 Rhyhm strip and see the rate

 See the number of boxes and see the heart rate (( normal 60-100) 300/ number of big squares between R-R)

• Identify the rhythm relationship btw P and QRS

 Regular
 Irregular
o regularly Irregular
o Irregularly irregular

• Regular –After every QRS complex the whole component of the complex repeated in regular interval

• If Irregularly irregular then think of AF or VF

Heart Rate

 Normal HR is sinus rhythm( normal 60-100) 300/ number of big squares between R-R)

• Sinus trachycardia – rhythm normal but HR is more than of > 100 bpm in adults Sinus bradycardia <60 bpm in adults

• Unstable patient with Trachycardia - DC shock

• Stable with trachycardia- < 3 boxes 3-5 normal > 5 bradycardia

• Narrow complex trachycardia < QRS (heart) small quares ---- AF

• SVT – any trachycardia above venticels (AF , A flutter, AVNRT, AVART)

Managements

• If regular rhythm – Carotid massage if normal then it means WPS ( delta wave after P ) accessory pathway goes in two
direction one from AV node and the other from accessory pathway. Rx Ablation

If not WPS then give IV Adenosine

• Atrial flutter is saw tooth pattern HR 150 as it is a 2:! Block , AV node act as filter

o Acute AF – CCB, B blocker Digoxin( 1st choice if associated with HF)

o Peroxysmal- Pill in the pocket flaconyte , Sotalol
o Chronic-repeated MI leading to fibrosis B blocker , CBB, Digoxin

• Ventricular trachycardia- amidarone if not then DC shock and Ventricular flutter ( death rhythm) DC shock

• Torse de Pointes ( QT interval prolonged) IV Mg SO4 if does not work then give Dc shock

Heat Block

1 degree- PR interval increased > 200 msec and will be seen in every QRS complex . The prolongation is constant

2 dgree-Mobiz type I ( Wenckebach )progressively prolong PR interval and it QRS complex suddenly drops and then again the
pattern continues

Mobiz type II PR interval remains the same but drops with 2:1 Or 3:1 QRS complex drops

3 degree P waves are completely unrelated with the QRS complex

Source : http://lifeinthefastlane.com/ecg-library

Normal Sinus Rhythm

Definition

 The default heart rhythm.

 Pacemaking impulses arise from the sino-atrial node and are transmitted to the ventricles via
the AV-node and His-Purkinje system.
 This results in a regular, narrow-complex heart rhythm at 60-100 bpm.

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 (unless a co-existent interventricular conduction delay is
present).

Normal heart rates in children

 Newborn: 110 – 150 bpm

 2 years: 85 – 125 bpm
 4 years: 75 – 115 bpm
 6 years+: 60 – 100 bpm
Sinus rhythm

Variations on sinus rhythm

 Sinus tachycardia = sinus rhythm with resting heart rate > 100 bpm in adults, or above the
normal range for age in children.
 Sinus bradycardia = sinus rhythm with resting heart rate < 60 bpm in adults, or below the normal
range for age in children.
 Sinus arrhythmia = sinus rhythm with a beat-to-beat variation in the P-P interval (the time
between successive P waves), producing an irregular ventricular rate.

Example ECG

Normal sinus rhythm in a healthy 18-year old male:

  Regular rhythm at 84 bpm.
 Normal P wave morphology and axis (upright in I and II, inverted in aVR).
 Narrow QRS complexes (< 100 ms wide).
 Each P wave is followed by a QRS complex.
 The PR interval is constant.

Sinus tachycardia

Definition

Sinus rhythm with a resting heart rate of > 100 bpm in adults, or above the normal range for age in
children.

Causes

Non-pharmacological

 Exercise
 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

Handy Tip

With very fast heart rates the P waves may be hidden in the preceding T wave, producing a
‘camel hump’ appearance.
Hidden P waves in sinus tachycardia ("camel hump" appearance)

Example ECG

Sinus tachycardia:

 Heart rate 150 bpm.

 P waves are hidden within each preceding T wave.
Sinus Bradycardia

Definition

 Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age
in children.

Causes

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

Differential Diagnosis

 Sinus bradycardia may be indistinguishable from type II sino-atrial block.

ECG Example

Sinus bradycardia secondary to anorexia nervosa

 Sinus bradycardia (35 bpm) in a 15-year old girl with anorexia nervosa.
 Note the prominent U waves in the precordial leads, a common finding in sinus bradycardia.
The P wave

The P wave is the first positive deflection on the ECG

 It represents atrial depolarisation

Characteristics of the Normal Sinus P Wave

Morphology

 Smooth contour
 Monophasic in lead II
 Biphasic in V1

Axis

 Normal P wave axis is between 0° and +75°

 P waves should be upright in leads I and II, inverted in aVR

Duration

 < 120 ms

Amplitude

 < 2.5 mm in the limb leads,

 < 1.5 mm in the precordial leads
Atrial abnormalities are most easily seen in the inferior leads (II, III and aVF) and lead V1,
as the P waves are most prominent in these leads.

The Atrial Waveform – Relationship to the 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.
 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.

Click image for source

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).
 Click image for source

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”).

Click image for source

Normal P-wave Morphology – Lead V1

The P wave is typically biphasic in V1, with similar sizes of the positive and negative
deflections.
 Normal P wave in V1

Right Atrial Enlargement – Lead V1

Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive
deflection of the P wave.

Click image for source

NB. This patient also has evidence of right ventricular hypertrophy.

Left Atrial Enlargement – Lead V1

Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep) in V1 of
the terminal negative portion of the P wave.
 Click image for source

Biatrial Enlargement

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:
 Reproduced from Wagner et al. (2007)

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.
Bifid P waves (P mitrale) in left atrial enlargement

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).

Peaked P waves (P pulmonale) due to right atrial enlargement

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):

Accelerated Junctional Rhythm

When the PR interval is ≥ 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm):

Ectopic Atrial 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:

Multifocal Atrial Rhythm

If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100, then multifocal atrial
tachycardia (MAT) is diagnosed:
Multifocal Atrial Tachycardia

First Degree Heart Block

Definition

 PR interval > 200ms (five small squares)

 ‘Marked’ first degree block if PR interval > 300ms

Examples

First degree heart block (PR interval > 200 ms)

Marked first degree heart block (PR interval > 300 ms, P waves are buried in the preceding T
wave)
Causes

 Increased vagal tone

 Athletic training
 Inferior MI
 Mitral valve surgery
 Myocarditis (e.g. Lyme disease)
 Electrolyte disturbances (e.g. Hyperkalaemia)
 AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)
 May be a normal variant

Clinical significance

 Does not cause haemodynamic disturbance

 No specific treatment is required

AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon)

Definition

 Progressive prolongation of the PR interval culminating in a non-conducted P wave

 The PR interval is longest immediately before the dropped beat
 The PR interval is shortest immediately after the dropped beat

Other Features

 The P-P interval remains relatively constant

 The greatest increase in PR interval duration is typically between the first and second beats of
the cycle.
 The RR interval progressively shortens with each beat of the cycle.
 The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

Mechanism

 Mobitz I is usually due to reversible conduction block at the level of the AV node.
  Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse.
This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly
(i.e. producing a Mobitz II block).

Causes

 Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone

 Increased vagal tone (e.g. athletes)
 Inferior MI
 Myocarditis
 Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

Clinical Significance

 Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low
risk of progression to third degree heart block.
 Asymptomatic patients do not require treatment.
 Symptomatic patients usually respond to atropine.
 Permanent pacing is rarely required.

ECG Examples

Example 1
  The first clue to the presence of Wenckebach AV block on this ECG is the way the QRS
complexes cluster into groups, separated by short pauses (This phenomenon usually represents
2nd-degree AV block or non-conducted PACs; occasionally SA exit block). At the end of each
group is a non-conducted P wave.
 The PR interval progressively increases from one complex to the next.
 The Wenckebach pattern here is repeating in cycles of 5 P waves to 4 QRS complexes (5:4
conduction ratio).
 The increase in PR interval from one complex to the next is subtle. However, the difference is
more obvious if you compare the first PR interval in the cycle to the last.
 The P-P interval is relatively constant despite the irregularity of the QRS complexes.

Example 2

Another example of a slowly-evolving Wenckebach cycle:

 QRS complexes cluster in groups, separated by non-conducted P waves.

 The P:QRS conduction ratio varies from 5:4 to 6:5.
 Note the difference in PR interval between the first and last QRS complex of each group.
Example 3

Wenckeback due to Inferior STEMI:

 The majority of the rhythm strip shows 2:1 AV conduction, which makes identification of the
type of block difficult (i.e. it could represent Mobitz I or Mobitz II).
 However, there is a single 3:2 Wenckebach cycle visible in the middle of the rhythm strip (QRS
complexes 5 + 6). If you look hard, you can see a non-conducted P wave deforming the
downslope of the T wave in complex 6.
 Continuous rhythm strip recording revealed that this patient was indeed in Mobitz I AV block.

AV block may occur in the context of an inferior STEMI due to ischaemia / infarction of the AV
node, or due to increased vagal tone (= the Bezold-Jarisch reflex).
An Interesting Case of Wenckebach

Mobitz I in an atrially-paced patient following mitral valve surgery

 Small atrial pacing spikes precede the QRS complexes.

 The interval between the pacing spikes increases progressively until there is a non-conducted
pacing spike.
 To find out the story behind this ECG, check out this chapter from the ECG Exigency series:”Post-
op Pacing Puzzler“

Diagnosis Wenckebach?

The ECG below was originally featured on this page as an example of Wenckebach AV block.
Can you spot the “deliberate” mistake?
AV block: 2nd degree, “fixed ratio” blocks

Definition

 Second degree heart block with a fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1).
 Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.

Examples

2:1 block

 The atrial rate is approximately 75 bpm.

 The ventricular rate is approximately 38 bpm.
 Non-conducted P waves are superimposed on the end of each T wave.
3:1 block

 The atrial rate (purple arrows) is approximately 90 bpm.

 The ventricular rate rate is approximately 30 bpm.
 Note how every third P wave is almost entirely concealed within the T wave.

Mobitz I or II?

 It is not always possible to determine the type of conduction disturbance producing a fixed ratio
block, although clues may be present.
 Mobitz I conduction is more likely to produce narrow QRS complexes, as the block is located at
the level of the AV node. This type of fixed ratio block tends to improve with atropine and has
an overall more benign prognosis.
 Mobitz II conduction typically produces broad QRS complexes, as it usually occurs in the context
of pre-existing LBBB or bifascicular block. This type of fixed ratio block tends to worsen with
atropine and is more likely to progress to 3rd degree heart block or asystole.
 However, this distinction is not infallible. In approximately 25% of cases of Mobitz II, the block is
located in the Bundle of His, producing a narrow QRS complex. Furthermore, Mobitz I may occur
in the presence of a pre-existing bundle branch block or interventricular conduction delay,
producing a broad QRS complex.
 The only way to be certain is to observe the patient for a period of time (e.g. watch the cardiac
monitor, print a long rhythm strip, take serial ECGs) and observe what happens to the PR
intervals. Often, periods of 2:1 or 3:1 block will be interspersed with more characteristic
Wenckebach sequences or runs of Mobitz II.

AV block: 3rd degree (complete heart block)

Definition

 In complete heart block, there is complete absence of AV conduction – none of the

supraventricular impulses are conducted to the ventricles.
 Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the
patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden
cardiac death (if prolonged).
  Typically the patient will have severe bradycardia with independent atrial and ventricular rates,
i.e. AV dissociation.

Example of complete heart block

 The atrial rate is approximately 100 bpm.

 The ventricular rate is approximately 40 bpm.
 The two rates are independent; there is no evidence that any of the atrial impulses are
conducted to the ventricles.

Mechanism

 Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block.
 It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to
increased vagal tone in the acute phase of an inferior MI).
 Alternatively, it may be due to sudden onset of complete conduction failure throughout the His-
Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute anterior MI).
 The former is more likely to respond to atropine and has a better overall prognosis.

Causes of complete heart block

The causes are the same as for Mobitz I and Mobitz II second degree heart block. The most
important aetiologies are:

 Inferior myocardial infarction

 AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin)
 Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease)

Clinical significance

 Patients with third degree heart block are at high risk of ventricular standstill and sudden
cardiac death.
 They require urgent admission for cardiac monitoring, backup temporary pacing and usually
insertion of a permanent pacemaker.
Differential diagnosis

Complete heart block should not be confused with:

 High grade AV block: A type of severe second degree heart block with a very slow ventricular
rate but still some evidence of occasional AV conduction.
 AV dissociation: This term indicates only the occurrence of independent atrial and ventricular
contractions and may be caused by entities other than complete heart block (e.g. “interference-
dissociation” due to the presence of a ventricular rhythm such as AIVR or VT).

ECG Examples

Example 1

Complete Heart Block:

 Atrial rate is ~ 85 bpm.

 Ventricular rate is ~ 38 bpm.
 None of the atrial impulses appear to be conducted to the ventricles.
 Rhythm is maintained by a junctional escape rhythm.
  Marked inferior ST elevation indicates that the cause is an inferior STEMI.

Example 2

Complete Heart Block:

 Atrial rate is ~ 60 bpm.

 Ventricular rate is ~ 27 bpm.
 None of the atrial impulses appear to be conducted to the ventricles.
 There is a slow ventricular escape rhythm.
Example 3

Complete Heart Block:

 Atrial rate 100 bpm

 Ventricular rate only 15 bpm!
 This patient needs urgent treatment with atropine / isoprenaline and pacing!
Example 4

Complete Heart Block with Isorhythmic AV Dissociation (long rhythm strip):

 Atrial rate ~ 85 bpm

 Ventricular rate ~ 42bpm
 There is a junctional escape rhythm.
 As the ventricular rate is approximately half the atrial rate, this rhythm at first glance appears to
be second-degree AV block with 2:1 conduction.
 However on closer inspection the PR interval varies, with some of the P waves superimposed on
the QRS complexes. The ventricular rate remains regular.
 This confirms that the atrial impulses are not being conducted to the ventricles.
 The apparent relationship between the P waves and QRS complexes occurs merely by chance (=
isorhythmic AV dissociation).
Left Axis Deviation

Left Axis Deviation

Definition

 QRS axis between -30 and -90 degrees

Left axis deviation: -30 to -90 degrees

How to recognise left axis deviation

 QRS is positive (dominant R wave) in leads I and aVL

 QRS is negative (dominant S wave) in leads II and aVF

Left Axis Deviation: leads I and aVL are positive; leads II and aVF are negative

Causes Causes of Left bundle branch

block(LBBB)
 Left anterior fascicular block
 Left bundle branch block  Ischemic heart disease (Recent or
 Left ventricular hypertrophy old MI)
 Inferior MI  Hypertention
 Ventricular ectopy  LVH
 Paced rhythm  Aotic valve disease
 Wolff-Parkinson White syndrome  Cardiomyopathy
 Myocarditis
 Post valve replacement
 Right ventricular pacemaker
 Trachycardia with aberrancy or
concealed conduction
 Ventricular ectopy
Right Axis Deviation

Right Axis Deviation

Definition

 QRS axis between + 90 and + 180 degrees

Right axis deviation: +90 to +180 degrees

How to recognise right axis deviation

 QRS is positive (dominant R wave) in leads III and aVF

 QRS is negative (dominant S wave) in leads I and aVL

Right axis deviation: leads III and aVF are positive; leads I and aVL are negative

Causes

 Infancy Causes of Right Bundle Branch Block

 Right Bundle Branch Block (RBBB) (RBBB)
 Right ventricular hypertrophy
 ( eg lung disease , pulmonary embolism,  Normal in young
large secundum ASD, Severe pulmonary Stennosis  Right ventricular strain (PE)
, Tetralogy of Fallot)  ASD
 IHD
 Myocarditis
 Idiopathic
 Trachycardia with abberancy or
concealed conduction
 Ventricular ectopy
Clinical diagnosis which can be made from the ECG of an Asymptomatic patient

 Atrial fibrillation
 Complete Heat Block
 HCM
 ASDs( with RBBB)
 Long Qt and Brugada syndromes
 Woff Parkinson- White Syndrome(Delta waves)
 Arrhythmogenic right ventricular dysplasia

Abnormal ECG in Atheletes

 Sinus Arrythmia
 Sinus Bradycardia
 First degree heart block
 Wenchebach phenomenon