Arrhythmias

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CONTENTS
TREATMENT
DIAGNOSIS
TYPES OF ARRYTHMIA

Supraventricular Arrhythmia
TYPES P WAVE QRS COMPLEX MANEUVOR
Rate Rhythm Shape Rate Rhythm Shape CSM &
IV Adenosine
Sinus
arrhythmia
0-100 Regular Normal 60-100 Regular Normal Gradual slowing and return to
former rate
Sinus
bradycardia
<60 Regular Normal <60 Regular Normal Gradual slowing and return to
former rate
Sinus
tachycardia
100-
180
Regular May be
peaked
100-180 Regular Normal Gradual slowing and return to
former rate

IV Adenosine
AV nodal re-
entry
150-
250
Very
regular
except at
onset and
terminati
on
Retrograde;
difficult to
see; lost in
QRS complex
150-250 Very regular
except at
onset and
termination
Normal Abrupt slowing caused by
termination of tachycardia or no
effect

IV Adenosine
Atrial flutter 250-
350
Regular Sawtooth 75-175 Generally
regular in
absence of
drugs or
disease
Normal Abrupt slowing and return to
former rate; flutter remains
Atrial
fibrillation
400-
600
Grossly
irregular
Baseline
undulation,
no P waves
100-160 Grossly
irregular
Normal Slowing; gross irregularity
remains

IV Adenosine
Atrial
tachycardia
100-
200
Regular
(except at
beginning
, where
there
could be
“warm
up”)
Abnormal,
but could be
similar to
sinus P wave
if origin near
sinus node
100-200 Generally
regular in
absence of
drugs or
disease, but
at faster rates
could have
some block
normal rate; tachycardia remains;
some may terminate with CSM or
adenosine

IV Adenosine
Atrial
tachycardia
with block
150-
250
Regular;
may be
irregular
Abnormal 75-200 Generally
regular in
absence of
drugs or
disease
normal rate; tachycardia remains

IV Adenosine
AV junctional
rhythm
40-100 Regular Normal 40-60 Fairly regular Normal None; may be slight slowing
AV junctional
tachycardia
100-
200
Regular Absent or
retrograde
100-200 Regular Normal Abrupt termination

IV Adenosine
Reciprocating
tachycardias
using an
accessory
(WPW)
pathway
150-
250
Very
regular
except at
onset and
terminati
on
Retrograde;
difficult to
see; monitor
the QRS
complex
150-250 Very regular
except at
onset and
termination
Normal Abrupt slowing caused by
termination of tachycardia or no
effect

Ventricular Arrhythmia
IV Adenosine
Ventricular
tachycardia
60-100 Regular Normal if
dissociated or
retrograde if
associated
(can be
difficult to
see)
110-250 Regular Abnormal,
>0.12 sec
None

Ventricular Arrhythmia
IV Adenosine
Accelerated
idioventricula
r rhythm
60-100 Regular Normal 50-110 Fairly regular;
may be
irregular
Abnormal,
>0.12 sec
None
Ventricular
flutter
60-100 Regular Normal;
difficult to
see
150-300 Regular Sine wave None
Ventricular
fibrillation
60-100 Regular Normal;
difficult to
see
400-600 Grossly
irregular
Baseline
undulation
s; no QRS
None

BRADY-ARRYTHMIA
IV Adenosine
First-degree
AV block
60-100 Regular Normal 60-100 Regular Normal Gradual slowing caused by sinus
Type I
second-
degree AV
block
60-100 Regular Normal 30-100 Irregular Normal Slowing caused by sinus slowing
and an increase in AV block
Type II
second-
degree AV
block
60-100 Regular Normal 30-100 Irregular Abnormal,
>0.12 sec
Gradual slowing caused by sinus
slowing
Complete AV
block
60-100 Regular Normal <40 Fairly regular Abnormal,
0.12 sec
None

BUNDLE BRANCH BLOCK
IV Adenosine
Right bundle
branch block
60-100 Regular Normal 60-100 Regular Abnormal,
0.12 sec
Gradual slowing and return to
former rate
Left bundle
branch block
60-100 Regular Normal 60-100 Regular Abnormal,
>0.12 sec
Gradual slowing and return to
former rate

SUPPORTS SVT SUPPORTS VT
Slowing or termination by vagal tone
Onset with premature P wave
RP interval ≤100 msec
P and QRS rate and rhythm linked to
suggest that ventricular activation
depends on atrial discharge, e.g., 2 : 1
AV block rSR′ V 1
Long-short cycle sequence
Fusion beats
Capture beats
AV dissociation
P and QRS rate and rhythm linked to
suggest that atrial activation depends on
ventricular discharge, e.g., 2 : 1 VA
block
“Compensatory” pause
Left axis deviation; QRS duration
>140 msec
Specific QRS contours (see text)
Differential Diagnosis of Wide-QRS Beats Versus Tachycardia

Right anteroseptal accessory pathway
• Normal to inferior axis
• The delta wave is upright in
leads I, II, and Avf and isoelectric
or negative in aVL; and negative
in aVR
• There is an rS in V 1 and V 2

Right posteroseptal accessory pathway
• Negative delta waves in leads II,
III, and aVF, upright in I and aVL,
localize this pathway to the
posteroseptal region
• The negative delta wave in V 1
with sharp transition to an
upright delta wave in V 2
pinpoints it to the right
posteroseptal area
• Atrial fibrillation is present.

Left lateral accessory pathway
• A positive delta wave in the anterior
precordial leads and in leads II, III, and
aVF, positive or isoelectric in leads I
and aVL, and isoelectric or negative in
leads V 5 and V 6 are typical of a left
lateral accessory pathway
• The relatively small amount of
preexcitation typical of left lateral
accessory pathways during sinus
rhythm, which is caused by the sinus
impulse taking longer to travel
through the entire right and left atria
to the accessory pathway than it does
from the sinus node to the AV node.

Right free wall accessory pathway
• The predominantly negative
delta wave in V 1
• the axis more leftward

Bradyarrhythmia
• Sinus bradycardia at a rate of 40
to 48 beats/min. The second and
third QRS complexes (
arrowheads ) represent
junctional escape beats. Note
the P waves at the onset of the
QRS complex.
• Non-respiratory sinus
arrhythmia occurring as a
consequence of digitalis toxicity.

SINUS ARREST
• The patient had a long-term
electrocardiographic recorder
connected when he died suddenly
of cardiac standstill. The rhythms
demonstrate progressive sinus
bradycardia and sinus arrest at
8:41 am . The rhythm then
becomes a ventricular escape
rhythm, which progressively slows
and finally ceases at 8:47 am . The
paired electrocardiographic strips
are continuous recordings.

Sinus nodal exit block
• Type I : The P-P interval shortens from the
first to the second cycle in each grouping,
followed by a pause. The duration of the
pause is less than twice the shortest cycle
length, and the cycle after the pause
exceeds the cycle before the pause. The
PR interval is normal and constant. Lead V
1 is shown
• TYPE II: The P-P interval varies slightly
because of sinus arrhythmia. The two
pauses in sinus nodal activity equal twice
the basic P-P interval and are consistent
with a type II 2 : 1 SA nodal exit block. The
PR interval is normal and constant. Lead
III recording is shown.

COMPLETE OR TYPE III SA EXIT BLOCK
• Sinus node exit block. After a
period of atrial pacing (only the last
paced cycle is shown), a sinus node
exit block developed. The tracing
demonstrates sinus node
potentials ( arrowheads ), recorded
with a catheter electrode, not
conducting to the atrium until the
last complex. Recordings are leads
I, II, III, and V 1 , right atrial
recording, sinus node recording,
and RV apical recording. The
bottom tracing is femoral artery
blood pressure

Wandering atrial pacemaker
• As the heart rate slows, the P
waves become inverted and then
gradually revert toward normal
when the heart rate speeds up
again. The PR interval shortens to
0.14 second with the inverted P
wave and is 0.16 second with the
upright P wave. This phasic
variation in cycle length with
varying P wave contour suggests a
shift in pacemaker site and is
characteristic of a wandering atrial
pacemaker

procainamide challenge
• After the prototypic changes on
the ECG are exaggerated, with
an increase in ST elevation, and
the ECG shows a type 1 pattern
with a downward-sloping coved
ST elevation and negative T
waves in V 1 to V 3 .

AV junctional rhythm
• AV junctional discharge occurs
fairly regularly at a rate of
approximately 50 beats/min.
Retrograde atrial activity follows
each junctional discharge. Bottom,
Recording made on a different day
in the same patient. The AV
junctional rate is slightly more
variable, and retrograde P waves
precede onset of the QRS complex.
The positive terminal portion of
the P wave gives the appearance of
AV dissociation, which was not
present.

Hypersensitive Carotid Sinus Syndrome
• Right carotid sinus massage (RCSM,
arrow ) results in sinus arrest and a
ventricular escape beat (probably
fascicular) 5.4 seconds later. Sinus
discharge then resumes. B, Carotid
sinus massage (CSM, arrow;
monitor lead) results in slight sinus
slowing but, more important,
advanced AV block. Obviously, an
atrial pacemaker without
ventricular pacing would be
inappropriate for this patient. HBE,
His bundle electrogram; HRA, high
right atrial electrogram.

Sick sinus syndrome with bradycardia-
tachycardia
• Sick sinus syndrome with
bradycardia-tachycardia. Top,
Intermittent sinus arrest is
apparent with junctional escape
beats at irregular intervals ( red
circles ). Bottom, In this continuous
monitor lead recording, a short
episode of atrial flutter is followed
by almost 5 seconds of asystole
before a junctional escape rhythm
resumes. The patient became
presyncopal at this point.

Atrioventricular Block (Heart Block)
• First-Degree Atrioventricular Block
• Second-Degree Atrioventricular Block
• Type I (Wenckebach) AV nodal block
• Type II (Mobitz) AV nodal block
• Third-Degree (Complete) Atrioventricular Block

First-degree AV block
• Left panel:The PR interval
measured 370 milliseconds (PA =
25 msec; A-H = 310 msec; H-V =
39 msec) during a right bundle
branch block. Conduction delay in
the AV node causes the first-degree
AV block
• Right panel:The PR interval is 230
milliseconds (PA = 39 msec; A-H =
100 msec; H-V = 95 msec) during a
left bundle branch block. The
conduction delay in the His-
Purkinje system is causing the first-
degree AV block.

Second-Degree Atrioventricular Block
• Typical 4 : 3 Wenckebach cycle. P waves (A tier)
occur at a cycle length of 1000 milliseconds. The PR
interval (AV tier) is 200 milliseconds for the first
beat and generates a ventricular response (V tier).
The PR interval increases by 100 milliseconds in the
next complex, which results in an R-R interval of
1100 milliseconds (1000 + 100). The increment in
the PR interval is only 50 milliseconds for the third
cycle, and the PR interval becomes 350
milliseconds. The R-R interval shortens to 1050
milliseconds (1000 + 50). The next P wave is
blocked, and an R-R interval is created that is less
than twice the P-P interval by an amount equal to
the increments in the PR interval. Thus the
Wenckebach features explained in the text can be
found in this diagram. If the increment in the PR
interval of the last conducted complex increased
rather than decreased (e.g., 150 msec rather than
50 msec), the last R-R interval before the block
would increase (1150 msec) rather than decrease
and thus become an example of an atypical
Wenckebach cycle

Type II AV block
• The sudden development of a His-Purkinje
block is apparent. The A-H and H-V intervals
remain constant, as does the PR interval. A
left bundle branch block is present. B,
Wenckebach AV block in the His-Purkinje
system. The QRS complex exhibits a right
bundle branch block morphology. However,
note that the second QRS complex in the 3 : 2
conduction exhibits a slightly different
contour from the first QRS complex,
particularly in V 1 . This finding is the clue that
the Wenckebach AV block might be in the His-
Purkinje system. The H-V interval increases
from 70 to 280 milliseconds, and then a block
distal to the His bundle results. HBE, His
bundle electrogram; HRA, high right atrium;
RV, right ventricle.

Third-Degree (Complete) Atrioventricular
Block
• The ventricular rate in acquired
complete heart block is less than
40 beats/min but can be faster
with congenital complete AV
block.

DEFINE VT
• Ventricular arrhythmias are characterized by a wide QRS (>120 msec)

SPRECTRUM
• Premature Ventricular Complexes
• NON SUSTAINED VT
• VT
• VFIB

SITE OF ORIGIN
• Ventricular rhythm disturbances are those rhythms whose driving
circuit or focus originates in ventricular tissue, including myocardium,
annuli, valve cusps, aorta, pulmonary artery, bundle branches, or
Purkinje fibres

VT- Anatomic Location
LOCATION ECG PATTERN
Outflow Tract VT LBBB morphology and inferior axis
Right ventricular outflow tract (RVOT) Later precordial transition (V 3 or later)
Narrower R wave duration and lower R/S wave
amplitude ratio in V 1 and V 2
Left ventricular outflow tract (LVOT) Early precordial transition (by V 3 )
Earlier precordial transition than SR
Broader R wave duration and greater R/S wave
amplitude ratio in V 1 and V 2
Notch (qrS) in V 1 or V 2
Left aortic cusp “M” or “W” pattern in V 1
Monophasic R by V 1 /V 2
Greater R wave II/III ratio
Lead I QS or rS

Right aortic cusp Monophasic R by V 2 /V 3
Positive notched R-wave in lead I
Aortomitral continuity qR in lead V 1
Positive concordance across precordium
Rs/rs complex in lead I
R wave ratio <1 in II/III
Epicardial MDI >55%
QS in lead I
QS in leads II, III, and aVF (if superiorly directed, near
MCV)
Q-wave ratio in aVL/aVR >1.4 or S wave amplitude
>1.2 mV
“Transition break,” specifically a loss of R from leads
V 1 to V 2 (QS or rS) with prominent R by V 3 (suggests
near anterior interventricular vein)
2 3

Pulmonary artery Tall R wave in the inferior leads
Larger Q wave ratio in aVL/aVR
Larger R/S amplitude in lead V 2
Larger Q wave ratio in aVL/aVR
Larger R/S amplitude in lead V 2
Tricuspid annular LBBB morphology and inferior or superior axis
R wave in lead I
R or r with overall positive polarity in aVL
Later precordial transition (>V 3 )
Tricuspid inflow or parahisian LBBB morphology and inferior axis
Large R wave in lead I
R wave with flat/positive polarity or “w” pattern in aVL
Mitral annular (MA) •RBBB pattern with concordance in leads V 1 to V 6
Anterior MAVT: positive QRS polarity in leads II, III, and
aVF and negative QRS polarity in leads I and aVL
•

Fascicular VT
Left posterior fascicle RBBB and left axis deviation (LAFB pattern)
rsR′ in V 1
q in I and aVL
Narrow QRS ≤140 msec
Left anterior fascicle RBBB and right axis deviation (LPFB pattern)
Narrow QRS <140 msec
Left septal Incomplete RBBB (QRSd ~100-110 msec) and normal
axis

Papillary Muscle VT
Posterior papillary muscle RBBB; can have varied axes
Posterior papillary muscle qR or R in V 1
Absent Q in leads I and aVL
Anterior papillary muscle qR or R in V 1
rS in leads I and aVL
Crux VT Leftward-superior axis QRS
Delayed intrinsicoid deflection
Basal crux: LBBB pattern with early precordial
transition
Apical crux: midprecordial transition with QS in V 5 /V 6

Accelerated idioventricular rhythm[AIR]
AIR competes with the sinus rhythm.
Wide QRS complexes at a rate of 110
beats/min fuse ( F ) with the sinus
rhythm, which takes control briefly,
generates the narrow QRS
complexes, and then yields once
again to the accelerated
idioventricular rhythm as the P
waves move “in and out” of the QRS
complex. This example of
isorhythmic AV dissociation may be
caused by hemodynamic modulation
of the sinus rate via the autonomic
nervous system.

Stepwise Criteria Favoring VT :Algorithms

WIDE QRS VS VT
KINDWALL WELLENS BRUGADA MILLER
R >30 msec in V1 or V 2→ VT AV dissociation → VT Absence of RS complex in all
precordial leads → VT
Initial R wave in aVR → VT
Any Q in V6 → VT QRS width >140 msec → VT Longest R/S interval >100 msec
in any precordial lead → VT
aVR with initial r or q >40 msec
in duration → VT
60 msec to S wave nadir in
V 1or V 2 → VT
Left axis deviation >−30
degrees → VT
AV dissociation → VT aVR with a notch on the
descending limb of a negative-
onset and predominantly
negative QRS in aVR → V
Notched downstroke S wave in
V 1 or V 2→ VT
If RBBB morphology,
monophasic or biphasic QRS in
V 1→ SVT or R-to-S ratio of <1
in V 6 → VT
If RBBB morphology,
monophasic R or qR in V1 →
VT
R taller than R′ → VT
rS in V 6 → VT
In aVR, mV of initial 40 msec
divided by terminal 40 msec
(v i /v t≤1) → VT
If LBBB morphology, S in V 1 -
V 2 → VT
If LBBB morphology, initial R
>40 msec in duration → VT
Slurred or notched S in V 1 or

Fusion and capture beats during VT
 The QRS complex is wide
 R-R interval is regular except for
occasional capture beats ( C ) that
have a normal contour and are
slightly premature. Complexes
intermediate in contour represent
fusion beats ( F )
 Even though atrial activity is not
clearly apparent, AV dissociation is
present during VT and produces
intermittent capture and fusion
beats

Heart stop in diastole when plasma K+ level rises?
• Normally, potassium has a tendency to move outside the cells due to the concentration gradient.
• As plasma potassium rises, this concentration gradient is reversed.
• So potassium will move into the cells.
• The cell's resting membrane potential is very sensitive to changes in extracellular potassium ion
concentration.
• Elevated potassium, or hyperkalemia, causes the resting electrical potential of the heart muscle
cells to be lower than normal (less negative).
• Without this negative resting potential, cardiac cells cannot repolarize.
• That means all your cells are depolarized.
• This inactivates sodium channels.
• Inactivated sodium channels means the cells can not fire.
• The heart can not contract.
• That's why, heart stops in diastole.

Cardiac arrhythmias due to digoxin toxicity
• Sinus bradycardia, tachycardia,
block, and arrest
• Ectopic atrial tachycardia with
block
• AV nodal block
• Junctional rhythm, tachycardia,
and bradycardia
• VPC,VT,VF
• Bidirectional ventricular
tachycardia
• Atrial flutter, atrial fibrillation,
and Mobitz type II second
degree AV block are the least
likely of all the arrhythmias to be
caused by digoxin toxicity

Cardiac arrhythmias Yellow Oleander poisoning
• Rhythms characteristic of Mobitz
type II AV conduction block,
although reported to be rare in
isolated digoxin poisoning,
occurred in several cases of the
oleander poisoning

Arrhythmogenic Right Ventricular (RV) Cardiomyopathy
Definite diagnosis 2 major criteria or
1 major and 2 minor criteria or
4 minor criteria from different categories
Probable 1 major and 1 minor criteria or
Possible 1 major or

Criteria
• Echocardiography/MRI
• Biopsy
• ECG
• Family history

Epsilon wave
• Normal sinus rhythm in a patient
with arrhythmogenic right
ventricular (RV) cardiomyopathy
(dysplasia). The arrowheads in V
1 and V 2 point to late RV
activation called an epsilon wave

VT in the same patient with RV dysplasia

Torsade's de pointes
• A demand ventricular pacemaker
(VVI) had been implanted because
of a type II second-degree AV block
• After treatment with amiodarone
for recurrent VT, the QT interval
became prolonged (approximately
640 msec during paced beats), and
episodes of TdP developed. In this
recording the tachycardia
spontaneously terminates, and a
paced ventricular rhythm is
restored

Torsade's de pointes
• A young boy with congenital
long-QT syndrome
• The QTU interval in the sinus
beats is at least 600
milliseconds. Note the TU wave
alternans in the first and second
complexes. A late premature
complex occurring in the
downslope of the TU wave
initiates an episode of VT[R-ON-
T]

Brugada Syndrome
• RBBB
• ST-segment elevation in the anterior precordial leads
• Often without evidence of structural heart disease

Twelve-lead ECG of a patient with BS
• RT bundle branch block pattern
and persistent ST elevation in
leads V 1 through V 3
• Shows a type 2 Brugada pattern
with a “saddleback” ST-segment
elevation greater than 1 mm and
a biphasic T wave in V 1 (positive
in V 2 -V 3 )

Characteristics of Brugada-Pattern
Electrocardiograms
YPE 1 TYPE 2 TYPE 3
J wave
amplitude
≥2 mm ≥2 mm ≥2 mm
T wave Negative Positive or
biphasic
Positive
ST-T
configuration
Coved Saddleback Saddleback
ST segment
(terminal
portion)
Gradually
descending
Elevated
≥1 mm
Elevated
<1 mm

Arrhythmias

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