In these presentation we explained about basic require knowledge for ECG who were working in area of critical care, Casualty,ICU. Here topic discussed is Basic ECG Presentation of each wave Some basic findings And how to interpret them.

1. PRESENTATION BY:-Dr Ankit
Agrawal

2. • ECG is the gold standard for the noninvasive
diagnosis of cardiac diseases and may
occasionally be the only marker for the
presence of heart disease

3. • P wave - <120mSec
• PR interval - <200mSec
• QRS complex - <110-120mSec
• QT interval - <440-450mSec

4. Normal Sinus Rhythm

5. Normal Sinus Rhythm
• ECG features of normal sinus rhythm
 Each QRS complex is preceded by a
normal P wave
 Normal P wave axis: P waves upright in
leads I and II, inverted in aVR
 The PR interval remains constant
 QRS complexes < 100 ms wide (unless
co-existent interventricular conduction
delay present)

6. STEMI
 ECG in STEMI
 Definition of STEMI
– ST segment elevation with subsequent Q wave formation
in precordial leads (V1-6) +/- high lateral leads. These
changes are often preceded by hyperacute T waves.
Reciprocal ST depression in inferior leads (mainly III and
aVF) Other conditions which are treated as a STEMI
– New or presumed new LBBB

9. STEMI

13. ATRIOVENTRICULAR BLOCK
(AV BLOCK)
• Atrioventricular block (AV block) is a type of heart block that occurs
when the electrical signal traveling from the atria, or the upper
chambers of the heart, to ventricles, or the lower chambers of the
heart, is impaired.
• Normally, the sinoatrial node (SA node) produces an electrical signal
to control the heart rate. The signal travels from the SA node to the
ventricles through the atrioventricular node (AV node). In an AV
block, this electrical signal is either delayed or completely blocked.
 THER ARE THREE TYPES OF AV BLOCK
 I st - Degree
 II nd - Degree
 IIIrd- Degree

14. 1 st degree :(Heart Block)
• PR interval > 200ms (five small squares)
 There is delay, without interruption, in
conduction from atria to ventricles
 ‘Marked’ first degree heart block is present if
PR interval > 300ms

15. P waves are buried in the preceding T wave

16. Causes of First Degree Heart Block
• 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

17. Second degree (AV block)
• ECG patterns that describe the behavior of the PR intervals (in sinus
rhythm) in sequences with at least 2 consecutively conducted PR intervals
in which a single P wave fails to conduct to the ventricles
• Mobitz Type I (Wenckebach AV block)
 PR interval is longest immediately before the dropped beat
 PR interval is shortest immediately after the dropped beat

18. • 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:
Other features

19. 2nd degree:(AV Block)
Definition of Mobitz II (Wenckebach AV block)
A form of 2nd degree AV block in which there is intermittent non-
conducted P waves without progressive prolongation of the PR interval
Arrows indicate “dropped” QRS complexes (i.e. non-conducted P waves)

20. Other features
 The PR interval in the conducted beats remains constant
 The P waves ‘march through’ at a constant rate
 The RR interval surrounding the dropped beat(s) is an exact multiple of the
preceding RR interval (e.g. double the preceding RR interval for a single
dropped beat, triple for two dropped beats, etc)
Mobitz type II rhythm strip demonstrating non-conducted P waves

21. 3rd degree: AV block
(Complete Heart Block)
• Complete Heart Block (CHB) Overview
 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.

22. Complete heart block strip
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
Features
Severe bradycardia due to absence of AV conduction
The ECG demonstrates complete AV dissociation, with independent
atrial and ventricular rates

23. Causes of complete heart block
 The causes are the same as for Mobitz I and Mobitz II second
degree heart block. The most important etiologies are:
 Inferior myocardial infarction
 AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-
blockers, digoxin)
 Idiopathic degeneration of the conducting system

24. Atrial Fibrillation
 Atrial Fibrillation (AF) is the most common sustained arrhythmia.
Characterized by disorganized atrial electrical activity and
contraction.
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).
 Fibrillatory waves may mimic P waves leading to misdiagnosis.

26. Treatment for A. Fibrillation
RACE protocol
• Rate Control – Beta Blocker, CCB
• Anticoagulated
• Chemical Cardioversion – Amiodarone
• Electrical cardioversion.

27. Ventricular Tachycardia
 Ventricular Tachycardia (VT) is a broad complex tachycardia originating in
the ventricles. There are several different varieties of VT
Duration
Sustained = Duration > 30 seconds or requiring intervention due to
hemodynamic compromise.
Non-sustained = Three or more consecutive ventricular complexes terminating
spontaneously in < 30 seconds.

28. Features suggestive of Ventricular
Tachycardia
 Features suggestive of VT 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.

30. ECG Features of Idiopathic Fascicular
Left Ventricular Tachycardia
• QRS duration 100 – 140 ms — this is narrower than
other forms of VT
• Short RS interval (onset of R to nadir of S wave) of 60-
80 ms — the RS interval is usually > 100 ms in other
types of VT
• RBBB Pattern
• Axis deviation depending on anatomical site of re-entry
circuit (see classification)

31. Broad-complex complex tachycardia with modest increase in
QRS width (~120 ms)
RBBB morphology (RSR’ in V1)
Left axis deviation (-90 degrees)
Narrow-complex capture beat (complex #6)
Several dissociated P waves are seen in the lead II rhythm
strip (associated with the 3rd, 10th, 14th, 18th and 22nd QRS
complexes)

34. MANAGEMENT

35. Ventricular Fibrillation (VF)
• Ventricular fibrillation (VF) is the the most important shockable cardiac
arrest rhythm.
 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.

36. ECG Findings
 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)

38. Supraventricular Tachycardia (SVT)
Definition
• The term supraventricular tachycardia (SVT) refers to any tachydysrhythmia arising
from above the level of the Bundle of His, and encompasses regular atrial, irregular
atrial, and regular atrioventricular tachycardias
 It is often used synonymously with AV nodal re-entry tachycardia (AVNRT), a
 form of SVT
 In the absence of aberrant conduction (e.g. bundle branch block), the ECG will
demonstrate a narrow-complex tachycardia
 Paroxysmal SVT (pSVT) describes an SVT with abrupt onset and offset –
characteristically seen with re-entrant tachycardias involving the AV node such as
AVNRT or atrioventricular re-entry tachycardia (AVRT).

39. Supraventricular tachycardia (SVT): Rhythm strip demonstrating a
regular, narrow-complex tachycardia
• Regular tachycardia ~140-280 bpm
• Narrow QRS complexes (< 120ms) unless there is co-
existing bundle branch block, accessory pathway, or
rate-related aberrant conduction
• P waves if visible exhibit retrograde conduction with P-
wave inversion in leads II, III, aVF. They may be buried
within, visible after, or very rarely visible before the
QRS complex

40. MANAGEMENT -CAROTID MASAGE

41. ADENOSINE
DOSE: 6 MG IV STAT
IF HEART RATE DOES NOT REVERT CAN GIVE 12 MG AS
NEXT DOSE
MAXIMUM: 30 MG

42. TORSADES DE. POINTES
• Torsades de pointes (TdP) is a specific form of
polymorphic ventricular tachycardia occurring
in the context of QT prolongation; it has a
characteristic morphology in which the QRS
complexes “twist” around the isoelectric line
• Management- BP recordable – MgSo4
• If BP un recordable - DC shock.

44. Left Bundle Branch Block (LBBB)
• ECG Diagnostic criteria
 QRS duration > 120ms
 Dominant S wave in V1
 Broad monophasic R wave in lateral leads
(I, aVL, V5-6)
 Absence of Q waves in lateral leads
 Prolonged R wave peak time > 60ms in
leads V5-6

45. LBBB: Left Bundle Branch Block
V1: Dominant S wave
V6: broad, notched (‘M’-shaped) R wave

46. • QRS Morphology in the Lateral Leads
 The R wave in the lateral leads may be either “M-shaped”, notched,
monophasic, or an RS complex
QRS Morphology in V1
The QRS complex in V1 may be either:
rS complex (small R wave, deep S wave)
QS complex (deep Q/S wave with no preceding R wave)

47. Right Bundle Branch Block (RBBB)
• Diagnostic criteria
• QRS duration >120ms
• RSR pattern in v1-3 (M-shaped QRS complex)
• Wide, slurred s wave in lateral leads (I, aVL, V5-6)

48. RBBB: Right Bundle Branch Block
V1: RSR’ pattern in V1, with (appropriate) discordant T
wave changes
V6: Widened, slurred S wave in V6

49. THANK
YOU