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Arrhythmia

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Arrhythmia
Other namesCardiac arrhythmia, heart arrhythmia, dysrhythmia, irregular heartbeat
Ventricular fibrillation(VF) showing disorganized electrical activity producing a spiked tracing on anelectrocardiogram(ECG)
SpecialtyCardiology
SymptomsPalpitations,dizzinessorlightheadedness,passing out,shortness of breath,chest pain,[1]decreased level of consciousness
ComplicationsStroke,heart failure[2][3]
Usual onsetOlder age[4]
TypesExtra beats,supraventricular tachycardias,ventricular arrhythmias,bradyarrhythmias[3]
CausesProblems with theelectrical conduction system of the heart[2]
Diagnostic methodElectrocardiogram,Holter monitor[5]
TreatmentMedications, medical procedures (pacemaker), surgery[6]
FrequencyMillions[4]

Arrhythmias,also known ascardiac arrhythmias,are irregularities in theheartbeat,including when it is too fast or too slow.[2]A restingheart ratethat is too fast – above 100 beats per minute in adults – is calledtachycardia,and a resting heart rate that is too slow – below 60 beats per minute – is calledbradycardia.[2]Some types of arrhythmias have nosymptoms.[1]Symptoms, when present, may includepalpitationsor feeling a pause between heartbeats.[1]In more serious cases, there may belightheadedness,passing out,shortness of breath,chest pain,ordecreased level of consciousness.[1]While most cases of arrhythmia are not serious, some predispose a person to complications such asstrokeorheart failure.[2][3]Others may result insudden death.[3]

Arrhythmias are often categorized into four groups:extra beats,supraventricular tachycardias,ventricular arrhythmiasandbradyarrhythmias.[3]Extra beats includepremature atrial contractions,premature ventricular contractionsandpremature junctional contractions.[3]Supraventricular tachycardias includeatrial fibrillation,atrial flutterandparoxysmal supraventricular tachycardia.[3]Ventricular arrhythmias includeventricular fibrillationandventricular tachycardia.[3][7]Bradyarrhythmias are due tosinus node dysfunctionoratrioventricular conduction disturbances.[8]Arrhythmias are due to problems with theelectrical conduction system of the heart.[2]A number of tests can help with diagnosis, including anelectrocardiogram(ECG) andHolter monitor.[5]

Many arrhythmias can be effectively treated.[2]Treatments may include medications, medical procedures such as inserting apacemaker,and surgery.[6]Medications for a fast heart rate may includebeta blockers,orantiarrhythmic agentssuch asprocainamide,which attempt to restore a normal heart rhythm.[6]This latter group may have more significant side effects, especially if taken for a long period of time.[6]Pacemakers are often used for slow heart rates.[6]Those with an irregular heartbeat are often treated withblood thinnersto reduce the risk of complications.[6]Those who have severe symptoms from an arrhythmia or are medically unstable may receive urgent treatment with acontrolled electric shockin the form ofcardioversionordefibrillation.[6]

Arrhythmia affects millions of people.[4]In Europe and North America, as of 2014, atrial fibrillation affects about 2% to 3% of the population.[9]Atrial fibrillation and atrial flutter resulted in 112,000 deaths in 2013, up from 29,000 in 1990.[10]However, in most recent cases concerning the 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.[11]Sudden cardiac deathis the cause of about half of deaths due tocardiovascular diseaseand about 15% of all deaths globally.[12]About 80% of sudden cardiac death is the result of ventricular arrhythmias.[12]Arrhythmias may occur at any age but are more common among older people.[4]Arrhythmias may also occur in children; however, the normal range for the heart rate varies with age.[3]

Classification[edit]

Broad classification of arrhythmias according to region of heart required to sustain the rhythm

Arrhythmia may be classified by rate (tachycardia,bradycardia), mechanism (automaticity, re-entry, triggered) or duration (isolatedpremature beats;couplets; runs, that is 3 or more beats; non-sustained = less than 30 seconds or sustained= over 30 seconds).[citation needed]

Arrhythmias are also classified by site of origin:[citation needed]

Atrial arrhythmia[edit]

Junctional arrhythmia[edit]

Ventricular arrhythmia[edit]

Heart blocks[edit]

These are also known asAVblocks, because the vast majority of them arise from pathology at theatrioventricular node.They are the most common causes of bradycardia:[citation needed]

First, second, and third-degree blocks also can occur at the level of the sinoatrial junction. This is referred to assinoatrial blocktypically manifesting with various degrees and patterns ofsinus bradycardia.[citation needed]

Sudden arrhythmic death syndrome[edit]

Sudden arrhythmic death syndrome(SADS), is a term used as part ofsudden unexpected death syndrometo describe suddendeathbecause ofcardiac arrestoccasioned 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 iscoronary artery diseasespecifically because of poor oxygenation of the heart muscle, that ismyocardial ischemiaor aheart attack[15]Approximately 180,000 to 250,000 people die suddenly of this cause every year in the US. SADS may occur from other causes. There are many inherited conditions and heart diseases that can affect young people which can subsequently cause sudden death without advance symptoms.[16]

Causes of SADS in young people includeviral myocarditis,long QT syndrome,Brugada syndrome,Catecholaminergic polymorphic ventricular tachycardia,hypertrophic cardiomyopathyandarrhythmogenic right ventricular dysplasia.[17][18]

Fetal arrhythmia[edit]

Arrhythmias may also occur in thefetus.[19]The normal heart rate of the fetus is between 110 and 160 beats per minute. Any rhythm beyond these limits is abnormal and classed as a fetal arrhythmia. These are mainly the result of premature atrial contractions, usually give no symptoms, and have little consequence. However, around one percent of these will be the result of significant structural damage to the heart.[19]

Signs and symptoms[edit]

The term cardiac arrhythmia covers a very large number of very different conditions.[citation needed]

The most common symptom of arrhythmia is an awareness of an abnormal heartbeat, calledpalpitations.These may be infrequent, frequent, or continuous. Some of these arrhythmias are harmless (thoughdistractingfor patients) but some of them predispose to adverse outcomes. Arrhythmias also causechest painandshortness of breath.[citation needed]

Some arrhythmias do not cause symptoms and are not associated with increased mortality. However, some asymptomatic arrhythmiasareassociated with adverse events. Examples include a higher risk of blood clotting within the heart and a higher risk of insufficient blood being transported to the heart because of a weak heartbeat. Other increased risks are ofembolizationand stroke, heart failure, and sudden cardiac death.[citation needed]

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.[20]

Some types of arrhythmia result incardiac arrest,or sudden death.[citation needed]

Medical assessment of the abnormality using anelectrocardiogramis one way to diagnose and assess the risk of any given arrhythmia.[citation needed]

Mechanism[edit]

Cardiac arrhythmia are caused by one of two major mechanism. The first of arrhythmia is a result of enhanced or abnormalimpulseformation originating at thepacemakeror theHis-Purkinjenetwork. The second is due tore-entryconduction disturbances.[21]

Diagnostic[edit]

Cardiac arrhythmia is often first detected by simple but nonspecific means:auscultationof the heartbeat with astethoscope,or feeling for peripheralpulses.These cannot usually diagnose specific arrhythmia 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.[citation needed]

The simplestspecificdiagnostic test for assessment of heart rhythm is theelectrocardiogram(abbreviated ECG or EKG).[22][23]AHolter monitoris an EKG recorded over a 24-hour period, to detect arrhythmias that may happen briefly and unpredictably throughout the day.[citation needed]

A more advanced study of the heart's electrical activity can be performed to assess the source of theaberrantheart beats. This can be accomplished in anelectrophysiology study,anendovascular procedurethat uses a catheter to "listen" to the electrical activity from within the heart, additionally if the source of the arrhythmias is found, often the abnormal cells can be ablated and the arrhythmia can be permanently corrected.Transesophageal atrial stimulation(TAS) instead uses an electrode inserted through theesophagusto a part where the distance to the posterior wall of theleft atriumis only approximately 5–6 mm (remaining constant in people of different age and weight).[24]Transesophageal atrial stimulation can differentiate betweenatrial flutter,AV nodal reentrant tachycardiaand orthodromicatrioventricular reentrant tachycardia.[25]It can also evaluate the risk in people withWolff–Parkinson–White syndrome,as well as terminatesupraventricular tachycardiacaused byre-entry.[25]

Differential diagnosis[edit]

Normal electrical activity[edit]

Each heartbeat originates as an electrical impulse from a small area of tissue in the rightatriumof the heart called thesinus node or sinoatrial node (SA node).The impulse initially causes both atria to contract, then activates theatrioventricular node (AV node),which is normally the only electrical connection between the atria and theventricles(main pumping chambers). The impulse then spreads through both ventricles via thebundle of Hisand thePurkinje fiberscausing a synchronized contraction of the heart muscle and, thus, the pulse.[citation needed]

In adults, 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, and be considered normal.[citation needed]

The termsinus arrhythmia[26]refers to a normal phenomenon of alternating mild acceleration and slowing of the heart rate that occurs with breathing in and out respectively. It is usually quite pronounced in children and steadily decreases with age. This can also be present duringmeditationbreathing exercises that involve deep inhaling and breath holding patterns.[27]

Bradycardias[edit]

Normal sinus rhythm, with solid black arrows pointing to normal P waves representative of normal sinus node function, followed by a pause in sinus node activity (resulting in a transient loss of heartbeats). Note that the P wave that disrupts the pause (indicated by the dashed arrow) does not look like the previous (normal) P waves – this last P wave is arising from a different part of the atrium, representing an escape rhythm.

A slow rhythm (less than 60 beats/min) is labelledbradycardia.This may be caused by a slowed signal from the sinus node (sinus bradycardia), 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 (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. Bradycardias may also be present in the normally functioning heart of endurance athletes or other well-conditioned persons. Bradycardia may also occur insome types of seizures.[citation needed]

Tachycardias[edit]

In adults and children over 15, resting heart rate faster than 100 beats per minute is labeledtachycardia.Tachycardia may result in palpitation; however, tachycardia is notnecessarilyan arrhythmia. Increased heart rate is a normal response to physical exercise or emotional stress. This is mediated by thesympathetic nervous systemon thesinus nodeand called sinus tachycardia. Other conditions that increase sympathetic nervous system activity in the heart include ingested or injected substances, such ascaffeineoramphetamines,and an overactive thyroid gland (hyperthyroidism) oranemia.[citation needed]

Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normalcardiac cycle.Abnormal impulses can begin by one of three mechanisms: automaticity, re-entry, or triggered activity. A specialized form of re-entry which is both common and problematic is termed fibrillation.[citation needed]

Although the term "tachycardia" has been known for over 160 years, bases for the classification of arrhythmias are still being discussed.[citation needed]

Heart defects[edit]

Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. Anyone can be affected by this because overall health does not play a role in the problem. Problems with the electrical pathway of the heart can cause very fast or even deadly arrhythmias.Wolff–Parkinson–White syndromeis due to an extra pathway in the heart that is made up of electrical muscle tissue. This tissue allows the electrical impulse, which stimulates the heartbeat, to happen very rapidly. Rightventricular outflow tracttachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals. This defect is due to an electrical node in the right ventricle just before the pulmonary artery. When the node is stimulated, the patient will go into ventricular tachycardia, which does not allow the heart to fill with blood before beating again.Long QT syndromeis another complex problem in the heart and has been labeled as an independent factor in mortality. There are multiple methods of treatment for these including cardiac ablations, medication treatment, or lifestyle changes to have less stress and exercise.[citation needed]

Automaticity[edit]

Automaticity refers to acardiac musclecell firing off an impulse on its own. All of the cells in the heart have the ability to initiate anaction potential;however, only some of these cells are designed to routinely trigger heartbeats. These cells are found in the conduction system of the heart and include the SA node, AV node, Bundle of His, and Purkinje fibers. Thesinoatrial nodeis a single specialized location in the atrium that has a higher automaticity (a faster pacemaker) than the rest of the heart and, therefore, is usually responsible for setting the heart rate and initiating each heartbeat.[citation needed]

Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called anectopicfocus and is, by definition, a pathological phenomenon. This may cause a single premature beat now and then, or, if theectopic focusfires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by theatrioventricular 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 different timing than usual and can be responsible for poorly coordinated contraction.[citation needed]

Conditions that increase automaticity includesympathetic nervous systemstimulation andhypoxia.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 may ensue.

Re-entry[edit]

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.[28][29]

Every cardiac cell can transmitimpulses of excitationin every direction but will do so only once within a short time. Normally, theaction potentialimpulse will spread through the heart quickly enough that each cell will respond only once. However, if there is some essential heterogeneity ofrefractory periodor if conduction is abnormally slow in some areas (for example in heart damage) so the myocardial cells are unable to activate the fast sodium channel, part of the impulse will arrive late and potentially be treated as a new impulse. Depending on the timing, this can produce a sustained abnormal circuit rhythm.

As a sort ofre-entry,vortices of excitation in the myocardium (autowave vortices) are considered to be the main mechanism of life-threatening cardiac arrhythmias.[30]In particular, theautowave reverberatoris common in the thin walls of the atria, sometimes resulting inatrial flutter.Re-entry is also responsible for mostparoxysmal supraventricular tachycardia,and dangerousventricular tachycardia.These types of re-entry circuits are different fromWPWsyndromes, which utilize abnormal conduction pathways.

Althoughomega-3 fatty acidsfromfish oilcan be protective against arrhythmias, they can facilitate re-entrant arrhythmias.[31]

Fibrillation[edit]

When an entire chamber of the heart is involved in multiple micro-re-entry circuits and is, 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 affects the upper chambers of the heart, known as theatria.Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by aphysician.It is not typically a medical emergency.
  • Ventricular fibrillation occurs in theventricles(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 ofcardiac arrest.An affected individual will not survive unlesscardiopulmonary resuscitation(CPR) anddefibrillationare provided immediately.

CPR can prolong the survival of thebrainin the lack of a normal pulse, but 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[edit]

Triggered beats occur when problems 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. They are relatively rare and can result from the action of anti-arrhythmic drugs, or afterdepolarizations.[citation needed]

Management[edit]

The method of cardiac rhythm management depends firstly on whether the affected person is stable or unstable. Treatments may include physical maneuvers, medications, electricity conversion, or electro- or cryo-cautery.[citation needed]

In the United States, people admitted to the hospital with cardiac arrhythmia and conduction disorders with and without complications were admitted to the intensive care unit more than half the time in 2011.[32]

Physical maneuvers[edit]

Several 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 several arrhythmias that originate above or at the AV node (see main article:supraventricular tachycardias). Parasympathetic nervous supply to the heart is via thevagus nerve,and these maneuvers are collectively known asvagal maneuvers.

Antiarrhythmic drugs[edit]

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 apro-arrhythmic,and so must be carefully selected and used under medical supervision.

Other drugs[edit]

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 the patient.[citation needed]

Some arrhythmias promote blood clotting within the heart and increase the risk of embolus and stroke.Anticoagulantmedications such aswarfarinandheparins,and anti-platelet drugs such asaspirincan reduce the risk of clotting.

Electricity[edit]

Arrhythmias 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.[33]

Cardioversionis either achieved pharmacologically or via the application of a shocksynchronizedto the underlying heartbeat. It is used for the treatment of supraventricular tachycardias. In elective cardioversion, the recipient is usually sedated or lightlyanesthetizedfor the procedure.

Defibrillationdiffers in that the shock is not synchronized. 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 animplantable cardioverter-defibrillator(ICD).

Electrical treatment of arrhythmias also includescardiac pacing.Temporary pacing may be necessary for reversible causes of very slow heartbeats, orbradycardia(for example, fromdrug overdoseormyocardial infarction). A permanentpacemakermay be placed in situations where the bradycardia is not expected to recover.

Electrical cautery[edit]

Some cardiologists further sub-specialize into electrophysiology. In specializedcatheter 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 by heat, cold, electrical, or laser probes in a process calledcatheter ablation.

This procedure may be completely curative for some forms of arrhythmia, but for others, the success rate remains disappointing.AV nodal reentrant tachycardiais often curable by ablating one of the pathways in theAV node(usually the slow pathway).Atrial fibrillationcan also be treated, by performing apulmonary veinisolation, but the results are less reliable.

Research[edit]

Arrhythmias due to medications have been reported since the 1920s with the use ofquinine.[34]In the 1960s and 1970s problems with antihistamines and antipsychotics were discovered.[34]It was not until the 1980s that the underlying issue,QTc prolongationwas determined.[34]Osborn wavesonelectrocardiogram(ECG) are frequent duringtargeted temperature management (TTM)aftercardiac arrest,particularly in patients treated with 33 °C.[35]Osborn wavesare not associated with increased risk ofventricular arrhythmia,and may be considered abenignphysiological phenomenon, associated with lowermortalityin univariable analyses.[35]

See also[edit]

References[edit]

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