Differential diagnosis and treatment of ventricular tachycardia, flutter, and ventricular fibrillation

1. Differential Diagnosis and Treatment of Ventricular
Tachycardia, Ventricular Flutter, and Ventricular
Fibrillation

2. Overview
►Ventricular tachycardia usually precedes ventricular flutter and ventricular fibrillation
►Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute
cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction
►Decreased cardiac output may result in decreased myocardial perfusion with degeneration to VF
►VT is a common health problem encountered in clinical practice
►VT is responsible for most of sudden cardiac deaths in US, at an estimated rate of approximately
300,000 deaths per year.
►ECG is used to differentiate types of ventricular tachycardia
►Risk factors for ventricular tachycardia are hypertension, previous myocardial infarction, chronic
obstructive pulmonary disease (COPD)
►The presence of pre-existing poor ventricular function is strongly associated with cardiovascular
compromise.
►The most common cause of VT is ischemic heart disease
►Monomorphic VT is the most common form

3. Ventricular Tachycardia
Occurs due to rapid discharge of an ectopic ventricular pacemaking focus
Wide complex rhythm QRS >0.12s
Series of three or more consecutive beats on ECG at a rate of 100 BPM or greater
Caused by significant heart disease: coronary artery disease, previous myocardial
infarction, cardiomyopathy, etc.
Could be life threatening
Can be monomorphic or polymorphic
Also can be classified as sustained or non-sustained VT. Sustained VT is any ventricular
tachycardia that lasts for more than 30 seconds or is symptomatic, seen in patients with
MI or chronic coronary artery disease. Non-sustained VT lasts for less than 30 seconds
and is asymptomatic. Is seen in ischemic or non-ischemic heart diseases, brugada
syndrome, metabolic problems including drug toxicity, and electrolyte imbalance

4. Classification and Causes of Ventricular Tachycardia
 Monomorphic Ventricular
Tachycardia (QRS complex
remains identical from beat-beat)
• Chronic coronary artery disease
• Idiopathic VT
• Right ventricular dysplasia
• Bundle branch reentry tachycardia
• Ventricular flutter
• Ventricular fibrillation
 Polymorphic Ventricular
Tachycardia (QRS complex
changes from beat-beat)
• Long QT interval (torsades de
pointes) – Congenital or acquired
(ischemic, drugs-induced,
hypokalemia)
• Normal QT interval – Brugada
syndrome, CPVT, acute ischemia or
infarction)

5. Clinical Presentation
• Hemodynamically stable: asymptomatic or minimal symptoms e.g. palpitations.
• Hemodynamically unstable —hypotension, tachypnea, chest pain, light headedness,
decreased consciousness, pallor, diaphoresis, syncope, sudden cardiac arrest or sudden
cardiac death
ECG features
Very broad complexes (>160ms)
AV dissociation: P wave and QRS complex at different rates
Capture beats
Fusion beats
Absence of typical RBBB or LBBB morphology.
Positive or negative concordance: absence of RS complex in all precordial leads

6. Monomorphic VT
• Regular rhythm.
• Originates from a single focus within the ventricles.
• Produces uniform QRS complexes within each lead — each QRS is identical
(except for fusion/capture beats).
Causes
• Ischemic heart disease
• Dilated cardiomyopathy
• Hypertrophic cardiomyopathy
• Chaga’s disease

8. Treatment
Non-sustained ventricular tachycardia
No therapy is required in asymptomatic patients without underlying cardiac
disease
Symptomatic patients: beta blockers, if episodes continue -> calcium channel
blockers e.g. verapamil or diltiazem can be used
Sustained monomorphic ventricular tachycardia
• Hemodynamically unstable:
immediate cardioversion with a 100-200J biphasic shock, and correction of
metabolic disturbances
In case of MI, it should be treated with lidocaine (2-3mg/kg)
• Hemodynamically stable:
Anti-arrhythmics: IV amiodarone or procainamide

9. Treatment, Continued….
First line therapy for ischemic heart disease and VT is a beta blocker which highly
reduces mortality (sudden cardiac death)
In case of recurrent VT despite beta-blockers therapy, amiodarone, or sotalol can be
used.
An implantable cardiac defibrillator (ICD) is very effective in preventing sudden
cardiac death and should be placed in those that survive sudden cardiac arrest, or
experience hemodynamically unstable or stable sustained ventricular tachycardia
Cardiac ablation through catheters is recommended for patients with a history of
myocardial infarction who continue to have sustained symptomatic VT and have
failed or are intolerant of amiodarone or other antiarrhythmic agents.

10. Polymorphic VT
• Multiple ventricular foci with the resultant QRS complexes varying in amplitude,
axis and duration.
• The commonest cause of PVT is myocardial ischemia.
• Biphasic VT: a form of polymorphic ventricular tachycardia with a QRS complex
that alternates from beat to beat. Associated with digoxin intoxication and long
QT syndrome.
• Torsades de pointes is a specific form of polymorphic ventricular tachycardia
with QT prolongation; it has a characteristic morphology in which the QRS
complexes twist around the isoelectric line (change axis).
Causes of Torsades de Pointes
• Congenital long QT syndrome
• Acquired long QT syndrome: secondary to multiple drugs’ effects, hypokalemia,
and other medical conditions.

12. Treatment of Tdp
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).
• 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.

13. Diagnosis of VT
• In a patient who is hemodynamically unstable or unconscious, the diagnosis
of VT is made from the physical findings and ECG rhythm strip only.
• ECG findings:
Absence of an RS complex in all precordial leads
RS interval >100 ms
AV dissociation or dissociation of P wave from QRS complex
Capture beats: sinus conducted impulse during ectopic ventricular beat
Fusion beats: occur when a sinus and ventricular beat coincide producing a
hybrid complex

17. Ventricular Flutter
Extreme form and a very rapid ventricular tachycardia (occurs at a rate of around 300
BPM), mostly caused by a reentry circuit.
The QRS complexes are regular and usually monomorphic.
The ventricles depolarize in a circular pattern, which prevents good function, this
results in a minimal cardiac output. Often deteriorates into ventricular fibrillation.
 Associated with rapid and profound hemodynamic compromise and is fatal within
minutes without intervention
ECG features:
 Continuous sine wave
 No identifiable P waves, QRS complexes, or T waves
 Rate >300 beats / min
Treatment: DC-defibrillation (200-360J) is the only treatment

20. Ventricular Fibrillation
Represents uncoordinated very rapid, irregular, and ineffective ventricular
contractions caused by many chaotic electric impulses. Terminal arrhythmia and
requires rapid initiation of management.
Mechanism
In the presence of ischemic heart disease VF may be preceded by:
Premature ventricular contractions (PVCs)
ST changes
R on T phenomenon or ventricular extrasystoles
Pauses
QT prolongation
Ventricular Tachycardia
Ventricular Flutter
Supraventricular arrhythmias

21. Causes of Ventricular Fibrillation
 Ischemic heart disease or coronary artery disease
 MI
 Cardiomyopathy (dilated, hypertrophic, restrictive)
 Aortic stenosis
 Aortic dissection
 Myocarditis
 Cardiac tamponade
 Blunt trauma (commotio cordis)
 Respiratory disorders
 Electrolyte disturbances: hypokalemia, hyperkalemia, acid base disturbances
 Drug-induced QT prolongation with torsades de pointes
 Environmental: electric shocks, hypothermia, drowning, sepsis
 Seizures, CVA

22. ECG Findings:
Chaotic irregular deflections of varying amplitude
No identifiable P waves, QRS complexes, or T waves
Heart rate 150 – 500 BPM
Amplitude decreases with duration, from coarse VF to fine VF which can resemble asystole.
Clinical Significance
• Ventricular fibrillation (VF) is the the most important shockable cardiac arrest rhythm.
• This rapid and irregular electrical activity renders the ventricles unable to contract in a
synchronized manner, resulting in immediate loss of cardiac output.
• VF gives rise to a mechanical standstill of the heart, because the heart is not able to
pump normally anymore. It’s fatal in all cases if treatment isn’t initiated immediately.
• Defibrillation is the only treatment for VF.

26. Bibliographies
www.ncbi.nlm.nih.gov
medscape.com
litfl.com
Textbookofcardiology.org
link.springer.com