Tachycardia

Sébastien Krul, MD, Louise Olde Nordkamp, MD, Jonas de Jong, MD

Introduction

Figure 1. Classification of tachyarrhythmias.[1]

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).

Supra-ventricular tachycardia

Atrial arrhythmias

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]

Sinus Tachycardia

Pathophysiology:

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]

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 (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.

Management:

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 (AT)

Pathophysiology:

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 of ≥ 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. Atrial flutter is a distinct type of AT, but due to its unique mechanism it is discussed separately.

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 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]

Management:

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 multifocal atrial tachyardia is difficult and therapy is usually directed at the management of underlying disease.[12][13]

Atrial Flutter (AFL)

Figure 2. The different atrial arrhythmias. Note the differences in P wave morphology or absence of P-waves in case of atrial fibrillation.[1]

Pathophysiology:

Atrial flutter (AFL) is the most common type of atrial tachycardia. The typical AFL 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 rate between 250-350 beats per minute. If the re-entry circuit moves counter clockwise a typical AFL is produced. If the re-entry circuit moves clockwise, a atypical AFL is seen.[14] The causes and risk are comparable with atrial fibrillation.

Clinical diagnosis:

An AFL 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 AFL typically has an atrial rate of 280-320 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 AFL 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 AFL the inferior leads have a positive vector. Atrial fibrillation is a common finding in patients with an AFL (up to 35%).[6][7][9][15]

Management:

A patient with an acute episode of AFL 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 AFL 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 AFL, especially in patients with heart failure or hemodynamic instability. AFL is amendable to catheter ablation and this is the treatment of choice in AFL. 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 AFL require anti-coagulation as in atrial fibrillation according to the CHADSVASc score.[22][23]

Atrial Fibrillation (AF)

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). During atrial standstill the atria does 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]

Classification of Atrial Fibrillation (AF) related symptoms based on the European Heart Rhythm Association (EHRA) score are: [30]
EHRA I	No symptoms
EHRA II	Mild symptoms; normal daily activity not affected
EHRA III	Severe symptoms; normal daily activity affected
EHRA IV	Disabling symptom; normal daily activity discontinued

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. hypertension, mitral valve disease, thyroid disease and diabetes.[31] 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.[32] 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.[33] AF is classified according to the clinical presentation of AF:[34]

• 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.

Management:

Acute Management:

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 most effective drug for chemical cardioversion is flecainide, although this drug is contra-indicated in patients with structural heart disease or ischemia.[35] Another option is ibutilide, but this is mostly used and more effective to terminate AFL, and has a small risk of ventricular arrhythmias.[18] In patients with severe structural heart disease amiodarone can be given.[36] 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.

Long-Term Management:

The management of AF consists of several key targets. Firstly, any underlying potential reversible cause of AF should be treated. Secondly, care should be taken to prevent the complications of AF. This means that adequate oral-anticoagulation should be initiated and rate control should be started to reduce heart rate. Thirdly, symptoms should be treated with medical or invasive therapy. There are two strategies to reduce symptoms of AF. Rate control is a strategy where a reduction of ventricular heart rate is the main goal. In rhythm control the aim is to maintain sinus rhythm and prevent recurrences of AF.[34] [37]

Rate control:

In AF the ventricle can have a fast irregular rate that can lead to complaints of palpitations and a tachycardiomyopathy. One of the strategies in managing AF is to control ventricular rate <110bpm.[38][39] In patients with persistent complaints or with heart failure a resting heart rate of <80 is advised. In this strategy no attempt is made to achieve sinus rhythm. This is the only treatment option in patients with permanent AF. Due to the fast irregular ventricular rate a dilated tachycardiomyopathy can develop and proper rate control can revert these ventricular changes. Rate control can be achieved with beta-blockers or non-dihydropyridine Ca-antagonists. Digoxine can be added to rate control, however a recent study showed an increase in mortality in patients using digoxine.[40] If rate control cannot be achieved with drugs, His ablation after pacemaker implant is indicated.

• His-Ablation with pacemaker implantation:

Patients with accepted AF and complaints of a high irregular ventricular rate who do not tolerate medication can be helped with a targeted His bundle ablation with catheter ablation to induce complete AV-block. Before His ablation a pacemaker should be implanted to assure an adequate ventricular rate and response to exercise.

Rhythm control:

In rhythm control all efforts are made to achieve and maintain sinus rhythm. This can be done with anti-arrhythmic drugs. Most effective are the Class IC and III anti-arrhythmic drugs.[41] Overall rhythm control is difficult and anti-arrhythmic drugs might have (pro-arrhythmic) side effects, if patients have contra-indications.[42][43] Therefore prescription of these drugs should occur with caution. If patients experience serious side effects of anti-arrhythmic drugs or have a low frequency of AF episodes a one month treatment with anti-arrhythmic drugs (especially flecainide combined with beta blocker or non-dihydropiridine calcium antagonist) after cardioversion can prevent the majority of recurrences.[44] Amiodarone is unsuitable for short-term treatment due to its pharmacological properties.[45]

Invasive treatment:[46]

Catheter ablation:

Medical therapy is not always sufficient to maintain sinus rhythm. In the last decade of 20th century it was discovered that AF is triggered from the pulmonary veins and that selective ablation of these trigger sites can reduce AF recurrence.[47] As this technique evolved it is now common to ablate an area around the pulmonary veins to isolate them from the atrial tissue. The left atrium is approached through the inter-atrial septum and with the use of imaging and electrocardiographic signals a 3D map is made to navigate the atria. The pulmonary vein isolation can be performed with multiple energy sources (cryo-cooling, radiofrequent energy). This is a complex procedure that depending on the technique used has a minor chance of (severe) complications (1-5%), primarily caused by damage of the surrounding structures. The one year success rate of the procedure varies on the experience of the operator and is a freedom of AF in 57-71% of the patients after one or more procedures.[48][49] Catheter ablation is suitable for patients with a with drug-refratory rhythm control strategy.[50] Certain selected patients with heart failure might benefit from catheter ablation, although success is lower.[51][52]

Surgical treatment:

Surgery is a more invasive, but effective modality to treat AF. The classical cut and sew Maze procedure is an open chest procedure that requires extra-corporeal circulation. In this procedure the atrium is cut and sewn again to compartmentalize the atrium en therefore prevent the atrium maintaining AF.[53][54] In recent years a less invasive procedure has developed to treat AF. This minimal invasive surgery is performed through thoracotomy or thoracoscopy and is performed on a beating heart.[55] A pulmonary vein isolation is performed with a clamp and if patients have persistent AF additional left atrial lesions are made on the atrium to compartmentalize the atrium. Finally the left atrial appendage is removed to reduce the occurrence of stroke. This procedure has a success rate of 68% after one year.[56][57][58] Recently hybrid surgical procedures have been described that combine the minimal invasive thoracoscopic surgery with (epicardial or endocardial) elektrophysiological measurement. Patients with a large left atrium (diameter>45mm) or a failed catheter ablation are eligible for AF surgery.[59][60]

Studies have shown no benefit of rhythm control over rate control, thus the selection of strategy is mainly dependent of patient and AF characteristics.[38][61][62][63][64][65][66] Patients with AF and heart failure have limited medical options of rate control, as most anti-arrhythmic drugs are contra-indicated, and no benefit of rate vs. rhythm control was detected in studies.[67][68] This means that, since rate control is easier to achieve, rate control should be the initial strategy in all patients, especially in old patients and patients with no or few symptoms of AF. The target heart rate to achieve in rest is <110 beats per minute.[69] In patients with persistent complaints of AF rhythm control can be initiated on top of rate control. Young patients with paroxysmal AF and no underlying heart disease might benefit from early (invasive) rhythm control to halt progression of the disease.[70] However, independent of the treatment strategy, proper anti-coagulation is important and necessary in patients with risk factors.[34][37]

CHA2DS2VASc score to estimate stroke risk
	Risk Factor	Points
C:	Congestive heart failure	1 point
H:	Hypertension	1 point
A:	Age>75years	2 point
D:	Diabetes	1 point
S:	Stroke/Embolism	2 points
V:	Vascular Disease	1 point
A:	Age>65years	1 point
Sc:	Female Sex	1 point

Anticoagluation treatment:

Proper anti-coagulation is important in patients with AF to reduce the occurrence of stroke.[28] 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.[71][72] 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)[73][74][75] 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

This section covers the arrhythmias in which the AV-node is critical in maintaining the arrhythmia. Most of these arrhythmias share the common characteristic that AV-node blocking or delaying manoeuvres or medication (adenosine) can terminate the arrhythmia.[2][3]

AV junctional tachycardia

An AV junctional tachycardia is a tachycardia resulting from regular frequent firing (110-250 bpm) of the AV-node. It has the characteristics of a small QRS with a retrograde or no P-wave. The P-wave is not always visible because it can be hidden in the QRS complex. If it is visible it is negative in the inferior leads and narrow, suggesting an AV-nodal origin. The small QRS is not preceded by a p-wave as atrium and ventricle are both activated from the AV-node. For management of this arrhythmia variable success is achieved with anti-arrhythmic drugs.

Atrioventricular Nodal Reciprocating Tachycardia (AVNRT)

Figure 3. The mechanism of AV-nodal re-entry.[1]

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.[6][76][77]

Clinical diagnosis:

It is a fast regular small complex tachycardia with a rate of 180-250 bpm. It is more common in women than in men (3:1) and has a sudden onset. Palpitations are experienced due to the fast regular heartbeat. The Frog sign can be observed; neck vein pulsations which occur due to simultaneous contraction of the atria and ventricles. The atria cannot empty into the ventricles and therefore expulse their contents into the venous circulation. A typical AVNRT can be diagnosed on the ECG by a RP distance of ≤ 100ms, resulting in a P wave hidden in the QRS complex or appearing directly after the QRS complex. An atypical AVNRT has a retrograde P appearing far away from the QRS, as it has to travel through the slow pathway. A registration of the onset can often be quite helpful in establishing the diagnosis AVNRT.[6][9]

Management:

Termination of acute episodes is possible by vagal manoeuvres (blowing on the wrist, carotid sinus massage) or medication (adenosine, verapamil, diltiazem).[78] If vagal manoeuvres or medication fail ECV can be performed. Catheter ablation can be the treatment of first choice in AVNRT. Electrophysiological studies can demonstrate dual AV-node physiology and evoke the arrhythmia in these patients. Selective ablation of the slow pathway has a high success rate (up to 98%) and the risk of inducing AV-block is low (<0,5%).[79] Long term medical therapy can be initiated in patients not suitable for catheter ablation, or who do not desire a catheter ablation. Calcium channel blocker, beta-blockers and digoxin are used as first option or in a pill in the pocket approach.[80] Other options are class IC or class III anti-arrhythmic drugs.

AV Re-entry Tachycardia (AVRT)

Figure 4. An example of orthodrome AVRT and antidrome AVRT. Note the differences in the direction of the arrhythmia.[1]

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.[81][82] 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:

If an accessory bundle excites the ventricle earlier than normal AV-conduction, thus has antegrade conduction properties, and can activate the ventricles, pre-excitation is visible on the ECG. Pre-excitation can be visible on the ECG by a shortened PQ interval and a widened QRS complex due to slurring of the initial part of the QRS complex (delta wave). This is also called the Wolf-Parkinson-White symptom and can occur intermittently. If a patient has pre-excitation and complaints of arrhythmia caused by an AVRT the combination of these two is called the Wolf-Parkinson-White syndrome.[83] Some patient have an AVRT, but no traces of pre-excitation. The bundle is then called a concealed bundle, which only conduct in one direction: from ventricles to atria. Patients can be asymptomatic if they only have pre-excitation and this ECG pattern is commonly an incidental finding.[6][9] When an arrhythmia develops using the AP, both types of AVRT can develop depending on the conduction characteristics of the bundle:

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.

Management:

The circuit of the arrhythmia uses the AV-node; therefore vagal maneuvers are able to terminate the AVRT. However adenosine should be used with care, as it may induce AF and cause 1:1 conduction.[84] Anti-arrhythmic drugs (Class IC, II, III, IV) can be useful to prevent paroxysms of arrhythmia, and a pill-in-the-pocket approach can be used for patients with infrequent episodes.[80] Catheter ablation can target the accessory pathway and destroy the bundle. The success of the procedure is dependent on the location of the bundle as not all anatomical positions can be easily targeted with ablation.[85][86] It is controversial if patients with an asymptomatic WPW ECG pattern and no co-morbidities should have an ablation. To determine the risk of 1:1 conduction, an exercise test can be performed to determine the response of the accessory bundle to an increased atria rate. If the pre-excitation persists an electrophysiological procedure can be performed to assess the conduction properties of the accessory bundle. While the characteristics of the bundle predict the risk for an event, the life-style and\or profession of the patient can influence the decision for ablation.[87][88][89]

Ventricular tachycardia

Auteur: Louise R.A. Olde Nordkamp

Supervisor: Jonas S.S.G. de Jong

Ventricular tachycardias (VT's) are rhythm disturbances that arise in the ventricles.

History

Symptoms can arise in every ventricular tachycardia, depending on the heart rate, the presence of underlying heart disease and the degree of systolic and diastolic heart failure. Various symptoms are:

• Palpitations
• Abnormal chest sensation
• Dyspnea
• Angina
• Presyncope (lightheadedness, weakness, diaphoresis)
• Syncope
• Cardiogenic shock

Additional information about drug use is mandatory. Toxic levels of digoxin and cocain can lead to VT's. Anti-arrhythmics such as amiodarone can influence VT rate. Also additional information about family history of sudden cardiac death is helpfull, as it is a strong predictor of susceptibility to ventricular arrhythmias and sudden cardiac death.

Physical Examination

Although the diagnosis of VT is generally made by a 12 lead ECG, the following physical symptoms may be present:

• Decreased or variable amplitude of the carotid or peripheral pulses. This is related to the intermittent periods of atrial and ventricular synchronization, which transiently augment cardiac output.
• Cannon "A" waves on the jugular venous pulse in the neck. These represent intermittent retrograde propulsion of blood into the jugular veins during right atrial contraction against a closed AV valve. This is evidence of AV dissociation.
• Variable intensity of the first heart sound (although this is difficult with a rapid heart rate).
• Variable splitting of the first and second heart sounds, and intermittent presence of a third and/or fourth heart sound.

Diagnostic Evaluation

• Exercise testing: Exercise testing is recommended in adult patients with ventricular tachycardias who have an intermediate or greater probability of having coronary heart disease by age, gender and symptoms. It is meant to provoke ischemic changes or ventricular arrhythmias.
• Ambulatory (Holter) ECG: An ambulatory ECG can be necessary if the diagnosis needs to be clarified, by detecting arrhythmias, QT-interval changes, T-wave alternans (TWA) or ST-segment changes.
• Echocardiography, Cardiac CT, MRI: Echocardiography is recommended in patients with ventricular tachycardias who are suspected of having a structural heart disease. If echocardiography does not provide accurate assessment of the left and right ventricular function and/or structural changes, cardiac CT or MRI can be done.
• Exercise testing with an image modality (echocardiography or nuclear perfusion): Some patients with ventricular arrhythmias have an intermediate probability of coronary heart disease, but their ECG is less reliable (because of digoxin use, LVH, greater than 1mm ST-segment depression at rest, WPW syndrome or LBBB). For detecting silent ischemia in these patients exercise testing with an image modality can be done. If patients are unable to perform exercise, a pharmacological stress test with an imaging modality can be done.
• Coronary angiography: Coronary angiography can diagnose or exclude the presence of significant obstructive coronary heart disease in patients with ventricular arrhythmias who have an intermediate or greater probability of having coronary heart disease.
• Electrophysiological testing: Electrophysiological testing can be performed to guide and assess the efficacy of VT ablation in patients with ventricular arrhythmias. It can also be done to clarify the mechanism of broad complex tachycardias in patients with coronary heart disease.

Overview of ventricular tachycardias

An overview of ventricular tachycardias, follow the Approach to the Wide Complex Tachycardia

	example	regularity	atrial frequency	ventricular frequency	origin (SVT/VT)	p-wave	effect of adenosine
Wide complex (QRS>0.12)
Ventricular Tachycardia	File:Vt small.svg	regular (mostly)	60-100 bpm	110-250 bpm	ventricle (VT)	AV-dissociation	no rate reduction (sometimes accelerates)
Ventricular Fibrillation	File:Vf small.svg	irregular	60-100 bpm	400-600 bpm	ventricle (VT)	AV-dissociation	none
Ventricular Flutter	File:Vflutt small.svg	regular	60-100 bpm	150-300 bpm	ventricle (VT)	AV-dissociation	none
Accelerated Idioventricular Rhythm	File:Aivr small.svg	regular (mostly)	60-100 bpm	50-110 bpm	ventricle (VT)	AV-dissociation	no rate reduction (sometimes accelerates)
Torsade de Pointes	File:Tdp small.svg	regular		150-300 bpm	ventricle (VT)	AV-dissociation	no rate reduction (sometimes accelerates)
Bundle-branch re-entrant tachycardia*		regular	60-100 bpm	150-300 bpm	ventricles (VT)	AV-dissociation	no rate reduction
* Bundle-branch re-entrant tachycardia is extremely rare

Ventricular tachycardia

Ventricular tachycardia (VT) is defined as a sequence of three or more ventricular beats. The rate is between 110-250 bpm. Ventricular tachycardias often origin around old scar tissue in the heart, e.g. after myocardial infarction. Also electrolyte disturbances and ischemia can cause ventricular tachycardias. The cardiac output is often strongly reduced during VT resulting in hypotension and loss of consciousness. VT is a medical emergency as it can deteriorate into ventricular fibrillation and thus mechanical cardiac arrest.

Definitions

• Non-sustained VT: three or more ventricular beats with a maximal duration of 30 seconds.
• Sustained VT: a VT of more than 30 seconds duration (or less if treated by electrocardioversion within 30 seconds).
• Monomorphic VT: all ventricular beats have the same configuration.
• Polymorphic VT: the ventricular beats have a changing configuration. The heart rate is 100-333 bpm.
• Biphasic VT: a ventricular tachycardia with a QRS complex that alternates from beat to beat. Associated with digoxin intoxication and long QT syndrome.

Localisation of the origin of a ventricular tachycardia

Determination of the location (or exit site) where a ventricular tachycardia originated can be helpful in understanding the cause of the VT and is very helpful when planning an ablation procedure to treat a ventricular tachycardia. The location can be determined with the QRS morphology:

• RBBB/LBBB morphology:
  • RBBB: origin in the left ventricle
  • LBBB: origin in the right ventricle

• Inferior/superior axis (lead II, III and aVF):
  • Inferior axis (positive in lead II, III and aVF): origin superior wall
  • Superior axis (negative in lead II, III and aVF): origin inferior wall

• Basal/apical (lead V5-V6):
  • Positive concordance in V5-6: basal origin
  • Negative concordance in V5-6: apical origin

Differential diagnosis

(Non)sustained VT may be idiopathic, but occurs most frequently in patients with underlying structural heart disease of various types including:

• Coronary heart disease (CHD) with prior myocardial infarction. This is the most frequent cause in developed countries
• Hypertrophic cardiomyopathy
• Dilated cardiomyopathy
• Mitral valve prolapse
• Aortic stenosis
• Complex congenital heart disease
• Cardiac sarcoidosis
• Arrhythmogenic RV cardiomyopathy/dysplasia

If no structural heart disease is present the differential diagnosis includes:

• Electrolyte disorders, especially hyper- / hypokalemia\
• Drugs: e.g. digoxin
• Channelopathies (e.g. long QT syndrome, Brugada syndrome, CPVT)
• Idiopathic ventricular tachycardia (e.g. RVOT tachycardia, idiopathic left ventricular tachycardia)
• Purkinje VT’s (e.g. Belhassen)

Treatment

Hemodynamical instability:

• Electrocardioversion

Haemodynamical stability in a regular monomorphic broadcomplex tachycardia (systolic blood pressure >100 mmHg):

• Pharmacological treatment can be considered with Procaïnamide or Amiodaron

Ventricular flutter

Ventricular flutter is a ventricular tachycardia that occurs at a very rapid rate (often around 300 bpm), mostly caused by re-entry. The QRS complexes are regular and usually monomorphic and show a typical sinusoidal pattern. During ventricular flutter the ventricles depolarize in a circular pattern, which prevents good function. Most often this results in a minimal cardiac output and subsequent ischemia. Often deteriorates into ventricular fibrillation. Treatment

Treatment

Electrocardioversion is the only treatment for ventricular flutter.

Ventricular fibrillation

Ventricular fibrillation (VF) is identified by the complete absence of properly formed QRS complexes and no obvious P waves. Instead of uniform activation of the ventricular myocardium, there are uncoördinated series of very rapid, ineffective contractions of the ventricle caused by many chaotic electrical impulses. In recent onset VF the QRS complexes are of high amplitude at rates greater than 320 bpm, which manifest random changes in morphology, width and height. It appears as a completely chaotic rhythm. If VF continues, the fibrillatory waves become fine and can resemble asystole in these cases.

Treatment

VF is lethal if the patient is not treated immediately. It gives rise to a mechanical standstill of the heart, because the heart is not able to pump normally anymore. Electrocardioversion is the only treatment for ventricular fibrillation.

Accelerated idio-ventricular rhythm

Accelerated idioventricular rhythm (AIVR) is a relatively benign form of ventricular tachycardia. It is (mostly) a regular repetitive ventricular rhythm with a rate around 60-120 bpm, but mostly 80-100. It is the result of an enhanced ectopic ventricular rhythm, which is faster than normal intrinsic ventricular escape rhythm (<40 bpm), but slower than ventricular tachycardia (over 100-120 bpm). It often occurs during reperfusion after a myocardial infarction. AIVR is not predictive marker for early VF; however, recent debate has started whether among patients with successfull coronary intervention, AIVR is a sign of ventricular dysfunction and therefore a slightly worse prognosis. AIVR can also occur in infants. By this definition, this is a ventricular rhythm of no more than 20% faster than the sinus rate and occuring in the absence of other heart disease. This arrhythmia typically resolves spontaneously during the first months of life (in contrast to an infant with incessant VT which can be due to discrete myocardial tumors or congenital cardiomyopathy).

Treatment

AIVR is generally a transient, self-limiting rhythm and resolves as sinus rate surpasses the rate of AIVR. It rarely causes hemodynamic instability and rarely requires treatment.

Torsades de Pointes

Torsade de Pointes, preceded by bigemini.

Torsade de pointes (TdP) is a ventricular tachycardia associated with a prolonged QTc interval on the resting ECG. The ECG is characterized by twisting of the peaks of the QRS complexes around the isoelectric baseline during the arrhythmia (changing axis). Torsade de pointes is initiated by a short-long-short interval. A ventricle extrasystole (first beat: short) is followed by a compensatory pause. The following beat (second beat: long) has a longer QT interval. If the next beat follows shortly thereafter, there is a good chance that this third beat falls within the QT interval, resulting in the R on T phenomenon and subsequent Torsades de pointes.

Causes of Torsade de Pointes

• Aquired long QT syndrome (complete list of drugs causing long QT syndrome: http://www.torsades.org http://www.torsades.org])
• Congenital long QT syndrome

Concomittant risk factors for medication induced torsade de pointes:
Female sex Hypokalemia Bradycardia Recent conversion of atrial fibrillation, especially if QT prolonging drugs were used (sotalol, amiodarone) Cardiac decompensation Digoxin treatment High or overdosing or rapid infusion of a QT prolonging drug Pre-existing QT prolongation Congenital QT syndrome

Notorious QT prolonging drugs:
Amiodarone Chloroquine Chlorpromazine Citalopram Claritromycin Disopyramide Dofetilide Erythromycin Flecainide Halofantrine Haloperidol Quinidine Sotalol

Treatment

Electrocardioversion is the first treatment for TdP. Additional treatments are:

• Withdrawal of any offending drugs and correction of electrolyte abnormalities (potassium repletion up to 4.5 to 5 mmol/liter).
• Acute and long-term cardiac pacing in patients with TdP presenting with heart block, symptomatic bradycardia or recurrent pause-dependent TdP
• Intravenous magnesium sulfate for patients with QT prolongation and few episodes of TdP.
• Beta blockers combined with cardiac pacing as acute therapy for patients with TdP and sinus bradycardia.
• Isoproterenol as temporary treatment in patients with recurrent pause-dependent TdP who do not have congenital long QT syndrome.

Differentiation between SVT and VT

To differentiate between supraventricular tachycardias and ventricular tachycardias a 12 lead ECG is the cornerstone of the diagnostic process. At first, the physician has to make a differentiation between a narrow or wide complex tachycardia.

Definitions

Narrow complex tachycardia: QRS duration < 120 ms.

A narrow complex tachycardia is most likely to be a SVT. However, also a septal VT or His-tachycardia can appear as a narrow complex tachycardia.

Wide complex tachycardia: QRS duration > 120 ms.

A wide complex tachycardia can be due to a SVT with aberration, pre-exited tachycardia (eg antidrome re-entry tachycardia) or VT.

Differentiation

These are the flow charts of a small and wide complex tachycardia to differentiate between the different rhythms:

Treatment

Haemodynamical instability (systolic blood pressure less than 100 mmHg):

• electrical cardioversion

Haemodynamical stability in a regular small complex tachycardia:

• Carotid massage (after palpation and ausculatation of carotid arteries for exclusion of carotid occlusion/stenosis)
• Vasalva manoeuvre
• Adenosine bolus (if patient is not asthmatic or having COPD)
• Verapamil (if patient is not having systolic heart failure)
• Beta-blocker (if patient is not having systolic heart failure)

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