Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
3. HYPERACUTE ANTEROSEPTAL STEMI:
ST ELEVATION AND HYPERACUTE T WAVES IN V2 -4
ST ELEVATION IN I AND AVL WITH RECIPROCAL ST DEPRESSION IN LEAD III
Q WAVES ARE PRESENT IN THE SEPTAL LEADS V1 -2
THESE FEATURES INDICATE A HYPERACUTE ANTEROSEPTAL STEMI
5. ACUTE STEMI(ANTERIOR)
THERE IS PROGRESSIVE ST ELEVATION AND Q WAVE FORMATION
IN V2-5
ST ELEVATION IS NOW ALSO PRESENT IN I AND AVL
THERE IS SOME RECIPROCAL ST DEPRESSION IN LEAD III
7. • ECG FEATURES OF ATRIAL FIBRILLATION
IRREGULARLY IRREGULAR RHYTHM
NO P WAVES
ABSENCE OF AN ISOELECTRIC BASELINE
VARIABLE VENTRICULAR RATE
QRS COMPLEXES USUALLY < 120MS, 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
9. ECG FEATURES OF COMPLETE HEART
BLOCK
SEVERE BRADYCARDIA DUE TO ABSENCE
OF AV CONDUCTION
THE ECG DEMONSTRATES COMPLETE AV
DISSOCIATION, WITH INDEPENDENT
ATRIAL AND VENTRICULAR RATES
11. THIS ECG DISPLAYS MANY OF THE FEATURES OF
HYPERKALAEMIA:
PROLONGED PR INTERVAL.
BROAD, BIZARRE QRS COMPLEXES — THESE MERGE WITH
BOTH THE PRECEDING P WAVE AND SUBSEQUENT T WAVE.
PEAKED T WAVES.
THIS PATIENT HAD A SERUM K+ OF 9.3
16. ECG FEATURES OF HYPOKALAEMIA (K < 2.7
MMOL/L)
INCREASED P WAVE AMPLITUDE
PROLONGATION OF PR INTERVAL
WIDESPREAD ST DEPRESSION AND T WAVE
FLATTENING/INVERSION
PROMINENT U WAVES (BEST SEEN IN THE
PRECORDIAL LEADS V2-V3)
APPARENT LONG QT INTERVAL DUE TO FUSION
OF T AND U WAVES (= LONG QU INTERVAL)
19. HIGH LATERAL STEMI
ST ELEVATION IS PRESENT IN THE HIGH LATERAL LEADS (I AND AVL).
THERE IS ALSO SUBTLE ST ELEVATION WITH HYPERACUTE T WAVES IN
V5-6.
THERE IS RECIPROCAL ST DEPRESSION IN THE INFERIOR LEADS (III
AND AVF) WITH ASSOCIATED ST DEPRESSION IN V1 -3 (WHICH COULD
REPRESENT ANTERIOR ISCHAEMIA OR RECIPROCAL CHANGE).
21. LBBB
QRS DURATION > 120MS
DOMINANT S WAVE IN V1
BROAD MONOPHASIC R WAVE IN LATERAL
LEADS (I, AVL, V5-6)
ASSOCIATED FEATURES INCLUDE:
LEFT AXIS DEVIATION (LAD);
POOR R WAVE PROGRESSION IN
PRECORDIAL LEADS
24. ACUTE PERICARDITIS
WIDESPREAD CONCAVE ST ELEVATION
AND
PR DEPRESSION THROUGHOUT MOST OF
THE LIMB LEADS (I, II, III, AVL, AVF) AND
PRECORDIAL LEADS (V2-6)
RECIPROCAL ST DEPRESSION AND PR
ELEVATION IN LEAD AVR (± V1)
26. PULMONARY EMBOLISM
SINUS TACHYCARDIA – THE MOST COMMON ABNORMALITY (SEEN IN 44% OF PATIENTS WITH PE)
COMPLETE OR INCOMPLETE RBBB (18%)
RIGHT VENTRICULAR STRAIN PATTERN – T WAVE INVERSIONS IN THE RIGHT PRECORDIAL
LEADS (V1-4) ± THE INFERIOR LEADS (II, III, AVF). THIS PATTERN IS ASSOCIATED WITH HIGH
PULMONARY ARTERY PRESSURES (34%)
RIGHT AXIS DEVIATION (16%). EXTREME RIGHT AXIS DEVIATION MAY OCCUR, WITH AXIS
BETWEEN ZERO AND -90 DEGREES, GIVING THE APPEARANCE OF LEFT AXIS DEVIATION
(“PSEUDO LEFT AXIS”)
DOMINANT R WAVE IN V1 – A MANIFESTATION OF ACUTE RIGHT VENTRICULAR DILATATION
RIGHT ATRIAL ENLARGEMENT (P PULMONALE) – PEAKED P WAVE IN LEAD II > 2.5 MM IN HEIGHT
(9%)
SI QIII TIII PATTERN – DEEP S WAVE IN LEAD I, Q WAVE IN III, INVERTED T WAVE IN III (20%). THIS
“CLASSIC” FINDING IS NEITHER SENSITIVE NOR SPECIFIC FOR PE
28. INFERIOR STEMI
ST ELEVATION IN II, III AND AVF.
Q-WAVE FORMATION IN III AND AVF.
RECIPROCAL ST DEPRESSION AND T WAVE INVERSION IN
AVL
29. 3 QUESTIONS TO DX ARRHYTHMIA
1.Is it narrow complex or broad complex?
2.Is it regular or irregular?
3.P wave – absent or present? If present
what’s the morphology?
30. If arrhythmia
present(abnormal/irregular
rate)
Narrow
complex
Normal P : Sinus tachy
Absent P: AF
Present but abnormal: AT
Saw-tooth: Flutter
Irregular
Absent/fibrillatory: AF
Present but variable: MAT
Sawtooth: Flutter with
block
Broad
complex
Regular
VT
SVT with BBB
Irregular
TDP
Polymorphic VT
AF with BBB
36. POLYMORPHIC VENTRICULAR
TACHYCARDIA (PVT) IS A FORM
OF VENTRICULAR TACHYCARDIA IN
WHICH THERE ARE MULTIPLE
VENTRICULAR FOCI WITH THE
RESULTANT QRS COMPLEX VARYING IN
AMPLITUDE, AXIS, AND DURATION. THE
MOST COMMON CAUSE OF PVT IS
MYOCARDIAL ISCHAEMIA/INFARCTION.
38. TDP SECONDARY TO HYPOKALAEMIA:
SINUS RHYTHM WITH INVERTED T WAVES, PROMINENT U WAVES AND
A LONG Q-U INTERVAL DUE TO SEVERE HYPOKALAEMIA (K+ 1.7)
A PREMATURE ATRIAL COMPLEX (BEAT #9 OF THE RHYTHM STRIP)
LANDS ON THE END OF THE T WAVE, CAUSING ‘R ON T’
PHENOMENON AND INITIATING A PAROXYSM OF POLYMORPHIC VT
40. ECG FINDINGS IN VENTRICULAR
FIBRILLATION (VF)
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)
46. MONOMORPHIC VT: REGULAR,
BROAD COMPLEX TACHYCARDIA
UNIFORM QRS COMPLEXES WITHIN
EACH LEAD — EACH QRS IS
IDENTICAL (EXCEPT FOR
FUSION/CAPTURE BEATS)
50. ATRIAL FLUTTER WITH A 3:1 BLOCK
ECG FEATURES OF ATRIAL FLUTTER
NARROW COMPLEX TACHYCARDIA
REGULAR ATRIAL ACTIVITY AT ~300 BPM
“SAW-TOOTH” PATTERN OF INVERTED
FLUTTER WAVES IN LEADS II, III, AVF
VENTRICULAR RATE DEPENDS ON AV
CONDUCTION RATIO
54. STEPS OF INTERPRETING AN ECG
1. First roll off the topmost part.
2. Start from the bottom – look at the rhythm strip
3. Find out the following a) rate b) rhythm – if there’s any arrhythmia
4. Then go upwards – look at the limb leads to determine axis.
5. Then the waves – start with p wave at lead II and V1
6. Then look for other waves at all the leads, read from left to right, top
to bottom. Look for q wave at all leads, r wave progression at chest
leads, T and U wave (if present) at all leads
7. Then start with intervals, look at PR/QT intervals at lead II, QRS
complex at all leads, ST INTERVAL AT ALL LEADS(DO IT AGAIN>
THEN AGAIN)
55.
56. HOW TO DESCRIBE A NORMAL ECG
•This is a 12-lead normal amplitude ecg of mr./mrs. -
---- , ---- y/o, presenting with ---- showing rate ---
with regular rhythm, and normal axis. (or between -
30 and +90 degree). All the waves look normal with
good R-wave progression and there is no Q-wave.
PR interval is 0.12s, QT interval is 0.4s and there is
no ST-elevation or depression.
57. FOR ABNORMAL ECGS
• Any abnormality in a wave/interval/unusual wave can
be of three types – amplitude/ duration / morphology
• Mention which leads are showing abnormality
• Always look at the corresponding leads
Hyperacute Anteroseptal STEMI:
ST elevation and hyperacute T waves in V2-4
ST elevation in I and aVL with reciprocal ST depression in lead III
Q waves are present in the septal leads V1-2
These features indicate a hyperacute anteroseptal STEMI
There is progressive ST elevation and Q wave formation in V2-5
ST elevation is now also present in I and aVL
There is some reciprocal ST depression in lead III
ECG Features of Atrial Fibrillation
Irregularly irregular rhythm
No P waves
Absence of an isoelectric baseline
Variable ventricular rate
QRS complexes usually < 120ms, 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
ECG features of complete heart block
Severe bradycardia due to absence of AV conduction
The ECG demonstrates complete AV dissociation, with independent atrial and ventricular rates
This ECG displays many of the features of hyperkalaemia:
Prolonged PR interval.
Broad, bizarre QRS complexes — these merge with both the preceding P wave and subsequent T wave.
Peaked T waves.
This patient had a serum K+ of 9.3
Hyperkalaemia:
Huge peaked T waves.
Sine wave appearance.
This patient had severe hyperkalaemia (K+ 9.0 mEq/L) secondary to rhabdomyolysis.
ECG features of hypokalaemia (K < 2.7 mmol/L)
Increased P wave amplitude
Prolongation of PR interval
Widespread ST depression and T wave flattening/inversion
Prominent U waves (best seen in the precordial leads V2-V3)
Apparent long QT interval due to fusion of T and U waves (= long QU interval)
High Lateral STEMI
ST elevation is present in the high lateral leads (I and aVL).
There is also subtle ST elevation with hyperacute T waves in V5-6.
There is reciprocal ST depression in the inferior leads (III and aVF) with associated ST depression in V1-3 (which could represent anterior ischaemia or reciprocal change).
This pattern is consistent with an acute infarction localised to the superior portion of the lateral wall of the left ventricle (high lateral STEMI).
The culprit vessel in this case was an occluded first diagonal branch of the LAD.
QRS duration > 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Associated features include:
Left axis deviation (LAD);
Poor R wave progression in precordial leads
Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6)
Reciprocal ST depression and PR elevation in lead aVR (± V1)
Sinus tachycardia – the most common abnormality (seen in 44% of patients with PE)
Complete or incomplete RBBB (18%)
Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF). This pattern is associated with high pulmonary artery pressures (34%)
Right axis deviation (16%). Extreme right axis deviation may occur, with axis between zero and -90 degrees, giving the appearance of left axis deviation (“pseudo left axis”)
Dominant R wave in V1 – a manifestation of acute right ventricular dilatation
Right atrial enlargement (P pulmonale) – peaked P wave in lead II > 2.5 mm in height (9%)
SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III (20%). This “classic” finding is neither sensitive nor specific for PE
Inferior STEMI:
ST elevation in II, III and aVF.
Q-wave formation in III and aVF.
Reciprocal ST depression and T wave inversion in aVL
Inferior STEMI:
ST elevation in II, III and aVF.
Q-wave formation in III and aVF.
Reciprocal ST depression and T wave inversion in aVL
Supraventricular tachycardia (SVT): Rhythm strip demonstrating a regular, narrow-complex tachycardia
Supraventricular tachycardia (SVT): Rhythm strip demonstrating a regular, narrow-complex tachycardia
Slow-Fast (Typical) AVNRT:
Narrow complex tachycardia at ~ 150 bpm
No visible P waves
Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction.
TdP secondary to hypokalaemia:
Sinus rhythm with inverted T waves, prominent U waves and a long Q-U interval due to severe hypokalaemia (K+ 1.7)
A premature atrial complex (beat #9 of the rhythm strip) lands on the end of the T wave, causing ‘R on T’ phenomenon and initiating a paroxysm of polymorphic VT
ECG findings in Ventricular Fibrillation (VF)
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)
“R on T” phenomenon causing Torsades de Pointes, which subsequently degenerates to VF
This patient is shocked out of VF five times in ten minutes!
Monomorphic VT: Regular, broad complex tachycardia
Uniform QRS complexes within each lead — each QRS is identical (except for fusion/capture beats)
Monomorphic VT:
Very broad QRS complexes (~ 200 ms) with uniform morphology
Fusion and capture beats are seen in the rhythm strip
Atrial flutter with a 3:1 block
ECG features of atrial flutter
Narrow complex tachycardia
Regular atrial activity at ~300 bpm
“Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF
Ventricular rate depends on AV conduction ratio