Cardiac dysrhythmia

Cardiac dysrhythmia (also known as arrhythmia or irregular heartbeat) is any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. The heartbeat may be too fast or too slow, and may be regular or irregular. A heart beat that is too fast is called tachycardia and a heart beat that is too slow is called bradycardia. 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-threatening medical emergencies and can result in cardiac arrest. Cardiac arrythmias are one of the most common causes of death when travelling to a hospital. 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/ventricular fibrillation, wire faults, and other technical or mechanical issues in cardiac pacemakers/defibrillators. Still others may not be associated with any symptoms at all, but may predispose the patient to potentially life threatening stroke or embolism. 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 decreases with age. This can also be present during meditation breathing exercises that involve deep inhaling and breath holding patterns. Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic 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

Arrhythmia may be classified by rate (normal sinus 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 ICD-9 MeSH I49.1 427.61 D018880

Premature atrial contractions (PACs), also known as atrial premature complexes (APC) or atrial premature beats (APB), are a commoncardiac dysrhythmia characterized by premature heartbeats originating in the atria. While the sinoatrial node typically regulates the heartbeat duringnormal sinus rhythm, PACs occur when another region of the atria depolarizes before 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

if the atrial beat is premature enough. the associated P wave appears different from those seen in normal sinus rhythm. it may reach the atrioventricular node during its refractory period. . although medications such as beta blockers can reduce the frequency of symptomatic PACs.[citation needed] In otherwise healthy people PACs usually disappear with adolescence. but occasionally they cause a sensation of palpitations. Diagnosis Premature atrial contractions are typically diagnosed with an electrocardiogram. Typically. no treatment other than reassurance is needed for PACs. the atrial impulse propagates normally through the atrioventricular node and into the cardiac ventricles. PACs are characterized by an abnormally shaped P wave. In most cases. in which case it will not be conducted to the ventricle and there will be no QRS complex following the P wave.These are usually gone by the end of third decade. However. Holter monitor. in patients with other underlying structural heart problems. Rarely. Electrocardiogram On an electrocardiogram (EKG).people without heart disease.[1][2] PACs are often completely asymptomatic and may be noted only with Holter monitoring. PACs can trigger a more serious arrhythmia such as atrial flutter or atrial fibrillation. narrow QRS complex. or cardiac event monitor. resulting in a normal. occasional premature atrial contractions are a common and normal finding and do not indicate any particular health risk. and by themselves are not considered an abnormal finding. Since the premature beat initiates outside the sinoatrial node. Prognosis In otherwise healthy patients.

nervousness and feelings of impending doom. nausea and. nocturnal breathlessness. or may be asymmetrical with a "sawtooth" shape. however.Atrial flutter Atrial flutter Classification and external resources Atrial flutter with varying A-V conduction (3:1 and 4:1) Atrial flutter (AFL) is an abnormal heart rhythm that occurs in the atria of the heart. it does rarely persist for months to years. its onset is often marked by characteristic sensations of regular palpitations. While this rhythm occurs most often in individuals with cardiovascular disease (e. resembling p-waves. coronary artery disease. If atrial flutter is suspected clinically but is not clearly evident on ECG.g. chest pains. acquiring a Lewis lead ECG may be helpful in revealing flutter waves. This may manifest as effort intolerance (exertional breathlessness). . Prolonged fast flutter may lead to decompensation with loss of normal heart function (heart failure). hypertension. it is usually associated with a fast heart rate or tachycardia (beats over 100 per minute).[2] and falls into the category of supra-ventricular tachycardias. it may occur spontaneously in people with otherwise normal hearts. and cardiomyopathy) and diabetes. which can include shortness of breath. or swelling of the legs or abdomen. in some patients.[1] When it first occurs. rising gradually and falling abruptly or vice versa. and frequently degenerates into atrial fibrillation (AF). Atrial flutter is usually well tolerated initially (a high heart rate is for most people just a normal response to exercise). lightheadedness or dizziness. Such sensations usually last until the episode resolves. Atrial flutter is recognized on an electrocardiogram by presence of characteristic flutter waves at a regular rate of 240 to 440 beats per minute. However. or until the heart rate is controlled. Atrial flutter was first identified as an independent medical condition in 1920 by the British physician Sir Thomas Lewis (1881–1945) and colleagues. Individual flutter waves may be symmetrical. It is typically not a stable rhythm.[3] Signs and symptoms While atrial flutter can sometimes go unnoticed. people with other underlying heart disease or poor exercise tolerance may rapidly develop symptoms.

this rate may be slowed by antiarrhythmic agents. If the flutter rate is 300/minute only half of these impulses will be conducted. for the example of a resting heart rate. there results an electric impulse that propagates through the atria. atrial flutter is propagated due to differences in refractory periods of atrial tissue. The impact and symptoms of atrial flutter depend on the heart rate of the patient. Due primarily to its longer refractory period.[4] Most individuals with atrial flutter will manifest only one of these. Typically initiated by a premature electrical impulse arising in the atria. Rarely someone may manifest both types. Heart rate is a measure of the ventricular rather than atrial activity. However. For each cycle around the loop. Classification There are two types of atrial flutter. also known as common atrial flutter or typical atrial flutter. This creates electrical activity that moves in a localized self-perpetuating loop. Impulses from the atria are conducted to the ventricles through the atrio-ventricular node. giving a ventricular rate of 150/minute. the common type I and rarer type II. the AV node exerts a protective effect on heart rate by blocking atrial impulses in excess of about 180 beats/minute. has an atrial rate of 240 to 340 beats/minute. or a 2:1 heart block. (This block is dependent on the age of the patient. and can be calculated roughly by subtracting patient age from 220). however. Type I Type I atrial flutter. The addition of rate-controlling drugs or conduction system disease can increase this block substantially (see image below). counterclockwise rotation with 3:1 and 4:1 AV nodal block. Type I atrial flutter. . they can only manifest one type at a time.Pathophysiology Atrial flutter is caused by a reentrant rhythm in either the right or left atrium.

passing through the cavo-tricuspid isthmus a body of fibrous tissue in the lower atrium between the inferior vena cava. Conversely. usually 340-440 beats/minute. Ablation of the isthmus. thus the flutter waves are upright in II. and the tricuspid valve. III.   Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen. The flutter waves in this rhythm are inverted in ECG leads II. atrial flutter should be managed the same as atrial fibrillation. and usually requires a lower energy shock. prevents the recurrence of the atrial flutter. Ablation Because of the reentrant nature of atrial flutter. known as counterclockwise atrial flutter and clockwise atrial flutter depending on the direction of current passing through the loop. and often deteriorates into atrial fibrillation prior to spontaneous return to sinus rhythm. and aVF.[5] Left atrial flutter is common after incomplete left atrial ablation procedures. there are some specific considerations particular to treatment of atrial flutter. as discussed above. and if successful. it is relatively resistant to chemical cardioversion. Additionally. and aVF. The re-entry loop cycles in the opposite direction in clockwise atrial flutter. it is often possible to ablate the circuit that causes atrial flutter.The reentrant loop circles the right atrium. Cardioversion Atrial flutter is considerably more sensitive to electrical direct-current cardioversion than atrial fibrillation. Catheter ablation of the isthmus is a procedure usually available in the electrophysiology laboratory. Complications . Eliminating conduction through the isthmus prevents reentry. Type II Type II flutter follows a significantly different re-entry pathway to type I flutter. III. Management In general. and is typically faster. 20-50J is commonly enough to revert to sinus rhythm. Type I flutter is further divided into two subtypes. This is done in the electrophysiology lab by causing a ridge of scar tissue that crosses the path of the circuit that causes atrial flutter. is a common treatment for typical atrial flutter. individuals with atrial flutter usually require some form of anticoagulation or anti-platelet agent. Because both rhythms can lead to the formation of thrombus in the atria. Both rhythms can be associated with dangerously fast heart rate and thus require medication for rate and or rhythm control.

There is paucity of published data directly comparing the two. runs lasting longer than three beats are generally referred to as ventricular tachycardia       Accelerated idioventricular rhythm Monomorphic Ventricular tachycardia Polymorphic ventricular tachycardia Ventricular fibrillation . but overall mortality in these conditions appears to be very similar.[ Junctional arrhythmias   Supraventricular tachycardia (SVT) AV nodal reentrant tachycardia is the most common cause of Paroxysmal Supraventricular 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". atrial flutter shares the same complications as the related condition atrial fibrillation.Although often regarded as a relatively benign rhythm problem.

Ventricular fibrillation is the most commonly identified arrhythmia in cardiac arrest patients.[1] While there is some activity. Despite considerable research. the underlying nature of ventricular fibrillation is still not completely understood. Such an arrhythmia is only confirmed by electrocardiography. the patient could sustain irreversible brain damage and possibly become brain dead due to the effects of cerebral hypoxia. The ventricular muscle twitches randomly rather than contracting in a coordinated fashion (from the apex of the heart to the outflow of the ventricles). it will likely degenerate further into asystole ("flatline"). On the other hand. Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world. death often occurs if normal sinus rhythm is not restored within 90 seconds of the onset of VF. As a consequence. While most episodes occur in diseased hearts. If this arrhythmia continues for more than a few seconds. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature). and so the ventricles fail to pump blood into the arteries and systemic circulation. and it is mostly caused by ischemic heart disease. sudden cardiac death (SCD) will result in a matter of minutes.Ventricular fibrillation Ventricular fibrillation Classification and external resources 12-lead ECG of ventricular fibrillation Ventricular fibrillation (V-fib or VF) is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart. This condition results in cardiogenic shock and cessation of effective blood circulation. Signs and symptoms Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. the lay person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. making them quiver rather than contract properly. especially if it has degenerated further into asystole. . others can afflict normal hearts as well.

Re-entry The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. The ionic basic automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV. Ventricular excitability may generate re-entry ventricular arrhythmia. a hyperpolarizing effect is lost and therefore there can be activation of funny current even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). the subsequent waves of depolarisation would pass around the ring. The product of a hypoxic myocardium can be hyperirritable myocardial cells. if a ring of excitable tissue was stimulated at a single point. Cellular depolarisation can be due to a raised external concentration of potassium ions K+. Normal cells may be exposed to hyperkalaemia. It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential. The ventricles are then being stimulated by more than one pacemaker.Cause Abnormal automaticity Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. the increased external K+ concentration. the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current. They were both able to show that. if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path. Myocardial cells are exposed to different environments.[2] When myocardial cell are exposed to hyperkalemia. increased permeability to Na+. it is necessary that there . In conditions such as myocardial ischaemia. This can lead to the instauration of automaticity in ischemic tissue. whose intensity and direction is strictly dependant on intracellular and extracellular potassium concentrations. Garrey cut out a similar ring from the turtle ventricle. then a selfsustaining circus movement phenomenon would result. the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Scar and dying tissue is inexcitable. a decreased intracellular concentration of sodium ions Na+. however. possible mechanism of arrhythmia generation include the resulting decreased internal K+ concentration. These may then act as pacemakers. For example. abnormal cells may be perfused by normal environment. with a healed myocardial infarction. abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia. but. For this to happen. or a decreased permeability to K+.[3] Mines created a ring of excitable tissue by cutting the atria out of the ray fish. That is. With Ik1 suppressed. The waves eventually meet and cancel each other out. norepinephrine release and acidosis.

be some form of non-uniformity. In addition.[4] Ventricular fibrillation most commonly occurs within diseased hearts. Ventricular fibrillation is also seen in those with cardiomyopathy. and. It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. It is evident that there are mechanisms at work that .[5] It follows then that. factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation. disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape. on the basis of the fact that ventricular fibrillation itself is common.[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. myocarditis. idiopathic ventricular fibrillation accounts for an appreciable mortality. In the Brugada syndrome. 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. 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. and other heart pathologies. in the vast majority of cases. and 14% of all ventricular fibrillation resuscitations in patients under the age of 40. magnitude and direction". or underlying scar tissue. Recently-described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias. Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-ofhospital arrest. this may be an area of ischaemic or infarcted myocardium. changes may be found in the resting ECG with evidence of right bundle branch block (RBBB) and ST elevation in the chest leads V1-V3. drugs which alter the length of the refractory period and areas of cardiac disease. with an underlying propensity to sudden cardiac death. In clinical practice. Pathophysiology Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et al. the so-called idiopathic ventricular fibrillation. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront. 1964). it is seen with electrolyte disturbances and overdoses of cardiotoxic drugs. as well as 3%-9% of the cases of ventricular fibrillation unrelated tomyocardial infarction. a short refractory period with a sufficient size of ring of conduction tissue. therefore. In practice. is a manifestation of underlying ischemic heart disease. A more complete definition is that ventricular fibrillation is a "turbulent. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause. Factors that promote re-entry would include a slow-propagation velocity. the substrate of ventricular fibrillation is transient or permanent conduction block. Therefore.

they can trigger another afterdepolarisation. Triggered activity Triggered activity can occur due to the presence of afterdepolarisations. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). as well as in imaging and acoustics.e. and thus self-perpetuate. This can be expressed as either the dominant or peak frequency. in Brugada Syndrome. such as amplitude and frequency.[8] Analysis of the fibrillation waveform is performed using a mathematical technique known as Fourier analysis. 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.we do not fully appreciate and understand. In certain forms of long QT syndrome. including analysis of heart rate variability and assessment of cardiac function. Gray has suggested an underlying mechanism for the frequency of the waveform that has puzzled investigators as possibly being a manifestation of the Doppler effect of rotors of fibrillation.[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.. the potassium inward rectifier channel is affected. More recently. For example. [9][10] . All waveforms can be described in terms of certain features. Frequency analysis has many other uses in medicine and in cardiology. Characteristics of the ventricular fibrillation waveform Ventricular fibrillation can be described in terms of its electrocardiographic waveform appearance. if they do. All afterdepolarisations may not reach threshold potential. the frequency with the greatest power or the median frequency. sodium channels are affected. 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. These are depolarising oscillations in the membrane voltage induced by preceding action potentials. i. 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. but. which divides the spectrum in two halves.

research has shown that the precordial thump releases no more than 30 joulesof energy[citation needed]. and. a precordial thump can be delivered at the onset of VF for a small chance to regain cardiac function. the use of an implantable cardioverter defibrillator has been shown to be beneficial.[12] During ventricular fibrillation. and its effects can be dramatic. . However. but.cardiac output drops to zero. or "heart attack". death usually ensues within minutes. Antiarrhythmic agents Antiarrhythmic agents like amiodarone or lidocaine can help. but is sometimes needed in cases where initial defibrillation attempts are not successful. ventricular fibrillation rarely reverses spontaneously in large adult mammals. this treatment is not used. it is not always successful. unless remedied promptly. Drug therapy with antiarrhythmic agents in ventricular fibrillation does not replace defibrillation and is not the first priority. and survival rates are only 2%. in the hospital setting. This is far less than the 200–360 J typically used to bring about normal sinus rhythm.Treatment Defibrillation Electric defibrillator The condition can often be reversed by the electric discharge of direct current from a defibrillator. unlike atrial fibrillation.000 to 90.[11] The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction.000 sudden cardiac deaths each year in the United Kingdom. Epidemiology Sudden cardiac arrest is the leading cause of death in the industrialised world. Although a defibrillator is designed to correct the problem. A precordial thump may only be delivered if a cardiac arrest is witnessed (someone sees the patient arrest) and if the arrest is monitored (as seen on a cardiac monitor). Implantable electric defibrillator In patients at high risk of ventricular fibrillation. Consequently. Precordial thump If no defibrillator is available. It exacts a significant mortality with approximately 70.

The most common symptom of arrhythmia is an abnormal awareness of heartbeat. or continuous. Sudden unexpected death syndrome) used to describe sudden death due to cardiac arrest brought on by an arrhythmia in the absence of any structural heart disease on autopsy. SADS SADS. long QT syndrome. and are not associated with increased mortality. Catecholaminergic polymorphic ventricular tachycardia.[A: 1] Signs and symptoms The term cardiac arrhythmia covers a very large number of very different conditions. is a term (as part of . also known as Mobitz I or Wenckebach Type 2 Second degree heart block. or sudden arrhythmic death syndrome. SADS occurs from other causes. hypertrophic cardiomyopathy andarrhythmogenic right ventricular dysplasia. Causes of SADS in young people include viral myocarditis. There are many inherited conditions and heart diseases that can affect young people and subsequently cause sudden death. Some arrhythmias do not cause symptoms. which manifests as PR prolongation Second degree heart block   Type 1 Second degree heart block. some asymptomatic arrhythmias are associated with adverse . They are the most common causes of bradycardia:   First degree heart block. also known as Mobitz II  Third degree heart block. Many of these victims have no symptoms before dying suddenly. The most common cause of sudden death in the US is coronary artery disease.000 people die suddenly of this cause every year in the US. Brugada syndrome.000 to 250. Some of these arrhythmias are harmless (though distracting for patients) but many of them predispose to adverse outcomes.[citation needed] Approximately 180. because the vast majority of them arise from pathology at the atrioventricular node. frequent. also known as complete heart block.HEART BLOCKS These are also known as AV blocks. However. called palpitations. These may be infrequent.

The impulse initially causes both atria to contract. Other increased risks are of embolisation and stroke. Note that the P wave that disrupts the pause (indicated by . 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. thus. 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 right atrium of the heart called the sinus node or Sino-atrial node or SA node. heart failure and sudden cardiac death. In athletes though. Medical assessment of the abnormality using an electrocardiogram is one way to diagnose and assess the risk of any given arrhythmia. then activates the atrioventricular (or AV) node which is normally the only electrical connection between the atria and the ventricles (main pumping chambers). If an arrhythmia results in a heartbeat that is too fast. this manifests as a lower blood pressure and may cause lightheadedness or dizziness. Bradycardias Normal sinus rhythm. and be considered as normal. The impulse then spreads through both ventricles via the Bundle of His and the Purkinje fibres causing a synchronised contraction of the heart muscle and. followed by a pause in sinus node activity (resulting in a transient loss of heart beats). the resting heart rate can be as slow as 40 beats per minute. In adults the normal resting heart rate ranges from 60 to 80 beats per minute. Some types of arrhythmia result in cardiac arrest. the pulse. too slow or too weak to supply the body's needs. or sudden death. or syncope (fainting). with solid black arrows pointing to normal P waves representative of normal sinus node function. The resting heart rate in children is much

and an overactive thyroid gland (hyperthyroidism). or by blocking of the electrical impulse on its way from the atria to the ventricles (AV block or heart block). representing an escape rhythm. is labelled bradycardia. Bradycardias may also be present in the normally functioning heart of endurance athletes or other wellconditioned persons. This may be caused by a slowed signal from the sinus node (sinus bradycardia). resting heart rate faster than 100 beats/minute is labelled tachycardia. which stimulates the heartbeat. however. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node.[B: 2] Heart defects causing tachycardia Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. Tachycardias In adults and children over 15. A slow rhythm (less than 60 beats/min). Increased heart rate is a normal response to physical exercise or emotional stress. Tachycardia may result in palpitation.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. basis for the classification of arrhythmias are still being discussed. tachycardia is not necessarily an arrhythmia. Although the term "tachycardia" is known over one hundred year. Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normal cardiac cycle. reentry or triggered activity. This tissue allows the electrical impulse. 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. Other things that increase sympathetic nervous system activity in the heart include ingested or injected substances. to happen very rapidly. Abnormal impulses can begin by one of three mechanisms: automaticity. This is mediated by the sympathetic nervous system on the sinus node and called sinus tachycardia. a pause in the normal activity of the sinus node (sinus arrest). such as caffeine or amphetamines. Right Ventricular Outflow Tract Tachycardia is the most common type of ventricular . A specialised form of re-entry problem is termed fibrillation. Wolf-Parkinson-White syndrome is due to an extra pathway in the heart that is made up of electrical muscle tissue. Heart block comes in varying degrees and severity.

All of the cells in the heart have the ability to initiate an action potential. These cells are found in the conduction system of the heart and include the SA node. or by theatrioventricular node. or.tachycardia in otherwise healthy individuals. or altering your lifestyle to have less stress and exercise.[A: 2][A: 3] . medication treatment. Rhythms produced by an ectopic focus in the atria. by definition. There are multiple methods of treatment for these including cardiac ablations. When the node is stimulated. but they can still produce a decrease in the heart's pumping efficiency. The resulting heart rhythm depends on where the first signal begins: If it is the sinoatrial node. Long QT Syndrome is another complex problem in the heart and has been labeled as an independent factor in mortality. is usually responsible for setting the heart rate and initiating each heart beat. which does not allow the heart to fill with blood before beating again. AV node. a pathological phenomenon. The sinoatrial node is a single specialized location in the atrium which has a higher automaticity (a faster pacemaker) than the rest of the heart and. if it is an ectopic focus. It is possible to live a full and happy life with these conditions. rather than moving from one end of the heart to the other and then stopping. however. therefore. only some of these cells are designed to routinely trigger heart beats. This defect is due to an electrical node in the right ventricle just before the pulmonary artery. it can produce a sustained abnormal rhythm. many types of dysrhythmia may ensue. the patient will go into ventricular tachycardia. are the least dangerous dysrhythmias. if the ectopic focus fires more often than the sinoatrial node. Re-entry Re-entrant arrhythmias occur when an electrical impulse recurrently travels in a tight circle within the heart. Automaticity Automaticity refers to a cardiac muscle cell firing off an impulse on its own. 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 include sympathetic nervous system stimulation and hypoxia. This may cause a single premature beat now and then. Bundle of His and Purkinje fibers. the rhythm remains normal but rapid. Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus and is.

V-fib is considered a form of cardiac arrest. It is not typically a medical emergency. Depending on the timing. When a heart goes into V-fib. Normally. ventricular fibrillation (VF. theautowave reverberator is a typical in thin walls of the atria. part of the impulse will arrive late and potentially be treated as a new impulse. Defibrillation is . with the atrial flutter producing. CPR can prolong the survival of the brain in the lack of a normal pulse. If left untreated. and dangerousventricular tachycardia. fish oil can worsen the arrhythmia. These types of re-entry circuits are different from WPW syndromes in which the real pathways existed.[A: 4] Fibrillation When an entire chamber of the heart is involved in a multiple micro-reentry circuits and. but defibrillation is the only intervention that can restore a healthy heart rhythm. effective pumping of the blood stops. [B: 1] In particular. However. Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation). the action potential impulse will spread through the heart quickly enough that each cell will only respond once. known as the atria. therefore. if there is some essential heterogeneity of refractory period or 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.  Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart. An individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately. Re-entry are also responsible for most paroxysmal supraventricular tachycardia. or V-fib) can lead to death within minutes.Every cardiac cell is able to transmit impulses of excitation in every direction but will only do so once within a short time.  Atrial fibrillation affects the upper chambers of the heart. in the case of re-entrant arrhythmias. this can produce a sustained abnormal circuit rhythm. Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by a physician. ventricular fibrillation is imminently life-threatening. As a sort of re-entry. Although omega-3 fatty acids from fish oil can be protective against arrhythmias. it is said to be in fibrillation. quivering with chaotic electrical impulses. it is always a medical emergency. the vortices of excitation in the myocardium (autowave vortices) is considered to be the main mechanism of life-threatening cardiac arrhythmias.

This can be accomplished in an Electrophysiology study. often the abnormal cells can be ablated and the arrhythmia can be permanently corrected. Diagnostic approach Cardiac dysrhythmias are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope. but can give a general indication of the heart rate and whether it is regular or irregular. Management The method of cardiac rhythm management depends firstly on whether or not the affected person is stable or unstable. See early and delayed Afterdepolarizations. This can slow down or stop a number of arrhythmias that originate above or at the AV node (see main . Triggered beats 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 sustained abnormal rhythm. They are relatively rare and can result from the action of antiarrhythmic drugs. A more advanced study of the heart's electrical activity can be performed to assess the source of the aberrant heart beats. resulting in blocking of electrical conduction through the AV node. Treatments may include physical maneuvers. A minimally invasive procedure that uses a catheter to "listen" to the electrical activity from within the heart. 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). or feeling for peripheral pulses. in many cardiac arrhythmias. additionally if the source of the arrhythmias is found. to detect dysrhythmias that may happen briefly and unpredictably throughout the day. These cannot usually diagnose specific dysrhythmias. permitting a normal beat to re-establish itself. electricity conversion. Physical maneuvers A number of physical acts can increase parasympathetic nervous supply to the heart. Not all the electrical impulses of the heart produce audible or palpable beats. which resets the cells. A Holter monitor is an EKG recorded over a 24-hour period. medications. or electro or cryo cautery.performed by applying an electric shock to the heart.

Often. and these maneuvers are collectively known as vagal maneuvers. the recipient is usually sedated or lightly anesthetized for the procedure. In elective cardioversion. It is used for treatment of supraventricular tachycardias. Some arrhythmias promote blood clotting within the heart. . Defibrillation differs in that the shock is not synchronised. Defibrillation or cardioversion may be accomplished by an implantable cardioverterdefibrillator (ICD). These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for the patient. without actually preventing an arrhythmia. and anti-platelet drugs such asaspirin can reduce the risk of clotting. more electricity is required for defibrillation than for cardioversion. Antiarrhythmic drugs Main article: Antiarrhythmic agents There are many classes of antiarrhythmic medications. In most defibrillation. or internally to the heart via implanted electrodes. Parasympathetic nervous supply to the heart is via the vagus nerve. Other drugs A number of other drugs can be useful in cardiac arrhythmias. and so must be carefully selected and used under medical supervision. Although the goal of drug therapy is to prevent arrhythmia. Cardioversion is either achieved pharmacologically or via the application of a shock synchronised to the underlying heartbeat. by applying a shock across the heart — either externally to the chest wall. with different mechanisms of action and many different individual drugs within these classes.article: supraventricular tachycardias). the recipient has lost consciousness so there is no need for sedation. Anticoagulant medications such as warfarin and heparins. Several groups of drugs slow conduction through the heart. nearly every antiarrhythmic drug has the potential to act as a pro-arrhythmic. It is needed for the chaotic rhythm of ventricular fibrillation and is also used for pulseless ventricular tachycardia. and increase risk of embolus and stroke. Electricity Dysrhythmias may also be treated electrically.

but for others. Temporary pacing may be necessary for reversible causes of very slow heartbeats. In specialised catheter laboratories. and subsequently destroyed with heat. or bradycardia. (for example. A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover. the success rate remains disappointing. cold. electrical or laser probes. This may be completely curative for some forms of arrhythmia. . pulmonary vein isolation).Electrical treatment of dysrhythmia also includes cardiac pacing. from drug overdose or myocardial infarction).g. AV nodal reentrant tachycardia is often curable. Atrial fibrillation can also be treated with this technique (e. 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. but the results are less reliable. Electrical cautery Some cardiologists further sub-specialise into electrophysiology.

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