Arrhythmias, also known as cardiac arrhythmias, heart arrhythmias, or dysrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow.

A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia.

Some arrhythmias have no symptoms.

Symptoms, when present, may include palpitations or feeling a pause between heartbeats.

Symptoms may include lightheadedness, passing out, shortness of breath, chest pain, or decreased level of consciousness.

Most cases of arrhythmia are not serious, some, however, predispose a person to complications such as stroke or heart failure, or sudden death.

Arrhythmias are  categorized into four groups: 

extra beats, supraventricular tachycardias, ventricular arrhythmias and bradyarrhythmias.

Extra beats include premature atrial contractions, premature ventricular contractions and premature junctional contractions.

Supraventricular tachycardias include atrial fibrillation, atrial flutter and paroxysmal supraventricular tachycardia.

Ventricular arrhythmias include ventricular fibrillation and ventricular tachycardia.

Bradyarrhythmias are due to sinus node dysfunction or atrioventricular conduction disturbances.

Arrhythmias are due to problems with the electrical conduction system of the heart.

Many arrhythmias can be effectively treated: medications, medical procedures such as inserting a pacemaker, and surgery.

Medications for a fast heart rate may include beta blockers, or antiarrhythmic agents such as procainamide, which attempt to restore a normal heart rhythm.

Pacemakers are often used for slow heart rates.

In patients with irregular heartbeats are often treated with anticoagulants reduce the risk of complications.

Those who have severe symptoms from an arrhythmia or are medically unstable may receive urgent treatment with a controlled electric shock in the form of cardioversion or defibrillation.

Atrial fibrillation affects about 2% to 3% of the population.

SARS-CoV‑2 pandemic, cardiac arrhythmias are commonly developed and associated with high morbidity and mortality among patients hospitalized with the COVID-19 infection, due to the infection’s ability to cause myocardial injury.

Sudden cardiac death is the cause of about half of deaths due to cardiovascular disease and about 15% of all deaths globally.

About 80% of sudden cardiac death is the result of ventricular arrhythmias, which may occur at any age but are more common among older people.

Arrhythmias may also occur in children.

The normal range for the heart rate varies with age.

Classification of arrhythmias may be according to region of heart required to sustain the rhythm.

Arrhythmia may be classified by rate:

tachycardia, bradycardia

By mechanism automaticity, re-entry, triggered

By duration-isolated premature beats; couplets; runs, that is 3 or more beats; non-sustained = less than 30 seconds or sustained= over 30 seconds/

Arrhythmias are also classified by site of origin:

Atrial arrhythmia

Sinus bradycardia

Sinus arrhythmia

Sinus tachycardia

Premature atrial contractions (PACs)

Wandering atrial pacemaker

Atrial tachycardia

Multifocal atrial tachycardia

Supraventricular tachycardia (SVT)

Atrial flutter

Atrial fibrillation (Afib)

AV nodal reentrant tachycardia

Junctional arrhythmia

AV nodal reentrant tachycardia

Junctional rhythm

Junctional tachycardia

Premature junctional contraction

Ventricular arrhythmia

Premature ventricular contractions (PVCs)

Premature ventricular beats occurring after every normal beat are termed ventricular bigeminy

PVCs that occur at intervals of 2 normal beats to 1 PVC, or 1 normal beat to 2 PVCs, are termed PVCs in trigeminy

Groups of three premature ventricular beats are called triplets and are considered a brief run of non-sustained ventricular tachycardia (NSVT); if the grouping lasts for more than 30 seconds, it is considered sustained ventricular tachycardia (VT).

Accelerated idioventricular rhythm

Monomorphic ventricular tachycardia

Polymorphic ventricular tachycardia

Ventricular fibrillation

Torsades de pointes

Arrhythmogenic right ventricular dysplasia

Re-entry ventricular arrhythmia

Heart blocks also known as AV blocks, as the vast majority of them arise from pathology at the atrioventricular node. 

Heart blocks ate the most common causes 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

First, second, and third-degree blocks also can occur at the level of the sinoatrial junction. 

This is referred to as sinoatrial block typically manifesting with various degrees and patterns of sinus bradycardia.

Sudden unexpected death syndrome to describe sudden death because of cardiac arrest occasioned by an arrhythmia in the presence or absence of any structural heart disease on autopsy. 

The most common cause of sudden death in the US is coronary artery disease specifically because of poor oxygenation of the heart muscle, that is myocardial ischemia or a heart attack.

Approximately 180,000 to 250,000 people die suddenly of this cause every year in the US. 

Sudden arrhythmic death may occur from other causes: inherited conditions and heart diseases that can affect young people which can subsequently cause sudden death without advance symptoms. viral myocarditis, long QT syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia, hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia.

Arrhythmias may occur in the fetus.

The normal heart rate of the fetus is between 110 and 160 beats per minute. 

Rhythms beyond these limits is abnormal and are classified as fetal arrhythmia. 

Fetal arrhythmia are mainly the result of premature atrial contractions, usually give no symptoms, and are without consequence. 

However, around one percent of fetal arrhythmias  will be the result of significant structural damage to the heart.

The most common symptom of arrhythmia is an awareness of an abnormal heartbeat, called palpitations. 

Heart palpitations may be infrequent, frequent, or continuous. 

Some of these arrhythmias are harmless.

 Some arrhythmia predispose to adverse outcomes. 

Arrhythmias also cause chest pain and shortness of breath.

Some arrhythmias do not cause symptoms and are not associated with increased mortality. 

Some asymptomatic arrhythmias are associated with adverse events, such as a higher risk of blood clotting within the heart and a higher risk of insufficient blood being transported to the heart, stroke, heart failure, and sudden cardiac death.

If an arrhythmia results in a heartbeat that is too fast, too slow, or too weak to supply the body’s needs, this manifests as lower blood pressure and may cause lightheadedness, dizziness, syncope, loss of consciousness, coma, persistent vegetative state, or brain death due to insufficient supply of blood and oxygen to the brain.

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

Cardiac arrhythmia are caused by one of two major mechanism. 

Enhanced or abnormal impulse formation originating at the pacemaker or the His-Purkinje network. 

The second is due to re-entry conduction disturbances.

Cardiac arrhythmia detection:

auscultation of the heartbeat with a stethoscope, or feeling for peripheral pulses. 

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.

 A Holter monitor is an EKG recorded over a 24-hour period, to detect arrhythmias that may happen briefly and unpredictably throughout the day.

Electrophysiology study is an endovascular procedure that uses a catheter to listen to the electrical activity from within the heart to identify the source of the arrhythmia.

 If the source of the arrhythmia is found the abnormal cells can be ablated and the arrhythmia permanently corrected. 

Transesophageal atrial stimulation (TAS) uses an electrode inserted through the esophagus to a part where the distance to the posterior wall of the left atrium is only approximately 5–6 mm.

Transesophageal atrial stimulation can differentiate between atrial flutter, AV nodal reentrant tachycardia and atrioventricular reentrant tachycardia, and can also evaluate the risk in people with Wolff–Parkinson–White syndrome, as well as terminate supraventricular tachycardia caused by re-entry.

Each heartbeat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node or sinoatrial node (SA node). 

The impulse initially causes both atria to contract, then activates the atrioventricular node (AV node), which is normally the only electrical connection between the atria and the ventricles.

The impulse then spreads through both ventricles via the bundle of His and the Purkinje fibers causing a synchronized contraction of the heart muscle and, thus, the pulse.

The normal resting heart rate ranges from 60 to 90 beats per minute. 

The resting heart rate in children is much faster. 

In athletes, however, the resting heart rate can be as slow as 40 beats per minute.

Sinus arrhythmia refers to the phenomenon of alternating mild acceleration and slowing of the heart rate that occurs with breathing in and out respectively. 

Sinus arrhythmia is usually quite pronounced in children and steadily decreases with age. 

A slow rhythm of less than 60 beats/min is labelled bradycardia. 

This may be caused by a slowed signal from the sinus node,known as sinus bradycardia, or by a pause in the normal activity of the sinus node (sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles, an AV block or heart block.

Heart block comes in varying degrees and severity. 

Heart block may be caused by reversible harm to the AV node with drugs that impair conduction at the AV or by irreversible damage to the node. 

Bradycardias may also be present in the normally functioning heart of endurance athletes or other well-conditioned persons. 

In adults and children over 15, resting heart rate faster than 100 beats per minute is labeled tachycardia. 

Tachycardia may result in palpitation.

Tachycardia is not necessarily an arrhythmia, a an increased heart rate is a normal response to physical exercise or emotional stress. 

Heart rate is mediated by the sympathetic nervous system on the sinus node and called sinus tachycardia. 

Other conditions that increase sympathetic nervous system activity in the heart include ingested or injected substances, such as caffeine or amphetamines, hyperthyroidism or anemia.

Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normal cardiac cycle. 

Such abnormal impulses can begin by one of three mechanisms: 

automaticity, re-entry, or triggered activity. 

A specialized form of re-entry is  fibrillation.

Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. 

Wolff–Parkinson–White syndrome is due to an extra pathway in the heart that is made up of electrical muscle tissue. 

This electrical muscle tissue allows the electrical impulse, which stimulates the heartbeat.

Right ventricular outflow tract tachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals, where a defect is due to an electrical node in the right ventricle just before the pulmonary artery. 

When this electrical node is stimulated, ventricular tachycardia will result, which does not allow the heart to fill with blood before beating again. 

Long QT syndrome is an independent factor in mortality.

Automaticity refers to a cardiac muscle cell firing off an impulse on its own. 

All of the cells in the heart have the ability to initiate an action potential, but, only some of these cells are designed to routinely trigger heartbeats. 

Such cells are found in the conduction system of the heart and include the SA node, AV node, Bundle of His, and Purkinje fibers. 

The sinoatrial node is a specialized location in the atrium that has a higher automaticity than the rest of the heart and.

The sinoatrial node is usually responsible for setting the heart rate and initiating each heartbeat.

A heart  that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus and is a pathological phenomenon. 

This may cause a single premature beat 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.

Such arrhythmias 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 different timing than usual and can be responsible for poorly coordinated contraction.

Automaticity is increased by sympathetic nervous system stimulation and hypoxia. 

The  heart rhythm that occurs 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 may follow..

Re-entrant arrhythmias occur when an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping.

All cardiac cells can transmit impulses of excitation in every direction but will do so only once within a short time. 

Normally, the action potential impulse will spread through the heart quickly enough that each cell will respond only once. 

If there is an essential heterogeneity of refractory period or if conduction is abnormally slow in some areas, part of the impulse will arrive late and potentially be treated as a new impulse: this can produce a sustained abnormal circuit rhythm.

Re-entry vortices of excitation in the myocardium are considered to be the main mechanism of life-threatening cardiac arrhythmias.

Autowave reverberator is common in the thin walls of the atria, sometimes resulting in atrial flutter. 

Re-entry is also responsible for most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia. 

Re-entry circuits differ from WPW syndromes, which utilize abnormal conduction pathways.

Omega-3 fatty acids from fish oil can facilitate re-entrant arrhythmias.

When a chamber of the heart is involved in multiple micro-re-entry circuits it quivers with chaotic electrical impulses, and 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 not typically a medical emergency.

If left untreated, ventricular fibrillation can lead to death within minutes. 

With aV-fib, effective pumping of the blood stops, and it is considered a form of cardiac arrest. 

An affected individual will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.

Defibrillation is the only intervention that can restore a healthy heart rhythm. 

Defibrillation is performed by applying an electric shock to the heart, which resets the cells, permitting a normal beat to re-establish itself.

Triggered beats occur at the level of the ion channels in individual heart cells result in abnormal propagation of electrical activity and can lead to a sustained abnormal rhythm. 

Triggered beats relatively rare and can result from the action of anti-arrhythmic drugs, or after depolarizations.

Management of arrhythmias depends on whether the affected person is stable or unstable. 

Treatments may include physical maneuvers, medications, electricity conversion, or electro- or cryo-cautery.

Certain physical acts can increase parasympathetic nervous supply to the heart, resulting in blocking of electrical conduction through the AV node, which can slow down or stop several arrhythmias that originate above or at the AV node.

Parasympathetic nervous supply to the heart is via the vagus nerve.

Such maneuvers are collectively known as vagal maneuvers.

Classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes are  efficacious.

Nearly every antiarrhythmic drug has the potential to act as a pro-arrhythmic.

Several  drugs slow conduction through the heart, without preventing an arrhythmia, and are used to control a fast rhythm and make it physically tolerable for the patient.

Some arrhythmias promote blood clotting within the heart, increasing the risk of embolus and stroke. 

Anticoagulant medications and anti-platelet drugs such as aspirin can reduce the risk of clotting.

Arrhythmias may also be treated electrically: applying a shock across the heart – either externally to the chest wall, or internally to the heart via implanted electrodes.

Cardioversion is achieved pharmacologically or via the application of a shock synchronized to the underlying heartbeat. 

It can be used for the treatment of supraventricular tachycardias. 

Defibrillation differs in that the shock is not synchronized. 

Defibrillation 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.

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

Electrical treatment of arrhythmias includes cardiac pacing. 

Temporary pacing may be necessary for reversible causes of bradycardia.

A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover.

Electrophysiology uses fine probes inserted through the blood vessels to map electrical activity from within the heart. 

This allows abnormal areas of conduction to be located and subsequently destroyed by heat, cold, electrical, or laser probes in a process called catheter ablation.

This procedure may be completely curative for some forms of arrhythmia, but for others, the success rate remains disappointing.

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