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Tachycardia: Difference between revisions
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[[File:overview.png|thumb|300px|'''Figure 1.''' Classification of tachyarrhythmias.<cite>ECGPedia</Cite>]] | [[File:overview.png|thumb|300px|'''Figure 1.''' Classification of tachyarrhythmias.<cite>ECGPedia</Cite>]] | ||
Differentiation between supraventricular tachycardias (SVT) and ventricular tachycardias (VT) can be challenging, especially in acute emergency settings. SVT's are rhythm disturbances in the atria or AV-nodal ring or rhythm disorders in which these structures are involved. Supraventricular arrhythmias are relatively common and rarely life-threatening. VT's are rhythm disorders that only involve the ventricles. | Differentiation between supraventricular tachycardias (SVT) and ventricular tachycardias (VT) can be challenging, especially in acute emergency settings. SVT's are rhythm disturbances in the atria or AV-nodal ring or rhythm disorders in which these structures are involved. Supraventricular arrhythmias are relatively common and rarely life-threatening. VT's are rhythm disorders that only involve the ventricles. VTs can both take place in the myocardial tissue and the conduction system tissue (Figure 1). | ||
=Supra-ventricular tachycardia= | =Supra-ventricular tachycardia= | ||
==Atrial arrhythmias== | ==Atrial arrhythmias== | ||
The following | The following arrhythmia arise in the atrium. Dependent on the refractory period of the AV-node the ventricles follow the atrial contraction. However, at higher atrial rates the AV-node starts to block conduction from atrium to ventricle.<cite>Blomstrom-Lundqvist, ESC</cite> | ||
===Sinus Tachycardia=== | ===Sinus Tachycardia=== | ||
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====Clinical diagnosis:==== | ====Clinical diagnosis:==== | ||
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.<cite>Robles, ECGpedia</cite> An inappropriate sinus tachycardia is diagnosed by when the sinus tachycardia is persistent (therefore non-paroxysmal) and no trigger can be identified. | 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).<cite>Robles, ECGpedia</cite> An inappropriate sinus tachycardia is diagnosed by when the sinus tachycardia is persistent (therefore non-paroxysmal) and no trigger can be identified. | ||
====Management:==== | ====Management:==== | ||
No treatment is indicated | No treatment is indicated; usually the sinustachycardia will pass when the external trigger is removed. If patients have persistent complaints, the trigger cannot be removed or in case of an inappropriate sinus tachycardia a beta-blocker can be administered. Patients with a contra-indication for beta-blockers can use nondihydropyridine calcium-channel blockers. | ||
===Atrial Tachycardia=== | ===Atrial Tachycardia (AT)=== | ||
====Pathophysiology:==== | ====Pathophysiology:==== | ||
Atrial tachycardia (AT) is a tachycardia resulting from fast firing in an ectopic focus or micro- | Atrial tachycardia (AT) is a tachycardia resulting from fast firing in an ectopic focus or micro re-entry circuit in the atria.<cite>Saoudi</cite> It has a 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 atrial flutter is a type of AT, but due to its unique mechanism it is discussed separately. | ||
====Clinical diagnosis:==== | ====Clinical diagnosis:==== | ||
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 | 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.<cite>Robles,Wellens,ECGpedia</cite> | ||
====Management:==== | ====Management:==== | ||
Vagal | Vagal manoeuvres or adenosine can be effective in terminating focal AT.<cite>Markowitz</cite> 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.<cite>Chen1</cite> The treatment of choice for symptomatic AT is catheter ablation. In an experienced centre up to 90% of the ATs can be ablated. Multifocal atrial tachyardia is difficult therapy is usually directed at the management of underlying disease.<cite>Chen2, Anguere</cite> | ||
[[File:atrial arrhythmias.svg|thumb|500px|'''Figure 2.''' The different atrial arrhythmias. Note the differences in P wave morphology or absence of P-waves in case of atrial fibrillation.<cite>ECGPedia</Cite>]] | [[File:atrial arrhythmias.svg|thumb|500px|'''Figure 2.''' The different atrial arrhythmias. Note the differences in P wave morphology or absence of P-waves in case of atrial fibrillation.<cite>ECGPedia</Cite>]] | ||
===Atrial Flutter=== | ===Atrial Flutter (AFT)=== | ||
====Pathophysiology:==== | ====Pathophysiology:==== | ||
Atrial flutter (AFT) is the most common type of atrial tachycardia. The typical | Atrial flutter (AFT) is the most common type of atrial tachycardia. The typical AFT is dependent of the cavotricuspid isthmus.<cite>Saoudi</cite> 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 between 250-350 beats per minute. If the re-entry circuit moves counter clockwise a typical AFT is produced. If the re-entry circuit moves clockwise, a atypical AFT is seen.<cite>Yang</cite> The causes and risk are comparable with atrial fibrillation. | ||
====Clinical diagnosis:==== | ====Clinical diagnosis:==== | ||
An AFT is usually paroxysmal, with a sudden onset, and is diagnosed on the ECG by it typical | An AFT 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 AFT has a frequency of 300 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 AFT 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 part slow (Figure 2). In an atypical AFT the inferior leads have a positive vector. Atrial fibrillation is a common finding in patients with an AFT (up to 35%).<cite>Robles,Wellens,Bochoeyer,ECGpedia</cite> | ||
====Management:==== | ====Management:==== | ||
A patient with an acute episode of AFT 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 AFT more clearly. Anti-arrhythmic drugs are modestly effective in the acute setting (ibutilide or dofetilide), but have the risk of pro-arrhythmic effects.<cite>Volgmann, Singh, Stambler</cite> DC cardioversion is an effective methods to cardiovert AFT, especially in patients with heart failure or hemodynamic instability. AFT is amendable to catheter ablation and this is the treatment of choice in AFT. 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.<cite>Kottkamp, Natale, Chen3</cite> 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 AFT require anti-coagulation as in atrial fibrillation according to the CHADSVASc score.<cite>Dunn, Lip5</cite> | |||
===Atrial Fibrillation=== | ===Atrial Fibrillation (AF)=== | ||
====Pathophysiology:==== | ====Pathophysiology:==== | ||
The pathophysiology of AF is complex and incompletely understood.<cite>Schotten</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>hais</cite> This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (e.i. the autonomic nerve system).<cite>Patterson</cite> These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change an 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.<cite>Wijfels</cite> 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 atrial standstill does not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.<cite>Watson</cite> 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 a irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>Packer</cite> | The pathophysiology of AF is complex and incompletely understood.<cite>Schotten</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>hais</cite> This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (e.i. the autonomic nerve system).<cite>Patterson</cite> These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change an 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.<cite>Wijfels</cite> 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 atrial standstill does not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.<cite>Watson</cite> 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 a irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>Packer</cite> | ||