ECG

• ECG tracings are recorded on grid paper.

• The horizontal axis of the EKG paper records time, with black marks at the
top indicating 3 second intervals.

Each second is marked by 5 large grid blocks. Thus each large block equals
0.2 second.
• The vertical axis records EKG amplitude (voltage). Two large blocks equal
1 millivolt (mV). Each small block equals 0.1 mV.

Within the large blocks are 5 small blocks, each representing 0.04 seconds
• P wave is the first deflection and is normally a positive (upward) waveform. It indicates atrial
depolarization.

QRS complex follows the P wave. It normally begins with a downward deflection, Q; a larger
upward deflection, R; and then a downward S wave. The QRS complex represents ventricular
depolarization and contraction.

T wave is normally a modest upward waveform, representing ventricular repolarization.

U wave indicates the recovery of the Purkinje conduction fibers. This wave component may
not be observable.
Indications
Heart disease: heart attack, arrhythmias, conduction disturbances, 
myocardial ischemia;
• metabolic disease: hypocalcemia or hypercalcemia, hypokalemia or
hyperkalemia;
• endocrine disease: diseases of the thyroid gland (hypothyroidism and 
hyperthyroidism).
Indications
• Chest pain
• Atypical chest pain
• Epigastric pain
• Back, neck, jaw or arm pain without chest pain
• Palpitations
• Syncope or near syncope
• Pulmonary edema
• Exertional dyspnea
• Weakness
• Diaphoresis unexplained by ambient temperature
• Feel of anxiety or impending doom
• Suspected diabetic ketoacidosis
are some examples of additional ECG leads[2]:              
lead

V7
location of the lead

posterior axillary line, on the same

level as V6, on the left

V8 scapulary line, in the same level as

V6, on the left

unipolar chest leads

paravertebral line on the left, on
V9 the same level as V6

VE just to the left of processus

xiphoideus
Electrical axis
• In electrocardiology, a vector represents both the magnitude and
direction of the action potential generated by an individual myocyte.
The sum of all the individual vectors generated by the depolarization
waves makes up the electrical axis.
• Because each myocyte can produce an action potential, an axis for
each wave and interval of the cardiac cycle can be determined.
Knowing the axis of each and how they interact can reflect certain
pathology.
• The ventricular axis can be determined by looking at the QRS
complex, which represents ventricular depolarization. Because the
QRS complex is used to determine the ventricular axis, it is also
referred to as the QRS axis. The ventricular (QRS) axis signifies the
sum of all individual vectors generated by the depolarization waves of
ventricular myocytes
• Wave: A positive or negative deflection from baseline that indicates a
specific electrical event. The waves on an ECG include the P wave, Q
wave, R wave, S wave, T wave and U wave.
• Interval: The time between two specific ECG events. The intervals
commonly measured on an ECG include the PR interval, QRS interval
(also called QRS duration), QT interval and RR interval.
• Segment: The length between two specific points on an ECG that are
supposed to be at the baseline amplitude (not negative or positive).
The segments on an ECG include the PR segment, ST segment and TP
segment.
P wave
• Atrial depolarisation proceeds sequentially from right to left, with the
right atrium activated before the left atrium.
• The right and left atrial waveforms summate to form the P wave.
• The first 1/3 of the P wave corresponds to right atrial activation, the
final 1/3 corresponds to left atrial activation; the middle 1/3 is a
combination of the two.
• In most leads (e.g. lead II), the right and left atrial waveforms move in
the same direction, forming a monophasic P wave
• As long as the atrial depolarization is able to spread through the
atrioventricular, or AV, node to the ventricles, each P wave should be
followed by a QRS complex
• The sinoatrial node lies high in the wall of the right atrium and
initiates atrial depolarisation, producing the P wave on the
electrocardiogram. Although the atria are anatomically two distinct
chambers, electrically they act almost as one. They have relatively
little muscle and generate a single, small P wave. P wave amplitude
rarely exceeds two and a half small squares (0.25 mV). The duration of
the P wave should not exceed three small squares (0.12 s)
• The wave of depolarisation is directed inferiorly and towards the left,
and thus the P wave tends to be upright in leads I and II and inverted in
lead aVR. Sinus P waves are usually most prominently seen in leads II
and V1. A negative P wave in lead I may be due to incorrect recording
of the electrocardiogram (that is, with transposition of the left and right
arm electrodes), dextrocardia, or abnormal atrial rhythms.
• The P wave in V1 is often biphasic. Early right atrial forces are directed
anteriorly, giving rise to an initial positive deflection; these are followed
by left atrial forces travelling posteriorly, producing a later negative
deflection
• However, in lead V1 the right and left atrial waveforms move in opposite
directions.
• This produces a biphasic P wave with the initial positive deflection
corresponding to right atrial activation and the subsequent negative
deflection denoting left atrial activation.
• This separation of right and left atrial electrical forces in lead V1 means that
abnormalities affecting each individual atrial waveform can be discerned in
this lead. Elsewhere, the overall shape of the P wave is used to infer the
atrial abnormality.
• Normal P-wave Morphology – Lead II
• The right atrial depolarisation wave (brown) precedes that of the left
atrium (blue).
• The combined depolarisation wave, the P wave, is less than 120 ms
wide and less than 2.5 mm high.
Right Atrial Enlargement – Lead II

• In right atrial enlargement, right atrial depolarisation lasts longer than

normal and its waveform extends to the end of left atrial depolarisation.
• Although the amplitude of the right atrial depolarisation current remains
unchanged, its peak now falls on top of that of the left atrial
depolarisation wave.
• The combination of these two waveforms produces a P waves that is
taller than normal (> 2.5 mm), although the width remains unchanged (<
120 ms).
• Left Atrial Enlargement – Lead II
• In left atrial enlargement, left atrial depolarisation lasts longer than
normal but its amplitude remains unchanged.
• Therefore, the height of the resultant P wave remains within normal
limits but its duration is longer than 120 ms.
• A notch (broken line) near its peak may or may not be present (“P
mitrale”).
• Normal P-wave
Morphology – Lead
V1
• The P wave is typically
biphasic in V1, with
similar sizes of the
positive and negative
deflections
• Right Atrial Enlargement – Lead V1
• Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial
positive deflection of the P wave
• Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep)
in V1 of the terminal negative portion of the P wave.
•
Biatrial enlargement is diagnosed when criteria for both right and left atrial
enlargement are present on the same ECG. The spectrum of P-wave changes in leads
II and V1 with right, left and bi-atrial enlargement is summarised in the following
diagram:
Common P Wave Abnormalities
Common P wave abnormalities include:
•P mitrale (bifid P waves), seen with left atrial enlargement.
•P pulmonale (peaked P waves), seen with 
right atrial enlargement.
•P wave inversion, seen with ectopic atrial and junctional rhythms.
•Variable P wave morphology, seen in multifocal atrial rhythms.
P mitrale
The presence of broad, notched (bifid) P waves in lead II is a sign of left atrial enlargement, classically due
to mitral stenosis
P Pulmonale
The presence of tall, peaked P waves in lead II is a sign of right atrial enlargement, usually due to pulmonary hypertension (e.g. cor pulmonale from chronic
respiratory disease).
Inverted P Waves
P-wave inversion in the inferior leads indicates a non-sinus origin of the P waves. When the PR interval is
< 120 ms, the origin is in the AV junction (e.g. accelerated junctional rhythm)
• Variable P-Wave Morphology
• The presence of multiple P wave morphologies indicates multiple
ectopic pacemakers within the atria and/or AV junction. If ≥ 3
different P wave morphologies are seen, then multifocal atrial
rhythm is diagnosed:
•
If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100,
then multifocal atrial tachycardia (MAT) is diagnosed:
QRS
• Q wave representing septal depolarisation
• R wave representing ventricular depolarisation
• S wave representing depolarisation of the Purkinje fibres.
• The first phase of ventricular depolarization is of relatively brief duration (shorter
than 0.04 sec) and small amplitude.
• It results from spread of the stimulus through the interventricular septum.
• The septum is the first part of the ventricles to be stimulated.
• Furthermore, the left side of the septum is stimulated first (by a branch of the left
bundle of His).
• Thus, depolarization spreads from the left ventricle to the right across the septum.
• Phase one of ventricular depolarization (septal stimulation) can
therefore be represented by a small arrow pointing from the left septal
wall to the right

• 2. The second phase of ventricular depolarization involves

simultaneous stimulation of the main mass of both the left and right
ventricles from the inside (endocardium) to the outside (epicardium) of
the heart muscle.
• In the normal heart the left ventricle is electrically predominant.
• In other words, it electrically overbalances the right ventricle.
The Normal QRS: Chest Leads
• 1. The first phase of ventricular stimulation, septal stimulation, is represented by an arrow pointing
to the right, reflecting the left-to-right spread of the depolarization stimulus through the septum
• This small arrow points toward the positive pole of lead V1.
• Therefore, the spread of stimulation to the right during the first phase produces a small positive
deflection
• (r wave) in lead V1.
• What does lead V6 show?
• The left-to-right spread of septal stimulation produces a small negative deflection (q wave) in lead
V6.
• Thus, the same electrical event (septal stimulation) produces a small positive deflection
• (or r wave) in lead V1 and a small negative deflection (q wave) in a left precordial lead, like
lead V6.
• The second phase of ventricular stimulation is represented by an
arrow pointing in the direction of the left ventricle
• This arrow points away from the positive pole of lead V1 and toward
the negative pole of lead V6.
• Therefore, the spread of stimulation to the left during the second
phase results in a negative deflection in the right precordial leads and
a positive deflection in the left precordial leads.
• Lead V1 shows a deep negative (S) wave, and lead V6 displays a tall
positive (R) wave.
• In summary, with normal QRS patterns, lead V1 shows an rS type of
complex.
• The small initial r wave represents the left-to-right spread of septal
stimulation.
• This wave is sometimes referred to as the septal r wave because it
reflects septal stimulation.
• The negative (S) wave reflects the spread of ventricular stimulation
forces during phase two, away from the right and toward the
dominant left ventricle.
• Conversely, viewed from an electrode in the V6 position, septal and
ventricular stimulation produce a qR pattern.
• The q wave is a septal q wave, reflecting the left-to-right spread of the
stimulus through the septum away from lead V6.
• The positive (R) wave reflects the leftward spread of ventricular
• stimulation voltages through the left ventricle
Increase in height of the R wave, which usually reaches a maximum
around lead V4 or V5, is called normal R wave progression.
• At some point, generally around the V3 or V4 position, the ratio of the
R wave to the S wave becomes 1.
• This point, where the amplitude of the R wave equals that of the S
wave, is called the transition zone
• In the ECGs of some normal people the transition may be seen as
early as lead V2.
• This is called early transition.
• In other cases the transition zone may not appear until leads V5 and
• V6.
• This is called delayed transition.
Extremity leads
• the extremity leads in normal ECGs can show a variable QRS pattern.
• Lead aVR normally always records a predominantly negative QRS
complex (Qr, QS, or rS).
• The QRS patterns in the other extremity leads vary depending on the
electrical position (QRS axis) of the heart.
• With an electrically vertical axis, leads II, III, and aVF show qR-type
complexes.
• With an electrically horizontal axis, leads I and aVL show qR
complexes.
Genesis of q wave
• Normal Q waves, when present, represent depolarization of the interventricular septum.
For this reason, they are referred to as septal Q waves and can be appreciated in the lateral
leads I, aVL, V5 and V6
•  The wave of depolarization spreads through the ventricles predominantly from the
endocardial area to the epicardium.
• The initial 0.01 second of the QRS complex is caused by depolarization of the middle of the
left side of the interventricular septum.
• The next few milliseconds of the QRS complex are produced by depolarization of the
endocardium of both ventricles, and the next few by depolarization of a decreasing amount
of the right ventricle and an increasing amount of the left ventricle.
• The last few milliseconds of the QRS complex are caused by depolarization of the basilar
portion of the left ventricle.
• A Q wave is any negative deflection that precedes an R wave
• The Q wave represents the normal left-to-right depolarisation of the interventricular
septum
• Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6)
•
Q waves in different leads
• Small Q waves are normal in most leads
• Deeper Q waves (>2 mm) may be seen in leads III and aVR as a normal variant
• Under normal circumstances, Q waves are not seen in the right-sided leads (V1-3)
• Pathological Q Waves
• Q waves are considered pathological if:
• > 40 ms (1 mm) wide
• > 2 mm deep
• > 25% of depth of QRS complex
• Seen in leads V1-3
• Pathological Q waves usually indicate current or prior myocardial
infarction
•The absence of small septal Q waves in leads V5-6 should be considered abnormal.
•Absent Q waves in V5-6 is most commonly due to LBBB.
• R wave Overview
• The R wave is the first upward deflection after the P wave. The R wave
represents early ventricular depolarisation
•
Abnormalities of the R wave
• There are three key R wave abnormalities:
• Dominant R wave in V1
• Dominant R wave in aVR
• Poor R wave progression
Dominant R wave in V1

• Causes of Dominant R wave in V1

• Normal in children and young adults
• Right Ventricular Hypertrophy (RVH)
• Pulmonary Embolus
• Persistence of infantile pattern
• Left to right shunt
• Right Bundle Branch Block (RBBB)
• Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9)
• Wolff-Parkinson-White (WPW) Type A
• Incorrect lead placement (e.g. V1 and V3 reversed)
• Dextrocardia
• Hypertrophic cardiomyopathy
• Dystrophy
S wave
• First downward deflection after R
• The amplitude gradually decreases from V1
T wave
• In electrocardiography, the T wave represents the repolarization of the 
ventricles. The interval from the beginning of the QRS complex to the
apex of the T wave is referred to as the absolute refractory period. The
last half of the T wave is referred to as the relative refractory
period or vulnerable period. The T wave contains more information than
the QT interval. The T wave can be described by its symmetry, skewness,
slope of ascending and descending limbs, amplitude and subintervals
like the Tpeak–Tend interval.[1]
• In most leads, the T wave is positive. This is due to the repolarization of
the membrane. During ventricle contraction (QRS complex), the heart
depolarizes. 
•  Repolarization of the ventricle happens in the opposite direction of
depolarization and is negative current, signifying the relaxation of the
cardiac muscle of the ventricles. This double negative of direction and
charge is why the T wave is positive; although the cell becomes more
negatively charged, the net effect is in the positive direction, and the
ECG reports this as a positive spike.[2] However, a negative T wave is
normal in lead aVR. Lead V1 may have a T wave with positive,
negative, or biphasic where positive is followed by negative, or vice
versa. In addition, it is not uncommon to have an isolated negative T
wave in lead III, aVL, or aVF. 
• Normally, T waves are upright in all leads, except aVR, aVL, III and V1
leads. Highest amplitude of T wave is found at V2 and V3 leads. The
shape of the T wave is usually asymmetrical with a rounded peak. T
wave inversions from V1 to V4 leads are frequently found and normal
in children. In normal adults, T wave inversions are less commonly
found, but can be normal from V1 to V3.[4] The depth of the T wave also
becomes progressively shallow from one to the next lead.[5] The height
of the T wave should not exceed 5 mm in limb leads and more than
10 mm in precordial leads.[4]
 • Biphasic T wave : MI and hypokalemia
Camel hump' T wave[edit]
The name of these T waves suggests the shape it exhibits (double peaks).
Since these T wave abnormalities may arise from different events, ie hypothermia and severe brain damage, they
have been deemed as nonspecific, making them much more difficult to interpret.[8]
U wave
• It comes after the T wave of ventricular repolarization and may not
always be observed as a result of its small size. 'U' waves are thought
to represent repolarization of the Purkinje fibers.
• U waves often register in all leads except V6, most frequently in V2
and V3 when the heart rate is greater than 96 beats per minute
• An inverted U wave may represent myocardial ischemia (and
especially appears to have a high positive predictive accuracy for 
left anterior descending coronary artery disease[7] ) or left ventricular 
volume overload
J point

• The point where the QRS complex meets the ST segment is the J-point.
The J-point is easy to identify when the ST segment is horizontal and
forms a sharp angle with the last part of the QRS complex. However,
when the ST segment is sloped or the QRS complex is wide, the two
features do not form a sharp angle and the location of the J-point is less
clear. There is no consensus on the precise location of the J-point in these
circumstances.[11] Two possible definitions are:
• The "first point of inflection of the upstroke of the S wave"[11]
• The point at which the ECG trace becomes more horizontal than vertical[12
• NORMAL ST SEGMENT
• the normal ST segment, representing the early phase of ventricular
repolarization, is usually isoelectric (flat on the baseline).
• Slight deviations (generally less than 1 mm) may be seen normally.
QRS axis
• The term mean QRS axis therefore describes the general direction in
the frontal plane toward which the QRS complex is predominantly
pointed.
• Because the QRS axis is being defined in the frontal plane, the QRS is
being described only in reference to the six extremity leads (the six
frontal plane leads).
• Therefore, the scale of reference used to measure the mean QRS axis
is the diagram of the frontal plane leads
• The mean QRS axis points midway between the axes of two extremity
leads that show tall Rwaves of equal amplitude.
• • The mean QRS axis points at 90° (right angles) to any extremity lead
that shows a biphasic (QR or RS) complex and in the direction of leads
that
• show relatively tall R waves.
• If the QRS complexes in both leads are positive, the axis must be
normal.
• If the QRS complexes is predominantly positive in lead I and negative
in lead II, LAD is present.
• If the QRS complex is predominantly negative in lead I and positive in
lead
• II, RAD (or at least borderline RAD) is present.
Clockwise and Counterclockwise rotation

• Clockwise and counterclockwise rotation refer to a change in the

electrical activity in a horizontal plane through the heart.
• Imagine the observer standing at the feet of the patient who is in bed.
If the electrical activity of the heart has turned more to the right side
of the patient this is called counterclockwise rotation.
• If the electrical activity of the heart has turned more to the left side of
the patient this is called clockwise rotation.
• Clockwise and counterclockwise rotation can be assessed only in the
chest-leads (V1 - V6). Normally the R wave amplitude increases from
V1 to V5. Around V3 or V4 the R waves become larger than the S
waves and this is called the 'transitional zone'. If the transition occurs
at or before V2, this is called counterclockwise rotation. If the
transition occurs after V4, this is called clockwise rotation
Causes of clockwise rotation
• intraventricular conduction abnormalities secondary to myocardial
degeneration
• right ventricular heart disease
• shift of the septum to the left
• dilated cardiomyopathy
• shift of the whole heart
• pulmonary emphysema
• vertical heart (usually thin and tall persons)
Causes of counterclockwise rotation
• electrical shift to the right
• right ventricular hypertrophy
• WPW Syndrome
• Posterior myocardial infarction
• Left septal fascicular block
• shift of the septum to the right
• hypertrophic cardiomyopathy
• Normal Axis = QRS axis between -30° and +90°.
• Left Axis Deviation = QRS axis less than -30°.
• Right Axis Deviation = QRS axis greater than +90°.
• Extreme Axis Deviation = QRS axis between -90° and 180° 
 Quadrant method

most efficient way to estimate axis is to look at LEAD I and LEAD aVF.

mine the QRS complex in each lead and determine if it is Positive, Isoelectric
uiphasic) or Negative:
• A positive QRS in Lead I puts the axis in roughly the same direction as
lead I.
• A positive QRS in Lead aVF similarly aligns the axis with lead aVF.
• Combining both coloured areas – the quadrant of overlap determines
the axis. So If Lead I and aVF are both positive, the axis is between 0°
and +90° (i.e. normal axis).
RAD
RAD: leads II, III and aVF are POSITIVE; Leads I and aVL are NEGATIVE

• Causes
• Left posterior fascicular block
• Lateral myocardial infarction
• Right ventricular hypertrophy
• Acute lung disease (e.g. Pulmonary Embolus)
• Chronic lung disease (e.g. COPD)
• Ventricular ectopy
• Hyperkalaemia
• Sodium-channel blocker toxicity
• WPW syndrome
• Normal in children or thin adults with a horizontally positioned heart
•
Leads I and aVL are positive; leads II and aVF are negative

• Causes of LAD
• Left anterior fascicular block
• Left bundle branch block
• Left ventricular hypertrophy
• Inferior MI
• Ventricular ectopy
• Paced rhythm
• Wolff-Parkinson White syndrome
• Characteristics of normal sinus rhythm
• Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in 
children).
• Each QRS complex is preceded by a normal P wave.
• Normal P wave axis: P waves should be upright in leads I and II,
inverted in aVR.
• The PR interval remains constant.
• QRS complexes are < 100 ms wide 
Sinus tachycardia

• Sinus rhythm with a resting heart rate of > 100 bpm in adults, or

above the normal range for age in children.
•Pain, anxiety
•Hypoxia, hypercarbia
•Acidaemia
•Sepsis, pyrexia
•Pulmonary embolism
•Hyperthyroidism
• Pharmacological
• Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine
• Sympathomimetics:  amphetamines, cocaine, methylphenidate
• Antimuscarinics:  antihistamines, TCAs, carbamazepine, atropine
• Others: caffeine, theophylline, marijuana
Sinus bradycardia
• Causes of bradycardia

• Non-pharmacological
• Normal during sleep
• Increased vagal tone (e.g. athletes)
• Vagal stimulation (e.g. pain)
• Inferior myocardial infarction
• Sinus node disease
• Hypothyroidism
• Hypothermia
• Anorexia nervosa
• Electrolyte abnormalities – hyperkalaemia, hypermagnesaemia
• Brainstem herniation (the Cushing reflex)
• Myocarditis
• Pharmacological
• Beta-blockers
• Calcium-channel blockers (verapamil & diltiazem)
• Digoxin
• Central alpha-2 agonists (clonidine & dexmedetomidine)
• Amiodarone
• Opiates
• GABA-ergic agents (barbiturates, benzodiazepines, baclofen, GHB)
• Organophosphate poisoning
• Sinus Node Dysfunction Overview

• A disease characterized by abnormal sinus node functioning with resultant bradycardia and cardiac
insufficiency.
• May be multi-factorial in origin. Causes can be considered either intrinsic or extrinsic.

• Intrinsic Causes
• Idiopathic Degenerative Fibrosis (commonest).
• Ischaemia.
• Cardiomyopathies.
• Infiltrative Diseases e.g. sarcoidosis, haemochromatosis.
• Congenital abnormalities.
• Extrinsic Causes
• Drugs e.g. digoxin, beta-blockers, calcium channel blockers.
• Autonomic dysfunction.
• Hypothyroidism.
• Electrolyte abnormalitites — e.g. hyperkalaemia.
• Bradycardia – tachycardia syndrome
• Alternating bradycardia with paroxysmal tachycardia, often
supraventricular in origin.
• On cessation of tachyarrhythmia may be a period of delayed sinus
recovery e.g. sinus pause or exit block.
• If significant this period of delayed recovery may result in syncope
• Clinical Manifestations
• Commonly seen in the elderly but sinus node dysfunction can affect all age groups.
• Symptoms are due to decreased cardiac output and end-organ hypoperfusion
associated with cardiac rhythm abnormality.
• Wide range of clinical symptoms including syncope, near-syncope, dizziness,
fatigue and palpitations
• Treatment
• Correction / removal of extrinsic causes e.g. non-essential drugs.
• Pacemaker insertion – requires correlation of both ECG abnormalities and clinical
symptoms.

• Ischaemic heart disease
• Hypertensive heart disease
• Rheumatic heart disease
• Thyrotoxicosis
• Alcohol misuse (acute or
chronic)
Causes of atrial fibrillation
• Cardiomyopathy (dilated or   hypertrophic)
• Sick sinus syndrome
• Post-cardiac surgery
• Chronic pulmonary disease
• Idiopathic (lone)
• Conduction of atrial impulses to the ventricles is variable and unpredictable.
• Only a few of the impulses transmit through the atrioventricular node to
produce an irregular ventricular response.
• This combination of absent P waves, fine baseline f wave oscillations, and
irregular ventricular complexes is characteristic of atrial fibrillation.
• The ventricular rate depends on the degree of atrioventricular conduction,
and with normal conduction it varies between 100 and 180 beats/min.
Slower rates suggest a higher degree of atrioventricular block or the patient
may be taking medication such as digoxin.
• ECG Features of Atrial Fibrillation
• Irregularly irregular rhythm.
• No P waves.
• Absence of an isoelectric baseline.
• Variable ventricular rate.
• QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory
pathway, or rate related aberrant conduction.
• Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or
coarse (amplitude >0.5mm).
Atrial flutter
• Atrial flutter is due to a re-entry circuit in the right atrium with secondary
activation of the left atrium. This produces atrial contractions at a rate of
about 300 beats/min—seen on the electrocardiogram as flutter (F) waves.
These are broad and appear saw-toothed and are best seen in the inferior
leads and in lead V1.
• The ventricular rate depends on conduction through the atrioventricular
node. Typically 2:1 block (atrial rate to ventricular rate) occurs, giving a
ventricular rate of 150 beats/min. Identification of a regular tachycardia with
this rate should prompt the diagnosis of atrial flutter. The non-conducting
flutter waves are often mistaken for or merged with T waves and become
apparent only if the block is increased. Manoeuvres that induce transient
atrioventricular block may allow identification of flutter waves
Flutter
• Narrow complex tachycardia
• Regular atrial activity at ~300 bpm
• Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF —
may be more easily spotted by turning the ECG upside down!
• Flutter waves in V1 may resemble P waves
• Loss of the isoelectric baseline
Tachycardia

• Atrial tachycardia typically arises from an ectopic source in the atrial muscle and
produces an atrial rate of 150-250 beats/min—slower than that of atrial flutter. The
P waves may be abnormally shaped depending on the site of the ectopic pacemaker.
Causes
• Cardiomyopathy
• Chronic obstructive pulmonary disease
• Ischaemic heart disease
• Rheumatic heart disease
• Sick sinus syndrome
• Digoxin toxicity
• Multifocal atrial tachycardia occurs when multiple sites in the atria are
discharging and is due to increased automaticity.
• It is characterised by P waves of varying morphologies and PR intervals
of different lengths on the electrocardiographic trace.
• The ventricular rate is irregular. It can be distinguished from atrial
fibrillation by an isoelectric baseline between the P waves.
• It is typically seen in association with chronic pulmonary disease. Other
causes include hypoxia or digoxin toxicity.
• Ashman phenomenon (1947) describes an aberrant ventricular conduction, usually
of RBBB morphology, which follows a short RR interval and is preceded by a
relatively prolonged RR interval.
• Ashman phenomenon is typically seen with atrial fibrillation but can also occur with
other supraventricular arrhythmias.
• Clinically, Ashman phenomenon by itself is asymptomatic and does not require any
specific treatment.

Ashman phenomenon. Occurs when a long RR interval is followed by a short RR

interval and terminated by the aberrant QRS complex
• Mechanism
• The refractory period of the His-Purkinje system is proportional to the RR interval of the
preceding beat.
•  So, when two beats are separated by a long RR interval, the subsequent refractory
period will be relatively long. 
• If a premature supraventricular stimulus (short RR interval) follows a long RR interval
whilst the His-Purkinje system is still refractory, then the conducted beat will appear
abnormal.
• As the refractory period of the right bundle is slightly longer than the left, the aberrantly-
conducted beat typically demonstrates a right bundle branch (RBBB) morphology.
Premature atrial contraction
• These arise from ectopic pacemaking tissue within the atria. There is an abnormal P wave, usually
followed by a normal QRS complex.
• Groups of pacemaker cells throughout the conducting system are capable of spontaneous depolarisation.
• The rate of depolarisation decreases from top to bottom: fastest at the sinoatrial node; slowest within
the ventricles.
• Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from
above.
• However, if an ectopic focus depolarises early enough — before the arrival of the next sinus impulse — it
may “capture” the ventricles, producing a premature contraction.
• Premature contractions (“ectopics”) are classified by their origin — atrial (PAC), junctional (PJC) or
ventricular (PVC).
CAUSES
• Anxiety.
• Sympathomimetics.
• Beta-agonists.
• Excess caffeine.
• Hypokalaemia.
• Hypomagnesaemia.
• Digoxin toxicity.
• Myocardial ischaemia
ECG

• An abnormal (non-sinus) P wave is followed by a QRS complex.

• The P wave typically has a different morphology and axis to the sinus
P waves.
• The abnormal P wave may be hidden in the preceding T wave,
producing a “peaked” or “camel hump” appearance — if this is not
appreciated the PAC may be mistaken for a PJC.
• PACS arising close to the AV node (“low atrial” ectopics) activate the
atria retrogradely, producing an inverted P wave with a relatively
short PR interval ≥ 120 ms 
• PACs that reach the SA node may depolarise it, causing the SA node to “reset” — this
results in a longer-than-normal interval before the next sinus beat arrives (“post-
extrasystolic pause”). Unlike with PVCs, this pause is not equal to double the preceding
RR interval (i.e. not a “full compensatory pause”).
• PACs arriving early in the cycle may be conducted aberrantly, usually with a RBBB
morphology (as the right bundle branch has a longer refractory period than the left).
They can be differentiated from PVCs by the presence of a preceding P wave.
• Similarly, PACs arriving very early in the cycle may not be conducted to the ventricles at
all. In this case, you will see an abnormal P wave that is not followed by a QRS complex
(“blocked PAC”). It is usually followed by a compensatory pause as the sinus node resets.
Ventricular tachycardia
• Ventricular tachycardia may impair cardiac output with consequent
hypotension, collapse, and acute cardiac failure. This is due to extreme heart
rates and lack of coordinated atrial contraction (loss of “atrial kick”).
• The presence of pre-existing poor ventricular function is strongly associated
with cardiovascular compromise.
• Decreased cardiac output may result in decreased myocardial perfusion with
degeneration to VF.
• Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is
required in all cases of VT.
Mechanism of ventricular tachycardia
• Reentry
• Commonest mechanism.
• Requires two distinct conduction pathways with a conduction block in one pathway, and a region of
slow conduction in the other.
• Develops due to abnormal myocardial scarring usually due to prior ischemia or infarction.
•
Triggered Activity
• Occurs due to early or late after-depolarisations.
• Examples include Torsades and digitalis toxicity.
• Abnormal Automaticity
• Accelerated abnormal impulse generation by a region of ventricular cells.
Clinical Features Suggestive of VT

• Age > 35 (positive predictive value of 85%)

• Structural heart disease
• Ischaemic heart disease
• Previous MI
• Congestive heart failure
• Cardiomyopathy
• Family history of sudden cardiac death 
ECG changes

• Very broad complexes (>160ms).

• Absence of typical RBBB or LBBB morphology.
• Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I + aVF.
• AV dissociation (P and QRS complexes at different rates).
• Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in
the midst of AV dissociation, to produce a QRS complex of normal duration.
• Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid
complex of intermediate morphology.
• Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely
positive (R) or entirely negative (QS) complexes, with no RS complexes seen
• Brugada’s sign – The distance from the onset of the QRS complex to
the nadir of the S-wave is > 100ms.
• Josephson’s sign – Notching near the nadir of the S-wave.
• RSR’ complexes with a taller “left rabbit ear”. This is the most specific
finding in favour of VT. This is in contrast to RBBB, where the right
rabbit ear is taller.
Ventricular flutter
• Extreme form of ventricular tachycardia (VT) with loss of organised
electrical activity
• Associated with rapid and profound hemodynamic compromise
• Usually short lived due to progression to ventricular fibrillation
• As with ventricular fibrillation rapid initiation of advanced life support
 is required
• Associated with rapid and profound hemodynamic compromise
• Usually short lived due to progression to ventricular fibrillation
• As with ventricular fibrillation rapid initiation of advanced life support
 is required
•
The ECG looks identical when viewed upside down
• Most often this results in a minimal cardiac output and subsequent
ischemia.
Ventricular fibrillation
• The ventricles suddenly attempt to contract at rates of up to 500 bpm.
• This rapid and irregular electrical activity renders the ventricles unable to
contract in a synchronised manner, resulting in immediate loss of cardiac output.
• The heart is no longer an effective pump and is reduced to a quivering mess.
• Unless advanced life support is rapidly instituted, this rhythm is invariably fatal.
• Prolonged ventricular fibrillation results in decreasing waveform amplitude, from
initial coarse VF to fine VF and ultimately degenerating into asystole due to
progressive depletion of myocardial energy stores.
ECG changes
• Chaotic irregular deflections of varying amplitude
• No identifiable P waves, QRS complexes, or T waves
• Rate 150 to 500 per minute
• Amplitude decreases with duration (coarse VF -> fine VF)