1. ECG
Jmin ooi

2. P wave
• Amplitude <2.5mm in limb lead ; <1.5mm in
precordial lead
• Width < 0.12s

3. Abnormality of p wave
• P mitrale/ bifid p wave
• P pulmonale/ peak p wave
• P inversion
• Multifocal atrial rhythm

4. PR interval
• N 0.12 – 0.2 s

5. Abnormality
• PR prolong = AV block
• Steps in determining type of AV block
1. Prolonged PR is fixed = first degree
2. see if got p wave not followed by QRS = second degree heart block
3. see if got prolonged PR interval = Mobitz type 1(WENCKEBACH)
4. see got QRS conduct on its own rate, independent of p wave
• First degree
• Second degree
• Third degree

6. Q wave
- Normal left to right interventricular depolarisation
- Small septal Q normally seen in left sided leads (1, avL v5 v6)
- Not seen in v1 to v3
- Pathological q wave- >1mm (1box) wide, >2mm (2 box) deep, >25% deep
of QRS, seen in v1 to 3
- DD
- MI****
- Cardiomypathies- hcom
- Rotation
- Lead placement
Loss of abnormal Q wave in v5 v6 normally due to LBBB

7. QRS
• Normal 0.06-0.10s
• >0.12 s suggest bundle branch block
• Look at width (0.06-0.10s)
• Look at voltage/height
– Low voltage (limb lead <5mm 一个大格) ,
(praecordial lead <10mm 两个大格)
– High voltage [(s1 + v5/v6) > 35mm]

8. • Narrow complex (<0.10s) *supraventricular
origin)
– SA (present of P wave)
– Atrial (abN P- atrial flutter/ atrial fibrillation)
– AV (no P or abN p with PR interval <0.12) normal
PR 0.12-0.2

9. • Broad complex ORS (>0.10 abN, >0.12 bundle
branch block)
– Bundle branch block
– Hyperkalaemia
– Tricyclic antidepressant
– Hypothermia
– Wolf- parkinson white syndrome

10. • Low voltage QRS [ (limb lead <5mm) (praecordial lead
<10mm) ]
• Mechanism
– “damping” effect of increased air/ fluid or fat between
lead and heart
– Loss of viable myocardium
– Infiltration of myxoedematous involvement of the heart
Causes
– pleural effusion, pericardial effusion, emphysema,
pneumothorax, constricitve pericarditis, obesity
– Previous massive MI, end stage dilated cardiomyopathies
– hypothyroidism

11. ST segment
Represents the interval between ventricular depolarisation and
repolarisation
ELEVATION
DD
- Acute MI (STEMI)
- Coronary vasospasm (Printzmetal’s angina)
- Pericarditis
- Others : benign early repolarisation, LBBB, LVH
STEMI
- Septal (v1 v2)
- Ant (v3 v4)
- Lat (I avL v5 v6)
- Inf (II III avF)

12. **prinzmetal angina – syndrome consist of
angina caused by vasospasm (contraction of
smooth muscle wall causing narrowing of
coronary arteries)

13. Site of infarct according to lead
- Inferior (avF II III)
- Anteroseptal (v1 to v4)
- Anterolateral (I avL v5 v6, v4)
- Posterior (tall R & ST depression in v1 v2)

14. DEPRESSION
DD
- Myocardial ischaemia (NSTEMI)
- Reciprocal change in STEMI
- Posterior MI
- Others : digoxin, hypoK+, supraventricular tachycardia, RBBB, RVH,
LBBB, LVH, ventricular paced rhythm
Morphology
- downsloping, upsloping or horizontal
- Downsloping and horizontal more or equal to 0.5mm for more than
or equal to 2 consecutive leads indicates Myocardial ischaemia

15. T wave
- Ventricular repolarisation
- Normally inverted in lead v1, avR, occasionally v2
- Abnormal if inverted in I, II, v4, v5, v6
- Abnormalities
- Inverted
- Hyperacute
- Flatten
- Biphasic
- Camel hump
Tall T wave
tall, narrow, symmetrically peaked T wave
hyperkalaemia

16. - Hyperacute T wave
-Broad asymmetrically peak or hyperactive
-seen in the early stages (hours) of STEMI,
precede the appearance of ST elevation
and Q wave.
-Also seen in printzmetal angina.

17. Irregularly irregular radial pulse
• DD
– Atrial fibrillation
– Multifocal ventricular ectopics
– Atrial flutter with varying block

18. AV block
• First degree
• Second degree
• Third degree

19. • First degree
– Prolonged PR
• Second degree – P not followed by QRS
– Mobitz I (Wenckebach)– progressively prolonged
PR and
-Mobitz II – PR constant
• Third degree- complete heart block
– QRS conducted at its own rate and is independent
of p wave

20. Sinus bradycardia
• Athlete
• Myxoedema
• hypothermia

21. Sinus tachycardia
• Exercise
• Pain
• Fear
• Thyrotoxicosis
• haemorrhage

22. Atrial tachyarrythmia
• Including
– Atrial fibrillation
– Atrial flutter
– Atrial ectopic beats
• Smiliarities
• Arise from atrial myocardium
• Share common etiology

23. • Etiology***********
(a)Cardiac
– IHD- ischaemic heart ds (coronary artery & MI)
– RHD- rheumatic heart ds
– valvular heart ds eg mitral stenosis/ regurg
– hypertension
(b)Non cardiac
– thyrotoxisosis
– pulmonary-disease (pneumonia, COPD) & vascular ds (pulm
embolism)
– e- imbalance (hypoK+)
– alcohol misused
Mneumonics: I HAVE A FIB- IHD/idiopathic(lone AF), HPT, Valvular heart
ds, Embolism(pulmonary), ASD, Failure (CHF), infection (pneumonia)

24. a) Atrial fibrillation
• History taking
– Signs & sx
– Etiology (Risk factor)
– Complications
• Sign and sx
– Palpitation
– Dyspnoea
– Chest pain
• Complications
– Stroke (systemic thromboembolism- blood pools in the atrium as the
atrial is not contracting efficiently, thus cause risk of blood clots in the
strium)
– Left ventricular failure (esp in fast atrial fib where the atrial cannot
filled with blood properly and pump efficiently to the ventricle, causing
raised left atrial pressure and LVF)
• exertional dyspnoea/orthopnoea[pillow!!!)/ Paroxysmal nocturnal dyspnoea
• peripheraal or central cyanosis dt red C.O.
– Exacerbation of angina

25. • Mechanisms
– Automatic foci that depolarize rapidly
– Located predominantly in pulmonary vein
– That supply the left atrium. Atrium respond electrically but
the mechanical action is not coordinated
– Only portion of the impulse is transmitted to the ventricle
• Clinical classification
– Paroxysmal (stop spontaneously within 7 days)
– Persistent (require cardioversion to stop)
– Permanent

26. Ix
1. ECG
– No p wave
– Irreg baseline
– Irreg and rapid QRS rhythm, vary btwn __to __bpm
2. (hyperthyroidism) TFT- low TSH, free T4 high
3. (Valvular heart ds) Echocardiography- valvular defects,
left atrial thrombus, left atrial size
4. (Paroxysmal AF) Holter monitoring
5. (Pulmonary ds-embolism&infection) CXR
6. (hypoK+) BUSE

27. • Mx
– Identify the underlying cause
– Treat arrhythmia by
• Cardioversion- electrical or pharmalogical
• Digoxin-control ventricular rate if cardioversion fails
– Anticoagulation- prevent thromboembolism, aim INR 2.0-3.0
INR
– http://www.myvmc.com/investigations/blood-clotting-
international-normalised-ratio-inr/
Anticoagulant
- CHADS2 (if more than 2 must use anticoagulant, if 1 assess by
CHADS2 VASc)- congestive heart failure, hypertension ,age above
75, diabetes mellitus, stroke/TIA (stroke/TIA scores 2)
- CHADS2 VASc - vascular heart disease, age 65-74, sex: female
(previous age above 75 and stroke score 2) (if more than 2 use
anticoagulant, if 1 consider anticoag or aspirin)

28. Atrial flutter
• Regular atrial rhythm with rate of 250-300
bpm
• ECG shows regular saw tooth appearance
between QRS complex

29. Left bundle branch block
• Normally Q wave form due to interventricular
depolarization thru septum from left to right,
produce Q wave in lateral leads. in LBBB septal
depo is reversed from right to left, RV is depo
first, to LV via the septum. This cause prolonged
QRS (>0.12s) And lost of Q wave
– Direction of depo from R to L cause tall R in lateral
leads (I, v5 v6) and deep S in R precordial leads (v1 v2
v3)
– Usually lead to L axis dev

30. Hypothyroidism
• Triads of
– Bradycardia (<60bpm)
– Low voltage QRS (<5mm for limb lead, <10mm for
praecordium)
– Widespread T inversion
• Machanism
• Myoedematous infiltration of heart
• Reduced thyroxin reduce inotropy(contraction of hear
muscle) and chronotropy(heart rate)
• Reduced sympathetic stimulation