reduce rate of phase 4 diastolic depolarization, at doses which have no other effects, causing a
reduction in spontaneous automaticity.
- class I drugs further subdivided by their effect on the duration of the action potential:
Ia
- lengthen action potential
- slow rate of rise of phase 0
- prolong repolarization
- prolong refractoriness by blocking several types of potassium channel
- prolong PR, QRS, QT
- moderate-marked sodium channel blockade
- eg quinidine, procainamide, disopyramide
Ib
- shorten action potential
- limited effect on rate of rise of phase 0
- shorten repolarization
- shorten QT
- raise fibrillation threshold
- mild-moderate sodium channel blockade
- little effect on refractoriness since there is essentially no blockade of potassium channels
- eg lignocaine, mexilitine, phenytoin, propafenone
Ic
- no effect on length of action potential
- markedly reduces rate of rise of phase 0
- little effect on repolarization
- markedly prolongs PR and QRS
- marked Na channel blockade
- prolong refractoriness by blocking outward-rectifying potassium channels
- eg flecainide
.Quinidine Like all other class I antiarrhythmic agents, quinidine primarily works by blocking
the fast inward sodium current (INa). Quinidine's effect on INa is known as a use dependent block.
This means that at higher heart rates, the block increases, while at lower heart rates the block
decreases. The effect of blocking the fast inward sodium current causes the phase 0
depolarization of the cardiac action potential to decrease (decreased Vmax).
- decrease maximum rate of rise of phase 0
- depresses spontaneous phase 4 depolarization in automatic cells (results in prolonged QT)
- in general slows conduction through atrial, ventricular and Purkinje fibres causing QRS
prolongation but usually has no effect on sinus rate or R interval
- antivagal action may accelerate AVN conduction