Tachycardia: Difference between revisions

Pathophysiology:

Clinical diagnosis:

Management:

Pathophysiology:

Atrial tachycardia (AT) is a tachycardia resulting from fast firing in an ectopic focus or micro re-entry circuit in the atria.<cite>8</cite> 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.

Clinical diagnosis:

====Atrial Flutter (AFTAFL)====

Pathophysiology:

Atrial flutter (AFTAFL) is the most common type of atrial tachycardia. The Ttypical AFTAFL is dependent of the cavotricuspid isthmus.<cite>8</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 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.<cite>14</cite> The causes and risk are comparable with atrial fibrillation.

Clinical diagnosis:

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%).<cite>6</cite><cite>7</cite><cite>9</cite><cite>15</cite>

Management:

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.<cite>16</cite><cite>17</cite><cite>18</cite> 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.<cite>19</cite><cite>20</cite><cite>21</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 AFTAFL require anti-coagulation as in atrial fibrillation according to the CHADSVASc score.[22, 23]

Pathophysiology:

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.<cite>29</cite>

Clinical diagnosis:

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.<cite>30</cite> 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.<cite>31</cite> 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.<cite>32</cite> AF is classified according to the clinical presentation of AF:<cite>33</cite>

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.<cite>34</cite> Another option is ibutilide, but this is mostly used and more effective to terminate AFTAFL, and has a small risk of ventricular arrhythmias.<cite>18</cite> In patients with severe structural heart disease amiodarone can be given.<cite>35</cite> 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.