The term arrhythmia, also known as dysrhytmia, is the condition when there are variations from the normal rhythm and sequence of excitation of the heart (Sherwood, 2007). Heartbeat that describes rapid irregular heartbeats is termed as tachycardia while heartbeat that is characterized by slow heart rhythms is called bradycardia. One of the ways to classify arrhythmia is by its site of origins such as atrial, atrioventricular and ventricular.
Atrial Fibrilation(AF) is one of the most common sympotomic sustained arrhythmias seen in clinical practice (Marriot J.L et al, 1998). AF is a condition whereby there is a desynchronization of the atrial electrical activity with consequent deterioration of atrial mechanical function causing a consequent irregular ventricular response. (Corino V.D.A et al, 2010). Symptoms in AF include palpitations and heart rate usually goes up to 100 to 180bpm. In AF, there is an unsynchronized atrial depolarization such that the P waves are absent and the QRS complexes are narrow and irregular. In AF, slower rate will indicate disease of atrioventricular(AV) conduction while faster rate suggests an accessory AV pathway or enhanced AV nodal conduction. Here, the ventricular rate is governed by the refractive period in the AV node. The mechanism of AF is mainly due to the constant conduction within the atria caused by multiple circuits. One of the known causes of AF is due to heart diseases in which atrial myocardium will induce or promote electrical disorganization of atrial depolarization. However, AF can also occur in individuals without any history of cardiac disorder which is also known as lone atrial fibrillation (LAF). LAF could occur due to reentrant supraventricular tachycardias, macro-reentrant atrial flutter and focal atrial tachycardia. (Wyndham.C, 2000). AF can be further designated into three classifications that are, paraxsomal atrial fibrillation, vagally mediated atrial fibrillation and persistant atrial fibrillation. AF may occur individually or also together with other arrhythmias such as atrial flutter or atrial tachycardia. AF will also result in atrial fibrosis and the loss of atrial muscle mass (Valentin F. et al, 2006).
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Another type of arrhythmia is called Ventricular Tachycardia (VT). Ventricular tachycardia is a condition where there is a rapid heart rate originating from the ventricles. It is a type of arrhythmia that is due to reentrant mechanisms that arises during the development of early afterdepolarization and critically slow conduction in a scarred heart tissue. Early after depolarization initiates the tachycardia and reentry sustains it (Marriot J.L et al, 1998). VT is further categorized into two that is monomorphic ventricular tachycardia and polymorphic tachycardia. Monomorphic ventricular tachycardia occurs when there are similar appearances in the beats generated due to increased automaticity within the ventricles because of reentry. Myocardial scarring will result in non-conduction of electrical activity and thus resulting in tachycardia. Polymorphic VT occurs when there is a continuous changing QRS complex in which polymorphic VT terminate spontaneously. Polymorphic VT waves results in a distinctive twisting configuration known as torsade de pointes. Torsade de pointes is an expression meaning twisting of the points in which the QRS peaks appear to be up and down (Marriot J.L et al, 1998). As of other tachycardia ECG recognition, there is an undulating pattern of the QRS complex appears to be twisted around the isoelectic line and that the heart rate being higher than 170bpm. VT is often hard to differentiate with supraventricular tachycardia. Lastly, VT most often requires medical attention as it would lead to ventricular fibrillation which is potentially life threatening.
Next, Premature Ventricular Contractions(PVC) or eitherwise known as Ventricular extrasystoles is a condition whereby there is a premature shaped QRS complexes that is broad an is not preceded by a P wave and the T wave is large and the direction is opposite the major deflection of the QRS (Aliot EM, et al). PVC usually occurs due to the ectopic cardia paecemaker originating from the ventricle. PVC is a type of premature (extra) beat arrhythmia which also includes Premature Atrial Contractions (PAC), instead of the ventrical, originates from the atrial. Mechanisms of the PVC are mainly thought due to reentry, triggered activity and enhanced automaticity of the heart. PVC is a common arrhythmia that can occur in patients with both existing and non-existing heart disease and is not usually a medical emergency.
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Unlike those above mentioned arrhythmia, sinus bradycardia involves the slowing down of the heart rate below 60bpm. ECG monitoring of sinus bradycardia will have a normal P wave amplitude and vector and is followed by a normal QRS complex and T waves. Thus, sinus bradycardia findings are incidental and not often observable. It is often associated with increased vagal tone or secondary to a failure of the sinoatrial (SA) node or atrioventricular (AV) block(Grantham H.J, 2007). AV block or heart block is also another form of arrhythmias will be explained further subsequently.
Heart block, also referred to as atrioventricular (AV) block, refers to a blockage in the electrical conducting system of the heart. Cardiac auto rhythmic cells initiate and conduct action potentials that lead to the contraction of the other contractile cardiac cells. These cells include the sinoatrial (SA) node (Heart's normal peacemaker), atrioventricular (AV) node, bundle of His (atrioventricular bundle) and Purkinje fibers (Sherwood, 2010). An action potential is started off at the SA node in the right atrium and transmitted to the AV node which transmits it to the bundle of His and Purkinje fibers in the ventricles. Heart block occurs when there is a blockage in this impulse conduction.
There are three levels of heart block of which are categorized differently. The first degree heart block occurs when the electrocardiographic PR interval of a PQRST complex takes 0.21 seconds or longer (Sornsin, 1987). In other words, the electrical impulse passes through the AV node at a slower pace. The etiologies include normal physiologic variance, idiopathic bundle branch fibrosis which is the unknown development of too much fibrous connective tissue, calcific valvular heart disease which involves the deposition of insoluble salts of calcium and magnesium in the valves in the heart , ischemic heart disease (heart disease caused by the lack of blood supply produced by obstruction or vasoconstriction), cardiomyopathies (myocardium disease associated with mechanical and/or electrical dysfunction that usually show inappropriate ventricular activity due to a myriad of causes mostly genetic (Basso et al, 2010)), infections resulting in the inflammation of the myocardium (myocarditis), drugs (especially type I antidysrhythmic medications), collagen vascular diseases, tumors, trauma and electrolyte imbalances to name a few. There are also many other causes which are idiopathic (Sornsin, 1987).
There are two types of second degree heart block, namely type I and type II also known as Mobitz type I (or Wenckebach's AV block) and Mobitz type II. The difference in these two types of heart block is that the site of blockage is situated below the AV node for Mobitz type II while for Mobitz type I it is localized within the AV node (Wogan, 1993). Second degree heart block, Mobitz type II, is characterized by a repetitive intermittent block of a single P wave; the preceding conducted sinus impulses have constant pulse rate (PR) intervals. 'High grade' or 'advanced' block occurs when there are consecutive blocked P waves (Wogan, 1993). In Mobitz type I, the PR interval varies, showing progressive PR prolongation before a dropped beat (Wenckebach phenomenon) after which the shortest PR interval occurs. Mobitz type I usually happens in patients with acute inferior wall myocardial infarction (heart attack) caused by the lack of blood supply of the AV node, adenosine release, increased vagal tone (the Bezold-Jarish reflex). Mobitz type I may even occur when sleeping when the parasympathetic tone is widespread and the sympaththetic tone is low (Neufeid, 1984). The etiology of Mobitz type II, if myocardial infarction is not a factor, is sclerodegeneration of the conduction system. This is more common in the aged where the lumens of the arteries are filled with lipid deposits throughout the system. Other etiologies of Mobitz type II would be the effects of drugs like calcium or betablockers and the proof of the bilateral bundle block (Haft, 1971).
Third degree heart block or complete heart block occurs when the impulse conduction is completely blocked resulting in independent pacemakers in the atrium and ventricles. The pacemaker in the ventricle (Purkinje fibers at 30mph) has a much slower rate than the SA node (70mph) in the atrium. The etiology could be a congenital heart block where the AV node is absent or damaged at birth, resulting in a broken conducting system (Lev, 1971). Other etiologies include the side effects of drug toxicity such as intramuscular ziprasidone (Tambyraja et al, 2010).
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In conclusion, most heart block are caused or elevated by a number of heart diseases such as hypotension and myocardial infarction.