Cardiac Dysrhythmia W

8/12/2019 Cardiac Dysrhythmia W

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Cardiac dysrhythmia

Cardiac dysrhythmia(also known as arrhythmiaor irregular heartbeat) is any of a

large and heterogeneous group of conditions in which there is abnormalelectrical

activityin theheart.Theheartbeatmay be too fast or too slow, and may be regular orirregular. A heart beat that is too fast is calledtachycardiaand a heart beat that is too

slow is calledbradycardia.Although many arrhythmias are not life-threatening, some

can cause cardiac arrest.

Arrhythmias can occur in the upper chambers of the heart, (atria), or in the lower

chambers of the heart, (ventricles). Arrhythmias may occur at any age. Some are barely

perceptible, whereas others can be more dramatic and can even lead to sudden cardiac

death.[1]

Some arrhythmias are life-threateningmedical emergenciesand can result incardiacarrest.Cardiac arrythmias are one of the most common causes of death when travelling

to ahospital.Others cause symptoms such as an abnormal awareness of heart beat

(palpitations)and may be merely uncomfortable. These palpitations have also been

known to be caused by atrial/ventricularfibrillation,wire faults, and other technical or

mechanical issues in cardiacpacemakers/defibrillators.Still others may not be

associated with any symptoms at all, but may predispose the patient to potentially life

threateningstrokeorembolism.

The termsinus arrhythmiarefers to a normal phenomenon of mild acceleration andslowing of the heart rate that occurs with breathing in and out. 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.Proarrhythmiais a new or more frequent occurrence of pre-existing

arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is

aside effectassociated with the administration of some existingantiarrhythmic drugs,

as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic

drugs to facilitate emergence of new arrhythmias. Some arrhythmias are minor and can

be regarded as normal variants. In fact, most people will on occasion feel their heart

skip a beat or give an occasional extra strong beat; neither of these is usually a cause

for alarm.[2]

Classification
https://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttps://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttps://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttps://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttps://en.wikipedia.org/wiki/Hearthttps://en.wikipedia.org/wiki/Hearthttps://en.wikipedia.org/wiki/Hearthttps://en.wikipedia.org/wiki/Cardiac_cyclehttps://en.wikipedia.org/wiki/Cardiac_cyclehttps://en.wikipedia.org/wiki/Cardiac_cyclehttps://en.wikipedia.org/wiki/Tachycardiahttps://en.wikipedia.org/wiki/Tachycardiahttps://en.wikipedia.org/wiki/Tachycardiahttps://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Atrium_(heart)https://en.wikipedia.org/wiki/Atrium_(heart)https://en.wikipedia.org/wiki/Atrium_(heart)https://en.wikipedia.org/wiki/Ventricleshttps://en.wikipedia.org/wiki/Ventricleshttps://en.wikipedia.org/wiki/Ventricleshttps://en.wikipedia.org/wiki/Sudden_cardiac_deathhttps://en.wikipedia.org/wiki/Sudden_cardiac_deathhttps://en.wikipedia.org/wiki/Sudden_cardiac_deathhttps://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-2https://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-2https://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-2https://en.wikipedia.org/wiki/Medical_emergencieshttps://en.wikipedia.org/wiki/Medical_emergencieshttps://en.wikipedia.org/wiki/Medical_emergencieshttps://en.wikipedia.org/wiki/Cardiac_arresthttps://en.wikipedia.org/wiki/Cardiac_arresthttps://en.wikipedia.org/wiki/Cardiac_arresthttps://en.wikipedia.org/wiki/Cardiac_arresthttps://en.wikipedia.org/wiki/Hospitalhttps://en.wikipedia.org/wiki/Hospitalhttps://en.wikipedia.org/wiki/Hospitalhttps://en.wikipedia.org/wiki/Palpitationshttps://en.wikipedia.org/wiki/Palpitationshttps://en.wikipedia.org/wiki/Palpitationshttps://en.wikipedia.org/wiki/Fibrillationhttps://en.wikipedia.org/wiki/Fibrillationhttps://en.wikipedia.org/wiki/Fibrillationhttps://en.wikipedia.org/wiki/Pacemakerhttps://en.wikipedia.org/wiki/Pacemakerhttps://en.wikipedia.org/wiki/Defibrillatorshttps://en.wikipedia.org/wiki/Defibrillatorshttps://en.wikipedia.org/wiki/Defibrillatorshttps://en.wikipedia.org/wiki/Strokehttps://en.wikipedia.org/wiki/Strokehttps://en.wikipedia.org/wiki/Strokehttps://en.wikipedia.org/wiki/Embolismhttps://en.wikipedia.org/wiki/Embolismhttps://en.wikipedia.org/wiki/Embolismhttps://en.wikipedia.org/wiki/Respiratory_sinus_arrhythmiahttps://en.wikipedia.org/wiki/Respiratory_sinus_arrhythmiahttps://en.wikipedia.org/wiki/Respiratory_sinus_arrhythmiahttps://en.wikipedia.org/wiki/Meditationhttps://en.wikipedia.org/wiki/Meditationhttps://en.wikipedia.org/wiki/Meditationhttps://en.wikipedia.org/wiki/Proarrhythmiahttps://en.wikipedia.org/wiki/Proarrhythmiahttps://en.wikipedia.org/wiki/Proarrhythmiahttps://en.wikipedia.org/wiki/Adverse_effecthttps://en.wikipedia.org/wiki/Adverse_effecthttps://en.wikipedia.org/wiki/Adverse_effecthttps://en.wikipedia.org/wiki/Antiarrhythmic_agenthttps://en.wikipedia.org/wiki/Antiarrhythmic_agenthttps://en.wikipedia.org/wiki/Antiarrhythmic_agenthttps://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-3https://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-3https://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-3https://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-3https://en.wikipedia.org/wiki/Antiarrhythmic_agenthttps://en.wikipedia.org/wiki/Adverse_effecthttps://en.wikipedia.org/wiki/Proarrhythmiahttps://en.wikipedia.org/wiki/Meditationhttps://en.wikipedia.org/wiki/Respiratory_sinus_arrhythmiahttps://en.wikipedia.org/wiki/Embolismhttps://en.wikipedia.org/wiki/Strokehttps://en.wikipedia.org/wiki/Defibrillatorshttps://en.wikipedia.org/wiki/Pacemakerhttps://en.wikipedia.org/wiki/Fibrillationhttps://en.wikipedia.org/wiki/Palpitationshttps://en.wikipedia.org/wiki/Hospitalhttps://en.wikipedia.org/wiki/Cardiac_arresthttps://en.wikipedia.org/wiki/Cardiac_arresthttps://en.wikipedia.org/wiki/Medical_emergencieshttps://en.wikipedia.org/wiki/Cardiac_dysrhythmia#cite_note-2https://en.wikipedia.org/wiki/Sudden_cardiac_deathhttps://en.wikipedia.org/wiki/Sudden_cardiac_deathhttps://en.wikipedia.org/wiki/Ventricleshttps://en.wikipedia.org/wiki/Atrium_(heart)https://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Tachycardiahttps://en.wikipedia.org/wiki/Cardiac_cyclehttps://en.wikipedia.org/wiki/Hearthttps://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttps://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_heart


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Arrhythmia may be classified by rate (normalsinus rhythm,tachycardia,bradycardia)or

mechanism (automaticity, reentry, junctional,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)

Premature atrial contraction

Premature atrial contraction

Classification and external resources

Two PACs as seen on a rhythm strip

ICD-10 I49.1

ICD-9 427.61

MeSH D018880

Premature atrial contractions(PACs), also known as atrial premature

complexes(APC) or atrial premature beats(APB), are a commoncardiacdysrhythmiacharacterized by premature heartbeats originating in theatria.While

thesinoatrial nodetypically regulates the heartbeat duringnormal sinus rhythm,PACs

occur whenanother region of the atria depolarizesbefore the sinoatrial node and thus

triggers a premature heartbeat. The exact cause of PACs is unclear; while several

predisposing conditions exist, PACs commonly occur in healthy young and elderly
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Pathophysiology

Atrial flutter is caused by areentrant rhythmin either the right or left atrium. Typicallyinitiated by a premature electrical impulse arising in the atria, atrial flutter is propagateddue to differences in refractory periods of atrial tissue. This creates electrical activity

that moves in a localized self-perpetuating loop. For each cycle around the loop, thereresults an electric impulse that propagates through the atria.

The impact and symptoms of atrial flutter depend on the heart rate of the patient. Heartrate is a measure of the ventricular rather than atrial activity. Impulses from the atria areconducted to the ventricles through theatrio-ventricular node.Due primarily to its longerrefractory period, the AV node exerts a protective effect on heart rate by blocking atrialimpulses in excess of about 180 beats/minute, for the example of a resting heart rate.(This block is dependent on the age of the patient, and can be calculated roughly bysubtracting patient age from 220). If the flutter rate is 300/minute only half of theseimpulses will be conducted, giving a ventricular rate of 150/minute, or a 2:1heart block.

The addition of rate-controlling drugs or conduction system disease can increase thisblock substantially (see image below).

Classification

There are two types of atrial flutter, the common type Iand rarer type II.[4]Mostindividuals with atrial flutter will manifest only one of these. Rarely someone maymanifest both types; however, they can only manifest one type at a time.

Type I

Type I atrial flutter, counterclockwise rotation with 3:1 and 4:1AV nodalblock.

Type I atrial flutter, also known as common atrial flutteror typical atrial flutter, hasan atrial rate of 240 to 340 beats/minute. However, this rate may be slowed byantiarrhythmic agents.
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The reentrant loop circles the right atrium, passing through thecavo-tricuspid isthmus-a body of fibrous tissue in the lower atrium between the inferior vena cava, and thetricuspid valve. Type I flutter is further divided into two subtypes, known ascounterclockwise atrial flutterand clockwise atrial flutterdepending on the directionof current passing through the loop.

Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is morecommonly seen. The flutter waves in this rhythm are inverted in ECG leads II, III,and aVF.

The re-entry loop cycles in the opposite direction in clockwise atrial flutter, thusthe flutter waves are upright in II, III, and aVF.

Catheter ablation of the isthmus is a procedure usually available in theelectrophysiology laboratory. Eliminating conduction through the isthmus preventsreentry, and if successful, prevents the recurrence of the atrial flutter.

Type II

Type II flutter follows a significantly different re-entry pathway to type I flutter, and istypically faster, usually 340-440 beats/minute.

[5]Left atrial flutter is common after

incomplete left atrial ablation procedures.

Management

In general, atrial flutter should bemanaged the same as atrial fibrillation.Because bothrhythms can lead to the formation ofthrombusin the atria, individuals with atrial flutterusually require some form of anticoagulation or anti-platelet agent. Both rhythms can be

associated with dangerously fast heart rate and thus require medication for rate and orrhythm control. Additionally, there are some specific considerations particular totreatment of atrial flutter.

Cardioversion

Atrial flutter is considerably more sensitive to electrical direct-current cardioversion thanatrial fibrillation, and usually requires a lower energy shock. 20-50J is commonly enoughto revert to sinus rhythm. Conversely, it is relatively resistant to chemical cardioversion,and often deteriorates into atrial fibrillation prior to spontaneous return to sinus rhythm.

Ablation

Because of the reentrant nature of atrial flutter, it is often possible to ablate the circuitthat causes atrial flutter. This is done in the electrophysiology lab by causing a ridge ofscar tissue that crosses the path of the circuit that causes atrial flutter. Ablation of theisthmus, as discussed above, is a common treatment for typical atrial flutter.

Complications
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Although often regarded as a relatively benign rhythm problem, atrial flutter shares thesame complications as the related conditionatrial fibrillation.There is paucity ofpublished data directly comparing the two, but overall mortality in these conditionsappears to be very similar.[

Junctional arrhythmias

Supraventricular tachycardia (SVT)

AV nodal reentrant tachycardiais the most common cause of Paroxysmal Supra-

ventricular Tachycardia (PSVT)

Junctional rhythm

Junctional tachycardia

Premature junctional contraction

Ventricular

Premature Ventricular Contractions (PVC)sometimes called Ventricular Extra Beats

(VEBs)

Premature Ventricular beats occurring after every normal beat are termed

"ventricular bigeminy" PVCs that occur at intervals of 2 normal beats to 1 PVC are termed "PVCs in

trigeminy"

Three premature ventricular grouped together is termed a "run of PVCs"; runs

lasting longer than three beats are generally referred to as ventricular

tachycardia

Accelerated idioventricular rhythm

Monomorphic Ventricular tachycardia

Polymorphic ventricular tachycardia

Ventricular fibrillation
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Classification and external resources

12-leadECGof ventricular fibrillation

Ventricular fibrillation(V-fibor VF) is a condition in which there is uncoordinated contraction of thecardiac

muscleof theventriclesin theheart,making them quiver rather than contract properly. Ventricular fibrillation is

the most commonly identified arrhythmia in cardiac arrest patients.[1]

While there is some activity, the lay

person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral

arteries. Such an arrhythmia is only confirmed byelectrocardiography.Ventricular fibrillation is amedical

emergencythat requires promptAdvanced Life Supportinterventions. If thisarrhythmiacontinues for more than

a few seconds, it will likely degenerate further intoasystole("flatline"). This condition results incardiogenic

shockand cessation of effective bloodcirculation.As a consequence,sudden cardiac death(SCD) will result in

a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room

temperature), the patient could sustain irreversible brain damage and possibly become brain dead due to the

effects of cerebralhypoxia.On the other hand, death often occurs if normalsinus rhythmis not restored within

90 seconds of the onset of VF, especially if it has degenerated further into asystole.

Signs and symptoms

Ventricular fibrillation is a cause ofcardiac arrestandsudden cardiac death.The ventricular muscle twitches

randomly rather than contracting in a coordinated fashion (from the apex of the heart to the outflow of the

ventricles), and so theventriclesfail to pump blood into thearteriesandsystemic circulation.Ventricular

fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, and it is mostly

caused byischemic heart disease.While most episodes occur in diseased hearts, others can afflict normal

hearts as well.

Despite considerable research, the underlying nature of ventricular fibrillation is still not completely understood.
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be some form of non-uniformity. In practice, this may be an area ofischaemicorinfarctedmyocardium, or

underlyingscar tissue.

It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of

the refractory period and the time taken for the dipole to travel a certain distance the propagation velocity

will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would

include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue.

These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with

continuation of thewavefront.

In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms

include increased heart size throughhypertrophyor dilatation, drugs which alter the length of the refractory

period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent

conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for

initiation and perpetuation of fibrillation through the phenomenon of re-entry.

Pathophysiology

Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et

al. 1964). A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity

of the heart in such a way that the recordedelectrocardiographicdeflections continuously change in shape,

magnitude and direction".[4]

Ventricular fibrillation most commonly occurs withindiseasedhearts, and, in the vast majority of cases, is a

manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those

withcardiomyopathy,myocarditis,and other heart pathologies. In addition, it is seen with electrolyte

disturbances and overdoses of cardiotoxic drugs. It is also notable that ventricular fibrillation occurs where

there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.

Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-

hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated tomyocardial infarction,and

14% of all ventricular fibrillation resuscitations in patients under the age of 40.[5]

It follows then that, on the basis

of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an

appreciable mortality. Recently-described syndromes such as theBrugada Syndromemay give clues to the

underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the

restingECGwith evidence ofright bundle branch block(RBBB) and ST elevation in the chest leads V1-V3, with

an underlying propensity to sudden cardiac death.[6]

The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for

the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work that
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we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and

understanding the underlying mechanisms of sudden cardiac death in these patients without pathological

evidence of underlying heart disease.[7]

Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death

are often the result of gene mutations that affect cellular transmembrane ion channels. For example, in

Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium

inward rectifier channel is affected.

Triggered activity

Triggered activity can occur due to the presence ofafterdepolarisations.These are depolarising oscillations in

the membrane voltage induced by preceding action potentials. These can occur before or after full

repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs).

All afterdepolarisations may not reach threshold potential, but, if they do, they can trigger another

afterdepolarisation, and thus self-perpetuate.

Characteristics of the ventricular fibrillation waveform

Ventricular fibrillation can be described in terms of its electrocardiographic waveform appearance. All

waveforms can be described in terms of certain features, such as amplitude and frequency. Researchers have

looked at the frequency of the ventricular fibrillation waveform to see if it helps to elucidate the underlying

mechanism of the arrhythmia or holds any clinically useful information. More recently, Gray has suggested an

underlying mechanism for the frequency of the waveform that has puzzled investigators as possibly being a

manifestation of theDoppler effectof rotors of fibrillation.

[8]

Analysis of the fibrillation waveform is performedusing a mathematical technique known asFourier analysis.

Power spectrum

Ventricular fibrillation as seen in lead II

The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the

contribution of different waveform frequencies to the waveform under analysis is measured. This can be

expressed as either the dominant or peak frequency, i.e., the frequency with the greatest power or the median

frequency, which divides the spectrum in two halves.

Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate

variability and assessment of cardiac function, as well as in imaging and acoustics.[9][10]
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HEART BLOCKS

These are also known asAVblocks, because the vast majority of them arise from

pathology at the atrioventricular node. They are 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 asMobitz IorWenckebach

Type 2 Second degree heart block,also known asMobitz II

Third degree heart block,also known ascomplete heart block.

SADS

SADS, or sudden arrhythmic death syndrome, is a term (as part of , Sudden

unexpected death syndrome)used to describe suddendeathdue tocardiac

arrestbrought on by an arrhythmia in the absence of any structural heart disease on

autopsy. The most common cause of sudden death in the US iscoronary artery

disease.[citation needed]Approximately 180,000 to 250,000 people die suddenly of this

cause every year in the US. SADS occurs from other causes. There are many inherited

conditions and heart diseases that can affect young people and subsequently cause

sudden death. Many of these victims have no symptoms before dying suddenly.

Causes of SADS in young people includeviral myocarditis,long QT syndrome,Brugada

syndrome,Catecholaminergic polymorphic ventricular tachycardia,hypertrophic

cardiomyopathyandarrhythmogenic right ventricular dysplasia.[A: 1]

Signs and symptoms

The term cardiac arrhythmia covers a very large number of very different conditions.

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

calledpalpitations.These may be infrequent, frequent, or continuous. Some of these

arrhythmias are harmless (though distracting for patients) 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 areassociated with adverse
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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 weak heartbeat.

Other increased risks are of embolisation and 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 a lower blood pressure and may cause lightheadedness

or dizziness, or syncope (fainting).

Some types of arrhythmia result incardiac arrest,or sudden death.

Medical assessment of the abnormality using anelectrocardiogramis one way to

diagnose and assess the risk of any given arrhythmia.

Differential diagnosis

Normal electrical activity

Main article:Electrical conduction system of the heart

Each heart beat originates as an electrical impulse from a small area of tissue in the

rightatriumof the heart called thesinus node or Sino-atrial node or SA node.The

impulse initially causes both atria to contract, then activates theatrioventricular (or AV)

nodewhich is normally the only electrical connection between the atria and

theventricles(main pumping chambers). The impulse then spreads through bothventricles via theBundle of Hisand thePurkinje fibrescausing a synchronised

contraction of the heart muscle and, thus, the pulse.

In adults the normal resting heart rate ranges from 60 to 80 beats per minute. The

resting heart rate in children is much faster. In athletes though, the resting heart rate

can be as slow as 40 beats per minute, and be considered as normal.

Bradycardias

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 heart beats). Note that the P wave that disrupts the pause (indicated by
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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), 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.

Tachycardias

In adults and children over 15, resting heart rate faster than 100 beats/minute islabelledtachycardia.Tachycardia may result in palpitation; however, tachycardia is

not necessarilyan arrhythmia. Increased heart rate is a normal response to physical

exercise or emotional stress. This is mediated by thesympathetic nervous systemon

the sinus node and called sinus tachycardia. Other things that increase sympathetic

nervous system activity in the heart include ingested or injected substances, such

ascaffeineoramphetamines,and an overactive thyroid gland (hyperthyroidism).

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, reentry or triggered activity. A specialised form of re-entry

problem is termed fibrillation.

Although the term "tachycardia" is known over one hundred year, basis for the

classification of arrhythmias are still being discussed.[B: 2]

Heart defects causing tachycardia

Congenital heart defects are structural or electrical pathway problems in the heart that

are present at birth. Anyone can be effected with 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. Wolf-Parkinson-White syndrome is 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. Right

Ventricular Outflow Tract Tachycardia is the most common type of ventricular
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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 Syndrome is 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 altering your

lifestyle to have less stress and exercise. It is possible to live a full and happy life with

these conditions.

Automaticity

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 heart beats. 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 which

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 heart beat.

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.

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

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.[A: 2][A: 3]
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Every cardiac cell is able to transmitimpulses of excitationin every direction but will

only do so once within a short time. Normally, theaction potentialimpulse will spread

through the heart quickly enough that each cell will only respond 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 of re-entry, the vortices of excitation in the myocardium (autowave vortices)is

considered to be the main mechanism of life-threatening cardiac arrhythmias.[B: 1]In

particular, theautowave reverberatoris a typical in thin walls of the atria, with theatrial

flutterproducing. Re-entry are also responsible for most paroxysmalsupraventricular

tachycardia,and dangerousventricular tachycardia.These types of re-entry circuits aredifferent fromWPWsyndromes in which the real pathways existed.

Althoughomega-3 fatty acidsfromfish oilcan be protective against arrhythmias, in the

case of re-entrant arrhythmias, fish oil can worsen the arrhythmia.[A: 4]

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 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 individual suffering

from it 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
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performed by applying an electric shock to the heart, which resets the cells, permitting a

normal beat to re-establish itself.

Triggered beats

Triggered beats occur when problems at the level of the ion channels in individual heartcells result in abnormal propagation of electrical activity and can lead to sustained

abnormal rhythm. They are relatively rare and can result from the action of anti-

arrhythmic drugs. See early and delayedAfterdepolarizations.

Diagnostic approach

Cardiac dysrhythmias are often first detected by simple but nonspecific

means:auscultationof the heartbeat with astethoscope,or feeling for

peripheralpulses.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 specificdiagnostic test for assessment of heart rhythm is

theelectrocardiogram(abbreviated ECG or EKG). AHolter monitoris an EKG recorded

over a 24-hour period, to detect dysrhythmias that may happen briefly and unpredictably

throughout the day.

A more advanced study of the heart's electrical activity can be performed to assess the

source of the aberrant heart beats. This can be accomplished in an Electrophysiology

study.A minimally invasive procedure that 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.

Management

The method of cardiac rhythm management depends firstly on whether or not the

affected person is stable or unstable. Treatments may include physical maneuvers,medications, electricity conversion, or 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 arrhythmias that originate above or at the AV node (see main
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Electrical treatment of dysrhythmia 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

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 tachycardiais often curable.

Atrial fibrillation can also be treated with this technique (e.g. pulmonary vein isolation),

but the results are less reliable.
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