ECG Interpretation
Cardiac Arrhythmias
Dr Safa Abdul Ghani
Coordinating the Pump: Electrical Signal Flow
Electrocardiography
• Electrical activity is recorded by electrocardiogram (ECG) using
electrodes
• P wave corresponds to depolarization of atrial
• QRS complex corresponds to ventricular depolarization
• T wave corresponds to ventricular repolarization
• Atrial repolarization record is masked by the larger QRS complex
The atria begin contracting
approximately 25 ms after
the start of the P wave
Heart Excitation Related to ECG
SA node generates impulse; Impulse delayed Impulse passes to Ventricular excitation
atrial excitation begins at AV node heart apex; ventricular complete
excitation begins
SA node AV node Bundle Purkinje
branches fibers
Figure 18.17
Coordinating the Pump: Electrical Signal Flow
• Delay for atrial emptying – atrioventricular (AV) node (posterior wall
of the right atrium).
• AV node to bundles of His, branches & Purkinje fibers
• Purkinje fibers:
- They are very large fibers.
- They transmit AP at a velocity of 1.5 to 4.0 m/sec (6x more than usual
ventricular muscle and 150x than the A-V nodal fibers).
- This allows almost instantaneous transmission of the cardiac impulse
throughout the entire remainder of the ventricular muscle.
Coordinating the Pump: Electrical Signal Flow
• Right and left ventricular contraction from apex upword
• Why the AP do not re-enter the Atrial muscle from the
ventricles?
1) One way conduction through the A-V bundle (except in
abnormal states).
2) The presence of a continuous fibrous barrier between the atrial
muscle and the ventricular muscle (except at the A-V bundle).
• The primary pacemaker therefore is the SA node and has an inherent
rate of 60-100 beats/minute. The SA node has the highest level of
automaticity, but escape pacemakers can exist.
• The AV node only generates an impulse if the SA node does not
function at its normal rate. The AV node fires electrical impulses at a
rate of 40-60 beats/ minute.
• bundle branches and the Purkinje network will become the initiating
pacemaker if the AV node is not able to function at its normal rate.
The inherent ventricular rate is 20-40 beats/minute
Electrocardiogram (ECG): Electrical Activity of the Heart
Einthoven's triangle:
1)Bipolar Limb Leads
– 1 positive and 1 negative electrode
• RA always negative
• LL always positive
– Provide a view from a vertical plane
– Three limb leads:
• Lead I: -ve terminal is connected to the right
arm/+ve terminal to the left arm
• Lead II:-ve terminal is connected to the right
arm/+ve terminal to the left leg
• Lead III:-ve terminal is connected to the left
arm/+ve terminal to the left leg
Electrocardiogram (ECG):
Electrical Activity of the Heart
ECG wave goes up
When an electrical
wave moving through
the heart is directed
toward the positive
electrode
ECG wave points
downward
If net charge
movement is toward
the negative electrode
2) Augmented Unipolar Limb leads
Two limbs are connected through electrical resistance to the negative
terminal of the ECG and the third limb is connected to the positive terminal
aVR when the +ve terminal on (R arm)
aVL when the +ve terminal on (L arm)
aVF when the +ve terminal on (left leg)
3) Unipolar chest leads (starting from the midline position)
V1, V2, V3, V4, V5, V6
The electrode on the anterior surface
of the chest is directly over the heart
and connected to the +ve terminal of
the ECG
The –ve electrode (the indifferent
electrode is connected through equal
resistances to the right arm, Left arm
and left leg at the same time
Twelve standard ECG leads that (((view))) the changing pattern
of the hearts electrical activity from different perspective
Components of the ECG Complex
Components of the ECG Complex
• P Wave • PR Interval
• QRS Complex
• first upward deflection • time impulse takes to
• Composition of 3 Waves move through atria and AV
• represents atrial • Q, R & S node
depolarization • represents ventricular • from beginning of P wave
• usually 0.10 seconds depolarization to the beginning of QRS
or less • much variability complex
• usually followed by • usually < 0.12 sec • normally 0.12 - 0.2 sec
QRS complex
• may be shorter with faster
rates
Components of the ECG Complex
• QRS Interval • ST Segment • T Wave
• time impulse takes to • early repolarization of • repolarization of ventricles
depolarize ventricles ventricles • concurrent with end of
• from beginning of Q • measured from end of S ventricular systole
wave to beginning of ST wave to onset of T wave
segment • elevation or depression
• usually < 0.12 sec may indicate abnormality
ECG Analysis
• A monitoring lead can tell you:
• How often the myocardium is depolarizing
• How regular the depolarization is
• How long conduction takes in various areas of the
heart
• The origin of the impulses that are depolarizing the
myocardium
• Heart Axis (normal !!! right or left axis deviation!!)
1) First ask yourself are there P waves?
2) What is the QRS width?
3) Is it a Regular rhythm?
4) Are P waves related to the QRS?
5) What is the Heart Rate?
Narrow
From beginning of P wave to
the beginning of QRS complex
(P wave)
(PR segment)
ECG interpretation: Heart Rate
From one P wave to the next P wave or from one R wave to the peak of the next R wave.
Normal resting heart rate = 60- 100 beats per minute (trained athletes often have slower
heart rates at rest)
A faster-than-normal rate is known as tachycardia
Slower-than-normal rate is called bradycardia
• Heart rate can be calculated simply with the following method:
Rule of 300: If the rhythm is regular, the heart rate can be "estimated" by using the
"Rule of 300"
• Work out the number of large squares in one R-R interval
• Then divide 300 by this number and you have your answer
e.g. if there are 4 squares in an R-R interval 300/4 = 75 beats per minute
ECG interpretation: Rhythm
• Measure R-R intervals across strip
• Should find regular distance between R waves
• Classification
• Regular
• Irregular
Can result from a benign extra beat or from atrial
fibrillation (SA node has lost control of the pacemaker)
6 6 6
4 8 4 8
(P wave)
(PR segment)
3 small boxes
Heart Axis??
The axis of the ECG is the major direction of the overall electrical activity of
the heart. It can be normal, leftward (left axis deviation, or LAD), rightward
(right axis deviation, or RAD) or indeterminate (northwest axis).
The direction of the average electrical depolarization with an arrow (vector). This is the heart axis. A
change of the heart axis or an extreme deviation can be an indication of pathology. To determine the
heart axis you look at the extremity leads only (not V1-V6). If you focus especially on leads I, II, and AVF
you can make a good estimate of the heart axis
ECG Analysis
• QRS Complex: Ventricular Depolarization
< 0.12 seconds (3 small boxes) is normal (((Narrow)))
(Atrial/supraventricular origin)
• Broad QRS Complex = Result from abnormal intraventricular conduction
Ventricular bundle branch block (Ventricular origin)
• Increase Height of QRS = Result from ventricular hypertrophy
In V1 = Right ventricular Hypertrophy
In V5+V6= Left ventricular Hypertrophy
• No QRS wave = Ventricular Fibrillation
• Q waves: Greater that 1mm across and 2mm deep= Indicate myocardial
infarction
(P wave)
(PR segment)
ECG Analysis
• P Waves
• Present?
• Do they all look alike?
• Regular interval
• Upright or inverted in Lead II?
• Upright = atria depolarized from top to
bottom
• Inverted = atria depolarized from
bottom to top
ECG Changes & Clinical Diagnosis
P wave: Atrial Depolarization
• Tall P wave= Result from right atrial Hypertrophy
(Due to tricuspid valve stenosis or pulmonary hypertension)
• Broad P wave= Result from left atrial hypertrophy
(Due to Mitral stenosis)
• No P wave= Junctional Escape, Junctional Extrasystoly, Junctional
Tachycardia, Ventricular Tachycardia, Atrial Fibrillation
P wave abnormality
Bifid/ mitrale
• ST segment:
- Elevated ST = Acute Myocardial Infarction, Pericarditis
- Depressed ST and T wave Inversion = Ischemia, Ventricular Hypertrophy
T
P
Elevated ST
1) First ask yourself are there P waves?
2) What is the QRS width?
3) Is it a Regular rhythm?
4) Are P waves related to the QRS?
5) What is the Heart Rate?
Cardiac Arrhythmias
• is a term for any of a large and heterogeneous group of conditions in which
there is abnormal electrical activity in the heart.
• The heart beat may be too fast or too slow, and may be regular or irregular.
• Normal Rhythm (Sinus Rhythm):
1. Heart rate 60-100 Bpm
2. SA node origin
3. Normal conduction pathway SAatriaAVHispurkenje
4. Normal velocity
Aetiology
1. Abnormal rhythmicity of the pacemaker
2. Shift of the pacemaker from the sinus node to another place in the heart
3. Blocks at different points in the spread of the impulse through the heart
4. Abnormal pathways of impulse transmission through the heart
5. Spontaneous generation of spurious impulses in almost any part of the heart
• Risk Factors:
Ischemia, Hypoxia, Acidosis/Alkalosis,
Electrolyte Abnormalities, Excessive Catecholamine Exposure, Autonomic
Influences, Drug Toxicity (e.g.antiarrhythmic drugs)
Manifestation
• The most common symptom of arrhythmia is an abnormal awareness of heartbeat,
termed palpitations.
• Some of these arrhythmias are harmless but many of them predispose to adverse
outcomes.
• If an arrhythmia results in a heart beat that is too fast, too slow or too weak to
supply the body's needs, this manifests as a lower blood pressure and may cause
lightheadedness or dizziness, or fainting.
• Some types of arrhythmia result in cardiac arrest, or sudden death.
• ECG is the best way to diagnose and assess the risk of any given arrhythmia.
Cardiac Arrhythmias
Abnormal rhythmicity of the pacemaker:
• Tachycardia: Heart rate in excess of 100bpm
• Bradycardia: Heart rate less than 60 bpm
• Sinus arrhythmia: Heart rate varies, can be either
faster or slower ---5% during respiratory cycle and
up to 30% during deep respiration
Abnormal rhythmicity of the pacemaker:
• Tachycardia: Heart rate in excess of 100bpm
• Bradycardia: Heart rate less than 60 bpm
Maybe due to: a normal response to sleep or in well Maybe the result of stress, exercise, pain, fever,
conditioned athlete, abnormal drops in rate could be pump failure, hyperthyroidism, drugs-caffeine,
caused by vagal stimulation, hypothyroidism or nitrates, atropine, epinephrine, and isoproterenol,
pharmacologic agents, such as digoxin nicotine
Sinus Arrhythmia
6 6 4 3
Rate: Usually 60-100 beats/min but may be either faster or slower
Commonly seen in the elderly and the young and usually does not
require treatment. Heart rate increases with inspiration and decreases
with expiration
Premature Contractions
• A premature contraction is a contraction of the heart before the time
that normal contraction would have been expected.
• This condition is also called extrasystole, premature beat, or ectopic beat
Premature contractions (“ectopics”) are classified by their origin —
atrial (PACs), junctional (PJCs) or ventricular (PVCs)
1. Premature atrial contractions: Occasional shortened intervals between
one contraction and succeeding, frequently occurs in healthy people.
Conditions such as smoking, lack of sleep, ingestion of too much coffee,
alcoholism, and use of various drugs can also initiate such contractions.
Premature Contractions
2. A-V Nodal or A-V Bundle Premature Contractions (Junctional):
These contractions have the same significance and causes as atrial
premature contractions.
3. Premature Ventricular Contractions:
• Some PVCs are relatively benign.
• They can result from factors as cigarettes, coffee, lack of sleep, various mild
toxic states, and even emotional irritability.
• PVCs also can result from signals that originate around the borders of
infarcted or ischemic areas of the heart. The presence of such PVCs can lead
to lethal ventricular fibrillation
Premature Atrial Complexes (PACs)
•These arise from ectopic
pacemaking tissue within the
atria.
•There is an abnormal P wave
(premature/ hidden), usually
followed by a normal QRS
complex
Irregular since the impulse occurs early
PAC occurs when an irritable site within the atria discharges before the next SA node is due to discharge
Premature Contractions
Premature beats are identified by their site of origin (atrial, junctional, and ventricular)
A-V nodal PC
PAC (Junctional)
PVC
•Broad QRS complex (≥ 120 ms) with abnormal
morphology.
•Premature — i.e. occurs earlier than would be
expected for the next sinus impulse.
•Discordant ST segment and T wave changes.
•Usually followed by a full compensatory pause.
Ventricular & Atrial Fibrillation
Fibrillation is a fast, chaotic beating of a heart chamber. If it's in the top
chamber, it's atrial fibrillation. If in the bottom chambers, it's ventricular
fibrillation
Ventricular fibrillation:
• The most serious of all cardiac arrhythmias, if not stopped within 1 to 3 minutes, is
almost fatal.
• It is a condition in which there is uncoordinated contraction of the cardiac muscle of
the ventricles in the heart, making them tremble rather than contract properly.
• Multiple factors can spark the beginning of ventricular fibrillation:
(1) sudden electrical shock of the heart, or
(2) ischemia of the heart muscle, of its specialized conducting system,
(3) both factors.
Ventricular Fibrillation (VF)
Rate: rapid and disorganized
Rhythm: irregular and chaotic
P Wave: absent but can be recognizable
PRI: not measurable
QRS: fibrillatory waves ((no wave)).
Ventricular Fibrillation
• ECG it is characterized by a chaotic irregular
appearance with complexes of varying amplitude
and morphology.
• Untreated, VF rapidly leads to death; the only
effective therapy is electrical defibrillation.
No P wave
Atrial rate usually > 400, Ventricular rate variable
Rhythm: Atrial and ventricular very irregular
P waves: No identifiable P waves, Erratic, wavy baseline
PRI: None
QRS: Usually <.10
The AV node protects the patient from having too high a ventricular response, and blocks the majority of the
impulses.
Blood may pool or stagnate in the atria and the patient is at risk for clot formation.
May be due to: ischemia, Myocardial Infarction hypoxia, or drug therapy.
Treatment may consist of beta-blockers (Inderal), calcium blockers (verapamil), or synchronized cardioversion
in an attempt to restore the patient to a sinus rhythm.
AV Block
• A problem with conduction of signals through the AV node may
exist.
• In heart block AP from the SA node fail to be transmitted
through the AV node to the ventricles. In these conditions, one
or more P waves may occur without initiating a QRS complex.
• In the most severe form of heart block (third-degree) the
atria depolarize regularly at one pace while the ventricles
contract at a much slower pace
First Degree AV Block:
PRI longer than 0.20 sec
There is No Block at all just a delay in conduction.
Every P wave is married to a QRS; no missed beats
P P P
Second Degree AV Block:
Type I (Mobitz I)
progressive prolongation of the PR interval, followed by a blocked P wave
1. decreasing RR intervals until pause
2. the pause is less than preceding 2 RR intervals
3. the RR interval after the pause is greater than the RR interval just prior to pause
QRS dropped after PRI progressive increase
Type II (Mobitz II)
PRI is fixed (no progressive increase in
PRI) QRS dropped without warning
QRS is dropped without warning; there
will always be more P Waves than QRS P
The P waves are married to the QRS
The level of conduction problem is usually
lower than the AV node, often involving
P
the Bundle of His P
Third Degree (Complete
Heart Block)
There is complete heart block so
that none of the impulses from
above are conducted to the
ventricles
The atria and the ventricles are
controlled independently by
separate pacemakers
P Waves are NOT married to the
QRS
.
