Understanding the ECG

• Normal conduction • Disease patterns

• Action potential • Ventricular hypertrophy
generation • Arrhythmias
• The 12 lead ECG • Heart Block
• Basic interpretation: • Myocardial ischemia
the 3 Rs : “Rate and infarction
Rhythm and • Interpretation
diRection”

D P NAIDOO
 The ECG Action Potential
• Current moves from negative to positive pole
• An electrode facing the current will record the
highest vector
– Towards the electrode: positive (above baseline)
– Away from the electrode: negative (below b/line)
 The direction of the current:
 Deflection

Current Electrode

Θ Deflection
avR avL

Std I

Std III Std II

avF
 The P- QRS rule

St II:

P is upright; precedes QRS = Sinus rhythm

PR interval
- 0.12 – 0.20 sec (3-5 small blocks).
QRS complex width
- 0.04 – 0.10 sec (1-2½ small blocks)
QT interval: 0.36-0.45 sec
AVR: PQRST complex always negative [if not:
leads wrongly placed; dextrocardia].
 AXIS

(in the direction

of the main
muscle mass –
LV)
 X axis

Y axis
The lead with the tallest
QRS complex indicates
the mean vector (AXIS)
By convention the ECG is recorded on paper at 25mm/sec.
This leads to a widening of the QRS complex
 Practical steps to interpretation of ECG
1. Check standardization and aVR
2. Rate and Rhythm: std lead II (P-wave scan)
3. diRection (qrs scan)
4. Measurements ( width and height scan)
- P-R interval
- QRS-duration and height (voltage)
- QT interval
6. Diagnostic patterns
- isoelectric baseline (ST-segment scan)
The QT interval
 The QT interval
• Ventricular activation time: ie from
depolarization and repolarization
• Measured from the beginning of the QRS to
the end of the T wave
• Normal: 0.36 to 0.44 seconds (9-11 boxes)
– normal QT Intervals is less than half of the R-R
Interval for heart rates <100/min
• Varies with gender, age and heart rate
below 100 bpm
 Case study
 Mrs NM, 73 years old.
 Known with scleroderma.
 2 week history of fatigue, intermittent
shortness of breath, nausea, dizziness and a
few episodes of pre-syncope.
 Presented to the base hospital after an episode
of syncope.
 Haemoglobin of 11.6 and platelets 72
 Cardiac markers were negative, magnesium 0.72 and
potassium 3.6.
 CXR showed mild cardiomegaly only.
 Pt developed an episode of ventricular fibrillation
(VF)/polymorphic ventricular tachycardia and was
defibrillated and started on an amiodarone infusion
 The ECG showed:
 Evaluation
 Complete heartblock – ventricular rate 37/min.
 QTc 397ms.
 Notched T waves.
 An episode of torsades de pointes that
terminates spontaneously
 Echocardiogram normal
 Of note was that she was allergic to penicillin.
 Patient was taking the following chronic medication:
 Methotrexate
 Chloroquine
 Paracod
 Calcium carbonate
 Vitamin D
 Folate
 Tear naturale
 Hydrochlorothiazide
 Enalapril
 Amlodipine
 A temporary pacemaker was immediately
inserted and followed 2 days later by insertion
of a permanent pacemaker
 She enjoyed an uneventful hospital stay and
was discharged a week later
 Introduction
 Long-QT syndrome is characterized by
abnormal QT-interval prolongation on the
surface ECG and an increased risk of sudden
death.
 The QT interval is considered to be prolonged
when it is >440ms in men and >460ms in
women.
 Long-QT syndrome can be congenital or
acquired.
 Long-QT syndrome is dangerous because it
can give rise to polymorphic ventricular
tachycardia – notably Torsades de pointes –
which can result in ventricular fibrillation,
asystole and death.
 Remember: the cardiomyocyte action potential
Failure to shorten
Long QTc
 Acquired long-QT
 Acquired long-QT syndrome is more common
than the genetic long-QT syndrome.
 The two main causes are electrolyte
disturbances and drugs.
 Miscellaneous causes form a very small part of
the total number of cases.
 Drug induced long QT
 Electrolyte disorders
 hypokalaemia
 hypomagnesaemia
 hypocalcaemia
 Drug-induced
 Antiarrhythmic drugs
 Quinidine
 Amiodarone
 Sotalol
 Procainamide
 Ranolazine
Drug induced long QT cont’d
 Antihistamines:Terfenadine/Astemizole
 Macrolides: Erythromycin

 Certain fluoroquinolone antibiotics

 Psychiatric agents
 Major tranquilizers
 Tricyclic antidepressants
 GI agents: Cisapride, Domperidone
 New investigational agents
 Clinical presentation
Common presentations of the long-QT syndrome
are:
 Palpitations

 Presyncope

 Syncope

 Polymorphic ventricular tachycardia (Torsades)

 Cardiac arrest

It is also common to have a prolonged QT interval

without any symptoms.
 Treatment
 Stop the offending agent
 Arrhythmia prevention
 involves the use of medication or surgery that attacks the
underlying cause for the prolongation.
 The most important medication in use for long-QT
syndrome is long acting beta blockers like atenolol and
nadolol. They do not decrease the QT interval but blunt the
exercise response
 Arrhythmia termination
 ICD
 ICD
 Arrhythmia termination is accomplished by
insertion of an inplantable cardioverter-
defibrillator (ICD).
 ICDs are commonly inserted for patients with
syncope on beta-blockers or for those who
have had a cardiac arrest and should also be
considered for people with a QTc longer than
500ms.
Torsade de pointes
 It is commonly seen in patients with diarrhoea,
malnourishment and chronic alcoholics
 The treatment is to defibrillate the patient, give
magnesium by infusion, anti-arrhythmic drugs
may be required and to treat the underlying
cause