Transcript Arrhythmias

Arrhythmia
Arrhythmias are abnormal beats of the heart.
Types of arrhythmias include:
According to heart rate :
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Heartbeats that are too slow ( bradycardia)
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Heartbeats that are too fast (tachycardia)
According to etiology
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Delayed after depolarization
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Heart block
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Abnormal pacemaker (Ectopic foci)
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Reentry circus movement
Risk Factors
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Excess caffeine ,stress ,tobacco use ,alcohol u
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Digitalis overdose
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High blood pressure & coronary artery disease
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Heart muscle damage after heart attack (MI)
Action Potential In Conducting Tissues
Symptoms:
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Some arrhythmias may occur without any symptoms. Others may cause
noticeable symptoms, such as:
Fainting
Dizziness, sensation of light-headedness
Palpitations
Sensation of a missed or extra heart beat
Shortness of breath & chest pain
Etiology of arrhythmias
1. Delayed after depolarization
Non pacemaker cells (non conducting fibers) normally have a stable
phase 4 (i.e. they do not fire unless they receive a signal from the
pacemakers)· In certain condition, non conducting cells have a slow,
rising phase 4, which allows them to fire without a signal from the
pacemaker. It is due to an increase in intracellular Ca2+ which ·
An increased intracellular Ca2+ occur in :
 A. Use of cardiac glycosides
 B. Increased sympathetic tone (adrenergic stress)
 C. Myocardial ischemia
3. Abnormal pacemaker (Ectopic foci)
 The pacemaker is the tissue which has the fastest rate of
firing Normally, this is the SA node· Sometimes, other tissues
in the heart can assume the role of pacemaker
 The main predisposing factors are
a-β adrenoceptor stimulation: causes increase in Ca2+ levels
b- Myocardial ischemia: There is a reflex increase in sympathetic tone as a
result of poor perfusion. This increase in sympathetic tone increases Ca2+
levels· Also, ischemia affects the Na+/K+ pump which requires ATP to
extrude Na+ out of the cell. If this pump fails to work (due to lack of ATP) Na+
concentrations increase in the cell, resulting in depolarization
4. Heart block
 Damage to nodal tissue, most commonly AV node (e.g. during
a myocardial infarct), prevents conduction of the signal to
other parts of the heart· The areas of the heart which
normally rely on normal SA node signal start to beat
independently, under the action of their own pacemakers.
Diagnosis
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Blood tests & urine tests
Electrocardiogram (EKG) :records the heart's activity by measuring electrical currents
through the heart muscle
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Normal heart ECG
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Atrial flutter
After depolarization
Ventricular fibrillation
Treatment
Antiarrhythmic Medications
 These will help slow down or speed up your heart rate, or return
your heart rhythm to normal , depending on your need.
Electrical Cardioversion or Defibrillation
These treatments involve placing paddles on the chest. An electrical
current is passed through the chest wall to the heart, in order to
re-set its electrical circuits, and attempt to return the heart rhythm
to normal.
 Class I drugs, those that act by blocking the sodium
channel, are subdivided into 3 subgroups, IA, IB, and
IC based on their effects on potency towards blocking
the sodium channel
 Subclass Ia drugs
 Subclass Ib drugs
 Subclass Ic drugs
 Class II (beta-adrenergic receptors blockers)
 Class III drugs prolong depolarization by blocking
outward potassium conductance (prolong QT interval),
 Class IV Ca channel blockers
 Miscellaneous In addition to the standard classes, IaIb,Ic, II, III, and IV, there is also a miscellaneous group
of drugs that includes digoxin, adenosine, atropine and
other compounds whose actions don't fit the standard
four classes
Antidysrhythmic drugs