The document outlines a systematic 7+2 step approach for interpreting electrocardiograms (ECGs) that involves analyzing the rhythm, rate, conduction, axes, wave morphologies, segment changes, and comparing to previous ECGs to form a clinical conclusion. The 7 steps examine the rhythm, rate, conduction intervals, axes, P wave, QRS, and ST-T wave morphologies. The +2 steps involve comparing the ECG to previous tracings and formulating a concluding statement.

1. When confronted with an ECG, always use a systematic
approach, following all steps to come to the correct
conclusion.
In this course we use the 7+2 step plan

2. 7+2 Step Plan
1.Rhythm
– Rate
– Conduction
– Heart axis
– P wave morphology
– QRS morphology
– ST morphology
1. Compare with previous ECG
2. Conclusion

3. Step 1: What is the Rhythm? P wave
Normal (conducted) sinus rhythm
• A P wave (atrial contraction) precedes I
every QRS complex.
• A QRS complex follows every P wave.
• The rhythm is regular, but varies slightly
during respirations. II
• The rate ranges between 60 and 100
beats per minute.
• The P waves maximum height is 2.5 mm
in II and/or III. AVF
• The P wave is positive in I and II, and
biphasic in V1.
• The PQ time is between 0,12 and 0,2
seconds.
V1

4. An example of normal sinus rhythm

5. Not sinus rhythm?
• If the rhythm is not sinus rhythm you proceed with the
arrhythmia algorithm (which you will learn with the next
topics) after determining the heart rate, heart axis and
conduction intervals.
• (A purist definition of sinus rhythm is that sinus rhythm is
present in the atria and not by definition in the ventricles,
e.g. there may be sinus rhythm in the atria, complete AV
block and a nodal escape rhythm in the ventricles).

6. Step 2: What is the heart rate?
Knowing the ECG paperspeed
(usually 25 mm/sec) allows us to
calculate the heart rate from the
ECG using any of these methods:
• Use the "square counting"
method
• Use a calculator
• Use a separate ECG ruler

7. The square counting method
The count method to determine the
The square counting method is ideal The second QRS
heart frequency.
for regular heart rates. Use the between 75 and 60 beats
complex is
sequence: per minute. This heartbeat is between
that, around 65 beats per minute.
300-150-100-75-60-50-43-37.
Count from the first QRS complex
(preferably occuring on a thick line). If
the next QRS complex would occur on
the next thick line, the heart rate would
be 300, 150 if at the second thick line,
100 if at the third thick line and so on.
When the second QRS complex is
between two lines, take the mean of the
two numbers from the sequence.

8. Step 3: Conduction
The speed of conduction of
the signal through the heart
results in conduction
intervals:
• PQ interval
• QRS duration
• QT interval

9. PQ interval
• Normal between 0.12 and 0.2 seconds.
• Starts at the beginning of the atrial complex and ends at
the beginning of the ventricular complex.
May be shortened if there is pre-excitation of the ventricles
through abnormal conduction between the atria and
ventricles (accessory pathway).
If the PQ interval is prolonged there is a degree of AV
block (which will be discussed later).

10. QRS duration
• Normal < 0.10 - 0.12 seconds
• Indicates how fast the ventricles depolarize
• QRS longer than 120 milliseconds may result from:
o Left bundle branch block
o Right bundle branch block
o Electrolyte disorders
o Idioventricular rhythm or paced rhythm

11. QT interval
• Indicates how fast the
ventricles are repolarized,
becoming ready for a new
cycle.
• The normal value for QTc is:
below 450ms for men and
below 460ms for women
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12. Correct assessment of the QTc
interval
The QT interval is comprised of the QRS-complex, the ST-
segment, and the T-wave. One difficultly of QT interpretation is
that the QT interval gets shorter as the heart rate increases. This
problem can be solved by correcting the QT time for heart rate
using the Bazett formula:
Correct QT measurements are important because QT prolongation
may make the patient prone to arrhythmias, especially when
combined with QT-prolonging drugs.

13. Stepwise approach to correct measurement of the QT
interval
1. Use lead II. Use lead V5 alternatively if lead II cannot be read.
– Draw a line through the baseline (PR segment, or TP alternatively)
– Draw a tangent against the steepest part of the end of the T wave. If the T
wave has two positive deflections, the taller deflection should be chosen. If the
T wave is biphasic, the end of the taller deflection should be chosen.
– The QT interval starts at the beginning of the QRS interval and ends where
the tangent and baseline cross.
– If the QRS duration exceeds 120ms, the amount surpassing 120ms should be
deducted from the QT interval (i.e. QT=QT-(QRS width-120ms) )
– Calculate QTc according to Bazett. You can use the QTc calculator for this.

14. Causes of QT prolongation
• Congenital long QT syndrome.
But QT prolongation can also occur as a consequence of
(a.o.):
• Medication (anti-arrhythmics, tricyclic antidepressants,
phenothiazides). See torsades.org for a full list.
• Electrolyte imbalances.
• Ischemia.

15. Step 4: Heart axis
The heart axis points in the direction of
the average electrical vector of all the
depolarizing heart cells.
A change of the heart axis or an extreme
deviation can be an indication of
pathology.
A positive QRS complex (more above
than below the baseline) in a certain lead
means that the heart axis is going (at
least slightly) in that lead's direction.
The heart axis is normal between -30
and +90 degrees.
Therefore, if QRS is positive in both
leads I and II, the heart axis is normal.

16. Interpretation
There are four areas where
the QRS vector can point:
• Left axis deviation (between
-30º and -90º)
• Normal axis between -30º and
90º
• Right lower quadrant --> right
axis deviation (between 90º
and -180º)
• Right upper quadrant -->
extreme right axis
deviation(between -90º and
-180º)
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17. Abnormal heart axis
Heart axis deviation to the left in Heart axis deviation to the right
case of an inferior infarct. Left can result from right
anterior hemiblock is another ventricular overload as in COPD
common cause. A left axis is or pulmonary embolism. A right
present between -30 and -90 axis is between +90 and +180
degrees. degrees.
A left - right arm lead exchange is
the most common cause of right
axis deviation!

18. Step 5: P Wave morphology
The P wave morphology can reveal I
right or left atrial dilatation or atrial
arrhythmias and is best determined
in leads II and V1 during sinus
rhythm. II
Normal P wave morphology :
• The maximal height of the P wave is 2.5 mm
in leads II and / or III. AVF
• The P wave is positive in II and AVF,
and biphasic in V1.
• The P wave duration is shorter than 0.12
seconds.
V1

19. Left atrial dilatation
Terminal part of V1 > 1mm2 and/or P >
0.12 seconds in I and/ or II

20. Right atrial dilatation
P > 2.5 mm in II and/ or III and/ or aVF
and/ or P > 1.5 mm in V1

21. Condition P Wave Morphology
Normal Sinus Rhythm
Right atrial enlargement
(= P Pulmonale)
Left Atrial Enlargement
(= P Mitrale)

22. Step 6: QRS Morphology
Check presence or absence of any of the following
abnormalities:
• Pathological Q waves
• LVH / RVH
• Microvoltages (QRS < 5 mm)
• Conduction problems (normal or prolonged)
• Abnormal R wave propagation
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23. Pathological Q wave
• Q waves point at electrically
silent areas and can be a sign of
previous myocardial infarction
• Definition of a pathologic Q
wave:
o Any Q wave in leads V2–V3
o Q wave ≥ 0.03 s and > 0.1 mV
deep in other leads.
o To be defined as pathologic, Q
waves need to be present in
two contiguous leads (e.g. II
and AVF or I and AVL or V1
and V2)

24. Left ventricular hypertrophy
Hypertrophic myocardium
has more electrical activity,
resulting in larger peaks.
Definition of LVH: R in V5 or
V6 + S in VI > 35mm
(Sokolow-Lyon criteria)
Often a "strain pattern" is
seen in V5 and V6.

25. Right ventricular hypertrophy
Right ventricular hypertrophy
is probably present when R is V1
larger than S in VI

26. Microvoltages
Microvoltages:
QRS < 5 mm in limb leads
QRS < 10 mm in chest leads
Occurs in infiltrative disease (e.g. amylodosis), and COPD

27. Conduction disorders
If the QRS duration is more than 0.12 seconds there may
be a block in the conductive tissue. Most often it will be
either right or left bundle branch block.
Rule of thumb: when distinguishing left
and right bundle branch block--look at
V1 only!
Does the signal end negative (below
the baseline) in V1? (away from V1)
>> the ventricle farther from V1 is
depolarized later>> it must be a left
bundle branch block
Does the signal end positive in V1?
(towards V1) >> the ventricle closer to
V1 is depolarized later >> it must be a
right bundle branch block

28. Conduction disorders: right bundle branch
block
• QRS > 0.12 seconds V1
• RSR'-pattern in V1 where
R' > R
• Slurred S wave in lead I
and V6

29. Conduction disorders: left bundle branch
block
• QRS > 0.12 seconds
• Broad monomorphic S waves in V1, may have a small
initial R wave
• Broad monomorphic R waves in I and V6 with no Q
waves

30. Normal R wave progression
Normally R waves become larger from V1-V5. At V5 it should be maximal. If
the R wave in V2 is larger than in V3, this could be a sign of a (previous)
posterior myocardial infarction.

31. Step 7
ST morphology
• The ST segment represents ventricular repolarization. During repolarization the
cardiomyocytes elongate and prepare for the next heartbeat. On the ECG, the
repolarization phase starts at the junctional, or J point, and continues until the T
wave. The ST segment is normally at or near the baseline.
• The T wave is usually concordant with the QRS complex. Thus if the QRS
complex is positive in a certain lead (the area under the curve above the
baseline is greater than the area under the curve below the baseline) then the T
wave usually is positive too in that lead. Accordingly the T wave is normally
upright or positive in leads I, II, AVL, AVF and V3-V6. The T wave is negative in
V1 and AVR. The T wave flips around V2, but there is likely some genetic
influence in this as in Blacks the T wave usually flips around V3.
• The T wave angle is the result of small differences in the duration of the
repolarization between the endocardial and epicardial layers of the left ventricle.
The endocardial myocytes need a little more time to repolarize (about 22 ms).
This difference causes an electrical current from the endocardium to the
epicardium, which reads as a positive signal on the ECG.

32. Step 7
ST morphology
• ST segment elevation
• Ischemia
• Pericarditis
• Aneurysma cordis
• Normal variant
• ST depression
• Ischemia
• LVH
• Digitalis
• Low potassium/ low magnesium
• Neurologic
• T wave changes
• Ischemia
• Pericarditis
• Myocarditis
• LVH / RVH
• Electrolyte changes (especially potassium)

33. Common causes of ST shift

34. ST elevation
normal
90% of healthy (young) men and women to a lesser extent
have ST elevation in precordial leads.
Normal variants of
ST segment elevation are:
• 1: normal
• 2: ‘early repolarization’
• 3: normal 'variant'

35. Abnormal ST segment elevation
1: LVH
2: LBBB
3: Pericarditis
4: High pottasium
5: Acute AS infarct
6: Acute AS infarct +
RBBB
7: Brugada syndrome

36. Diffuse ST elevation in pericarditis
ST segment elevation (upper ECG) due to pericarditis. The lower ECG
shows PTa depression, which is typically seen in pericarditis.

37. ST depression
The most important cause of ST segment depression is ischemia. Causes of
ST segment depression include:
 Reciprocal ST segment depression during ischemia. If one lead shows
ST segment elevation then usually the lead "on the other side" shows ST
segment depression.
 Left ventricular hypertophy with "strain" or depolarization abnormality
 Digoxin effect
 Low potassium/low magnesium
 Heart rate-induced changes (post tachycardia), 'cardiac memory'
 During acute neurologic events
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38. ST segment elevation due to high potassium levels

39. T wave
• The T wave is quite labile and long lists of possible causes of T wave
changes exist. A changing T wave can be a sign that something is
abnormal, but it doesn't say much about the severity. T waves can be
peaked, normal, flat, or negative. Flat and negative T waves are defined as:
• flat T wave:
< 0.5 mm negative or positive T wave in leads I, II, V3, V4, V5 or V6
• negative T wave:
> 0.5 mm negative T wave in leads I, II, V3, V4, V5 or V6
Possible causes of T wave changes
o Ischemia and myocardial infarction
o Pericarditis, myocarditis
o Cardiac contusion
o Acute neurologic events, such as subarachnoid bleeding (SAB)
o Digoxin effect
o Right and left ventricular hypertrophy with strain
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41. Prominent U wave
Sometimes a U wave is present: an extra wave following the T wave. During
hypokalemia (and hypocalcemia) the U wave can become more prominent:

42. Step 7+1
Compare with previous ECG
• New LBBB?
• Change in heart axis?
• New pathologic Q?
• Decreased R wave height?
All of these can exist as chronic abnormalities, but when
the are new it can be a sign of acute ischemia or another
condition.
more about this topic on ECGpedia...

43. Step 7+2
Conclusion
Try to formulate one sentence that summarizes your
finding with a clinical useful conclusion.
Examples:
 "Sinus tachycardia with ST elevation in V2-V5, likely
caused by acute anterior myocardial infarction"
 "Supraventricular tachycardia of 200 beats per minute
caused by an AV nodal re-entry"
 "Previous infarction combined with an acute lateral
myocardial infarction with widening of the QRS
complexes"
 "Normal ECG"