Arrythmias (heart)

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Cardiac arrhythmia

ICD-10	I47 - I49
ICD-9	427
OMIM	[1]
DiseasesDB	15206
MedlinePlus	001101
eMedicine	/
MeSH	{{{MeshNumber}}}

Cardiac arrhythmia (also dysrhythmia) is a term for any of a large and heterogenous group of conditions in which there is abnormal electrical activity in the heart. The heart beat may be too fast or too slow, and may be regular or irregular.

Some arrhythmias are life-threatening medical emergencies that can result in cardiac arrest and sudden death. Others cause aggravating symptoms such as an abnormal awareness of heart beat, and may be merely annoying. Others may not be associated with any symptoms at all, but pre-dispose toward potentially life threatening stroke or embolus.

Some arrhythmias are very minor and can be regarded as variants of normal. In fact, most people will sometimes feel their heart skip a beat, or give an occasional extra strong beat - neither of which are usually a cause for alarm.

The term sinus arrhythmia refers to a normal phenomenon of mild acceleration and slowing of the heart rate that occurs with breathing in and out. It is usually quite pronounced in children, and steadily lessens with age.

Manifestations

The term cardiac arrhythmia covers a very large number of very different conditions, many of which receive separate articles in depth elsewhere in Wikipedia.

The commonest symptom of arrhythmia is an abnormal awareness of heartbeat, termed palpitations. These may be infrequent, frequent, or continuous. Some of these arrhythmias are harmless (though annoying) but many of them predispose to adverse outcomes.

Some arrhythmias do not cause symptoms, and are not associated with increased mortality. However, some asymptomatic arrhythmias are associated with adverse events. Examples include increase in risk of blood clotting within the heart, and thus increase the risk of embolisation and stroke, or increase in the risk of heart failure, or increase in the risk of sudden cardiac death.

If an arrhythmia results in a heart beat that is too fast, too slow or too weak to supply the body's needs, this manifests as a lower blood pressure and may cause lightheadedness or dizziness, or fainting.

Some types of arrhythmia result in cardiac arrest, or sudden death.

Medical assessment of the abnormality using an electrocardiogram is the best way to diagnose and assess the risk of any given arrhythmia.

Mechanisms and aetiology

Normal electrical activity in the heart

Main article: Electrical conduction system of the heart

Each heart beat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node. The impulse initially causes both of the atria to contract, then activates the AV node which is the only electrical connection between the atria and the ventricles or main pumping chambers. The impulse then spreads through both ventricles via the His Purkinje fibres causing a synchronised contraction of the heart muscle, and thus, the pulse.

Tachycardias

In adults the normal resting heart rate ranges from 60 to 100 beats per minute. The resting heart rate in children is much faster.

Any heart rate faster than 100 beats/minute is labelled tachycardia. Tachycardia may result in palpitation, however, tachycardia is not necessarily an arrhythmia. Increased heart rate is a normal response to physical exercise or emotional stress. This is mediated by the sympathetic nervous system on the sinus node, and is called sinus tachycardia. Other things that increase sympathetic nervous system activity in the heart include ingested or injected substances such as caffeine or amphetamines, and an overactive thyroid gland (hyperthyroidism).

Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normal cardiac cycle. Abnormal impulses can begin by one of two mechanisms: automaticity or reentry. A specialised form of re-entry problem is termed fibrillation.

Automaticity

Automaticity refers to a cardiac muscle cell firing off an impulse on its own. Only specialized cells in the heart have the ability to fire off an action potential - these cells are found in the 'conduction system' of the heart and include the SA node, AV node, Bundle of HIS and Purkinje fibers. A single specialized location in the atrium, the sinoatrial node, has a higher automaticity (a faster pacemaker) than the rest of the heart, and therefore is usually the one to start the heartbeat.

Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus, and is by definition a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart's pumping efficiency, because the signal reaches the various parts of the heart muscle with slightly different timing than usual and causes a poorly coordinated contraction.

Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm depends on where the first signal begins: if it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus, many types of dysrhythmia can result.

Re-entry

Re-entry dysrhythmias occur when an electrical impulse travels in a circle within the heart, rather than moving outward and then stopping. Every cardiac cell is able to transmit impulses in every direction, but will only do so once within a short period of time. Normally the impulse spreads through the heart quickly enough that each cell will only respond once, but if conduction is abnormally slow in some areas, part of the impulse will arrive late and will be treated as a new impulse, which can then spread backward. Depending on the timing, this can produce a sustained abnormal rhythm, such as atrial flutter, a self-limiting burst of supraventricular tachycardia, or the dangerous ventricular tachycardia.

By analogy, imagine a room full of people all given these instructions: "If you see anyone starting to stand up, then stand up for three seconds and sit back down." If the people are quick enough to respond, the first person to stand will trigger a single wave which will then die out; but if there are stragglers on one side of the room, people who have already sat down will see them and start a second wave, and so on.

Fibrillation

When an entire chamber of the heart is involved in a multiple micro-reentry circuits, and therefore quivering with chaotic electrical impulses, it is said to be in fibrillation.

Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation); ventricular fibrillation is imminently life-threatening.

Atrial fibrillation is the quivering, chaotic motion in the upper chambers of the heart, known as the atria. Atrial fibrillation is often due to serious underlying medical conditions, and should be evaluated by a physician. It is not typically a medical emergency.

Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest, and an individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.

CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the intervention which is most likely to restore a more healthy heart rhythm. Defibrillation is performed by applying an electric shock to the heart, which sometimes causes the heart to revert to a rhythm that can once again pump blood.

Bradycardias

A slow rhythm, (less than 60 beats/min), is labelled bradycardia. This may be caused by a slowed signal from the sinus node (termed sinus bradycardia), a pause in the normal activity of the sinus node (termed sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles (termed AV block or heart block). Heart block comes in varying degrees and severity. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node.

Classification of common cardiac arrhythmias

Arrhythmia may be classified by rate (normal, tachycardia, bradycardia), or mechanism (automaticity, reentry, fibrillation).

It is also appropriate to classify by site of origin:

Atrial

• Premature Atrial Contractions (PACs)
• Wandering Atrial Pacemaker
• Multifocal atrial tachycardia
• Atrial flutter
• Atrial fibrillation (Afib)

Junctional arrhythmias

• Supraventricular tachycardia (SVT)
• AV nodal reentrant tachycardia is the commonest cause of Paroxysmal Supra-ventricular Tachycardia (PSVT)
• Junctional rhythm
• Junctional tachycardia
• Premature junctional complex

Atrio-ventricular

• AV reentrant tachycardia occurs when a re-entry circuit crosses between the atria and ventricles somewhere other than the AV node:
  • Wolff-Parkinson-White syndrome
  • Lown-Ganong-Levine syndrome

Ventricular

• Premature Ventricular Contractions (PVC) sometimes called Ventricular Extra Beats (VEBs)
  • Premature Ventricular beats occurring after every normal beat are termed ventricular bigeminy
  • Two premature ventricular beats for each normal beat is termed ventricular trigeminy
• Accelerated idioventricular rhythm
• Monomorphic Ventricular tachycardia
• Polymorphic ventricular tachycardia
• Ventricular fibrillation

Heart blocks

These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They are the commonest cause of bradycardia:

• First degree heart block, which manifests as PR prolongation
• Second degree heart block
  • Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
  • Type 2 Second degree heart block, also known as Mobitz II
• Third degree heart block, also known as complete heart block

Diagnosis

Cardiac dysrhythmias are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope, or feeling for peripheral pulses. These cannot usually diagnose specific dysrhythmias, but can give a general indication of the heart rate and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats.

The simplest specific diagnostic test for assessment of heart rhythm is the electrocardiogram (abbreviated ECG or EKG). A Holter monitor is an EKG recorded over a 24-hour period, to detect dysrhythmias that may happen briefly and unpredictably throughout the day.

SADS

SADS, or sudden arrhythmia death syndrome, is a term used to describe sudden death due to cardiac arrest brought on by an arrhythmia. The most common cause of sudden death in the US is coronary artery disease^{[How to reference and link to summary or text]}. Approximately 300,000 people die suddenly of this cause every year in the US^{[How to reference and link to summary or text]}. SADS can also occur from other causes. Also, there are many inherited conditions and heart diseases that can affect young people that can cause sudden death. Many of these victims have no symptoms before dying suddenly^{[How to reference and link to summary or text]}.

Causes of SADS in young people are long QT syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia and hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia ("arrythmia"-causing, "right ventricle"-involving, pre-cancerous malformation).

Treatment

Because arrhythmias are such a heterogenous group of conditions, treatment needs to be carefully selected by a patient with their physician. Some arrhythmias require no treatment at all. Others require immediate emergency treatment if death is to be avoided.

Treatments include physical maneuvers, antiarrhythmic drugs, other drugs, electricity, and electro or cryo cautery.

Physical maneuvers

A number of physical acts can increase parasympathetic nervous supply to the heart, resulting in blocking of electrical conduction through the AV node. This can slow down or stop a number of arrhytmias that originate above or at the AV node (see main article: supraventricular tachycardias). Parasympathetic nervous supply to the heart is via the vagus nerve, and these maneuvers are collectively known as vagal maneuvers.

Antiarrhythmic drugs

See main article on antiarrhythmic agents.

There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every antiarrhythmic drug has the potential to act as a pro-arrhythmic, and so must be carefully selected and used under medical supervision.

Other drugs

A number of other drugs can be useful in cardiac arrhythmias.

Several groups of drugs slow conduction through the heart, without actually preventing an arrhythmia. These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for a patient.

Some arrhythmias promote blood clotting within the heart, and increase risk of embolus and stroke. Anticoagulant medications such as warfarin and heparins, and anti-platelet drugs such as aspirin can reduce the risk of clotting.

Electricity

Dysrhythmias may also be treated electrically, by applying a shock across the heart - either externally to the chest wall, or internally to the heart via implanted electrodes.

Cardioversion is the application of a shock synchronised to the underlying heartbeat. It is used for treatment of supraventricular tachycardias. In elective cardioversion, the recipient is usually sedated or lightly anesthetized for the procedure.

Defibrillation differs in that the shock is not synchronised. It is needed for the chaotic rhythm of ventricular fibrillation and is also used for pulseless ventricular tachycardia. Often, more electricity is required for defibrillation than for cardioversion. In most defibrillation, the recipient has lost consciousness so there is no need for sedation.

Defibrillation or cardioversion may be accomplished by an implantable cardioverter-defibrillator (ICD).

Electrical treatment of dysrhythmia also includes cardiac pacing. Temporary pacing may be necessary for reversible causes of very slow heartbeats, or bradycardia, (for example, from drug overdose or myocardial infarction). A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover.

Electrical cautery

Some cardiologists further sub-specialise into electrophysiology. In specialised catheter laboratories, they use fine probes inserted through the blood vessels to map electrical activity from within the heart. This allows abnormal areas of conduction to be located very accurately, and subsequently destroyed with heat, cold, electrical or laser probes.

This may be completely curative for some forms of arrhythmia, but for others, the success rate remains disappointing. AV nodal reentrant tachycardia is often curable. Atrial fibrillation can also be treated with this technique (e.g. pulmonary vein isolation), but the results are less reliable.

See also

• Clinical cardiac electrophysiology
• Antiarrhythmic agents
• Artificial pacemaker
• Electrical conduction system of the heart
• Implantable cardioverter-defibrillator.
• Tachycardia

External links

• International Winter Arrhythmia School
• Arrhythmia information from Seattle Children's Hospital Heart Center
• SADS Foundation
• Cardiac Risk in the Young (UK)
• Rhythms and Arrhythmia from Cardionetics
• Block Party and Other Cardiac Arrhythmias from eLeaP Healthcare Courses