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{{DevelopmentPhase}}
<div align="right">
''Sébastien Krul, MD, Louise Olde Nordkamp, MD, Jonas de Jong, MD''
''Sébastien Krul, MD, Louise Olde Nordkamp, MD, Jonas de Jong, MD''
</div>
==Introduction==
==Introduction==
[[Image:overview.png|thumb|300px|'''Figure 1.''' Classification of tachyarrhythmias.<cite>ECGPedia</cite>]]
[[Image:overview.png|thumb|300px|'''Figure 1.''' Classification of tachyarrhythmias.<cite>ECGPedia</cite>]]
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====Atrial Tachycardia (AT)====
====Atrial Tachycardia (AT)====
=====Pathophysiology:=====
=====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 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.
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 of &ge; 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:=====
=====Clinical diagnosis:=====
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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:=====
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{| class="wikitable" border="0" width="400px"
{| class="wikitable" border="0" width="400px"
|-
|-
! colspan="3" |CHA2DS<sub>2</sub>VASc score to estimate stroke risk
! colspan="3" bgcolor="#cfefcf"|CHA2DS<sub>2</sub>VASc score to estimate stroke risk
|-
|-
!
!
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==Ventricular tachycardia==
==Ventricular tachycardia==
''Auteur: Louise R.A. Olde Nordkamp''
''Supervisor: Jonas S.S.G. de Jong''
[[Image:SR_VT.svg|thumb|right|400px]]
[[Image:SR_VT.svg|thumb|right|400px]]


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


===History===
==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.  
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:  
 
'''Various symptoms are:'''
*Palpitations  
*Palpitations  
*Abnormal chest sensation  
*Abnormal chest sensation  
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*Cardiogenic shock  
*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.  
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===
==Physical Examination==
Although the diagnosis of VT is generally made by a 12 lead ECG, the following physical symptoms may be present:  
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.  
*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.  
*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 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.  
*Variable splitting of the first and second heart sounds, and intermittent presence of a third and/or fourth heart sound.  


===Diagnostic Evaluation===
===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.  
*'''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:''' 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.  
*'''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 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.  
*'''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.  
*'''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.  
*'''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.  
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==Ventricular tachycardia==
==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.  
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===
===Definitions===
*'''Non-sustained VT:''' Three or more ventricular beats with a maximal duration of 30 seconds.  
*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).  
*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.  
*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.  
*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.  
*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===
===Localisation of the origin of a ventricular tachycardia===
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===Differential diagnosis===
===Differential diagnosis===
(Non)sustained VT may be idiopathic, but occurs most frequently in patients with underlying structural heart disease of various types including:  
(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)
*Coronary heart disease (CHD) with prior myocardial infarction. This is the most frequent cause in developed countries
*Hypertrophic cardiomyopathy  
*Hypertrophic cardiomyopathy  
*Dilated cardiomyopathy  
*Dilated cardiomyopathy  
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*Complex congenital heart disease  
*Complex congenital heart disease  
*Cardiac sarcoidosis  
*Cardiac sarcoidosis  
*Arrhythmogenic RV cardiomyopathy/dysplasia  
*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===
===Treatment===
'''Hemodynamical instability:'''
Hemodynamical instability:  
*Electrocardioversion  
*Electrocardioversion  
 
Haemodynamical stability in a regular monomorphic broadcomplex tachycardia (systolic blood pressure >100 mmHg):  
'''Haemodynamical stability in a regular monomorphic broadcomplex tachycardia (systolic blood pressure >100 mmHg):'''
*Pharmacological treatment can be considered with Procaïnamide or Amiodaron
*Pharmacological treatment can be considered with Procaïnamide or Amiodaron  


==Ventricular flutter==
==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.  
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===
===Treatment===
Electrocardioversion is the only treatment for ventricular flutter.  
Electrocardioversion is the only treatment for ventricular flutter.


==Ventricular fibrillation==
==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.  
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===
===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.  
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 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).  
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===
===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.  
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==
==Torsades de Pointes==
[[Image:Torsades_de_Pointes.png|thumb|400px|Torsade de Pointes, preceded by bigemini.]]
[[Image:Torsade_de_Pointes.png|thumb|400px|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
 
{| class="wikitable" border="0" cellspacing="0" cellpadding="0" width="400px"
|-
!
===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
 
|}
 
{| class="wikitable" border="0" cellspacing="0" cellpadding="0" width="400px"
|-
!
===Notorious QT prolonging drugs:===
|-
|
#Amiodarone
#Chloroquine
#Chlorpromazine
#Citalopram
#Claritromycin
#Disopyramide
#Dofetilide
#Erythromycin
#Flecainide
#Halofantrine
#Haloperidol
#Quinidine
#Sotalol


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===
===Treatment===
Electrocardioversion is the first treatment for an unconcious patient with incessant TdP.  
Electrocardioversion is the first treatment for TdP.  
 
Additional treatments are:  
'''Additional treatments are:'''
*Withdrawal of any offending drugs and correction of electrolyte abnormalities (potassium repletion up to 4.5 to 5 mmol/liter).  
*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  
*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.
*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. This prevents extrasystoles and thereby short-long-short sequences.
*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.  
*Isoproterenol as temporary treatment in patients with recurrent pause-dependent TdP who do not have congenital long QT syndrome.


==Differentiation between SVT and VT==
==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.  
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===
===Definitions===
*'''Narrow complex tachycardia:''' QRS duration < 120 ms.
 
'''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.  
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.
'''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.  
 
A wide complex tachycardia can be due to a SVT with aberration, pre-exited tachycardia (eg antidrome re-entry tachycardia) or VT.


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


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===Treatment===
===Treatment===
*'''Haemodynamical instable (systolic blood pressure less than 100 mmHg):'''
'''Haemodynamical instability (systolic blood pressure less than 100 mmHg):'''  
**Electrical cardioversion (with anesthesia when concious)
*electrical cardioversion  


*'''Haemodynamically stable regular narrow complex tachycardia:'''
'''Haemodynamical stability in a regular small complex tachycardia:'''  
**Carotid massage (after palpation and ausculatation of carotid arteries for exclusion of carotid occlusion/stenosis)  
*Carotid massage (after palpation and ausculatation of carotid arteries for exclusion of carotid occlusion/stenosis)  
**Vasalva manoeuvre  
*Vasalva manoeuvre  
**Adenosine bolus (if patient is not asthmatic or having COPD)  
*Adenosine bolus (if patient is not asthmatic or having COPD)  
**Verapamil (if patient is not having systolic heart failure)  
*Verapamil (if patient is not having systolic heart failure)  
**Beta-blocker (if patient is not having systolic heart failure)  
*Beta-blocker (if patient is not having systolic heart failure)


==References==
==References==
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# Bochoeyer pmid=12835225  
# Bochoeyer pmid=12835225  
# Heemstra pmid=21761194
# Heemstra pmid=21761194
# EHRA pmid=20802247
</biblio>
</biblio>
Retrieved from "https://www.textbookofcardiology.org/wiki/Special:MobileDiff/2131...2365"

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