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 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 every QRS complex.
A QRS complex follows every P wave.
The rhythm is regular, but varies slightly during respirations.
The rate ranges between 60 and 100 beats per minute.
The P waves maximum height is 2.5 mm in II and/or III.
The P wave is positive in I and II, and biphasic in V1.
The PQ time is between 0,12 and 0,2 seconds. I II
AVF 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 square counting method is ideal for regular heart rates. Use the sequence:
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.
The count method to determine the heart frequency. The second QRS complex is between 75 and 60 beats per minute. This heartbeat is between that, around 65 beats per minute.

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:
Left bundle branch block
Right bundle branch block
Electrolyte disorders
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
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 case of an inferior infarct. Left anterior hemiblock is another common cause. A left axis is present between -30 and -90 degrees.
Heart axis deviation to the right can result from right ventricular overload as in COPD or pulmonary embolism. A right axis is between +90 and +180 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 right or left atrial dilatation or atrial arrhythmias and is best determined in leads II and V1 during sinus rhythm. 
Normal P wave morphology :
The maximal height of the P wave is 2.5 mm in leads II and / or III.
The P wave is positive in II and AVF,
       and biphasic in V1.
The P wave duration is shorter than 0.12 seconds. I II
AVF 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:
Any Q wave in leads V2–V3 
Q wave ≥ 0.03 s and > 0.1 mV deep in other leads.
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 larger than S in VI V1

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 blockV1
QRS > 0.12 seconds
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 ST depression T wave changes
Ischemia
Pericarditis
Aneurysma cordis
Normal variant
ST depression
LVH
Digitalis
Low potassium/ low magnesium
Neurologic
T wave changes
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
Ischemia and myocardial infarction
Pericarditis, myocarditis
Cardiac contusion
Acute neurologic events, such as subarachnoid bleeding (SAB)
Digoxin effect
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.
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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"