What is Arrhythmias?

The improper beating of the heart, whether irregular, too fast, or too slow.

An arrhythmia is a problem with the rate or rhythm of your heartbeat. It means that your heart beats too quickly, too slowly, or with an irregular pattern. When the heart beats faster than normal, it is called tachycardia. When the heart beats too slowly, it is called bradycardia. The most common type of arrhythmia is atrial fibrillation, which causes an irregular and fast heart beat.



What is Arrhythmia?
At rest, the heart is normally activated at a rate of 50–100 bpm. Abnormal rhythms of the heart (arrhythmias) can be classified as either too slow (bradycardias) or too fast (tachycardias).

Bradycardia
Bradycardia can arise from two basic mechanisms. First, reduced automaticity of the sinus node can result in slow heart rates or pauses. If sinus node pacemaker activity ceases, the heart will usually be activated at a slower rate by other cardiac tissues with pacemaker activity. Reduced sinus node automaticity can occur during periods of increased vagal tone (sleep, carotid sinus massage, “common faint”), with increasing age, and secondary to drugs (beta blockers, calcium channel blockers).


Second, slow heart rates can occur if the cardiac impulse is prevented from activating the ventricles normally because of blocked conduction. Because the fibrous valvular annulus is electrically inert, the AV node and His bundle normally form the only electrically active connection between the atria and the ventricles. Although this arrangement is useful for preventing feedback between the two chambers, it also makes the AV node and His bundle vulnerable sites for blocked conduction between the atria and ventricles. 

Although a block can be observed in either the left or right bundle branches, bradycardia does not necessarily occur because the contralateral bundle can still activate the ventricles. Atrioventricular block has been classified as first degree when there is an abnormally long atrioventricular conduction time (PR interval >0.22 s) but activation of the atria and ventricles still demonstrates a 1:1 association. In second-degree atrioventricular block, some but not all atrial impulses are conducted to the ventricles. 

Finally, in third-degree block, there is no association between atrial and ventricular activity. Atrioventricular block can occur with increasing age, with increased vagal input, and as a side effect of certain drugs. Atrioventricular block can sometimes also be observed in congenital disorders, such as muscular dystrophy, tuberous sclerosis, and maternal systemic lupus erythematosus, and in acquired disorders, such as sarcoidosis, gout, Lyme disease, systemic lupus erythematosus, ankylosing spondylitis, and coronary artery disease.

Bradycardia resulting from either decreased automaticity or blocked conduction requires evaluation to search for reversible causes. However, the implantation of a permanent pacemaker is often required. 

Tachycardia
Tachycardias can be caused by one of three basic cellular mechanisms. First, increased automaticity caused by faster phase 4 depolarization can result in a faster heart rate. Second, if repolarization is delayed (due to a longer plateau period), spontaneous depolarizations (caused by reactivation of sodium or calcium channels) can occur in phases 3 or 4 of the action potential. These depolarizations are referred to as triggered activity because they are dependent on the presence of a previous action potential. Tachycardia can occur in certain pathologic conditions if these depolarizations reach a threshold. Third, and most frequently, tachycardias can be caused by a re-entrant circuit.


A re-entrant circuit can be formed by any condition that results in parallel but electrically separate regions with different conduction velocities (for example, the border zone of myocardial infarction or an accessory atrioventricular connection).

Tachyarrhythmias can be caused by one of three different mechanisms. First, increased automaticity from faster phase 4 depolarization can result in arrhythmias. Second, under certain conditions, spontaneous depolarizations during phase 3 (early after-depolarizations [EAD]) or phase 4 (delayed after-depolarizations [DAD]) can repeatedly reach a threshold and cause tachycardia. This appears to be the mechanism of polymorphic ventricular tachycardia (torsades de pointes) observed in some patients taking procainamide or quinidine, as well as the arrhythmias associated with digoxin toxicity. Third, re-entry is the most common mechanism for tachyarrhythmia. There are two parallel pathways with different conduction properties during re-entry (perhaps at the border zone of myocardial infarction or a region of myocardial ischemia).

The electrical impulse normally travels down both the fast and slow pathways (shaded region), but when the two pathways converge, the impulse traveling down the slow pathway is blocked because the tissue is refractory to the recent depolarization via the fast pathway (a). When a premature beat enters the circuit, the fast pathway can become blocked, and the impulse travels down the slow pathway (shaded region) (b). After passing through the slow pathway, the impulse can enter the fast pathway retrogradely (with recovered excitability due to the delay) and then re-enter the slow pathway to begin a continuous loop of activation, or re-entrant circuit (c).

What are the symptoms of an arrhythmia?
An arrhythmia may be “silent” and not cause any symptoms. A doctor can detect an irregular heartbeat during an examination by taking your pulse, listening to your heart or by performing diagnostic tests. If symptoms occur, they may include:
  • Palpitations: A feeling of skipped heartbeats, fluttering, "flip-flops" or feeling that the heart is "running away"
  • Pounding in the chest
  • Dizziness or feeling lightheaded
  • Shortness of breath
  • Chest discomfort
  • Weakness or fatigue (feeling very tired)


What causes Arrhythmias?

Arrhythmias can be caused by:
  • Coronary artery disease
  • High blood pressure
  • Changes in the heart muscle (cardiomyopathy)
  • Valve disorders
  • Electrolyte imbalances in the blood, such as sodium or potassium
  • Injury from a heart attack
  • The healing process after heart surgery
  • Other medical conditions

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