Tachycardia: Difference between revisions

Differentiation between supraventricular tachycardias (SVT) and ventricular tachycardias (VT) can be challenging, especially in acute emergency settings. SVT's are arrhythmias in the atria or AV-node or arrhythmias in which these structures are involved. Supraventricular arrhythmias are relatively common and rarely life-threatening. VT's are rhythm disorders that origin from the ventricles. VTs can both take place in the myocardial tissue and the conduction system tissue (Figure 1).

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>6</cite><cite>7</cite> An inappropriate sinus tachycardia is diagnosed by when the sinus tachycardia is persistent (therefore non-paroxysmal) and no trigger can be identified.

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>6</cite><cite>7<cite><cite>9</cite>

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. 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 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>

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! colspan="3" | CHA2DS₂VASc score to estimate stroke risk

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Anticoagluation treatment: Proper anti-coagulation is important in patients with AF to reduce the occurrence of stroke.<cite>28</cite> In patients with AF the indication of anti-coagulation is based on certain patient-related risk-factors. A score is created to facilitate the clinical decision making. The CHADS2VASc2 score incorporates these risk factors. A patient has no indication for anti-coagulation if there is a low-risk of thromboembolic complications.<cite>70</cite><cite>71</cite> These patients are defined as males or females <65 years old with no other risk factors. This translates ins a CHADSVASc score of 0, or a CHADSVASc score of 1, where 1 point is based on the female sex. In all other cases anti-coagulation with coumarins or other new anticoagulation drugs (dabigatran, rivaroxiban, apixaban)<cite>72</cite><cite>73</cite><cite>74</cite> is indicated if no strong bleeding-risk exist. It is important to note that anti-coagulation is independent of the underlying rhythm.

==AV-nodal arrhythmias==

===AV junctional tachycardia===

===Atrioventricular Nodal Reciprocating Tachycardia (AVNRT)===

====Pathophysiology:====

AVNRT is a regular arrhythmia relying on the dual AV-physiology for its maintenance. The AV-node usually has two pathways in these patients; a fast pathway with fast conduction times and a slow pathway, which conducts slowly. The fast pathway has a longer refractory period than the slow pathway. Due to these characteristics re-entry formation is possible. Normally the impulse from the atria is conducted through the fast pathway to the ventricle. The impulse also travels through the slow pathway, but reaches tissue still in the refractory period at the end of the AV-node (as the fast pathway has already conducted the impulse and activated this part of the AV-node). When an extra premature atrial contraction occurs it encounters a refractory fast-pathway (which has a longer refractory period). It enters the slow pathway and when it reaches the end of this pathway it can conduct to the (now restored) end of the AV-node to the ventricles and back up into the fast pathway. The result is a ventricular activation with a retrograde P-wave. If the slow pathway is restored when the impulse reaches the beginning (atrial side) of the fast pathway, the impulse can re-enter the slow-pathway and a re-entry mechanism is established. This is the mechanism of a typical AVNRT, which is found in 90% of the patient with an AVNRT (Figure 3). Two other forms of AVNRT exist that take a different route through the AV-node. Firstly there is an atypical AVNRT in which the impulse travels through the fast pathway and returns through the slow pathway. The result of this AVNRT is a retrograde P-wave which appears far from the QRS complex. Finally there is a rare AVNRT which in patients with two slow pathways. The impulse enters en re-enters through a slow pathway.<cite>6</cite><cite>75</cite><cite>76</cite>

====Clinical diagnosis:====

====Management:====

===AV Re-entry Tachycardia (AVRT)===

====Pathophysiology:====

AVRT are tachycardias with a re-entry circuit comprising the entire heart. The atria, AV-node, ventricles and an extra bundle (accessory pathway, AP) are essential parts of this circuit. The pre-requisite for an AVRT is the existence of an AP between the atrium and the ventricle. This bundle can bypass the AV-node and connect directly to the His bundle, ventricular myocardium or one of the fascicles. Bundles have variety of anatomical locations and can run epicardially.<cite>80</cite><cite>81</cite> The conduction direction of these bundles can be anterograde (atrium-ventricle), retrograde (ventricle-atrium) or bidirectional. Some of the bundles exhibit AV-nodal conduction properties, these are also known as Mahaeim fibres. If a bundle can conduct anterograde at a high rate (a refractory period of <260ms), then a risk of VF exists if the patients develops AF due to fast conduction of fibrillatory activity. Depending on the conduction characteristics of the bundle and the direction of conduction two different AVRT circuits can manifest (Figure 4):

*'''Orthodrome AV re-entry tachycardia:''' The impulse travels through the normal conduction system in the standard direction and returns to the atria via the accessory bundle.

*'''Antidrome AV re-entry tachycardia:''' The impulse travels antrograde through the accessory bundle and activates the ventricles. The impulse returns through the normal conduction system to the atria.

====Clinical diagnosis:====

*'''Orthodrome AV re-entry tachycardia:''' There is a P-wave (other morphology than sinus rhythm) followed by a narrow QRS-complex

*'''Antidrome AV re-entry tachycardia:''' This is a wide-complex tachycardia, where the wide QRS complex is followed by a retrograde P-wave originating from the AV-node.

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