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=====Pathophysiology:=====
=====Pathophysiology:=====
The pathophysiology of AF is complex and incompletely understood.<cite>24</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>25</cite> 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).<cite>26</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 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.<cite>27</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). During atrial standstill the atria does  not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.<cite>28</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 an irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>29</cite>
The pathophysiology of AF is complex and incompletely understood.<cite>24</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>25</cite> 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).<cite>26</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 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.<cite>27</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). During atrial standstill the atria does  not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.<cite>28</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 an irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>29</cite>
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
|-
|colspan="2" bgcolor="#cfefcf"|'''Classification of Atrial Fibrillation (AF) related symptoms based on the European Heart Rhythm Association (EHRA) score are: <cite>EHRA</cite>'''
|-
!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:=====
=====Clinical diagnosis:=====
Line 156: Line 173:


=====Pathophysiology:=====
=====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>
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
 
=====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 &le; 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.<cite>6</cite><cite>9</cite>
 
=====Management:=====
Termination of acute episodes is possible by vagal manoeuvres (blowing on the wrist, carotid sinus massage) or medication (adenosine, verapamil, diltiazem).<cite>77</cite> 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%).<cite>78</cite> 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.<cite>79</cite> Other options are class IC or class III anti-arrhythmic drugs.
 
====AV Re-entry Tachycardia (AVRT)====
[[Image:OCT_ACT.svg|thumb|400px|'''Figure 4.''' An example of orthodrome AVRT and antidrome AVRT. Note the differences in the direction of the arrhythmia.<cite>ECGPedia</Cite>]]
 
=====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'''):
 
{| class="wikitable" width="100%"
|-
|bgcolor="#cfefcf"|'''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.
{| class="wikitable" width="100%"
|-
|bgcolor="#cfefcf"|'''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.<cite>82</cite> 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.<cite>6</cite><cite>9</cite> When an arrhythmia develops using the AP, both types of AVRT can develop depending on the conduction characteristics of the bundle:
 
{| class="wikitable" width="100%"
|-
|bgcolor="#cfefcf"|'''Orthodrome AV re-entry tachycardia:'''
|}
There is a P-wave (other morphology than sinus rhythm) followed by a narrow QRS-complex
{| class="wikitable" width="100%"
|-
|bgcolor="#cfefcf"|'''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.<cite>83</cite> 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.<cite>79</cite> 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.<cite>84</cite><cite>85</cite> 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.<cite>86</cite><cite>87</cite><cite>88</cite>
 
==Ventricular tachycardia==
[[Image:SR_VT.svg|thumb|right|400px]]
 
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
 
The patient’s age and previous medical history are essential. The chance that a wide complex tachycardia in a 70 year old man with previous myocardial infarction is a VT (vs. SVT with aberrancy) is >90%. Additional information about drug use is mandatory. Toxic levels of digoxin and cocain can lead to VT's. Also additional information about family history of sudden cardiac death is helpful, 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 intermittant 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 are now in sinus rhythm to detect coronary heart disease. It is meant to provoke ischemic changes or ventricular arrhythmias.
*'''Ambulatory (Holter) ECG:''' Ambulatory ECG is 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 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==
{| class="wikitable" font-size="90%"
|- style="text-align:center;background-color:#6EB4EB;"
|+'''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
|-
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Wide complex (QRS>0.12)'''
|-
! [[Ventricular Tachycardia]]
| [[Image:vt_small.svg|200px]]
| regular (mostly)
| 60-100 bpm
| 110-250 bpm
| ventricle (VT)
| [[AV-dissociation]]
| no rate reduction (sometimes accelerates)
|-
! [[Ventricular Fibrillation]]
| [[Image:vf_small.svg|200px]]
| irregular
| 60-100 bpm
| 400-600 bpm
| ventricle (VT)
| [[AV-dissociation]]
| none
|-
! [[Ventricular Flutter]]
| [[Image:vflutt_small.svg|200px]]
| regular
| 60-100 bpm
| 150-300 bpm
| ventricle (VT)
| [[AV-dissociation]]
| none
|-
! [[Accelerated Idioventricular Rhythm]]
| [[Image:aivr_small.svg|200px]]
| regular (mostly)
| 60-100 bpm
| 50-110 bpm
| ventricle (VT)
| [[AV-dissociation]]
| no rate reduction (sometimes accelerates)
|-
! [[Torsade de Pointes]]
| [[Image:tdp_small.svg|200px]]
| regular
|
| 150-300 bpm
| ventricle (VT)
| [[AV-dissociation]]
| no rate reduction (sometimes accelerates)
|-
! [[Bundle-branch re-entrant tachycardia]]*
| [[Image:bb_reentry_small.svg|200px]]
| regular
| 60-100 bpm
| 150-300 bpm
| ventricles (VT)
| [[AV-dissociation]]
| no rate reduction
|-
|colspan="8"|* 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 often 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 (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
 
===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) and results from 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 at a high rate, which prevents good function. Most often this results in a minimal cardiac output and subsequent ischemia. Often deteriorates into ventricular fibrillation.
 
===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. 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 electrical activity is of higher 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 there is no pump function. 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 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 a predictive marker for early VF; however, recent debate has started whether among patients with successful coronary intervention, AIVR is a sign of ventricular dysfunction and therefore a slightly worse prognosis. AIVR can also occur in infants. By definition, AIVR 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==
[[Image:Torsades_de_Pointes.png|thumb|400px|Torsade de Pointes, preceded by bigemini.]]
 
Torsades de pointes (TdP) is a ventricular tachycardia associated with a prolonged QTc interval on the resting ECG. The ECG during TdP is characterized by twisting of the peaks of the QRS complexes around the isoelectric line during the arrhythmia (changing axis). Torsade de pointes is typically 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 (third beat: short), 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.
 
See the chapter on [[LQTS]] for a list of medication and genes that can cause QT prolongation and TdP.
 
===Treatment===
Electrocardioversion is the first treatment for an unconcious patient with incessant TdP.
 
'''Additional treatments are:'''
*Withdrawal of any offending drugs and correction of electrolyte abnormalities (potassium repletion up to 4.5 to 5 mmol/liter, the goal should be to make the patient slightly hyperkalemic).
*Acute and long-term cardiac pacing in patients with TdP presenting with heart block, symptomatic bradycardia or recurrent pause-dependent TdP
*Intravenous magnesium sulfate can be helpful to cardiovert TdP in the acute phase in patients with few TdP episodes. If recurrence occurs a continues infusion may be beneficial.
*Beta blockers combined with cardiac pacing as acute therapy for patients with TdP and sinus bradycardia. This prevents extrasystoles and thereby short-long-short sequences.
*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 small or broad 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:
 
{| class="wikitable"
|-
|[[Image:SmallTachydiff.png|500px|left|Small complex differentation]]
||[[Image:BroadTachydiff.png|500px|right|Wide-complex differentation]]
|}
 
===Treatment===
*'''Haemodynamical instable (systolic blood pressure less than 100 mmHg):'''
**Electrical cardioversion (with anesthesia when concious)
 
*'''Haemodynamically stable regular narrow 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)
 
==References==
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# Wyse pmid=12466506
# Ogawa pmid=19060419
# IonescuIttu pmid=22664954
# Heeringa pmid=16527828
# Shelton pmid=19282313
# Roy1 pmid=10738049
# Roy2 pmid=18565859
# Wijfels pmid=7671380
# Patterson pmid=15922271
# Nieuwlaat pmid=16204266
# Packer pmid=3953440
# Watson pmid=19135613
# Friberg pmid=19176537
# Jahangir pmid=17548732
# Martinez pmid=11053705
# Chevalier pmid=12535819
# Stambler pmid=9416896
# Kirchof pmid=22713626
# Ahmed pmid=18854540
# Ghuran pmid=11532824
# Robles isbn=9789031313983
# Cossu pmid=9717859
# Alboni pmid=11216977
# Clague pmid=11133213
# Akhtar pmid=8319342
# Wellens isbn=9781416002598
# Pappone pmid=12535816
# Priori pmid=11482917
# Jackman pmid=2030716
# Mazgelev pmid=11390334
# WPW pmid=17040283
# Cosio pmid=10430823
# Wu pmid=12212708
# Becker pmid=639209
# Tebbenjohanns pmid=7596861
# Saoudi pmid=11440490
# Markowitz pmid=10355690
# Anguere pmid=11274945
# Chen2 pmid=9581952
# Chen1 pmid=8087935
# Volgmann pmid=9581743
# Singh pmid=11067793
# Dunn pmid=9732894
# Lip5 pmid=11428832
# Kottkamp pmid= 11044424
# Natale pmid=10841241
# Chen3 pmid=8613615
# Yang pmid=11425774
# Bochoeyer pmid=12835225
# Heemstra pmid=21761194
</biblio>
NiloferT
467

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