TEST EKG

Supraventricular tachycardia

• Abbreviated SVT
• “Supra” means “above”
• Supraventricular tachycardia comes from above the
ventricles
• DO NOT CONFUSE with NSVT (non-sustained
ventricular tachycardia)
• (Essentially) all narrow-complex tachycardia has a
supraventricular origin
 SVT possible sites of origin

• Sinus node
• Atria
• Atrioventricular node
• His bundle

• Or some combination of the above

 Categorizing tachycardia
•Mechanism
•Location
•Frequency
Mechanism

Re-entrant Automatic
Atrial Atrial flutter Automatic atrial tachycardia
Atrial fibrillation Chaotic atrial tachycardia
AV Node and AV node re-entry Junctional tachycardia
His Bundle
Location

Atrium and WPW

Ventricle Concealed AP
PJRT
Mahaim
 Classifying tachycardia:
• Re-entrant
mechanism
• Automatic
(1) reentrant atrial • (1) automatic atrial
• tachycardia • tachycardia
• (atrial flutter)
• (2) automatic
• (2) AV reentry • junctional tachycardia
• a. WPW • (3) chaotic (multifocal) atrial
• orthodromic tachycardia
• antidromic
• “two pathway”
• b. concealed accessory
• pathway
• c. PJRT
• d. Mahaim
• (3) AV node reentry
• a. typical
• b. atypical
• (4) atrial fibrillation
 Classifying tachycardia:
•Atrium
location
• automatic atrial tachycardia
• reentrant atrial tachycardia
• chaotic atrial tachycardia
• atrial fibrillation

AVN and His bundle

AV node reentry tachycardia
automatic junctional tachycardia

• Atrium and ventricle

• accessory pathway tachycardia
• concealed
• WPW
• PJRT
• Mahaim
 Differentiating AF from AFl

• AFl is a macroreentrant atrial rhythm with a

reentry circuit that involves a large area of
atrial myocardium

• AF is caused by multiple wandering

wavelets, a hodgepodge of microreentrant
circuits, often located in the pulmonary veins
Atrial flutter
 Atrial flutter
• P waves exhibit a “sawtooth” pattern referred
to as flutter waves or “F” waves
• Atrial rate is typically 250-350 beats per
minute (bpm)
Atrial flutter (with 4:1 response)
 Atrial fibrillation
• Rapid and irregular atrial activity at a rate of
350-600 impulses per minute
• Usually irregularly irregular ventricular
response
• There are no P waves
• Sometimes the F waves are so fine, the
surface EKG cannot detect them
Atrial fibrillation
Wolf Parkinson White
 Wolff-Parkinson-White
Syndrome

Delta Wave

Wide QRS
Short PR
Multifocal Atrial Tachycardia
Supraventricular Tachycardia
Typical AVNRT and normal sinus rhythm after conversion.

Richard L. Page et al. Circulation. 2016;133:e506-e574

Copyright © American Heart Association, Inc. All rights reserved.

 Atypical AVNRT. Arrows point to the P wave.

Richard L. Page et al. Circulation. 2016;133:e506-e574

Copyright © American Heart Association, Inc. All rights reserved.

Right Bundle Branch Block
LBBB
 Left Bundle Branch Block

• Left ventricle gets a delayed impulse

• QRS is widened (at least 3 boxes)
• V5 and V6 have RR’ (rabbit ears)
• Be careful not to miss any hiding q waves!
• Pacemaker if syncope occurs
 Sick Sinus Syndrome

• Conduction problem with no junctional escape

during sinus pause
• Diagnose with ECG or Holter. If inconclusive, need
electrophysiologic testing.
• If asymptomatic, leave alone. If symptomatic,
needs pacemaker.
 First Degree AV Block

• Delay at the AV node results in prolonged PR

interval
• PR interval>0.2 sec.
• Leave it alone
Wolf Parkinson White
 WPW
• Ventricles receive partial signal normally and
partially through accessory pathway
• Symptomatic tachycardia, short PR interval
(<0.12), a delta wave and prolonged QRS (>0.12)
• Electrophysiologic testing helps to identify the
reentry pathway and location of the accessory
pathway
 Atrial tachycardia.

Richard L. Page et al. Circulation. 2016;133:e506-e574

Copyright © American Heart Association, Inc. All rights reserved.

 Permanent form of junctional reciprocating tachycardia (PJRT).

Richard L. Page et al. Circulation. 2016;133:e506-e574

Copyright © American Heart Association, Inc. All rights reserved.

Atrial Flutter
Atrial Fibrillation
Ventricular Tachycardia
 Ventricular Tachycardia

• Impulse is initiated from the ventricle itself

• Wide QRS, Rate is 140-250
• If unstable DC cardiovert
• If not, IV Amiodarone and/or DCCV
• Consider procainamide
• Nonsustained ventricular tachycardia needs no treatment
 Torsades de Pointes

• “Twisting of the points” is usually caused by medication

(quinidine, disopyramide, sotalol, TCA), hypokalemia or
bradycardia especially after MI
• Has prolonged QT interval
• Acute: Remove offending medication. Shorten the QT
interval with magnesium, lidocaine, isoproterenol, or
temporary overdrive pacing
• Chronic: may need pacemaker/ICD, amiodarone, beta-
blockers
 Ventricular Fibrillation

• Most common in acute MI, also drug overdose,

anesthesia, hypothermia & electric shock can
precipitate
• Absence of ventricular complexes
• Usually terminal event
• Use Amiodarone if refractory to DCCV.
 Atrial fibrillation
accounts for 1/3 of all 6%
patient discharges PSVT

with arrhythmia as 6%
PVCs 18%
principal diagnosis. Unspecified
4%
Atrial
Flutter

9% 34%
SSS Atrial
Fibrillation

8%
Conduction
Disease
10% VT
3% SCD

2% VF
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
 Atrial Flutter
• Treatment:
– Same as atrial fibrillation but often harder to slow the
ventricular rate
– Long term treatment is ablation and NOT drugs!
 Sinus tachycardia

There is one P with one QRS

Regular rhythm
 Atrial Tachycardia

•P before QRS. (may have different p morphology)

•May be indistinguishable from sinus tachycardia

•Usually abrupt onset and offset (as opposed to gradual with sinus

tachycardia
 Multifocal atrial tachycardia

• One P wave with one QRS

• Irregular rhythm
• Varying p wave morphology and PR segments
• Usually Seen in patients with lung disease
 Atrial fibrillation

 No clear visible P waves

 Irregular rhythm
Atrial Fibrillation
 Supraventricular tachycardia

 Narrow complex, regular

 Starts and stops suddenly, usually with PAC

 May see inverted p waves in the ST

segment or T wave
 P waves may be invisible
Ventricular tachycardia
 Ventricular tachycardia

•Wide complex tachycardia

•May be monomorphic or polymorphic

•Usually preceded by PVC

•Look for more QRS then P

 Ventricular tachycardia

•Wide complex tachycardia

•May be monomorphic or polymorphic

•Usually preceded by PVC

•Look for more QRS then P

Polymorphic VT/Torsade de Pointes

• Classic pattern of “twisting” of QRS in an axis

•Can be seen with electrolyte abnormalities- Hypo K,

Hypo Mg or Long QT syndrome

•Typical onset- bradycardia, long R-R interval followed by

premature ventricular complex (PVC)

Ventricular Fibrillation

No clear
visible P
Very fast

> 300
bpm
** This may not be ASYSTOLE
•ALWAYS check that leads are properly put on

•ALWAYS check gain is not too low!

Wide Complex tachycardia
EKG
 EKG – 12 Leads
• Anterior Leads - V1, V2, V3, V4
• Inferior Leads – II, III, aVF
• Left Lateral Leads – I, aVL, V5, V6
• Right Leads – aVR, V1
 Intervals
• Measure length of PR interval, QT interval,
width of P wave, QRS complex
 QTc
• QTc = QT interval corrected for heart rate
– Uses Bazett’s Formula or Fridericia’s Formula

• Long QT syndrome – inherited or acquired

(>75 meds); torsades de ponites/VF; syncope,
seizures, sudden death
Axis
 Bundle Branch Blocks
• Diagnosed by looking at width and
configuration of QRS complexes
Bundle Branch Blocks
 Preexcitation
• Wolff-Parkinson-White (WPW) Syndrome
– 1. PR interval < 0.12 sec
– 2. Wide QRS complexes
– 3. Delta waves seen in some leads
• Lown-Ganong-Levine (LGL) Syndrome –
– 1. PR interval < 0.12 sec
– 2. Normal QRS width
– 3. No delta wave
• Common Arrhythmias
– Paroxysmal Supraventricular Tachycardia (PSVT) – narrow QRS’s
are more common than wide QRS’s
– Atrial Fibrillation – can be rapid and lead to ventricular
fibrillation
 Preexcitation
WPW LGL
Supraventricular Arrhythmias
Ventricular Arrhythmias

PVC’s
Torsades de Pointes
 Atrial Enlargement
• Look at P waves in leads II and V1
• Right atrial enlargement (P pulmonale)
– 1. Increased amplitude in first portion
of P wave
– 2. No change in duration of P wave
– 3. Possible right axis deviation of P wave
• Left atrial enlargement (p mitrale)
– 1. Occasionally, increased amplitude of terminal part
of P wave
– 2. More consistently, increased P wave duration
– 3. No significant axis deviation
 Myocardial Infarction
• Dx – Hx, PE, serial cardiac enzymes, serial
EKG’s
• 3 EKG stages of acute MI
– 1. T wave peaks and
then inverts
– 2. ST segment elevates
– 3. Q waves appear
 Q Waves
• Criteria for significant Q waves
– Q wave > 0.04 seconds in duration
– Q wave depth > ⅓ height of R wave in same QRS
complex
• Criteria for Non-Q Wave MI
– T wave inversion
– ST segment depression persisting > 48 hours in
appropriate clinical setting
 Electrolyte Abnormalities on EKG
• Hyperkalemia – peaked T waves, prolonged
PR, flattened P waves, widened QRS, merging
QRS with T waves into sine wave, VF
• Hypokalemia – ST depression, flattened T
waves, U waves
• Hypocalcemia – prolonged QT interval
• Hypercalcemia – shortened QT interval
 Drugs
• Digitalis
– Therapeutic levels – ST segment and T wave changes
in leads with tall R waves
– Toxic levels – tachyarrhythmias and conduction blocks;
PAT with block is most characteristic.
• Multiple drugs associated with prolonged QT
interval, U waves
– Sotalol, quinidine, procainamide, disopyramide,
amiodarone, dofetilide, dronedarone, TCA’s,
erythromycin, quinolones, phenothiazines, various
antifungals, some antihistamines, citalopram (only
prolonged QT interval – dose-dependent)
 EKG ∆’s in other Cardiac Conditions
• Pericarditis – Diffuse ST segment elevations and
T wave inversions; large effusion may cause low
voltage and electrical alternans (altering QRS
amplitude or axis and wandering baseline)
• Myocarditis – conduction blocks
• Hypertrophic Cardiomyopathy – ventricular
hypertrophy, left axis deviation, septal Q waves
EKG ∆’s in Pulmonary Disorders
• COPD – low voltage, right axis deviation, and
poor R wave progression.
• Chronic cor pulmonale – P pulmonale with
right ventricular hypertrophy and
repolarization abnormalities
• Acute pulmonary embolism – right ventricular
hypertrophy with strain, RBBB, and S1Q3T3
(with T wave inversion). Sinus tachycardia and
atrial fibrillation are common.
EKG ∆’s in Pulmonary Disorders
• COPD – low voltage, right axis deviation, and
poor R wave progression.
• Chronic cor pulmonale – P pulmonale with
right ventricular hypertrophy and
repolarization abnormalities
• Acute pulmonary embolism – right ventricular
hypertrophy with strain, RBBB, and S1Q3T3
(with T wave inversion). Sinus tachycardia and
atrial fibrillation are common.
 Case 1
• 53 year old caucasian female with 4 day hx
of severe central chest pain on exertion,
previously alleviated with rest; now
worsened over last 24 hours and sustained
at rest
• PMHx – DM2, HTN, hyperlipidemia
• Appears unwell, in pain, sweaty, and grey
 Case 1

• Diagnosis? EKG findings?

 Case 1
• Acute anterior ST-elevation MI with
“tombstone” or “fireman’s hat” in V1-V4
• Tx? Localization?
 Case 1
• PCI stenting of LAD

• Post-procedure = resolving ST elevation; loss of

ominous tombstone effect; Q waves developing
 Case 2
• 45 yo male presents with acute SOB s/p long
vacation in Paris
• PMHx - asthma, Crohn’s disease, anxiety,
GERD, tobacco abuse
• VS 37, 148/92, 130, 26
• Patient appears uncomfortable but otherwise
unremarkable exam
 Case 2

• Diagnosis? EKG findings?

 Case 2
• Acute PE with sinus tachycardia, a PVC, and
S1Q3T3 pattern
 Case 4

• Diagnosis? EKG findings?

 Case 3

• Diagnosis? EKG findings?

 Case 5

• Diagnosis? EKG findings?

 Case 6

• Diagnosis? EKG findings?

 Case 7

• Diagnosis? EKG findings?

 Case 8

• Diagnosis? EKG findings?

 Case 9

• Diagnosis? EKG findings?

 Case 10

• Diagnosis? EKG findings?

 Case 10
• Monomorphic sustained ventricular
tachycardia (VT) – could rapidly deteriorate
into VF, torsades de pointes, asystole, or
sudden death
 Case 12

• Diagnosis? EKG findings?

 Case 12
• Hyperkalemia – tall peaked T waves present
throughout; other progressive EKG changes
may follow with increasing potassium levels –
prolonged PR interval, flattened P waves,
widening QRS, sine waves
• Sinus tachycardia also present
 Bonus Case

• Diagnosis? EKG findings?

 41M weakness

Irregular wide complex rhythm, peaked T, no P = hyperkalemia

 61M fever, cough, dyspnea

Regular WCT, P waves in V1 = atrial tachycardia + LBBB

 64F SOB, hypotension, PMH: a fib

Regular WCT, bidirectional = Digoxin toxicity

What can you see?
 Atrial Flutter
 SVT, regular
 Saw-tooth flutter waves.
 Flutter waves rate = 300 bpm
 Ventricular rate = 150 bpm or 100 bpm, due to AVN block ratio
of 2:1 or 3:1
 Ectopic atrial beat causes a re-entrant circuit within the atria.
 Causes
 As for AF
 Hyperkalaemia
 Digoxin toxicity.
 Treatment
 As for AF (discussed later)
 Can be differentiated from Fast AF with vagal manouvres/adenosine.
What can you see?
 Ventricular tachycardia
• Broad complex tachycardia

• Causes
» Electrolyte derangement (hypokalaemia, hypomagnesaemia,
hypocalcaemia)
» Myocardial ischaemia/infarct
» Cardiomyopathy
» Congenital (HOCM, long QT)

• Treatment
» Amiodarone
» ICDs
What can you see?
 Atrial Fibrillation
 Types
Paroxysmal (acute onset, spontaneous termination within 1 week)
Persistent (>7 days, can be cardioverted)
Permanent (> 1 year not terminated by cardioversion)

 Causes
Cardio (HTN, valvular disease, CAD, myositis)
Pulmonary (PE, pneumonia, COPD, lung Ca)
Metabolic (hyperthyroidism)
Infection
Drugs (alcohol, illicit drugs)
 AF
 Investigations
 Bedside – ECG/24 hour tape
 Bloods – FBC, U&Es, LFTs, TFTs, coag screen
 Imaging – CXR, echo

 Management (Rate vs Rhythm)

 Rate –
 Beta blockers
 Digoxin

 Rhythm
 Cardioversion
 Sotalol
 Amiodarone (HF)
 AF - CHA2DS2-VASc score
 Thromboprophylaxi
s
C – cardiac failure (1)
H – HTN (1)
A - >75 (2, 1 if 65-74)
D – diabetes (1)
S- stroke/TIA (2)
Va – vascular disease
Sc – female (1)
0 = Low Risk
1 = Moderate risk
2 or more = high risk
 MANIFESTASI KLINIK
Aritmia Asimptomatis:
Aritmia Simptomatis:
• Palpitasi/berdebar
• Pusing
• Pingsan
• Sesak nafas
• Nyeri dada
• Lemah, cepat capek
 EPS procedure
• Vascular access (Venous – arterial)
• Electrode catheter (contact mapping – pacing)
• Catheter position
• Multichannel recording system +
programmable stimulator
 Electrode catheter Connecting port

4 3 12 1

Dist.
Prox.

Bipolar intracardiac recording

(localized leectrical activity-
depolarization of tissue)
Ablation catheter RF-current
applic.
 Catheter position
RAO LAO

His

CS
RV
 Challenge of deploying newer therapies optimally
Equality of access to treatment options..?

• Anti-arrhythmic management
– Dronedarone / Vernakalant
DDDRP
– Pacing & AV-nodal ablation
– Catheter ablation

• Stroke Prevention
- Warfarin vs Dabigatran
- Left atrial occlusion devices

• Newer options in valve disease

- Mitral valve clips for MR
- TAVI for AS
- Timing of surgical MVR
◊ Presence of AF was associated with worse NYHA-FC (p < 0.0001)
◊ Improved in 6-minute walk test in rhythm control group (p = 0.049)

Effect of rate & rhythm control on left ventricular function & cardiac dimensions in
patients with persistent atrial fibrillation: RACE Study

◊ Routine rate controlEcho studydeterioration

prevents with 1-2 year of
follow-up (N = 335)
LV-function.
In rhythm control group LV-function compared between SR & AF pts at study end
◊ Maintenance of sinus rhythm improves LV-function & reduces atrial sizes
Hagens et al. Heart Rhythm 2005, 2:19-24
Circulation 2004, 109:1509-15

◊ Variables associated with increased risk of death

- Increasing age
- Coronary artery disease
- Congestive cardiac failure; Left ventricular dysfunction
- Diabetes mellitus or smoking
- Stroke or TIA
- Mitral regurgitation

◊ Variables associated with reduced risk of death

- Maintenance or sinus rhythm
- Warfarin therapy

◊ Anti-arrhythmic drugs ≠ improved survival

- any benefits are offset by adverse effects
Cardiac resynchronisation therapy
+ ICD component

CRT
&
CRTD
3

2
Pacing to improve coordination of cardiac contraction
(atrio-ventricular; inter- & intra-ventricular resynchronisation)
Pacing to improve LV-function

RA

LV

RVA
Electrical

resynchronization
 MADIT-CRT Trial
To assess whether CRT-D reduces mortality &
heart failure events in patients with:
NYHA class I-II
QRS > 130ms
LVEF < 30%

■ 34% reduced all-cause mortality

or 1st heart failure event with CRT-D
(p < 0.001) p < 0.001

■ 41% reduction in HF events

(p < 0.001)

■ Benefits IHD = DCM

 Surgical options
• MAZE procedure
-Routinely done during mitral valve surgeries;
often done other times
• LA appendage ligation
• Percutaneous left atrial appendage occlusion
(PLAATO) and others
MAZE
PLAATO
 PLAATO

• Very cool; effectiveness studies of this and

competing devices are underway