ECG Made Easy –An abnormal

look
BY: Abdallah Adel Farah
RRT, RT, CCRN, RN, HF Specialist
AHA, ERC, ASHI, SCCM Instructor
Disaster Medical Director from SESRIC
James Cook University hospital
Hypertrophy
• Left ventricular
hypertrophy :-
#.R wave inV5 or V6+S
wave in V1or
V2>35mm.
#.R wave V5 or V6
>25mm.
#.ass e- inverted T wave
in lead 1,VL,V5-V6
• Right
ventricular
hypertrophy :-
-Tall R wave in V1.
-deep S wave in V6.
-right axis
deviation.
Left atrial
enlargement:-
Either:-
#.P wave with a broad
(>0,04 sec or 1 small
square) and deeply
negative (>1 mm)
terminal part in V1. or
#.P wave duration >0,12
sec in laeds I and / or II.
#,seen in mitral valve
stenosis.
Right atrial enlargement:-
#.peak P wave >2,5 mm in II /
III and / or aVF .
#. results
from increased
pressure in the
pulmonary artery,
e.g.pulmonary
embolism, tricuspid
stenosis.
Infarction & Ischemia
 Non-ST Elevation Myocardial
Infarction (NSTEMI) or ischemia

• Symptoms suggesting MI

• Non-specific ECG abnormalities

– ST segment depression
– T wave inversion
• Elevated cardiac enzymes in case of
NSTEMI
Acute ST depression
T wave inversion
 Evolution of AMI
1.Hyper acute T wave:-
#.Earliest sign is an increase in T wave
amplitude.
#.T wave pointed.
#.Most evident in anterior chest leads.
#.Changes are usually only present for 5-30
minutes.
#.ST segment change follows.
Hyper acute T waves
 Evolution of AMI
2.ST segment elevation:-
#.occurs within the first few hours of
symptom onset.
#.Degree of ST elevation varies.
#.ST elevation>1mm in 2 contiguous limb
leads or >2mm in 2 contiguous chest
leads is an indication for thrombolysis.
ST Elevation
 How To Measure ST
Segment Elevation
J point

PT baseline
 Evolution of AMI
3. Pathological Q wave:-
#.As AMI evolves pathological Q waves
develop due to Loss of viable myocardium
beneath the recording electrode.
#.May develop within 1-2 hours.
#.Q waves act as a permanent marker of
myocardial necrosis.
• Pathologic Q-wave (any Q in V1-V3 or Q
width > 30ms in I, II, AVL, V4-V6; minimal
in 2 contiguous leads, minimal depth 1
mm): previous MI. Leads III and AVR may
have a Q wave, which is non-pathological.
Pathological Q Waves
 Evolution of AMI
4.Resolution of changes:-
#.ST segment elevation diminishes.
#.T waves invert.
#.ST segment elevation can take weeks to
diminish.
#.T wave inversion may persist for many
months.
 Evolution of AMI

Normal

Peaked T wave

Degree of ST
segment elevation

Q wave formation
and loss of R wave

T wave inversion
Site of infarction
(Septum)
Site of infarction
(Anterior Wall)
Site of infarction
(Lateral Wall)
Site of infarction
(Inferior Wall)
Site of infarction
Anterolateral Myocardial
Infarction
Posterior Myocardial
Infarction
 Contraindications to fibrinolytic
therapy
Absolute Relative
Hemorrhagic stroke or stroke of unknown origin at Refractory hypertension (SBP > 180)
any time.
Ischemic stroke in the preceding 6 months. TIA in preceding 6 months

Central nervous system damage or neoplasm. Oral anticoagulant treatment

Recent major trauma/surgery/head injury (within the
preceding 3 weeks).
Internal or Gastro-intestinal bleeding within the last
month.
Previous allergy to used fibrinolytic
Non-compressible vascular puncture
Pregnancy or < 1 week postpartum.

Known bleeding disorder. Active peptic ulcer disease (PUD)

Aortic dissection. Advanced liver disease

Infective endocarditis
 Differential diagnosis ST elevation
1.acute ischemia.

2. Acute pericarditis: ST elevation in all leads except

aVR.

3.PE: ST elevation in V1 and aVR.

4.Hypothermia: ST elevation in V3-V6, II, III and

aVF.

5.Hypertrophic cardiomyopathy: V3-V5 .

6.Hyperkalemia : V1-V2 (V3).

7.Ventricular aneurythm.

8.Acute sympathic stress: all leads, especially V1.

Differential diagnosis ST depression

1.Digoxin.

2. Strain pattern due to Rt, Lt ventricular overload.

3. Tachycardia.

4. Hypokalaemia.

5.Bundle branch block.

6. Cardiomyopathies.
 Differential diagnosis of T wave inversion

1.Normal in lead III,VR,V1and V2-V3 in black.

2.Ventricular rhythm.
3.Bundle branch block.
4.Myocardial infarction.
5.Rt or Lt ventricular hypertrophy.
6.WPW syndrome.
 ECG change in hyperkalemia:-
1.Tall and tented T wave.
2.Small or absent P wave.
3.Wide QRS complex.
4.Shortened or absent ST segment.
 Hyperkalaemia

Tall tented T wave

Small/absent P waves

Wide QRS
 ECG change in hypokalemia:-
1.Small or absent T wave.
2.Prominent U wave.
3.Prolonged PR interval.
4.Slight ST segment depression.
Hypokalaemia

Small/Absent T

U Wave
 ECG change in pericarditis
#.saddle-shappe ST-elevation in most lead.
#.PR depression.
Acute pericarditis
Any Questions?
 Congrats,
Now You are Competent in ECG
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