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Internal Medicine > OHCEPS - ECG > Flashcards

OHCEPS - ECG Flashcards

1
Q

The 6 chest leads examine the heart how?

A

In a TRANSVERSE plane:

  1. V1-V2 –> looking at the RV.
  2. V3-V4 –> At the septum and anterior aspects of the LV.
  3. V5-V6 –> At the anterior and lateral aspects of the LV.
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2
Q

P wave represents atrial depolarization and it a positive (upwards) deflection - except?

A

In aVR.

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3
Q

Q wave?

A

So called if the first QRS deflection is negative (downwards).
Pathological Q waves may be seen in infarction.

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4
Q

R wave?

A

The first positive (upwards) deflection - may or may not follow a Q wave.

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5
Q

S wave?

A

A negative (downwards) deflection following the R wave.

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6
Q

HR - How to calculate from ECG?

A

HR can be calculated by dividing 300 by the number of large squares between each R wave (with machine trace running at the standard speed of 25mm/sec and deflection of 1cm/1mV.

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7
Q

3 large squares between R waves = ?

A

100 HR.

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8
Q

5 large squares between R waves = ?

A

60 HR.

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9
Q

Normal rate ?

A

60-100/min.

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10
Q

PR interval?

A
  1. From the start of the P wave to the start of the QRS complex.
  2. This represents the inbuilt delay in electrical conduction at the AV node.
  3. Normally <0.20 sec (5 small squares at standard recording speed).
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11
Q

QRS complex?

A

Width of the QRS complex - Normally <0.12sec (3 small squares at standard rate).

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12
Q

R-R interval?

A
  1. From the peak of one R wave to the next.

2. This is used in the calculation of HR.

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13
Q

QT interval?

A
  1. From the start of the QRS complex to the end of the T wave.
  2. Varies with HR.
  3. Corrected QT=QT/square root of the R-R interval.
  4. Corrected QT should be 0.38-0.42sec.
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14
Q

Rhythm of the ECG - What to look?

A

Is the rhythm (and the time between successive R waves) regular or irregular?

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15
Q

Cardiac axis - what is it?

A

Refers to the overall direction of depolarization through the ventricular myocardium in the coronal plane.

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16
Q

Normal cardiac axis?

A

Lies between -30 and +90 degrees.

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17
Q

Cardiac axis deviation - Can be seen in healthy individuals?

A

Yes:
Right axis deviation if tall and thin.
Left axis deviation if short and stocky.

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18
Q

Which leads should be used to accurately determine the cardiac axis?

A

Leads I, II, III.

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19
Q

Etiology of axis deviation - Left axis deviation (

A
  1. LV hypertrophy
  2. LBBB
  3. Left anterior hemiblock (anterior fascicle of the left bundle).
  4. Inferior MI
  5. Cardiomyopathies
  6. TV atresia
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20
Q

Etiology of axis deviation - Right axis deviation (>+90).

A
  1. RV hypertrophy
  2. RBBB
  3. Anterolateral MI
  4. RV strain (pulm. embolism)
  5. Cor pulmonale
  6. Fallot’s tetralogy (PV stenosis)
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21
Q

What is a heart block?

A

Disturbance of the normal conduction through the AV junction.

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22
Q

Etiology of heart block?

A
  1. IHD
  2. Idiopathic fibrosis of conduction system
  3. Cardiomyopathies
  4. Inferior/anterior MI
  5. Drugs
  6. Physiological (1st degree) in athletes
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23
Q

Drugs that cause heart block?

A
  1. Digoxin
  2. Beta blockers
  3. Verapamil
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24
Q

First degree heart block?

A

PR interval fixed but prolonged at >0.20 sec (5small squares at standard ratee).

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25
Q

Second degree heart block - Mobitz I?

A
  1. PR interval becomes progressively longer after each P wave until an impulse fails to be conducted at all.
  2. The interval then returns to the normal length and the cycle is repeated.
  3. Also known as the Wenkenbach phenomenon.
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26
Q

Second degree heart block - Mobitz II?

A
  1. PR interval is fixed but NOT EVERY P wave is followed by a QRS.
  2. The relationship betweenP waves and QRS complex may be 2:1, 3:1, or random.
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27
Q

Third degree heart block?

A

Also called complete heart block.

  1. There is no conduction of the impulse through the AV junction.
  2. Atrial and ventricular depolarization occur independently of one another.
  3. Each has a separate pacemaker triggering electrical activity at different rates.
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28
Q

QRS complex shape in 3rd degree heart block?

A

The QRS complex is an abnormal shape as the electrical impulse does not travel through the ventricles via the normal routes (see ventricular escape).

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29
Q

Hint about 3rd degree block?

A

In 3rd degree heart block P waves may be seen “merging” with QRS complexes if they coincide.

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30
Q

Hint about 3rd degree heart block?

A

If in doubt about the pattern of P waves and QRS complexes, mark out the P wave intervals and the R-R intervals separately, then compare.

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31
Q

P waves best seen in?

A

Leads II and V1.

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32
Q

What happens in RBBB?

A

Conduction through the AV node, bundle of His, and left bundle branch will be normal but depolarization of the RV occurs BY THE SLOW ELECTRICAL CURRENT THROUGH THE MYOCARDIAL CELLS.

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33
Q

What is the result of RBBB?

A

The result is delayed right ventricular depolarization giving a second R wave known as “R prime” (R’).

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34
Q

RBBB suggests what?

A

Pathology in the right side of the heart, but can be a normal variant.

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35
Q

RBBB - ECG changes?

A
  1. “RSR” pattern seen in V1.
  2. Cardiac axis usually remains normal unless left anterior fascicle is also blocked (“bifascicular block”) which results in left axis deviation.
  3. T wave is DOWN in anterior chest leads (V1-V3).
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36
Q

Some causes of RBBB?

A
  1. Hyperkalemia
  2. Congenital heart disease (Fallot)
  3. Pulmonary embolus
  4. Cor pulmonale
  5. Fibrosis of conduction system
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37
Q

LBBB what happens?

A

Conduction through the AV node, bundle of His, and right bundle branch will be normal but depolarization of the LV occurs by the slow spread of electrical current through myocardial cells.

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38
Q

LBBB result?

A

The result is delayed LV depolarization.

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39
Q

Can LBBB be seen in normal individual?

A

ALWAYS PATHOLOGICAL.

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40
Q

LBBB - ECG changes?

A
  1. M pattern seen in V6.

2. T wave down in lateral chest leads (V5-V6).

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41
Q

Some causes of LBBB?

A
  1. HTN
  2. IHD
  3. Acute MI
  4. AV stenosis
  5. Cardiomyopathies
  6. Fibrosis of the conducting system
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42
Q

Some causes of sinus bradycardia?

A
  1. Drugs
  2. Sick sinus rhythm
  3. Hypothyroidism
  4. Inferior MI
  5. Hypothermia
  6. Incr. intracranial pressure
  7. Physiological (athletes)
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43
Q

Drugs that cause bradycardia?

A
  1. Beta blockers
  2. Verapamil
  3. Amiodarone
  4. Digoxin
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44
Q

Sinus tachycardia - ECG features?

A
  1. Ventricular rate >100 (usually 100-150 beats per minute).

2. Normal P wave before each QRS.

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45
Q

Drugs that cause tachycardia?

A
  1. Epinephrine
  2. Caffeine
  3. Nicotine
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46
Q

Some causes of sinus tachycardia?

A
  1. Drugs
  2. Pain
  3. Exertion
  4. Anxiety
  5. Anemia
  6. Thyrotoxicosis
  7. Pulmonary embolus
  8. Hepatic failure
  9. Cardiac failure
  10. Hypercapnia
  11. Pregnancy
  12. Constrictive pericarditis
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47
Q

Supraventricular tachycardias are?

A

Tachycardias (>100) arising in the atria or in the AV node.
–> As conduction through the bundle of His and ventricles will be normal (unless there is other pathology in the heart), the QRS complexes appear normal.

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48
Q

4 main causes of supraventricular tachycardia that you should be aware of?

A
  1. A-fib
  2. A-flutter
  3. Junctional tachycardia
  4. Re-entry tachycardia
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49
Q

A-fib - What is it?

A

Disorganized contraction of the atria in the form of rapid, irregular twitching. There will, therefore, be NO P WAVES on the ECG.

50
Q

A-fib - what happens?

A

Electrical impulses from the twitches of the atria arrive at the AV node randomly, they are then conducted via the normal pathways to cause ventricular contraction.
–> Characteristic rhythm that is irregularly irregular with no discernable pattern.

51
Q

A-fib - ECG features?

A
  1. No P waves. Rhythm is described as irregularly irregular.
  2. Irregular QRS complexes.
  3. Normal appearance of QRS.
  4. Ventricular rate may be UP (“fast AP”) - typically 120-160 per minute.
52
Q

Etiology of A-fib?

A
  1. Idiopathic
  2. IHD
  3. Thyroid disease
  4. HTN
  5. MI
  6. Pulmonary embolus
  7. Rheumatic mitral or tricuspid valve disease
53
Q

A-flutter - What is it?

A

Abnormally rapid contraction of the atria.

  1. The contractions are NOT DISORGANIZED/RANDOM, unlike AF, but are fast and inadequate for a normal movement of blood.
  2. Instead of P waves, the baseline will have a typical “saw-tooth” appearance - sometimes known as F waves.
54
Q

A-flutter - What happens?

A
  1. The AV node is unable to conduct impulses faster than 200/min.
  2. Atrial contraction faster than that leads to impulses failing to be conducted –> Atrial rate of 300 –> HR 150. –> Called 2:1 block.
  3. Other ratios of atrial to ventricular contractions may occur.
55
Q

A-flutter + a variable block at the AV node?

A

May lead to an irregularly irregular pulse indistinguishable from that of AF on clinical examination.

56
Q

A-flutter - ECG changes?

A
  1. “Saw-tooth” appearance baseline.

2. Normal appearance of QRS complexes.

57
Q

A-flutter - etiology?

A

Similar to A-fib.

58
Q

Junctional (nodal) tachycardia - What happens?

A
  1. The area in or around the AV node depolarizes spontaneously, the impulse will be immediately conducted to the ventricles.
  2. The QRS complex will be of normal shape but no P waves will be seen.
59
Q

Junctional (nodal) tachycardia - ECG features?

A
  1. No P waves
  2. QRS complexes are regular and normal shape.
  3. Rate may be fast or may be of normal rate.
60
Q

Etiology of junctional (nodal) tachycardia?

A
  1. Sick sinus syndrome (including drug-induced).
  2. Digoxin toxicity
  3. Ischemia of the AV node, especially with acute INFERIOR MI
  4. Acutely after cardiac surgery
  5. Acute inflammatory processes (acute RF) which may involve the conduction system.
  6. Diphtheria
  7. Other drugs (most anti-arrhythmics)
61
Q

WPW syndrome - Main problem?

A

There is an extra conducting pathway between the atria and the ventricles –> The bundle of Kent.
A break in the normal electrical insulation.
–> Not specialized to delay the impulse as the AV node does.
–> Not linked to the normal conduction pathways of the bundle of His.

62
Q

WPW syndrome is an example of what type of beat?

A

A fusion beat - Normal + Abnormal ventricular depolarization combine to give distortion of the QRS complex.

63
Q

Re-entry tachycardia - What is the problem?

A

The accessory pathway may allow electrical activity to be conducted from the ventricles back up to the atria.
–> Electrical activity may be conducted down the bundle of His, across the ventricles and UP THE ACCESSORY PATHWAY into the atria causing them to contract again…and the cycle is repeated.

64
Q

Classification of WPW syndrome?

A
  1. The bundle of Kent may connect the atria with either the right or the left ventricle.
  2. Thus WPW is classically divided into 2 groups according to the resulting appearance of the QRS complex in the anterior chest leas.
  3. In practice, this classification is rather simplistic as 11% of patients may have more than one accessory pathway.
65
Q

Type A WPW syndrome?

A
  1. Upright delta wave and QRS in V1.

2. May be mistaken for RBBB or posterior MI.

66
Q

Type B WPW syndrome?

A
  1. Downward delta wave and QRS in V1, positive elsewhere.

2. May be mistaken for LBBB or anterior MI.

67
Q

Ventricular rhythms - main feature?

A

Most of them originate outside the usual conduction pathways meaning that excitation spreads by an abnormal path through the ventricular muscle to give broad or unusually shaped QRS complexes.

68
Q

Ventricular tachycardia (VT) - what happens?

A

Here, there is a focus of ventricular tissue depolarizing rapidly within the ventricular myocardium.

69
Q

VT - definition?

A

3 or more successive ventricular extrasystoles at a rate of >120/min.
Sustained VT lasts for > 30sec.

70
Q

Monomorphic and polymorphic VT?

A

Monomorphic VT –> Repetitive QRS shape.

Polymorphic VT –> Unstable with varying patterns of the QRS complex.

71
Q

VT may be impossible to be distinguished from what?

A

SVT + bundle branch block.

72
Q

VT - ECG features?

A
  1. Wide QRS complexes which are irregular in rhythm and shape.
  2. AV dissociation - independent atria/ventricular contraction.
  3. May seen FUSION and CAPTURE beats on ECG as signs of atrial activity independent of ventricular activity –> Said to be pathognomonic.
  4. Rate can be up to 130-300/min.
  5. QRS concordance: all the QRS complexes in the chest leads are either mainly positive or mainly negative –> ventricular origin of the tachycardia.
  6. EXTREME axis deviation (far negative or far positive).
73
Q

Etiology of VT?

A
  1. Ischemia (AMI)
  2. Electrolyte abnormalities (Low K, Low Mg)
  3. Aggressive adrenergic stimulation (eg cocaine use)
  4. Drugs - especially antiarrhythmics.
74
Q

VF - what is it?

A

Disorganized, uncoordinated depolarization from multiple foci in the ventricular myocardium.

75
Q

VF - ECG features?

A
  1. No discernible QRS complexes.

2. A completely disorganized ECG.

76
Q

VF - Etiology?

A
  1. Coronary artery disease
  2. Cardiac inflammatory disease
  3. Abnormal metabolic states
  4. Pro-arrhythmic toxic exposures
  5. Electrocution
  6. Tension pneumothorax, trauma, and drowning
  7. Large pulm. embolism
  8. Hypoxia and acidosis
77
Q

Fine VF?

A

This is VF with a small amplitude waveform.
It may resemble asystole on the ECG monitor, particularly in an emergency situation.
–> You should remember to increase the gain on the monitor to ensure what you think is asystole is not really fine VF as the management for each is very different.

78
Q

Ventricular extrasystoles (ectopics) - what happens?

A

These are ventricular contractions originating from a focus of depolarization within the ventricle.
As conduction is via ABNORMAL PATHWAYS, the QRS complex will be unusually shaped.

79
Q

Ventricular extrasystoles - Harmless?

A

They are COMMON + HARMLESS if there is no structural heart disease.
–> If they occur at the same time as a T wave, the “R on T” phenomenon –> VF.

80
Q

Ventricular escape rhythm - When does this occur?

A

This occurs as a back-up when conduction between the atria and the ventricles is interrupted (as in complete heart block).

81
Q

Intrinsic pacemaker in ventricular myocardium - rate?

A

30-40/min.

82
Q

Ventricular escape rhythm - features?

A

The ventricular beats will be abnormal and wide with abnormal T waves following them.
–> This rhythm can be stable but may suddenly fail.

83
Q

Asystole - what happens?

A

This is complete absence of electrical activity and is not compatible with life.

84
Q

Asystole - Hint?

A

There may be a slight wavering of the baseline which can be easily confused with fine VF in emergency situations.

85
Q

Agonal rhythm - What happens?

A

This is a slow, irregular rhythm with wide ventricular complexes which vary in shape.

86
Q

Agonal rhythm - When do we see it?

A

Often seen in the later stages of unsuccessful resuscitation attempts as the heart dies.

87
Q

Agonal rhythm - Course?

A

The complexes become progressively broader before all recognizable activity is lost (asystole).

88
Q

Torsades de pointes - What is it?

A

Literally meaning “twisting of points.
A form of polymorphic VT characterized by a gradual change in the amplitude and twisting of the QRS axis.
In the US, it is known as “cardiac ballet”.

89
Q

Torsades - Course?

A

Usually terminates spontaneously but frequently recurs and may degenerate into sustained VT and VF.

90
Q

Torsades - Etiology?

A

Results from prolonged QT interval.

  1. Congenital long-QT syndromes
  2. Drugs (antiarrhythmics
  3. K and Mg may also be down.
91
Q

P wave - Normal?

A
  1. In sinus rhythm each P wave is closely associated with a QRS complex.
  2. P waves are usually upright in most leads EXCEPT aVR.
  3. P waves are <3 small squares high.
92
Q

P wave - Abnormal?

A
  1. Right atrial hypertrophy –> Tall, peaked P waves (P pulmonale)
  2. Left atrial hypertrophy –> Wider and twin-peaked or “bifid” P wave. (P mitrale).
93
Q

T wave - most commonly affected by?

A

Ischemic changes.

94
Q

T wave - MC abnormality?

A

Inversion, which has a number of causes.

95
Q

T wave - normal?

A
  1. Commonly inverted in V1 and aVR.

2. May be inverted in V1-V3 as normal variant.

96
Q

T wave - Abnormal - Ischemia or MI?

A

Non-Q wave MI can cause T wave inversion. Changes need to be interpreted in light of clinical picture.

97
Q

T wave - Abnormal - Ventricular hypertrophy?

A

Ventricular hypertrophy causes T inversion in those leads focused on the ventricle in question.
–> For example, LV hypertrophy will give T changes in V5, V6, II, aVL.

98
Q

T wave - Abnormal - Bundle branch block?

A

Causes abnormal QRS complexes due to abnormal pathways of ventricular depolarization.
–> The corresponding abnormal repolarization gives unusually shaped T waves which have no significance in themselves.

99
Q

T wave - Abnormal - Digoxin?

A

Digoxin causes a characteristic T wave inversion with a downsloping of the ST segment known as the “reverse tick” sign.
–> This occurs at therapeutic doses and it NOT a sign of digoxin toxicity.

100
Q

T wave - Abnormal - Electrolyte imbalances?

A
  1. UP K –> Tall tented T waves.
  2. DOWN K –> Small T waves and U waves (broad, flat waves occurring after the T waves).
  3. DOWN Ca –> Small T waves with prolongation of the QT interval. (UP Ca has the reverse effect).
101
Q

T wave - Abnormal - Other causes?

A
  1. Subarachnoid hemorrhage

2. Lithium use

102
Q

ST elevation - importance?

A

The degree + extent of ST elevation is of crucial importance in ECG interpretation as it determines whether reperfusion therapy (thrombolysis or PCI) is considered in AMI.

103
Q

ST elevation - Etiology?

A
  1. AMI - Convex ST elevation in affected leads (the “tomb-stone” appearance), often with reciprocal ST depression in opposite leads.
  2. Pericarditis - Widespread concave ST elevation (“saddle-shaped”).
  3. LV aneurysm - ST elevation may persist over time.
104
Q

ST depression - Patterns?

A

Can be horizontal, upward sloping, or downward sloping.

105
Q

ST depression - etiology?

A
  1. Myocardial ischemia - Horizontal ST depression and an upright T wave. May be the result of CAD or other causes (anemia, AV stenosis).
  2. Digoxin toxicity - downward sloping (“reverse tick”).
  3. “Non-specific” changes - ST depression which is often upward sloping may be a normal variant and is NOT thought to be associated with any underlying significant pathology.
106
Q

Exercise ECG testing and ST changes?

A

Test looks to induce ischemic changes –> Extent + Timing + Nature of ST changes can help quantify the probability of ischemic heart disease.

107
Q

AMI - ECG changes in 1st hr?

A

ECG can remain normal.

108
Q

AMI - ECG changes?

A

In order:

  1. ST elevation and T waves become peaked.
  2. Pathological Q waves develop.
  3. ST returns to baseline and T waves invert.
109
Q

ECG changes in AMI - Help what?

A

The leads in which these changes take place allow you to identify which part of the heart has been affected and, therefore, which coronary artery is likely to be occluded.

110
Q

Anterior MI - Leads?

A

V2-V5

111
Q

Anterolateral MI - Leads?

A

I, aVL, V5, V6

112
Q

Inferior MI - Leads?

A

III, aVF (sometimes also II)

113
Q

Posterior MI - Leads?

A

The usual depolarization of the posterior of the LV is lost, giving a dominant R wave in V1.
Imagine it as a mirror image of the Q wave you would expect with an anterior MI.

114
Q

Right ventricular MI - Leads?

A

Often no changes on the 12-lead ECG.
If suspected clinically, leads are placed on the right of the chest, mirroring the normal pattern and are labeled V1R, V2R, V3R, and so on.

115
Q

Atrial hypertrophy - ECCG changes?

A

Changes to the P wave.

116
Q

Ventricular hypertrophy - ECG changes?

A

This can lead to changes to the cardiac axis, QRS complex height/depth, and the T wave.

117
Q

LV hypertrophy - ECG changes?

A
  1. Tall R wave in V6 and deep S wave in V1.
  2. May also see left axis deviation.
  3. T wave inversion in V5, V6, I, aVL.
118
Q

Voltage criteria for LV hypertrophy include?

A
  1. R wave > 25mm (5 large squares) in V6.

2. R wave in V6 + S wave in V1>35mm (7 large squares).

119
Q

RV hypertrophy - ECG changes?

A
  1. “Dominant” R wave in V1 (ie R wave bigger than S wave).
  2. Deep S wave in V6.
  3. May also see right axis deviation.
  4. T wave inversion in V1-V3.
120
Q

How are the 6 limb leads look at the heart?

A

In the CORONAL plane:

  1. aVR –> Looking at the right atrium.
  2. aVF, II, III –> Inferior septum and anterior aspects of LV.
  3. I, aVL –> Left lateral aspect.

Internal Medicine (106 decks)

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