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Published byAlexia Barber Modified over 9 years ago
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Arrhythmia Arrhythmias are abnormal beats of the heart.
Types of arrhythmias include: According to heart rate : Heartbeats that are too slow ( bradycardia) Heartbeats that are too fast (tachycardia) According to etiology Delayed after depolarization Heart block Abnormal pacemaker (Ectopic foci) Reentry circus movement Risk Factors Excess caffeine ,stress ,tobacco use ,alcohol u Digitalis overdose High blood pressure & coronary artery disease Heart muscle damage after heart attack (MI)
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Action Potential In Conducting Tissues
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Etiology of arrhythmias
Symptoms: 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
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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.
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Diagnosis Blood tests & urine tests
Electrocardiogram (EKG) :records the heart's activity by measuring electrical currents through the heart muscle Normal heart ECG After depolarization Atrial flutter Ventricular fibrillation
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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.
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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, Ia-Ib,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
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Antidysrhythmic drugs
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