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Cardiology > ECG > Flashcards

ECG Flashcards

1
Q

Describe the Eletricity through the heart

A
  • Sa node
  • AV node
  • Bundle of His
  • R + L bundle branches
  • Purkinje fibres
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2
Q

Describe the correlation of ECG waves with the systole and diastole>

A
  • P wave = contraction on atria
  • QRS complex = contraction of ventricles
  • T wave = reploarisation
  • U wave = repolarisation of papillary muscles
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3
Q

How many leads are there in a 12 lead ECG and what are they?

A

10 leads in total

Limb Leads

  • 4 (1 to each limb - aVR, aVL, avF, neutral )

Chest leads

  • 6 (V1 to V6)
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4
Q

What are the colours of the Limb leads and where do they go?

A

Traffic lights

  • RED- Right limb lead
  • Yellow - Left limb lead
  • Green - Left leg
  • Black - Right leg - neutral lead

The sun and the grass are on the same side

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5
Q

Which views of the heart can be seen from each lead?

A

Limb leads look at the heart in a coronal plane

Chest leads look at the heart in a horizontal plane

Anterior - V3,V4

Lateral - I, AVL V5, V6

Septal - V1, V2

Inferior - II, III, aVF

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6
Q

Where are the chest leads placed on the chest?

A

V1 – 4th intercostal space – right sternal edge

V2 – 4th intercostal space – left sternal edge

V3 – 5th rib ( between two and four)

V4 – 5th intercostal space – mid clavicular

V5 – anterior axillary line – 5th intercostal space

V6 – mid-axillary – 5th intercostal space

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7
Q

The direction of deflection depends on?

A
  • direction of spread of the electrical force
  • location of the electrode

An electrical signal travelling towards an electrode is recorded as a positive deflection

An electrical signal travelling away from an electrode is recorded as a negative deflection

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8
Q

Systematic approach to the ECG?

A
  • Rate
  • Rhythm
    • regular or irregular?
  • P waves
    • specific rhythm diagnosis
    • (look in leads II & V1)
  • Intervals and durations – PR, QRS, QT
  • QRS complexes (axis and morphology)
  • ST segment / T wave changes
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9
Q

How do you calculate the rate?

A

Dividing 300 by the number of large squares between each R wave

Or 6 seconds worth of rhythm strip (30 big squares) then count the number of QRS complexes and multiply by 10

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10
Q

What is the standard speed of the paper?

A

25mm/sec

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11
Q

What is the size and speed of a large square and how many large squares are there per second?

A

Large square = 5mm = 0.2 second

5 large squares per second

Therefore, 300 squares per minute

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12
Q

Normal heart rate ?

Bradycardia ?

Tachycardia?

A

Normal heart rate = 60-100bpm

Rate< 60 = bradycardia

rate>100= tachycardia

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13
Q

Intervals

A
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14
Q

Rhythm

A

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

  • If irregular but in a clear pattern, then it is said to be ‘regularly irregular’ (e.g. types of heart block)
  • If irregular but no pattern, then it is said to be ‘irregularly irregular’ (e.g. atrial fibrillation).
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15
Q

QRS complex

A

Depolarisation of right and left ventricles

Nomeclature: R wave is the first positive deflection. Q wave is a negative deflection that precedes R wave and S is a negative deflection that follows R wave

not every QRS complex contains a Q wave, R wave or S wave.

  • Capital letters for large amplitude (>5mm),
  • lowercase letters for small amplitude waves.

The depolrisation spreads to the atrium and out to the epicardium in all directions

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16
Q

ST segment

A
  • Flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.
  • It represents the interval between ventricular depolarization and repolarization.
  • ST elevation : STEMI, Prinzmetal’s angina, pericarditis, ventricular aneurysm, early repolarization (benign), hyperkalemia, hypothermia
  • ST depression: ischaemia or NSTEMI (note can be upsloping, downsloping or horizontal)
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17
Q

QT interval

A

total time taken for depolarisation and repolarisation of the ventricles

QT interval is inversely proportional to heart rate

A normal QT is less than half the preceding RR interval

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18
Q

T wave

A
  • The T wave is the positive deflection after each QRS complex. It represents ventricular repolarisation.
  • Upright in all leads except aVR and V1
  • Abnormal P wave: Hyperacute, Inverted, Biphasic, ‘Camel Hump’, Flattened
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19
Q

U wave

A

Repolarisation of mid-myocardial cells

can be present or absent

Abnormal U waves (>2mm in height):

  • Hypokalaemia
  • cardiomyopathy
  • left ventricular enlargement
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20
Q

What is the normal cardiac axis?

A

The cardiac axis, or ‘QRS axis’, refers to the overall direction of depolarization through the ventricular myocardium in the coronal plane.

Zero degrees is taken as the horizontal line to the left of the heart (the right of your diagram).

The normal cardiac axis lies between –30 and +90 degrees (see Fig. 19.6). An axis outside of this range may suggest pathology, either congenital or acquired.

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21
Q

How to calculate the cardiac axis?

A
  • Draw a diagram showing the 3 leads—be careful to use the correct angles.
  • Look at the ECG lead I. Count the number of mm above the baseline that the QRS complex reaches.
  • Subtract from this the number of mm below the baseline that the QRS complex reaches.
  • Now measure this number of centimetres along line I on your diagram and make a mark (measure backward for negative numbers).
  • Repeat this for leads II and III.
  • Extend lines from your marks, perpendicular to the leads (see Fig. 19.6).
  • The direction from the centre of the diagram to the point at which all these lines meet is the cardiac axis.
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22
Q

Cause of left axis deviation

A
  • Left ventricular hypertrophy
  • left bundle branch block (LBBB)
  • left anterior hemiblock
  • inferior MI

<-30 degrees = left axis deviation

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23
Q

Causes of right axis deviation

A
  • right ventricular hypertrophy
  • RBBB
  • anterolateral myocardial infarction
  • cor pulmonale

>+90 degrees = right axis deviation

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24
Q

Reason for cardiac deviation in healthy individuals

A

Right axis deviation - tall and thin

left axis deviation - short and stocky

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25
Q

Right atrial enlargement

A
  • RA depolarisation lasts longer and its waveform extends to the LA depolairsation. The combination of these two waveforms produces a P wave that is taller and normal >2.5mm
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26
Q

Definition of AV conduction abnormalities

A

In the normal ECG each P wave is followed by a QRS complex.

The isoelectric gap between is the PR interval and represents slowing of the impulse at the AV junction.

Disturbance of the normal conduction here, leads to ‘heart block

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27
Q

What are the four different types of heart block?

A

First Degree AV Block

Every evening Mrs P awaits for QRS to come home, and although he does return at the same time every night, it’s later than usual. Prolonged but constant P-R interval. Caused by delayed conduction through the AV node and/or conducting system

Second Degree AV block Type I (Wenckebach or MobitzI)

The relationship is getting worse. Mrs P still waits for QRS to come home, he is now coming home later and later every night, and roughly one night a week he doesn’t come home at all. Progressive prolongation of the PR interval in cycles, preceding or being followed by a dropped beat. Caused by intermitted failure of atrial depolarisations to reach the ventricles.

Second Degree AV block Type II (MobitzII)

Things are not looking good for P and QRS’s relationship and P suspects QRS is cheating. When he does come home it is always at the same time, however he is more often and unexpectedly he is not coming home at all. PR-interval is constant. More frequent and intermittent dropped beats.

Third Degree AV Block

Looks like a divorce is on the cards for Mrs P and QRS - they no longer communicate at all and are completely dissociated from one another. Complete heart block. Charactarised by a complete dissociation between P-waves and QRS complexes

28
Q

What type of heart block is this?

A

Second degree Heart block Mobitz type 2

29
Q

What type of heart block is this?

A

Second degree heart block Mobitz 1

30
Q

What type of heart block is this?

A

First degree heart block

31
Q

What type of heart block is this?

A

Complete third degree heart block

32
Q

Causes of heart block?

A

Causes of heart block include

  • ischaemic heart disease,
  • idiopathic fibrosis of the conduction system,
  • cardiomyopathies,
  • inferior and anterior MI,
  • drugs (digoxin, ?-blockers, verapamil), and
  • physiological (1st degree) in athletes.
33
Q

Extra tips for identifying 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.
  • P waves are best seen in leads II and V1.
34
Q

Definition of ventricular conduction abnormalities

A

Depolarization of both ventricles usually occurs rapidly through left and right bundle branches of the His–Purkinje system

If this process is disrupted as a result of damage to the conducting system, depolarization will occur more slowly through non-specialized ventricular myocardium.

The QRS complex—usually <0.12 seconds’ duration—will become prolonged and is described as a ‘broad’

35
Q

Right bundle branch block

A

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

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

ECG changes - QRS complex in V1 looks like an M and a W

MarroW

36
Q

Causes of RBBB

A
  • Hyperkalaemia.
  • Congenital heart disease (e.g. Fallot’s tetralogy).
  • Pulmonary embolus.
  • Cor pulmonale.
  • Fibrosis of conduction system.

Note can be a normal variant

37
Q

Left bundle branch block

A

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

The result is delayed left ventricular depolarization

ECG changes: QRS complex in V1 looks like an W and an M in V6 respectively

38
Q

Causes of LBBB

A
  • Hypertension.
  • Ischaemic heart disease.
  • Acute myocardial infarction.
  • Aortic stenosis.
  • Cardiomyopathies.
  • Fibrosis of conduction system

Always pathological

39
Q

Bundle branch block mnemonic

A

LBBB, the QRS complex in V1 looks like a ‘W’ and an ‘M’ in V6. This can be remembered as ‘WiLLiaM’. There is a W at the start, an M at the end and ‘L’ in the middle for ‘left’

Conversely, in the case of RBBB, the QRS complex in V1 looks like an ‘M’ and a ‘W’ in V6. Combined with an ‘R’ for right, you have the word ‘MaRRoW

40
Q

Which bundle branch block is this?

A

left bundle branch block

41
Q

Which bundle branch blocK

A

Right bundle branch block

42
Q

Two types of arrthymias

A

Arrhytmias: sinus arrhytmias resulting from disturbances in impulse discharge or impulse conduction from the sinus node

Arrhythmias are generally divided into two categories:

  • ventricular
  • Supraventricular.

Ventricular arrhythmias occur in the lower chambers of the heart, called the ventricles.

Supraventricular arrhythmias occur in the area above the ventricles, usually in the upper chambers of the heart, called the atria. T

he irregular beats can either be too slow (bradycardia) or too fast (tachycardia)

43
Q

Definition of

Sinus bradycardia

sinus tachycardia

A

This is a bradycardia (rate <60 beats per minute) at the level of the SA node. The heart beats slowly but conduction of the impulse is normal.

This is a tachycardia at the level of the SA node—the heart is beating too quickly but conduction of the impulse is norma

44
Q

What does this show?

A

Sinus bradycardia

P waves: normal in size, shape and direction. Positive in II One P wave preceding every QRS complex

PR interval: normal

QRS complex: Normal (<0.12)

45
Q

Sinus tachycardia

A

Sinus Tachycardia

Rhythm: regular

Rate: 100-160bpm

P waves: normal in size, shape and direction. Positive in II. One P wave preceds each QRS

PR interval normal

QRS complex: normal

46
Q

Causes of Sinus tachycardia

A
  • Drugs (epinephrine/adrenaline, caffeine, nicotine).
  • Pain.
  • Exertion
47
Q

Causes of sinus bradycardia

A

Drugs (?-blockers, verapamil, amiodarone, digoxin).

  • Sick sinus syndrome.
  • Hypothyroidism.
  • Inferior M
48
Q

Definition of supraventricular tachycardias and causes?

A

These are tachycardias (rate >100bpm) arising in the atria or 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 norma

Causes

  • Atrial fibrillation
  • Atrial flutter
  • Wolf Parkinsons White syndrome
  • Premature atrial contractions
  • Wandering atrial pacemaker
49
Q

Atrial fibrillation definition

A

This is disorganized contraction of the atria in the form of rapid, irregular twitching. There will, therefore, be no P waves on the ECG.

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. The result is a characteristic ventricular rhythm that is irregularly irregular with no discernible pattern

ECG

  • no p waves
  • Irregularly irregular
  • Normal QRS appearance
  • Ventricular rate fast
50
Q

Causes of AF

A
  • Idiopathic.
  • Ischaemic heart disease.
  • Thyroid disease.
  • Hypertension.
  • MI
51
Q

Atrial flutter definition

A

This is the abnormally rapid contraction of the atria. The contractions are not disorganized or random, unlike AF, but are fast and inadequate for the normal movement of blood. Instead of P waves, the baseline will have a typical ‘saw-tooth’ appearance (sometimes known as F waves).

ECG appearances:

  • ‘Saw-tooth’ appearance of baseline.
  • Normal appearance of QRS complexes.
52
Q

Definition of Wolf-Parkinson-White syndrome

A

Wolff-Parkinson-White (WPW) syndrome is a group of abnormalities caused by extra muscle pathways between the atria and the ventricles. The pathways cause the electrical signals to arrive at the ventricles too soon, and the signals are sent back to the atria. The result is a very fast heart rate. People with this syndrome may feel dizzy, have chest palpitations, or have episodes of fainting. People with WPW may also be more likely to have episodes of paroxysmal supraventricular tachycardia (PSVT)

53
Q

Definition of premature supraventricular contractions

A

Also called “premature atrial contractions” (PACs), they happen when the atria contract too soon, causing the heart to beat out of sequence.

54
Q

Ventricular arrhytmias definition and causes

A

Most ventricular rhythms 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

Causes:

  • ventricular tachycardia
  • Ventricular Fibrillation
  • Premature ventricular contractions
55
Q

Ventricular tachycardia definition

A

Here, there is a focus of ventricular tissue depolarizing rapidly within the ventricular myocardium. VT is defined as 3 or more successive ventricular extrasystoles at a rate of >120/min. ‘Sustained’ VTs last for >30 secs.

VT may be ‘stable’ showing a repetitive QRS shape (‘monomorphic’) or unstable with varying patterns of the QRS complex (‘polymorphic’).

It may be impossible to distinguish VT from an SVT with bundle branch block on a 12-lead ECG

ECG changes

  • Wide QRS complexes which are irregular in rhythm and shape.

• A-V dissociation—independent atrial and ventricular contraction

56
Q

Ventricular fibrillation definition

A

This is disorganized, uncoordinated depolarization from multiple foci in the ventricular myocardium

ECG

  • no discernible QRS complexes
  • disorgganised ECG
57
Q

Premature ventricular contractions

A

A less serious type of ventricular arrhythmia is a premature ventricular contraction (PVC). As the name suggests, the condition happens when the ventricles contract too soon, out of sequence with the normal heartbeat. PVCs (sometimes called PVB for premature ventricular beat) generally are not a cause for alarm and often do not need treatment. But if you have heart disease or a history of ventricular tachycardia, PVCs can cause a more serious arrhythmia. Although most PVCs happen quickly and without warning, they can also happen in response to caffeine, which is found in coffee, tea, sodas, and chocolate. Some kinds of over-the-counter cough and cold medicines may also cause PVCs.

58
Q

Abnormal P waves

A

Represents depolarization of the small muscle mass of the atria. The P wave is thus much smaller in amplitude than the QRS complex.

Normal

  • In sinus rhythm each P wave is closely associated with a QRS complex.
  • P waves are usually upright in most leads except aVR.
  • P waves are <3 small squares wide and <3 small squares high.

Abnormal

• Right atrial hypertrophy will cause tall, peaked P waves.

  • Causes include pulmonary hypertension (in which case the wave is known as ‘P pulmonale’) and tricuspid valve stenosis.

• Left atrial hypertrophy will cause the P wave to become wider and twin-peaked or ‘bifid’.

  • Usually caused by mitral valve disease—in which case the wave is known as ‘P mitrale
59
Q

Abnormalities of the T wave

A

Represents repolarization of the ventricles. The T wave is most commonly affected by ischaemic changes. The most common abnormality is ‘inversion’ which has a number of causes.

Normal

  • Commonly inverted in V1 and aVR.
  • May be inverted in V1–V3 as normal variant.

Abnormal

  • Myocardial ischaemia or MI (e.g. non-Q wave MI) can cause T wave inversion. Changes need to be interpreted in light of clinical picture (Fig.19.20).
  • Ventricular hypertrophy causes T inversion in those leads focused on the ventricle in question. For example, left ventricular hypertrophy will give T changes in leads V5, V6, II, and aVL.
  • Bundle branch block 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.
  • 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 is not a sign of digoxin toxicity.
  • Electrolyte imbalances cause a number of T wave changes:
  • Raised K+ can cause tall tented T waves
  • Low K+ can cause small T waves and U waves (broad, flat waves occurring after the T waves)
  • Low Ca2+ can cause small T waves with a prolongation of the QT interval. (Raised Ca2+ has the reverse effect)
  • Other causes of T wave inversion include subarachnoid haemorrhage and lithium use
60
Q

ST segment abnormalities

A

This is the portion of the ECG from the end of the QRS complex to the start of the T wave and is an isoelectric line in the normal ECG. Changes in the ST segment can represent myocardial ischaemia and, most importantly, acute MI

ST elevation - The degree and extent of ST elevation is of crucial importance in ECG interpretation as it determines whether reperfusion therapy (thrombolysis or primary PCI) is considered in acute M

ST depression- ST depression can be horizontal, upward sloping, or downward sloping

61
Q

Causes of ST elevation

A
  • Acute MI—convex ST elevation in affected leads (the ‘tomb-stone’ appearance), often with reciprocal ST depression in opposite leads.
  • • Pericarditis—widespread concave ST elevation (‘saddle-shaped’).
  • • Left ventricular aneurysm—ST elevation may persist over time
62
Q

Causes of ST depression

A
  • Myocardial ischaemia—horizontal ST depression and an upright T wave. May be result of coronary artery disease or other causes (e.g. anaemia, aortic stenosis).
  • Digoxin toxicity—downward sloping (‘reverse tick’).
  • ‘Non-specific’ changes—ST segment depression which is often upward sloping may be a normal variant and is not thought to be associated with any underlying significant pathology
63
Q

Changes on the ECG in MI

A

In the first hour following a MI, the ECG can remain normal. However, when changes occur, they usually develop in the following order:

  • ST segment becomes elevated and T waves become peaked.
  • Pathological Q waves develop.
  • ST segment returns to baseline and T waves invert.

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.

  • Anterior: V2–V5.
  • Antero-lateral: I, aVL, V5, V6.
  • Inferior: III, aVF (sometimes II also).
  • Posterior: the usual depolarization of the posterior of the left ventricle 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 infarction.
  • Right ventricular: 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 labelled V1R, V2R, V3R, and so on.
64
Q

Changes in teh ECG with hypertrophy

A

If the heart is faced with having to overcome pressure overload (e.g. left ventricular hypertrophy in hypertension or aortic stenosis) or higher systemic pressures (e.g. essential hypertension) then it will increase its muscle mass in response. This increased muscle mass can result in changes to the ECG.

Atrial hypertrophy

This can lead to changes to the P wave.

Ventricular hypertrophy

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

Left ventricular hypertrophy (LVH)

  • Tall R wave in V6 and deep S wave in V1.
  • May also see left axis deviation.
  • T wave inversion in V5, V6, I, aVL.
  • Voltage criteria for LVH include:
  • R wave >25mm (5 large squares) in V6
  • R wave in V6 + S wave in V1 >35mm (7 large squares).

Right ventricular hypertrophy

  • ‘Dominant’ R wave in V1 (i.e. R wave bigger than S wave).
  • Deep S wave in V6.
  • May also see right axis deviation.
  • T wave inversion in V1–V3.
65
Q

Left atrial enlargement

A

LA depolarisation lasts longer than normal. The resultant P wave last >120msec. A notch may appear (P Mitrale)

66
Q

Wandering atrial pacemaker

A

PM site shifts back and forth between SN and ectopic atrial sites.

Cardiology (12 decks)

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