ECG READING for FINAL YEAR

ECG: A graphical waveform representation of Electrical activity of myocardial tissue.

GIVES INFORMATION about: RRAHI (mnemonic)

RATE
RHYTHM
AXIS
HYPERTROPHY
ISCHEMIA/INFARCTION

PLACEMENT OF ECG LEADS

3 limb leads and 6 chest leads.

RA (avR)on right arm

LA (avL) on left arm
LL (avF) on left leg
RL(neutral lead) on right leg
V1 on right sternal border 4th IC space
V2 on Left sterna border 4th IC space
V4 in middle clavicular line 5th IC space
V3 in b/w v2 and v4
V5 in anterior axillary line
V6 in mid axillary line

(rest of 3 LEADS..I,II and III are recorded by reversal of these electrodesimp viva question)
current flowing towards a lead produces positive upward deflection and vice versa.
FIRST STEP is to know whether ECG given is standardized or not.

The arrowed column at start should be 2 large squares in height and 1 large square in width
(@normal speed of 25mm/sec).
(The given ECG is recorded at high paper speed thus showing 2 large squares in width)
Faster paper speed is used in diagnosing different tachyarrhythmias.
ECG PAPER PARAMETERS:
1 large square = 5 small squares
1 small square = 1 x 1 mm
Along horizontal (X AXIS); 1 small square = 0.04 seconds at Normal ECG PAPER SPEED of 25mm/sec
(again faster paper speed is used in different tachyarrhythmias)
Along vertical (Y AXIS); 1 small square = 0.1 millivolts

RATE:
If rhythm is regular then most commonly used method is to count # of large squares b/w two R waves
and use this formula:
Heart rate=300/# of large squares

# of large squares
1
2
3
4
5
6
7

Approximate heart rate

300
150
100
75
60
50
43

If rhythm is Irregular then use 6 second rhythm strip of lead 2 present at bottom of ECG.
Heart rate = total # of R waves in rhythm strip x 10.

RHYTHM:
LEAD 2 is known as RHYTHM STRIP.
Paper and pencil method is used to check the regularity of rhythm. Mark two adjacent R waves on a
white paper and use it as standard to check the interval b/w next R waves. If interval is equal rhythm is
regular and vice versa.
Normal ECG has two important intervals.
PR interval: from start of P wave to start of R wave. Normal value: 0.12-0.20 seconds. Prolonged (>0.20
seconds) in heart blocks.
QT interval: from start of Q wave to start of T wave. Normal is <0.42 sec
QTc (corrected QT) = QT (observed)/ square root of RR interval
QT interval is prolonged by hypokalemia, hypocalcaemia, hypomagnesaemia and various Drugs e.g.
Class 1A (Quinidine, Procainamide) and Class 3 (Sotalol) antiarrhythmics which can lead to Torsade de
pointes.
QT interval is shortened by hypercalcaemia.

AXIS:
Thumbs method is used to check axis. Hold ECG paper in front of you as you place your left thumb on
lead 1 and right thumb on lead aVF in the direction of QRS complex in respective leads..

Both thumbs UP >> Normal AXIS

Both thumbs DOWN >> Extreme right Axis deviation
Otherwise thumb which is upright denotes the axis deviation to its side.

As a general rule, AXIS deviates AWAY FROM INFARCT but TOWARDS THE HYPERTROPHY (loves the bulk
:P )
P.S. in BUNDLE branch blocks QRS complexes attain certain morphologies. Imp to know esp. for M4.
WiLLiaM in left bundle branch block. QRS is W shaped in lead V1 and M shaped in lead V6.
MaRROW in right bundle branch block QRS M shaped in lead V1 and W shaped in Lead V6.
Bi fascicular block: right bb block + Axis deviation
Tri fascicular block: bi-fascicular block + AV block

AV BLOCKS very very important.

PR interval is prolonged. Normal is less than 3- 5 s.s. or 0.12-0.20 seconds. QRS is normal.
First degree: fixed prolongation of PR interval i.e. more than 0.20 seconds BUT NO beat is dropped. No
treatment needed
Second Degree: beat is dropped.
2 types

Mobitz type 1 (wenckeback phenomenon): progressive prolongation of PR interval until a beat

is dropped. No treatment needed
Mobitz Type 2: fixed prolongation of PR interval, like first degree BUT beat is DROPED here
after every 2 or 3 normal beats. Risk of progression to 3rd degree block and ultimately ASYSTOLE.
Treat with atropine or pacemaker.

Third degree (Complete Heart Block): No atrial beat is conducted to ventricles. Both chambers beat
independent
of each other. PP and RR interval are fixed, but PR INTERVALS ARE NOT FIXED (difference
from 2nd degree type 2 block). Symptomatic with spells of dizziness (STOKES ADAM syndrome)
CHARACTERISTIC CANNON A waves on JVP. Treat with atropine or PACEMAKER.

HYPERTROPHY:
Assess P waves for ATRIAL size and QRS complex for ventricular size.
Normal P waves < 0.12 seconds and < 2.5 mm on Y axis.
P Pulmonale: first half of P wave represents right atrium, so it increases in voltage to more than 2.5 s.s.
along Y axis. Seen in cor pulmonale (right atrial enlargement)
P Mitrale: Second half of P wave represents Left atrium, so it can increase in duration along X axis with
notched M shaped P wave. Seen in Mitral STENOSIS (left Atrial enlargement)
NORMAL QRS complex < 0.12 sec in duration
In LEFT VENTRICULAR HYPERTROPHY:
Left axis deviation,
S wave in V1 + R wave in V6 are >> 7 LARGE squares (35 s.s.)
In RIGHT VENTRICULAR HYPERTROPHY:
Right axis deviation,
positive R wave in lead V1 >> 7 small squares (Normally R wave Absent in V1)

ISCHEMIA/INFARCT: Most Important

for ISCHEMIA: look for

ST segment depression,
Inverted T waves and,
No pathological Q waves

for INFARCT: look for

ST segment elevation,
Hyper acute broad based T waves and,
Pathological Q waves (signifies DEAD tissue)
P.S. Physiological Q waves are less than 25% of R waves in height, and less than 1 s.s. duration.

How to look for ST segment ELEVATION:

In Services hospital, J point elevation is considered as ST segment elevation. J point is end point of QRS
complex and mark the junction between the termination of the QRS complex and the beginning of the
ST segment.
Reference point for elevation is ISOELECTRIC LINE i.e. PR SEGMENT. 2 s.s. elevation on limb leads and 1
s.s. elevation on chest leads is significant.
ATLEAST 2 contiguous limb leads should show ST segment Changes if to be considered significant,
EXCEPT in posterior wall MI where only lead V1 will show ST depression (not elevation).
LEAD representation of MYOCARDIAL AREAS:
Leads V1, V2: Ventricular septum
Leads V3, V4: Anterior wall
Leads V1-V4: Anteroseptal area
Leads V5, V6, aVL: Lateral wall
Leads II, III and aVF: Inferior wall (most common STEMI and very common in exams).
Mechanism of Bradycardia in Inferior Wall MI: Inferior wall is supplied by RCA which also supplies SA
and AV nodes (in most individuals). Also there is vagal stimulation as inferior aspect of the heart has rich
innervation of vagal nerve terminals, which lead to G.I. Symptoms (nausea, vomiting etc.) and
bradycardia.
Hyperacute T waves of MI versus Hyperkalemia Tall T waves:
Hypercute Tall T wave is first ECG change seen in STEMI. These are broad based and slightly
asymmetrical ascending and descending limbs. ST segment changes may also be present
Hyperkalemia Tall T waves. These are narrow based and have very symmetrical limbs. ST
segment is normal.
OTHER T wave abnormalities:
T wave flattening or inversion along with ST depression, QT prolongation and U waves in
Hypokalemia (also with class 3 potassium channel blockers).
T wave inversion also seen in ISCHEMIA, ventricular hypertrophy.

CARDIAC ARRHYTMIAS
Classification:

Sinus tachycardia (anxiety, fever, anemia, hyperthyroidism, drugs e.g. epinephrine)

Sinus bradycadia (athletes, hypothermia, hypothyroidism, vagal stimulation and
vasovagal syncope and Drugs e.g. beta blockers). Relative bradycadia in typhoid, viral
infections and raised ICP (Cushing reflex in raised intracranial pressure). Bradycardia
plus hypertension imp to note vitals in meningitis).
SUPRA-Ventricular Arrhythmia: consist of SVT, MAT, Atrial flutter and
fibrillation.QRS complex is MOSTLY narrow/normal in these i.e. less than 0.12 sec
duration
Ventricular Arrhythmias may be V.tachycardia or V.fibrillation. QRS complex is
ALWAYS wide i.e. 0.12 sec or more duration
AV junctional blocks: 3 degrees described above.

Atrial Fibrillation: Most important to know.

Irregularly irregular rhythm. No P waves. Narrow QRS. Pulsus deficit on examination.

3 basic steps in management

RATE control: most important is to bring ventricular rate below 100. With beta blockers,
Ca channel blockersndor DIGOXIN (best drug if symptoms of Heart failure are present too)
Anticoagulation: 2 most important thing if A.fib persists for more than 48 hours.
Assess CHADS2 score and if its 2+ use warfarin (add heparin for first week) to bring INR
to 2-3. If score is 1 use Aspirin or warfarin..

Rhythm control: Least important. 2 types of cardioversion.

-Chemical with amiodarone, procainamide or sotalol
-Electrical synchronized cardioversion.
Before both cardioversions give anticoagulation cover to avoid thromboembolism.

Golden rule In any kind of arrhythmia, if pt is unstable i.e. complains of chest pain,
hypotension, syncope, confusion, heart failure, shortness of breath, next best step is
ELECTRICAL Cardioversion.

Paroxysmal SVT:

Sudden onset and abrupt termination.

Presents with palpitations.
No P waves.
Rhythm is regular and,
QRS complex is narrow (only difference from ventricular tachycardia)

Best initial treatment: Vagal maneuvers e.g. carotid massage, valsalva etc.
I/V ADENOSINE is the drug of choice if pt is stable. Others options are beta blockers and
CCB (verapamil)
If pt is UNSTABLE then Shock him (Cardioversion).

MAT (multifocal atrial tachycardia):

IRREGULAR rhythm.
Narrow complex QRS.
More than 3 different morphologies of P waves (diagnostic).
Seen in elderly with chronic lung diseases.

Treatment: with verapamil. Avoid beta blockers because of coexisting COPD. Treat underlying
condition.

ATRIAL FLUTTER

Usually regular rhythm.

SAW TOOTH flutter waves instead of P waves.
Narrow QRS complex

Treatment: If unstable, Shock.

If stable, beta blockers or CCBs or Digoxin.

WPW syndrome (aka VENTRICULAR PRE-EXCITATION Syndrome)

Presence of accessory conduction pathways (Kent bundle) b/w atria and ventricles that bypass
AV node. So no normal AV delay. Its associated with SVT or A. fib and flutter.
Short PR interval << 0.12 sec. (Absence of normal AV delay)
WIDE QRS complex.

 DELTA wave (slurred initial deflection of QRS) that represents early ventricular
activation.
DRUGS that DELAY AV conduction (b blockers, CCBs, Digoxin, Adenosine) can cause DEATH so
better avoid them.
TREATMENT: PROCAINAMIDE (class IA) is drug of choice in Stable patient. Other option is class
3 drug amiodarone.
Cardioversion in unstable.
Catheter ablation of accessory pathway is definitive.

TORSADE de POINTES (French word meaning twisting of points)

Atypical V. tachycardia with undulating amplitude.
V.tachycardia plus polymorphic QRS complexes that twist around the isoelectric line.

CAUSES include

Hypomagnesaemia, hypokalemia, hypocalcaemia.

Prolonged QT interval due to any cause.
Drugs that PROLONG vent. repolarization e.g. Class IA and Class III antiarrhythmics
(except amiodarone), tricyclic antidepressants.
Congenital LONG QT syndrome e.g. Jervell and Lange-Nielsen syndrome (due to defects
in cardiac sodium or potassium channels, can be associated with congenital sensorineural
deafness)

TREATMENT:
Maintain ABC.
Correct underlying electrolyte imbalance Mg++ etc.
Discontinue the culprit drug.
If unstable, SHOCK him.

V. TACHYCARDIA:
Defined as 3 or more consecutive beats of ventricular origin at a rate greater than 120 beats per
min.
WIDE QRS complex >> 0.12 sec. (differentiates from SVT)
NO P waves.
Regular rhythm.
Present with palpitations, hypotension, angina, syncope.

TREATMENT:
If STABLE, maintain ABC and give amiodarone, lidocaine or procainamide (prolong
repolarization)
If unstable, SHOCK the pt.

V.FIBRILLATION:

Aberrant, very strong electrical activity seen on ECG but no signs of any kind of organized
pattern.

TREATMENT
Follow BLS, and DEFIBRILLATE i.e. unsynchronized cardioversion (one of few indications )

Digoxin toxicity (v.imp viva question)

Digoxin competes with K at Na-K ATPase so Hypokalemia increases toxicity and so does renal
failure.
Presents with
Nausea, vomiting, diarrhea (increased vagal stimulation),
Blurred vision with YELLOW color halos around objects and
Arrhythmias.
Gynecomastia is an important side effect seen in males.
TREATMENT:
STOP digoxin
Administer K (if hypokalemia present)
Lidocaine and phenytoin for arrhythmias.
Digibind (digoxin immune Fab) ONLY in acute overdose with CNS and EKG
abnormalities

Sinus Arrhythmia:
Physiological variation in heart rate with respiration. INspiration INcreases the heart rate.

Produced By: Muhammad Hassaan Amjad

Directed By: Soban Ahmad

SIMS, LHR.