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Catecholaminergic Ventricular Tachycardia

Cathecholaminergic Polymorphic Ventricular Tachycardia

Catecholaminergic Polymorphic Ventricular Tachycardia
Bidirectional Ventricular Tachycardia
ECG and Catecholaminergic Polymorphic VT

Catecholaminergic Polymorphic Ventricular Tachycardia

Patients have a congenital genetic calcium channel disorder (the action potential in cardiomyocytes is impaired)
Intracellular calcium concentration increases (similarly to digoxin overdose)
CPVT occurs during stress (either physical or emotional) when catecholamines (adrenaline, noradrenaline) are released

Catecholamines in the context of the genetic calcium channel disorder trigger CPVT
The mechanism is early afterdepolarization
On EKG, there is bidirectional ventricular tachycardia (polymorphic ventricular tachycardia)
CPVT is present only during stress (it disappears at rest)

Causes 15% of unexplained sudden deaths in young people (under 20 years old)
Occurs mainly in young people under 20 years of age, it is a pediatric tachycardia
Patients do not have structural heart damage

Sometimes CPVT is classified among idiopathic ventricular tachycardias

Bidirectional Ventricular Tachycardia

Bidirectional Ventricular Tachycardia

Bidirectional ventricular tachycardia is a type of polymorphic ventricular tachycardia
There are active 2 ectopic foci in the ventricles, which alternately generate impulses

Ventricular extrasystole (VES) in the right ventricle triggers VES in the left ventricle
This process repeats continuously (ping-pong theory)

On the ECG, QRS complexes rotate in the frontal plane in two directions (180°)
The mechanism is early afterdepolarization
Bidirectional ventricular tachycardia arises

Most commonly due to digoxin intoxication
The second most common cause is Catecholaminergic polymorphic ventricular tachycardia
Andersen-Tawil syndrome
Metastatic heart involvement
Poisoning from plants in the Aconite genus (Aconite poisoning)

Bidirectional ventricular tachycardia is not ventricular bigeminy

In ventricular bigeminy, sinus rhythm alternates with ventricular extrasystole in a 1:1 ratio
In bidirectional ventricular tachycardia, 2 ventricular extrasystoles alternate in a 1:1 ratio

ECG Bidirectional ventricular tachycardia (BVT)

Bidirectional Ventricular Tachycardia

Heart rate: 130/min.
All QRS complexes are wide > 0.12s

Because they have a ventricular origin

Heart axis changes by approximately 180° after each beat
P waves are absent before the QRS complexes
The tachycardia occurred during physical exertion and the patient was not taking digoxin

This is a catecholaminergic polymorphic ventricular tachycardia

ECG premature ventricular complex (PVC), ventricular bigemini

Ventricular Bigeminy

On the ECG, it is not bidirectional ventricular tachycardia because

After each sinus beat (narrow QRS complex with a P wave)
It is followed by a ventricular extrasystole (wide QRS complex)

This is ventricular bigeminy

ECG and Catecholaminergic Polymorphic VT

The patient has a congenital calcium channel disorder (altered action potential)
During sinus rhythm

A U wave may be present

During exercise (physical or emotional) the following occur

Ventricular extrasystoles
Bidirectional ventricular tachycardia

Frequency: 110-130/min.
Wide QRS complexes (> 0.12s)
Frontal axis of QRS complexes changes by 180°
Disappears at rest
May progress to ventricular fibrillation and sudden cardiac death

ECG sinus rhythm, U wave, Bidirectional ventricular tachycardia (BVT)

Sinus Rhythm and U Wave

The ECG shows sinus rhythm
The patient had catecholaminergic polymorphic ventricular tachycardia during physical exertion

The patient was not digoxin-overdosed
The tachycardia spontaneously resolved at rest

The patient has a congenital calcium channel disorder

Sometimes seen during sinus rhythm as U waves (red arrows)

ECG digoxim toxicity, Bidirectional ventricular tachycardia (BVT)

Bidirectional Ventricular Tachycardia

Heart rate: 130/min.
Wide QRS complexes (> 0.12s)
Heart axis changes by approximately 180° (best seen on continuous II lead)
The patient was digoxin-intoxicated

Therefore, this ECG does not show catecholaminergic polymorphic ventricular tachycardia

ECH exercise, Cathecholaminergic Polymorphic Ventricular Tachycardia

Catecholaminergic Polymorphic Ventricular Tachycardia

This concerns a 20-year-old patient with no structural heart damage
During ergometry - cycling, the patient experienced an abnormal ECG and palpitations (heart pounding)

After 30 seconds of exercise, the ECG showed ventricular bigeminy
After 1 minute, paroxysms of bidirectional ventricular tachycardia appeared
At 4 minutes, the patient stopped cycling

This led to the development of polymorphic ventricular tachycardia, which gradually began transitioning to sinus rhythm

This is catecholaminergic polymorphic ventricular tachycardia

Bidirectional tachycardia occurred during physical exertion and subsided at rest
The patient was not digoxin-intoxicated

ECG Multifocal ectopy and bidirectional VT secondary to digoxin poisoning

Bidirectional Ventricular Tachycardia

Heart Rate: 150/min.
Wide QRS complexes (> 0.12s)
Heart Axis changes by approximately 180° (II lead)
AV Dissociation

P waves (stars in V1) are independent of QRS complexes
AV dissociation is a key feature of ventricular tachycardia

The patient was digoxin-intoxicated

Therefore, this ECG does not show catecholaminergic polymorphic ventricular tachycardia

Sources

ECG from Basics to Essentials Step by Step
litfl.com
ecgwaves.com
metealpaslan.com
medmastery.com
uptodate.com
ecgpedia.org
wikipedia.org
Strong Medicine
Understanding Pacemakers

Catecholaminergic Ventricular Tachycardia

Cathecholaminergic Polymorphic Ventricular Tachycardia

Catecholaminergic Polymorphic Ventricular Tachycardia
Bidirectional Ventricular Tachycardia
ECG and Catecholaminergic Polymorphic VT

Catecholaminergic Polymorphic Ventricular Tachycardia

Patients have a congenital genetic calcium channel disorder (the action potential in cardiomyocytes is impaired)
Intracellular calcium concentration increases (similarly to digoxin overdose)
CPVT occurs during stress (either physical or emotional) when catecholamines (adrenaline, noradrenaline) are released

Catecholamines in the context of the genetic calcium channel disorder trigger CPVT
The mechanism is early afterdepolarization
On EKG, there is bidirectional ventricular tachycardia (polymorphic ventricular tachycardia)
CPVT is present only during stress (it disappears at rest)

Causes 15% of unexplained sudden deaths in young people (under 20 years old)
Occurs mainly in young people under 20 years of age, it is a pediatric tachycardia
Patients do not have structural heart damage

Sometimes CPVT is classified among idiopathic ventricular tachycardias

Bidirectional Ventricular Tachycardia

Bidirectional ventricular tachycardia is a type of polymorphic ventricular tachycardia
There are active 2 ectopic foci in the ventricles, which alternately generate impulses

Ventricular extrasystole (VES) in the right ventricle triggers VES in the left ventricle
This process repeats continuously (ping-pong theory)

On the ECG, QRS complexes rotate in the frontal plane in two directions (180°)
The mechanism is early afterdepolarization

Bidirectional Ventricular Tachycardia

Bidirectional ventricular tachycardia arises

Most commonly due to digoxin intoxication
The second most common cause is Catecholaminergic polymorphic ventricular tachycardia
Andersen-Tawil syndrome
Metastatic heart involvement
Poisoning from plants in the Aconite genus (Aconite poisoning)

Bidirectional ventricular tachycardia is not ventricular bigeminy

In ventricular bigeminy, sinus rhythm alternates with ventricular extrasystole in a 1:1 ratio
In bidirectional ventricular tachycardia, 2 ventricular extrasystoles alternate in a 1:1 ratio

ECG Bidirectional ventricular tachycardia (BVT)

Bidirectional Ventricular Tachycardia

Heart rate: 130/min.
All QRS complexes are wide > 0.12s

Because they have a ventricular origin

Heart axis changes by approximately 180° after each beat
P waves are absent before the QRS complexes
The tachycardia occurred during physical exertion and the patient was not taking digoxin

This is a catecholaminergic polymorphic ventricular tachycardia

ECG premature ventricular complex (PVC), ventricular bigemini

Ventricular Bigeminy

On the ECG, it is not bidirectional ventricular tachycardia because

After each sinus beat (narrow QRS complex with a P wave)
It is followed by a ventricular extrasystole (wide QRS complex)

This is ventricular bigeminy

ECG and Catecholaminergic Polymorphic VT

The patient has a congenital calcium channel disorder (altered action potential)
During sinus rhythm

A U wave may be present

During exercise (physical or emotional) the following occur

Ventricular extrasystoles
Bidirectional ventricular tachycardia

Frequency: 110-130/min.
Wide QRS complexes (> 0.12s)
Frontal axis of QRS complexes changes by 180°
Disappears at rest
May progress to ventricular fibrillation and sudden cardiac death

ECG sinus rhythm, U wave, Bidirectional ventricular tachycardia (BVT)

Sinus Rhythm and U Wave

The ECG shows sinus rhythm
The patient had catecholaminergic polymorphic ventricular tachycardia during physical exertion

The patient was not digoxin-overdosed
The tachycardia spontaneously resolved at rest

The patient has a congenital calcium channel disorder

Sometimes seen during sinus rhythm as U waves (red arrows)

ECG digoxim toxicity, Bidirectional ventricular tachycardia (BVT)

Bidirectional Ventricular Tachycardia

Heart rate: 130/min.
Wide QRS complexes (> 0.12s)
Heart axis changes by approximately 180° (best seen on continuous II lead)
The patient was digoxin-intoxicated

Therefore, this ECG does not show catecholaminergic polymorphic ventricular tachycardia

ECH exercise, Cathecholaminergic Polymorphic Ventricular Tachycardia

Catecholaminergic Polymorphic Ventricular Tachycardia

This concerns a 20-year-old patient with no structural heart damage
During ergometry - cycling, the patient experienced an abnormal ECG and palpitations (heart pounding)

After 30 seconds of exercise, the ECG showed ventricular bigeminy
After 1 minute, paroxysms of bidirectional ventricular tachycardia appeared
At 4 minutes, the patient stopped cycling

This led to the development of polymorphic ventricular tachycardia, which gradually began transitioning to sinus rhythm

This is catecholaminergic polymorphic ventricular tachycardia

Bidirectional tachycardia occurred during physical exertion and subsided at rest
The patient was not digoxin-intoxicated

ECG Multifocal ectopy and bidirectional VT secondary to digoxin poisoning

Bidirectional Ventricular Tachycardia

Heart Rate: 150/min.
Wide QRS complexes (> 0.12s)
Heart Axis changes by approximately 180° (II lead)
AV Dissociation

P waves (stars in V1) are independent of QRS complexes
AV dissociation is a key feature of ventricular tachycardia

The patient was digoxin-intoxicated

Therefore, this ECG does not show catecholaminergic polymorphic ventricular tachycardia

Sources

ECG from Basics to Essentials Step by Step
litfl.com
ecgwaves.com
metealpaslan.com
medmastery.com
uptodate.com
ecgpedia.org
wikipedia.org
Strong Medicine
Understanding Pacemakers