Tachycardia: Difference between revisions

[[File:overview.png|thumb|300px|'''Figure 1.''' Classification of tachyarrhythmias.<cite>ECGPedia</Cite>]]

The following arrhythmias arise in the atrium. Dependent on the refractory period of the AV-node the ventricles follow the atrial activation at the same rate at higher atrial rates the AV-node starts to block conduction from atrium to ventricle.[2, 3]

When the sinus node fires with a frequency rate between 100-180bpm, the term sinustachycardia is used. The maximum heart rate a person can achieve during exercise can be calculatedbe estimated by subtracting the age in years from 210, although it is not uncommon for sinus rates to peak above 200/min during vigorous exercise. Usually it is a physiological reaction to stress (exercise, inflammation, stress). External factors can increase the heart rate like coffee and alcohol or drugs.[4] The term inappropriate sinus tachycardia is a persistent increase in resting heart rate or sinus rate unrelated to or an exaggerated response to stress in a person without structural heart disease.[5]

A sinus tachycardia usually has a gradual start and ending. Diagnosis on the ECG can be made by the morphology of the P-wave. The P-wave has the same morphology during sinus tachycardia as during normal sinus rhythm (Figure 2).[6, 7] An inappropriate sinus tachycardia is diagnosed by when the sinus tachycardia is persistent (therefore non-paroxysmal) and no trigger can be identified.

Atrial tachycardia (AT) is a tachycardia resulting from fast firing in an ectopic focus or micro re-entry circuit in the atria.[8] It has a rate frequency of above the> 100bpm. In some patients the tachycardia has multiple foci (multifocal atrial tachycardia). This results in different P-wave morphologies on the ECG during the arrhythmia. Atrial tachycardia can be caused by all the mechanisms of arrhythmia formation. Patients after earlier surgery or catheter ablation usually present with macro re-entry AT located around functional or anatomical sides of block. The Aatrial flutter is a distinct type of AT, but due to its unique mechanism it is discussed separately.

ATs have a wide range clinical presentation. They can occur in paroxysms or can be the permanent underlying rhythm. Complaints of palpitation and a fast regular heart rate are common and as a result of the tachycardia complaints of dizziness, dyspnoea and syncope can be experienced. Focal AT that with a progressive increase at onset and decrease before termination are likely based on abnormal automaticity. Digoxine intoxication is a common cause for ATs. On the ECG an atrial tachycardia can be detected through the P-wave morphology. The P-wave has a different morphology depending on the foci of the atrial tachycardia (Figure 2). An ECG in resting condition of sinus rhythm can help distinguish different morphologies and help in localization of the source of the atrial tachycardia. Vagal manoeuvres or administration of adenosine can block the AV-conduction and reveal firing from the atrium, thereby clearly identifying the atrial source of the tachycardia. Some ATs are sensitive to adenosine and will terminate after administration of adenosine. However sometimes only an electrophysiological study can differentiate between the different SVT and localize the precise location or circuit of the AT.[6, 7, 9]

Vagal manoeuvres or adenosine can be effective in terminating focal AT.[10] If AT persist and is drug-resistant DC cardioversion can be indicated. Recurrent episodes of AT can be prevented with anti-arrhythmic medication, for instance with beta-blockers or calcium antagonists. However not all AT are sensitive to medication and success rate of medication is usually low. If these drugs are unsuccessful Class IC in combination with AV-nodal-blocking agents or Class III drugs can be tried.[11] The treatment of choice for symptomatic AT is catheter ablation. In an experienced centre up to 90% of the ATs can be ablated, recurrence rate is relatively high often due to a new focus of AT. Treatment of mMultifocal atrial tachyardia is difficult and therapy is usually directed at the management of underlying disease.[12, 13]

Atrial flutter (AFTAFL) is the most common type of atrial tachycardia. The Ttypical AFTAFL is dependent of the cavotricuspid isthmus.[8] The isthmus between the caval vein and tricuspid is an area of slow conduction. Due to this slow conduction counter clockwise re-entry around the tricuspid annulus can exist. This re-entry produces a typical arrhythmia with activates the atria at a frequency rate between 250-350 beats per minute. If the re-entry circuit moves counter clockwise a typical AFTAFL is produced. If the re-entry circuit moves clockwise, a atypical AFTAFL is seen.[14] The causes and risk are comparable with atrial fibrillation.

An AFTAFL is usually paroxysmal, with a sudden onset, and is diagnosed on the ECG by it typical saw tooth pattern. Patients experience complaints of palpitations, dyspnoea, fatigue or chest pain. An AFTAFL typically has a frequency atrial rate of 280-32300 bpm, which conducts to the ventricles in 2:1, 3:1 or 4:1 manner. The P-wave morphology has a saw tooth like appearance and in a typical AFTAFL has a negative vector in the inferior leads. The upstroke or down stroke of the first part of the P-wave is fast, the second path slow (Figure 2). In an atypical AFTAFL the inferior leads have a positive vector. Atrial fibrillation is a common finding in patients with an AFTAFL (up to 35%).[6, 7, 9, 15]

A patient with an acute episode of AFTAFL requires cardioversion. This can be achieved with anti-arrhythmic drugs or electrical cardioversion. Vagal manoeuvres increase the AV-block on the ECG and demonstrate the AFTAFL more clearly. Anti-arrhythmic drugs are modestly effective in the acute setting (ibutilide or dofetilide) and, but  have the risk of pro-arrhythmic effects.[16, 17, 18] DC cardioversion is an effective methods to cardiovert AFTAFL, especially in patients with heart failure or hemodynamic instability. AFTAFL is amendable to catheter ablation and this is the treatment of choice in AFTAFL. Targeted ablation of the area between the inferior vena cava and the tricuspid annulus can block the re-entry circuit. This is a very successful procedure, with few complications in the hands of an experienced electrophysiologist.[19, 20, 21] If patients are not eligible for ablation, anti-arrhythmic drugs class IC or III can be started. However they are of limited efficacy and class IC drugs not be administered without AV-nodal slowing agent because of atrial slowing can result in 1:1 AV conduction. Patients with AFTAFL require anti-coagulation as in atrial fibrillation according to the CHADSVASc score.[22, 23]

The pathophysiology of AF is complex and incompletely understood.[24] In most patients the trigger of AF results from extra beats in from the pulmonary veins.[25] This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (i.e. the autonomic nerve system).[26] These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change and move through the atria. The ability of the atria to sustain AF is dependable on atrial structural changes (fibrosis/inflammation). AF induces electromechanical changes in the atrium. These changes make it easier for AF to perpetuate: ; AF begets AF.[27] Due to the fast and rapid activation of the atria, there is no functional mechanical activity left. This results in the most feared complication of AF, namely forming of blood clots (with for instance stroke as a result). The During atrial standstill the atria ddoes  not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.[28] The strokes resulting from AF are often more severe than other causes of stroke. Another complication of AF is a tachycardiomyopathy. Due to the constant chaotic activity in the atria, the AV-node can conduct these signals at high rate. The result is an irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.[29]

AF is the most common supraventricular arrhythmia in Western society. Patients can experience complaints from palpitations, dyspnoea and dizziness. Prevalence increases with age and reaches 7-10% in 80 year olds. It is characterized by the absence of clear P-waves on the surface ECG and an irregular ventricular rate (Figure 2). On physical examination an irregular pulse can be felt, however this is not diagnostic of AF as other causes can cause an irregular pulse (mainly atrial or ventricular extra systoles). The cardiac output is 10% reduced due to lack of atrial kick. Furthermore due to the higher ventricular rate the heart has not enough time to completely fill with blood thereby reducing stroke volume. The development of AF is associated with different diseases, e.g. for instance hypertension, mitral valve disease, thyroid disease and diabetes.[30] AF usually starts with short single isolated episodes of AF which are self terminating. Progressively over time these episodes are of longer duration and occur more frequently. These episodes progress to persistent AF, which is defined as AF lasting last longer than 7 days or which can only be terminated by cardioversion. In the end AF is permanent and cardioversion is not possible or duration of sinus rhythm is short.[31] Episodes of AF can be symptomatic, but patients can experience no symptoms during AF. However it is important to note that the risks of complications of AF are unrelated to the duration of the episodes. [32] AF is classified according to the clinical presentation of AF:[33]

? Paroxysmal atrial fibrillation: Episodes AF lasting shorter than 7 days and terminating spontaneously usually within 48 hours.

? Persistent atrial fibrillation: Episodes of AF not terminating spontaneously or lasting longer than 7 days or requires cardioversion

? Long standing persistent atrial fibrillation: Persistent AF for more than one year.

? Permanent atrial fibrillation: Accepted AF, no strategies of rhythm control are pursued.

The acute management of AF depends on the presentation of the patient. In stable patients with little complaints, rate control can be initiated with beta-blockers, non-dihydropyridine Ca-antagonists and digoxine. If the patient has recent onset of AF, is highly symptomatic or hemodynamicly compromised, cardioversion is indicated. Cardioversion can be performed medically or with electricity. The mMost effective drug for chemical cardioversion is flecainide, although this drug is contra-indicated in patients with structural heart disease or ischemia.[34] Another option is ibutilide, but this is mostly used and more effective to terminate AFTAFL, and has a small risk of ventricular arrhythmias.[18] In patients with severe structural heart disease amiodarone can be given.[35] Electrical cardioversion can achieved by a DC shock after sedation of the patient. If the AF persist for longer than >48 hours or the start of the episode is not clear, anti-coagulation should be initiated before (medical or electrical) cardioversion. Three weeks of adequate anti-coagulation is advised before cardioversion and it should be continued after cardioversion for 4 weeks to minimize thromboembolic risk.