Electrocardiography

( ecg )

Presented by :
Fahad I. Hussien
Definitions
• Electrocardiography
• Electrocardiograph
• Electrocardiogram

• Is there any deference ??

Anatomy of the heart
• To understand the ECG we first should take a review to the
anatomy of the heart
• The heart is located in the thoracic cavity and occupy less than
half of the inner diameter
• It’s composed of atria and ventricles which is divided into right
and left.
• There are four valves which separates the atria from the
ventricles and the ventricles from the circulation.
• These valves called ; mitral , tricuspid , aortic and pulmonary
valves.
• The function of heart valves is to prevent the blood from
returning back and to act as electrical insulator.
Physiology of the heart
• The action potential of the heart differ from the rest of the
body is that it has the platue phase.
• It depends on the K, Na, Ca
Circulation of blood
• The heart receives blood from systemic circulation through the
superior and inferior vena cava and coronary sinuses in the
right atrium and pump it through the right ventricle to
pulmonary arteries.
• Then it receive that blood through the pulmonary veins to the
left atrium and pump it through the left ventricle to the
systemic circulation through the aorta
Coronary circulation
• Left main : LAD in AV groove and supply ant. Lat. Apical LV and
ant septal perforator . CX AA. Supply post. Lat. Inferior LV.
• Right : in Rt. AV groove supply RA, RV and inferioposterior LV
• Post. Descending AA. From RCA in 90% and from LCA in 10%
• Occlusion of RCA >> bradycardia if paroxysmal and if
permanent >> inferior LV and RV infarction.
• Occlusion of LCA >> infarction in the corresponding areas
Conducting system of the heart
• SA node act as pacemaker under ANS and catecholamine
control.
• AV node conduct at slower rate to give the time needed for
ventricular filling.
• His- Purkinji system ; depolarize very rapidly to allow near
simultaneous contraction of the ventricles.
Electrocardiogram
• Used to assess the cardiac electrical rhythm and conduction.
• Provides information about the chamber size and ischemic
changes.
• Atrial depolarization produce P wave and repolarization is
undetectable because it’s to small.
• Ventricular depolarization produce the QRS complex and it’s
repolarization produce T wave.
• Interval: interval mean is that the previous wave included.
• Segment: it means that the previous and next wave is NOT included.
• Examples : P-R interval; from the starting of P wave to the beginning
of QRS complex, while S-T segment calculated from the end of S
wave to the starting of T wave.
Times
• ECG paper is divided into large and small squares.
• Large square = 5mm = 0.2 second.
• Small square = 1mm = 0.04 second.
• P-R interval = 3-5 small squares.
• QRS = 3 small squares or less.
• R-R distance = heart rate.
• 1cm height = 1 mV.
Shape of QRS
• It will be mainly positive if the electrical current moves toward
it, so the R > S
• It will be mainly negative if the electrical current moves away
from it, so the R < S
• Or isoelectric of the current are in right angle to the electrode
so R=S
QRS complex in chest leads
• V1 / V2 overlies the right side of the heart.
• V3 / V4 overlies the septum.
• V5 / V6 overlies the left side.

• Transition point normally occur in V3-V4, if moved to the left it

signify chronic lung disease ( clockwise rotation ).
How to read an ECG paper???
• Rhythm, Rate.
• Axis.
• P wave.
• P-R interval ( conduction interval ).
• QRS complex.
• S-T segment.
• T wave.
• Additional waves.
Rhythm
• Whether it’s regular or not ?
• Irregular rhythm subdivided into:
1. Regular irregularity.
2. Completely irregular ( irregular irregularity )
Rate
• Calculated as the distance between R-R or S-S as the follow:
• R-R distance = 300 / large squares OR
• R-R distance = 1500/ small squares OR
• In AF = number of R wave in 10 large squares *** 30
Heart axis
• Normal heart axis lie between -30 to 90 degree.
• Left axis deviation caused by LVH and anterior fascicular block.
• Right axis deviation caused by RVH and posterior fascicular
block.
• Lead l and lead ll will determine the axis.
• If lead l +ve and lead ll –ve then there is left axis deviation, and
the opposite is true.
P wave
• First we should check for the presence of P wave.
• Then we will assess it and see if it’s normal.
• Normal P wave vary in different leads and best seen at lead ll
and V1.
• It should be < 3 small squares in width and 1.5 – 2.5 small
squares in depth.
• Tall P wave indicate hypertrophy of the right atrium.
• Notched P wave indicates hypertrophy of the left atrium P
( pulmonale and Mitrale respectively )
PR interval
• The PR interval refer to conduction through the AV node; so
and defect in the conduction speed will prolong the PR
interval.
• Normal PR interval should be :
• 3-5 small squares
• Less than this could occur ??!!!
QRS complex
• Should be :
1. Not more than 3 small squares in width.
2. Right ventricular leads; the S wave should be greater than R
wave and vice versa.
3. R wave in left ventricular leads should be less than 25mm
caliber.
4. Left ventricular leads may show Q wave.
QRS complex
• Q wave:
1. Occur due to depolarization of the septum.
2. Usually present in V5-V6.
3. Normally should be: less than 1 mm in width and less than
2mm in depth.
ST segment
• It starts at the end of S wave and the beginning of T wave.
• It should be isoelectric ( at the same level with the base line.
• It could be elevated or depressed by diseases that affect the
heart.
T wave
• Has a variable caliber and width.
• It could be normal or inverted under normal circumstances.
• T wave is inverted normally in aVR , V1 .
• Variable in lead lll , V2 and V3.
• And upright in other leads.
• T inversion in one lead considered normal, but in more than
one lead can signify ischemic changes.
Sinus arrhythmia
• Occur normally in healthy subjects during respiration.
 Table 1: effect of respiration on the heart

state INspiration EXpiration

Blood pressure Decrease up to 10 mmHg Increase

Jugular venous pressure Decrease Increase

Pulse rate Increase Decrease

2nd heart sound split fuse

Abnormalities of an ECG
There are many diseases that will cause a change in the ECG, here
we will discuss the main and common ECG abnormalities.
1. Abnormalities of rate and rhythm.
2. Abnormalities of axis.
3. Abnormalities of P wave.
4. Abnormalities of PR interval.
5. Abnormalities of QRS complex.
6. Abnormalities of ST segment.
7. Abnormalities of T wave.
Abnormalities of heart rate and rhythm
• Normal heart rate is 60 – 100 beats per min.
• Tachycardia is a heart rate of more than 100 bpm.
• Bradycardia is a heart rate slower than 60 bpm.
• Each P wave should be followed by QRS complex.
Abnormalities of heart rate and rhythm
• The abnormalities can be divided into supraventricular and
ventricular rhythms.
• Supraventricular rhythm has ………………. QRS.
• Ventricular rhythm has …………………. QRS.

• N.B. an exception of this rule is supraventricular rhythm with

RBBB or LBBB or WPW.
Bradycardia
• Sinus bradycardia is a well known condition and can be
physiological or pathological
• Physiological bradycardia occur in:
1. Rest.
2. Sleep.
3. Athletes.
Bradycardia
• Pathological causes of bradycardia:
1. MI.
2. SSS.
3. Hypothermia.
4. Hypothyroidism.
5. Raised ICP.
6. Jaundice.
7. Drugs.

• Treatment is with atropine if symptomatic 0.6-1.2 mg , or

pacemaker as definitive treatment.
Escape rhythm
When the SA node fail to control the heart ; the generation of
depolarization will occur from another focus, could be the
atrium , junctional or ventricular areas.

these waves escape the normal inhibitory mechanism of the

heart. So called escape rhythm.
Ectopic beats ( Extrasystoles, premature
beats )
• What's the deference between it and escape rhythm ??

• Here the heart beat comes early while escape beat comes late.
Tachycardia
• It’s a term used to refer to a fast heart rate > 100 bpm.
• Divides into:
1. Sinus tachycardia.
2. Atrial tachycardia.
3. Junctional tachycardia.
4. Ventricular tachycardia.
Sinus tachycardia
• Heart rate of more than 100 bpm.
• Occur due to sympathetic activation.
• Physiological causes include; exercise , emotion , stress and
pregnancy .
• Pathological causes include; fever , anemia, thyrotoxicosis,
pheochromocytoma and drugs.

• Heart failure will cause ??????

Atrial tachycardia
• Due to increases automaticity , sss or digoxin toxicity.
• Produce narrow complex tachycardia with abnormal P wave
morphology.
• May be associated with heart block as a protective
mechanism.
• Rx with B blockers or class l , lll antiarhythmic.
• Catheter ablation is curative.
Atrial flutter
• Large ( macro ) re-entry circuit, originate from the right atrium.
• Atrial rate = 300 / min.
• Usually there is 2:1 , 3:1 , 4:1 heart block.
• Rarely in young; all beats are conducted.
• Saw toothed appearance on ECG.
• Always should be suspected when there is narrow complex
tachycardia of 150 bpm.
• Carotid pressure or adenosine may help in Dx by increasing heart
block.
• Rx is with digoxin, B blockers, verapamil as rate control and it is
preferred to restore the heart rhythm by DC or IV amiodarone.
• Flecainide can slow the flutter wave and enhance 1:1 conduction
• Catheter ablation is the definitive treatment.
AV nodal re-entrant tachycardia
• There is a re-entry circle that involve the AV node.
• The upper fast and lower slow pathway will produce 120-240
bpm.
• Signs of low cardiac output.
• Polyuria due to ????
• ECG show tachycardia with narrow QRS complex , no P wave or
near the QRS complex.
• Carotid sinus pressure could be curative or valsalvae maneuver.
• Adenosine 3-12 mg rapidly through IV line or verapamil 5mg
over 1 min. will terminate the attack, B blockers and flecainide
could be used instead.
• Catheter ablation is curative.
Wolf Parkinson white syndrome
• Here; there is an accessory pathway with the AV node.
• Concealed accessory pathway conduct from the ventricles to
the atria , no ECG changes yet.
• Manifest accessory pathway. The pathway will conduct with
the AV node and there will be a circle that include the AV node
and will produce a narrow complex tachycardia.
• If AF occur; it’s called pre-excited AF and will produce a wide
complex tachycardia which will cause hemodynamic
compromise and even death.
• DC shock may be needed to terminate the attack.
• Catheter ablation is the defenitive treatment.
• Prophylactic anti arrhythmic drugs may be used.
Ventricular tachycardia
• VT occur most commonly in the setting of previous CAD and
cardiomyopathies.
• Presented with hemodynamic compromise and VF.
• Signs of low cardiac output.
• ECG shows tachycardia , wide , abnormal QRS complexes and a
rate of more than 120 bpm.
• VT vs. SVT with BBB or WPW
1. Hx of MI
2. Axis deviation.
3. Wide QRS > 140 ms.
4. No response to carotid sinus massage or IV adenosine.
Fibrillation
• Atrial fibrillation.
• Ventricular fibrillation.
Atrial fibrilation
• The most common sustained cardiac arrhythmia.
• Due to increased automaticity and re-entry circuit.
• Heart rate is determined by the conduction through AV node.
• Atrial contraction is irregular and ineffective.
• Three main types; paroxysmal , persistent and permanent.
• ECG finding are;
1. No P wave.
2. Irregular irregularity.
3. Normal QRS.
4. Fibrilation waves at the baseline could be present.
Management of AF
• Rhythm control :
1. If <48 hrs ; give heparin ------- cardio version .
2. If > 48 hrs ; give heparin and warfarin ……… stop heparin
after 1 week and do INR……… continue at warfarin with INR
=2 for 1 month ………… cardio version ……… warfarin for 3
months.

• Cardioversion is either chemical or electrical ,

1. Chemical cardio version is done by flecainide 2mg/ kg over
30 minutes ; MAX. 150 mg . …. Amiodarone can be used
instead in LVF.
2. Electrical cardio version is done by DC shock ( synchronized )
• Rate control :
1. Digoxin
2. B blockers
3. Rate limiting Ca channel blockers ( verapamil and deltiazem )

• Some resistant patients need pace and ablate strategy.

• Prevention of thromboembolic phenomenon by

CHA2 DS2 VASc

Ventricular fibrillation
• Pulseless ventricular tachycardia.
• Disorganized ECG .
• Loss of consciousness.
• DC shock should be given without delay.
• BLS should be done early.
• Survival rate is 90% when early DC shock is given.
• Each minute delay there will be a drop of not less than 10%
Abnormalities of P wave
• First we should check for it’s presence.
• Absent P wave occur in Atrial fibrillation.
• Peaked P wave in right atrial enlargement.
• Bifid P wave in left atrial enlargement.
Abnormalities of PR interval
• It measures the time taken for the electrical current to be
transmitted from the SA node to the ventricles.
• Increment in its time is usually due to heart block.
Atrioventricular block
• 1st degree AV block: there will be a delay in the PR interval.
• 2nd degree is divided into mobitz type l and mobitz type ll
1. Mobitz type l is associated with Wenckebach phenomenon ,
could occur in athletes with high vagal tone. AV node
disease
2. Mobitz type ll is presented with non transmitted P wave and
carry a risk of asystole . Purkinji system disease.
• 3rd degree AV block is called AV dissociation, ventricular
contraction is occur by escape rhythm. And produce 25-50
bpm.

• Rx is with pacemaker , atropine or isoprenaline.

QRS abnormalities
• Width
• Calibre
ST segment abnormalities
• Elevated or depressed.
• Elevated in MI and pericarditis.
• Horizontal depression with upright T wave is a sign of ischemia
not infarction.
• Down slopping depression indicate myocardial ischemia and
could be due to digoxin treatment.
T wave abnormalities
• T inversion is seen in :
1. Normal.
2. Ischemia.
3. Hypertrophy.
4. BBB.
5. Digoxin Rx.
 CAD
Coronary artery disease is the most common form of heart
disease. Its divided into:
• Acute
• Chronic
Definitions
• Stable angina: ischemia due to fixed atheromatous stenosis of
one or more coronary arteries.

• Unstable angina: ischemia due to rupture atheromatous

plaque or erosion with superimposed thrombosis.

• Myocardial infarction: myocardial necrosis caused by acute

occlusion due to plaque rupture or erosion and superimposed
thrombosis.
Angina pectoris
• Is the symptom complex caused by transient myocardial
ischemia and constitutes a clinical syndrome rather than a
disease. Atheroma ‘ being the most common’ , aortic valve
stenosis and hypertrophic cardiomyopathy is the underlying
causes.
Clinical features
• History
1. Central chest pain.
2. Breathlessness or discomfort.
These symptoms present or precipitated by exertion or stress
and relieved by rest. Some patients complain from warm up
angina.

• Clinical examination:
1. Evidence of aortic valve disease.
2. Hypertension and D.M.
3. Anemia and thyrotoxicosis.
4. Left ventricular dysfunction.
Investigations
• Resting ECG:
1. Normal
2. Previous MI
3. T- inversion or flattening in some leads.
4. Reversible ST segment depression or elevation “ at time of
symptoms or during exercise.
• Exercise ECG:
1. Planer or down slopping ST depression is usually indicates
ischemia , up sloping ST depression is less specific and often
occur normally.
2. There is false-positive results in the presence of digoxin
therapy, LVH , BBB and WPW syndrome.
Manegment
• General measures.
• Antiplatelet therapy: aspirin or clopidogril 75 mg per day.
• Antianginal therapy:
1. Nitrates: GTN sublingual tab. 300-500 mic. Relieve
symptoms within 2-3 minutes.
2. Beta blockers: bisoprolol 5-15mg or metoprolol 50-200 mg
daily.
3. Calcium channel blockers: dihydropyridine used with beta
blockers, rate limiting ca chennel blockers can be used alone.
• Invasive treatment: percutaneous coronary intervention and
coronary artery bypass grafting.
Acute Coronary syndrome
• Unstable angina
• STEMI
• No STEMI
Unstable angina
• There will be an ST elevation during the episode of chest pain,
when the pain resolved there will be a normal ECG.
STEMI
• There will be an ST elevation in the corresponding leads
• Anterior leads: V1-V4
• Lateral leads: lead ll , aVL , V5 and V6.
• Inferior leads: lead lll and aVF.
• Posterior leads: reciprocal changes in the anterior leads.

When we suspect acute myocardial infarction we should see an

ECG changes in at least two leads of the same view and the ST
elevation should be more than 1 mm in limbs lead and 2mm in
chest leads.
• Treated as an emergency with primary PCI or thrombolytic
therapy.
Consequences of STEMI
• After the development of ST elevation, there will be T
inversion and pathological Q wave in the affected leads.
• If primary PCI was made for the patient there will be no
changes.

• To confirm the diagnosis we should send for cardiac

biomarkers like troponin ( daily ) with the history and ECG
changes ; there will be a complete picture of the disease.
Investigations
• ECG
• Cardiac biomarkers
1. Troponin : released within 4-6 hours and remain high for up
to 2 weeks.
2. Creatine kinase : rise after 4-6 hours and peak about 12
hours and fall to normal within 48-72 hours. Also present in
skeletal muscle.
Management
• Urgent admission to the hospital ( ICU ).
• Analgesia: to relief pain and reduce sympathetic drive; so
reduce vascular resistance, IV morphine sulfate 5-10mg or
diamorphine 2.5-5mg , with antiemetic agent like
metoclopramide 10 mg . IM injection should be avoided !!!
• Antithrombotic therapy:
1. Antiplatlets: aspirin 75-325mg daily improve survival given
within 12 hours, clopidogril can be used in combination of a
dose of 600mg , then 150 mg daily for one week then 75
daily indefinitely.
2. Anticoagulant : heparin , LMWH (enoxaparin 1mg/kg twice
daily ) and pentasaccharides ( fondaparinux 2.5 mg daily).
• Anti anginal therapy:
1. nitrate (GTN) 300-500 mic. For first aid and IV nitrate or
isosorbid dinitrate used in left ventricular failure.
2. Beta blockers: IV atenolol 5-10mg or metoprolol 5-15mg
over 5 minutes
3. Ca channel blockers either with or without beta blockers.

• Reperfusion therapy: beneficial in STEMI; sign of success is

pain relief , ST become normal and idioventricular rhythm.
1. Primary percutaneous coronary intervention ( PCI ) used if
the facility is available and within 48 hours of the symptoms.
2. Thrombolytic therapy: alteplase ( given over 90 minutes ;
bolus of 15mg followed by 0.75 mg/kg Max. 50 mg over 30
minutes; then 0.5mg/kg Max. 35mg over 60minutes ) should
be given withen 12 hours of the onset of the symptoms.
NSTEMI
• Here ; there is only T inversion in the corresponding leads.
• The Q wave will not develop after the returning of the T wave.
• There could be an ST depression.
• Treatment same as STEMI but without reperfusion therapy.