This document provides guidance on diagnosing ventricular tachycardia (VT) versus supraventricular tachycardia (SVT). It discusses evaluating the patient's history, physical exam findings, ECG characteristics including QRS morphology, and using pharmacological interventions to help differentiate the two. Features that suggest VT over SVT include the presence of AV dissociation, irregular RR intervals, and negative or discordant QRS complexes in precordial leads.

1. VENTRICULAR
TACHYCARDIA-Diagnosis

2. Ventricular tachycardia
 Ventricular tachycardia is the most common
cause of WCT, accounting for up to 80
percent of cases
 The frequency is even higher in patients
with structural heart disease
 monomorphic or polymorphic

3. GENERAL DIAGNOSTIC
APPROACH
 Immediate determination of whether the
patient is hemodynamically stable or
unstable
 In patients with significant hemodynamic
instability or compromise emergent
cardioversion is the treatment of choice

4. History
 Age — A WCT in a patient over the age of
35 years is likely to be VT
 SVT is more likely in the younger patient
 Duration of the tachycardia — SVT is
more likely if the tachycardia has recurred
over a period of greater than three years
 The first occurrence of the tachycardia after
an MI strongly implies VT

5.  Underlying heart disease- strongly
suggests VT as an etiology
 Other medical conditions -diabetes
mellitus increases CAD and with it VT
 Hyperkalemia

6.  Medications —The most common drug-
induced tachyarrhythmia is a form of
polymorphic VT,
 associated with QT interval prolongation
when the patient is in sinus rhythm, called
torsade de pointes (TdP).
 antiarrhythmic drugs such as sotalol and
quinidine and antimicrobial drugs such as
erythromycin.

7.  Diuretics - cause hypokalemia and
hypomagnesemia, which may predispose to
ventricular tachyarrhythmias, particularly
TdP
 class I antiarrhythmic drugs, especially class
IC agents

8.  Digoxin can cause almost any cardiac arrhythmia,
especially with plasma concentrations above 2.0
ng/mL (2.6 mmol/L).
 more frequent if hypokalemia is also present.
 The most common digoxin-induced arrhythmias
include
 monomorphic VT
 bidirectional tachycardia
 nonparoxysmal junctional tachycardia.

9. Physical examination
 Blood pressure and heart rate,
 Evidence of underlying cardiovascular disease
should be sought
 Presence of AV dissociation strongly suggests VT,
although its absence is less helpful
 Cannon "A" waves - intermittent and irregular -
They reflect simultaneous atrial and ventricular
contraction; contraction of the right atrium against
a closed tricuspid valve

10.  Cannon A waves must be distinguished from
the continuous and regular prominent A
waves seen during some SVTs
 Highly inconsistent fluctuations in the blood
pressure
 Variability in the occurrence and intensity of
heart sounds

11. Carotid sinus pressure
 sinus tachycardia will gradually slow with carotid
sinus pressure and then accelerate upon release.
 The ventricular rate of atrial tachycardia and atrial
flutter will transiently slow with carotid sinus
pressure (due to increased AV nodal blockade).
 An SVT (either AVNRT or AVRT) will either
terminate or remain unaltered with carotid sinus
pressure.
 VT is generally unaffected

12. Pharmacologic interventions
 Termination of the arrhythmia with lidocaine
suggests. Rarely SVT, especially AVRT, may
terminate with lidocaine
 Termination of the arrhythmia with digoxin,
verapamil, diltiazem, or adenosine strongly
implies SVT. However, VT may also rarely
terminate.

13.  Unless the etiology for the wide complex
tachycardia is definitely established,
verapamil, diltiazem, and even adenosine
should not be administered
 Termination of the arrhythmia with
procainamide or amiodarone does not
distinguish between VT and SVT.

14. Laboratory tests
 Plasma potassium and magnesium
 In patients taking digoxin, quinidine, or
procainamide, plasma concentrations of
these drugs should be measured
 Chest X-ray —structural heart disease, such
as cardiomegaly,. presence of a pacemaker
or ICD

15. EVALUATION OF THE
ELECTROCARDIOGRAM
 WCT should be presumed to be VT in the
absence of contrary evidence.
 VT accounts for up to 80 percent of cases of
WCT
 guards against inappropriate and potentially
dangerous therapy

16.  Rate — The rate of the WCT is of limited
use.
 There is wide overlap in the distribution of
heart rates for SVT and VT

17. Regularity
 Slight irregularity of RR intervals, especially
during the onset of a WCT ("warm-up
phenomenon"), suggests VT.
 More marked irregularity of RR intervals
occurs in polymorphic VT and in atrial
fibrillation with aberrant conduction.
 Most SVT is characterized by the total and
persistent uniformity of the RR intervals.

18. RBBB versus LBBB pattern
 An RBBB-like pattern (QRS polarity is
positive in leads V1 and V2)
 An LBBB-like pattern (QRS polarity is
negative in leads V1 and V2)

19. QRS axis
 A marked rightward or leftward shift in axis (more
than 40 degrees) when compared with a previous
ECG in normal sinus rhythm suggests VT
 A right superior axis (axis from -90 to +/- 180
degrees), sometimes called a "northwest" axis,
strongly suggests VT
 In a patient with a RBBB-like WCT, a QRS axis to
the left of -30 degrees suggests VT.
 In a patient with an LBBB-like WCT, a QRS axis to
the right of +90 degrees suggests VT

20. QRS duration
 A wider QRS favors VT.
 In the setting of RBBB-like WCT, a QRS
duration >140 msec suggests VT
 In the setting of LBBB-like WCT, a QRS
duration >160 msec suggests VT
 A QRS duration less than 140 msec is not
helpful for excluding VT( for example in
fascicular tachycardia.)

21.  A QRS complex wider than 160 msec is not
helpful in identifying VT in several settings
like
 Preexisting bundle branch block
 SVT with AV conduction over an
accessory pathway (preexcitation
 the presence of drugs capable of
slowing intraventricular conduction

22. Precordial QRS concordance
 QRS complexes in precordial leads (V1 through
V6) are either all positive in polarity (tall R waves)
or all negative in polarity (deep QS complexes).
 Negative concordance is strongly suggestive of VT
 Positive concordance is most often due to VT;
however, this pattern also occurs in the relatively
rare case of AVRT with a left posterior accessory
pathway

23. Variation in QRS and ST-T shape
 Subtle, non-rate related fluctuations or
variations in QRS and ST-T wave
configuration suggest VT
 SVT, because it follows a fixed conduction
pathway, is characterized by complete
uniformity of QRS and ST-T shape unless
the rate changes.

24. AV dissociation
 AV dissociation is a feature of most VT
 atrial rate is usually slower than the
ventricular rate
 AV dissociation does not occur in SVT
 Absence is not as helpful for two reasons:
 AV dissociation may be present but
not obvious on the ECG
 Some patients with VT do not have AV
dissociation

25. AV dissociation

26. Dissociated P waves
 If P waves can be clearly seen, and the
atrial rate is unrelated to, and slower than,
the ventricular rate, AV dissociation
consistent with VT is present.
 An atrial rate that is faster than the
ventricular rate is more often seen with SVT
with AV conduction block.

27.  Fusion beats -Intermittent fusion beats
during a WCT are diagnostic of AV
dissociation and therefore of VT.
 Dressler beats (capture beat)
 Fusion and capture beats are more
commonly seen when the tachycardia rate is
slower

29. QRS morphology
V1 positive (RBBB) pattern
 A monophasic R or biphasic qR complex in lead
V1 favors VT.
 In contrast, a triphasic RSR' complex in lead V1
favors SVT.
 A double-peaked R wave in lead V1 favors VT if
the left peak is taller than the right peak (the so-
called "rabbit ear" sign)
 Findings in lead V6 — An rS complex (R wave
smaller than S wave) in lead V6 favors VT

31. V1 negative (LBBB) pattern
 A broad initial R wave of 40 msec or more in
lead V1 or V2 favors VT.
 A slurred or notched downstroke of the S
wave in lead V1 or V2 favors VT
 duration from the onset of the QRS complex
to the nadir of the QS or S wave of 70 msec
in lead V1 or V2 favors VT

33. Brugada criteria
 1)All precordial leads are inspected to detect
the presence or absence of an RS complex
(with R and S waves of any amplitude).
 If an RS complex cannot be identified in
any precordial lead, the diagnosis of VT can
be made with 100 percent specificity.

34.  2)If an RS complex is clearly distinguished in one
or more precordial leads, the interval between the
onset of the R wave and the deepest part of the S
wave (RS interval) is measured.
 The longest RS interval is considered if RS
complexes are present in multiple precordial
leads.
 If the RS interval is >100 msec, the diagnosis of
VT can be made with a specificity of 98 percent.

35.  3)If the RS interval is <100 msec, either a
ventricular or supraventricular site of origin
of the tachycardia is possible
 the presence or absence of AV dissociation
must be determined.
 Evidence of AV dissociation is 100 percent
specific for the diagnosis of VT, but this
finding has a low sensitivity.

36.  4)If the RS interval is <100 msec and AV
dissociation cannot clearly be demonstrated,
the QRS morphology criteria for V1-positive
and V1-negative wide QRS complex
tachycardias are considered

39. VT versus AVRT
 second algorithm was developed by
Brugada and Brugada et al
 1)The predominant polarity of the QRS
complex in leads V4 through V6 is defined
either as positive or negative.
 If predominantly negative, the diagnosis of
VT can be made with 100 percent
specificity.

40.  2)If the polarity of the QRS complex is
predominantly positive in V4 through V6,
look for a qR complex in one or more of
precordial leads V2 through V6.
 If a qR complex can be identified, VT can
be diagnosed with a specificity of 100
percent.

41.  3)If a qR wave in leads V2 through V6 is
absent, the AV relationship is then evaluated
(AV dissociation).
 If a 1:1 AV relationship is not present and
there are more QRS complexes present
than P waves, VT can be diagnosed with a
specificity of 100 percent.