ECGs Flashcards
1
Q
Which leads are the anterior leads?
A
V1, V2
2
Q
Which leads are the septal leads?
A
V3, V4
3
Q
Which leads are the lateral leads?
A
I
aVL
V5, V6
4
Q
Which leads are the inferior leads?
A
II, III
aVF
5
Q
Of the praecordial leads, which ones have an isoelectric QRS complex?
A
V3, V4
6
Q
Which leads must be looked at to figure out if there is any axis deviation?
A
I and aVF
(as these are perpendicular)
7
Q
- What does the PR interval represent?
- What is its normal length?
A
- PR interval = time taken for excitation to spread from SAN, through atrial muscle, the AVN, down the bundle of His and into ventricular muscle (start of p wave to start of QRS complex)
- normal length of PR interval = 120-220ms (3-5 small squares)
8
Q
- What does the QRS complex represent?
- What is its normal length?
A
- duration of the QRS complex shows how long excitation takes to spread through the ventricles
- normal length = 120ms (3 small squares)
9
Q
- What does the ST segment represent?
- What is its normal length?
A
- interval between ventricular depolarization and repolarization (end of s wave to start of t wave)
- should be ~ 80ms (but more than length, whether its elevated or depressed tells us more about pathology)
10
Q
How might you recognise left ventricular hypertrophy (i.e. left axis deviation) on:
a) limb leads
b) praecordial leads
A
a) I and aVF : if the waves are ‘leaving’ each other
b) V1 and V2 are the isoelectric leads (QRS complex)
11
Q
How might you recognise right ventricular hypertrophy (i.e. right axis deviation) on:
a) limb leads
b) praecordial leads
A
a) I and aVF: waves are ‘coming together’
b) V5 and V6 are the isoelectric leads (QRS complex)
12
Q
Which lead shows the P wave most clearly?
A
II
or V1
13
Q
What is 1st degree heart block w.r.t. electrical conduction?
A
- If each wave of depolarization that originates in SA node is conducted to ventricles
- but there is a delay somewhere along conduction pathway
- –> the PR interval is prolonged
14
Q
How do you identify 1st degree heart block on an ECG?
A
PR intervals are lengthened (>220ms)
PR interval = time taken for excitation to spread from SAN, through atrial muscle, the AVN, down the bundle of His and into ventricular muscle
normal length of PR interval = 120-220ms (3-5 small squares)
15
Q
What is the clinical significance of 1st degree heart block?
A
Can be a sign of:
- coronary artery disease
- aute rheumatic carditis
- digoxin toxicity
- electrolyte disturbances.
16
Q
What is the Tx for 1st degree heart block?
A
No specific action required
17
Q
What is 2nd degree heart block w.r.t. to electrical conduction?
A
- excitation completely fails to pass through AV node or the bundle of His
- 2nd degree heart block = this occurs intermittently
18
Q
What is 2nd degree heart block (Mobtiz type 1) w.r.t. to electrical conduction
A
- progressive lengthening of PR interval
- –> failure of conduction of an atrial beat
- followed by a conducted beat w a shorter PR interval
- then a repetition of this cycle.
19
Q
How do you identify 2nd degree heart block (Mobitz type 1/Wenkelback) on an ECG?
A
see image
20
Q
What is 2nd degree heart block (Mobtiz type 2) w.r.t. to electrical conduction?
A
- Most beats are conducted with a constant PR interval*
- but occasionally there is atrial depolarization without a subsequent ventricular depolarization.
21
Q
How do you identify 2nd degree heart block (Mobitz type 2) on an ECG?
A
see image
22
Q
What is the clinical significance of 2nd degree heart block?
A
- Usually indicates heart disease;
- often seen in acute MI
23
Q
During heart blocks, how may a p wave present?
A
as a distortion of a t wave
24
Q
What is 3rd degree heart block w.r.t. to electrical conduction?
A
- = complete heart block
- atrial contraction is normal but no beats are conducted to the ventricles
- When this occurs the ventricles are excited by a slow ‘escape mechanism’ from a depolarizing focus within the ventricular muscle
25
What is the clinical significance of 3rd degree heart block?
**always** indicates **conducting tissue disease**
**acute phenomenon**
* MI (when it is usually transient)
**chronic**
* fibrosis around the bundle of His.
* block of both bundle branches.
26
How do you identify 3rd degree heart block on an ECG?
see image
(must look at PR intervals and recognise that there is no consistency)
27
What is the Tx for 3rd degree heart block?
Permanent/temp. pacemaker
28
What is the principle of bundle branch block as seen on an ECG?
* If the depolarization wave reaches the interventricular septum normally, interval between the beginning of the P wave and the first deflection in the QRS complex (the PR interval) will be normal.
* However, if there is abnormal conduction through either the right or left bundle branches (‘bundle branch block’) there will be a delay in the depolarization of part of the ventricular muscle.
* The extra time taken for depolarization of the whole of the ventricular muscle --\> **widening of QRS complex******
* *conduction within the ventricles must have occurred by an abnormal, and therefore slower, pathway.*
29
Which ECG leads are useful when determining bundle branch block?
Praecordial leads (as they're in the horizontal plane)
* V1
* V6
30
What is the similaritiy and difference between depolarisation starting from the ventricles (i.e. an arrythmia), and bundle branch block on an ECG?
**similarity**
* both have widened QRS complexes
**difference**
* bundle branch block (sinus rhythm)=
* normal P waves are present
* a constant PR interval
* arrythmia =
*
31
What is seen on an ECG if both bundle branches are blocked?
has the same effect as block of the His bundle
## Footnote
**--\> complete (third degree) heart block.**
32
What is RBBB a sign of?
problem w right side of heart
33
What does RBBB indicate clinically?
possible atrial septal defect
34
What does a RBBB pattern with a QRS complex of normal duration indicate?
quite common in healthy people
35
What does LBBB indicate clinically?
* **always** an indication of **left ventricular disease**
* **aortic stenosis**
* **ischaemic disease**.
* if presents w _recent chest pain_:
* **acute MI**
36
What is the Tx for LBBB?
**asymptomatic**:
* none required
if **indication of recent acute MI:**
* follow MI guidelines
37
What is the implication on further ECG interpretation if LBBB is present?
LBBB **prevents further interpretation of ECGs**
38
What is the implication on further ECG interpretation if RBBB is present?
makes interpretation more difficult
39
How do you identify LBBB on an ECG?
**W**illia**M**
* V1 - W
* V6 - M
* Sinus rhythm, rate 100/min
* Normal PR interval
* Normal cardiac axis
* **Wide QRS complexes (160 ms)**
* M pattern in the QRS complexes, best seen in leads I, VL, V5 and V6
* **Inverted T waves in leads I, II, VL**
40
How do you identify RBBB on an ECG?
**M**arro**W**
* V1 - M
* V6 - W
* Sinus rhythm, rate 60/min
* Normal PR interval
* Normal cardiac axis
* **Wide QRS complexes (160 ms)**
* RSR1 pattern in lead V1 and deep, wide S waves in lead V6
* **Normal ST segments and T waves**
41
What is the clinical significance of
## Footnote
**left axis deviation + RBBB?**
**severe conducting tissue disease**
right bundle branch + left anterior fascicle = blocked
*(see image)*
* no specific Tx required
* Pacemaker required if pt has symptoms suggestive of intermittent complete heart block
* i.e. right bundle branch + both fascicles of left bundle branch = blocked
* --\> complete heart block occurs just as if main His bundle had failed to conduct.
42
What is the meaning of sinus rhythm?
When depolarization begins in the SA node
43
What is an arrhythmia?
When depolarisation begins anywhere other than the SAN
* the rhythm is named after the place of origin
44
Broadly speaking, how is an arrhythmia identified?
from the lead in which the P waves can be seen most easily (leads II or V1)
45
Which part of the heart controls the rate of ventricular contraction?
part of the heart that is depolarizing most frequently (i.e. highest rate of electrical discharge)
* in sinus rhythm, this is the SAN
46
1. What is sinus arrhythmia
2. give some examples of sinus arrhythmia
1. Sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate.
2. respiratory sinus arrhthymia
47
Where can abnormal cardiac rhythms originate?
* atrial muscle
* the region around the atrioventricular (AV) node (this is called ‘nodal’ or, more properly, junctional’)
* ventricular muscle.
48
What are the supraventricular rhythms?
* sinus (SAN origin)
* atrial rhythm
* junctional rhythm
49
What is the electrical pathway in supraventricular rhythms?
depolarization wave spreads to the ventricles in the normal way via the His bundle and its branches
* so QRS complex is normal
*
50
What is the electrical pathway in ventricular rhythms?
depolarization wave spreads through the ventricles by an abnormal and slower pathway, via Purkinje fibres
* QRS complex is wide & abnormally shaped.
Repolarization is also abnormal
* so the T wave is also of abnormal shape
51
What is the shape of the QRS complex in
a) supraventricular rhythms
b) ventricular rhythms
a) narrow QRS complexes
* exception: supraventricular rhythm with right or left bundle branch block, or the Wolff–Parkinson–White (WPW) syndrome
* --\> wide QRS complex
b) wide QRS complexes.
52
What are escape rhythms?
slow and protective rhythms in case the SAN fails
occurs during sinus **bradycardia**
* they occur when secondary sites for initiating depolarization escape from their normal inhibition by the more active SA node
* not primary disorders, but are the response to problems higher in the conducting pathway.
53
When is ventricular escape most commonly seen?
when conduction between the atria and ventricles is interrupted by complete heart block
* BUT Ventricular escape rhythms can occur without complete heart block
54
How do you identify atrial escape on an ECG?
abnormal p wave (II or V1)
55
How do you identify junctional escape on an ECG?
absence of p waves (V1, V2 - septal leads)
56
How do you identify ventricular escape on an ECG?
wide abnormal QRS complex, not following a p wave
57
What is **paroxysmal** tachycardia?
When a tachycardia occurs **intermittently**
58
Name some supraventricular tachycardias
* Atrial tachycardia
* Atrial flutter
* Junctional (nodal) tachycardia
* AVRT
* AV re-entry tachycardia
* AVNRT
* AV nodal reentrant tachycardia
59
How would you identify atrial tachycardia on an ECG?
p waves are superimposed on preceding t waves
atrial rate \> 150/min
60
What is the physiological basis surrounding atrial flutter?
re-entry rhythm, atrial depolarisation (continuous loop) overrides the SAN
61
How do you identify atrial flutter on an ECG?
* atrial rate \>250/min
* no flat baseline between the P waves:
* p waves \> 350 bpm = 'sawtooth waves'
* seen best on inferior leads (II, III, aVF) + aVR
62
How do you identify junctional tachycardia on an ECG?
no p waves in any lead
QRS complexes are of normal shape (normal route of depolarisation)
QRS complexes - rate = high
* If the area around AVN depolarizes frequently, P waves may be seen very close to the QRS complexes OR may not be seen at all
63
What is ventricular tachycardia?
If a focus in the ventricular muscle depolarizes with a high frequency
Excitation has to spread by an abnormal path through the ventricular muscle, and the QRS complex is therefore wide and abnormal
64
How do you recognise ventricular tachycardia on an ECG?
* broad QRS complexes
* tachycardia
* no identifiable t waves
65
How do you distinguish between ventricular tachycardia and supraventricular tachycardia + BBB on an ECG?
ventricular tachycardia
* very wide QRS complexes (\>4squares)
* Left axis deviation during tachycardia
66
What is fibrillation?
individual muscle fibres contracting independently
67
What is the physiological basis behind atrial fibrillation?
Atrial muscle fibres contract independently
* no P waves on ECG, only an irregular line
AV node is continuously bombarded with depolarization waves of varying strength, and depolarization spreads at irregular intervals down the His bundle. The AV node conducts in an ‘all or none’ fashion, so that the depolarization waves passing into the His bundle are of constant intensity.
* QRS complexes present
However, these waves are irregular, and the ventricles therefore contract irregularly.
* irregular QRS complexes - e.g. not every 3 secs
Because conduction into and through the ventricles is by the normal route
* QRS complex is of normal shape.
68
How do you recognise atrial fibrillation on an ECG?
best seen on inferior leads (II, III, aVF)
69
How do you recognise ventricular fibrillation on an ECG?
ECG is totally disorganised in **every lead**
patient will be unconscious (cardiac arrest)
70
What is Wolff-Parkinson-White syndrome?
The only normal electrical connection between the atria and ventricles is the His bundle.
Some people, however, have an **extra or ‘accessory’ conducting bundle,** a condition known as the Wolff–Parkinson–White syndrome
* accessory bundles form a **direct connection between the atrium and the ventricle**
* usually on the left side of the heart
* in these bundles there is **no AV node to delay conduction**
71
How do you identify WPW syndrome on an ECG?
* **Slurred upstroke** of the QRS complex, best seen in leads V3 and V4.
* **Wide QRS complex** due to this ‘**delta’ wave**
* Dominant R wave in lead V1
* **Short PR interval**
72
What is the clinical significance of WPW syndrome?
it can **cause** **paroxysmal tachycardia**
* Depolarization can spread down the His bundle and back up the accessory pathway, and so reactivate the atrium.
* A ‘re-entry’ circuit is thus set up, and a sustained tachycardia occurs
73
Apart from p wave abnormalities in rhythm changes, what 2 other things may cause p wave abnormalities?
* left atrial hypertrophy
* right atrial hypertrophy
74
What may cause left atrial hypertrophy?
mitral stenosis
75
How do you recognise left atrial hypertrophy on an ECG?
* **_broad_ P wave +**
* **_bifid_ P wave**
76
What may cause right atrial hypertrophy?
* tricuspid stenosis
* pulmonary hypertension
77
How do you recognise right atrial hypertrophy on an ECG?
**_peaked_ P waves**
78
What may cause right ventricular hypertrophy?
* **pulmonary hypertension**
* due to COPD, pulmonary embolism, other restrictive lung diseases
* **tricuspid insufficiency**
* **pulmonary** **stenosis**,
79
How do you recognise right ventricular hypertrophy on an ECG?
* best seen on anterior leads (e.g. _V1_)
* **height of R wave \> depth of S wave**
* lead _V6_
* **deep S wave**
usually accompanied by:
* right axis deviation
* right atrial hypertrophy i.e. peaked p wave
80
What may cause left ventricular hypertrophy?
The left ventricle hypertrophies in response to pressure overload secondary to conditions such as
* aortic stenosis
* aortic insufficiency
* hypertension
primary causes:
* hypertrophic cardiomyopathies
81
How do you recognise left ventricular hypertrophy on an ECG?
lateral leads: (V5 or V6)
* **tall R wave** (greater than 25 mm)
anterior leads: (V1 or V2)
* **deep S wave**
82
How do you recognise **severe** left ventricular hypertrophy on an ECG?
* _lateral leads_ (I, aVL, V5, V6) + *sometimes septal V4*
* **inverted T waves**
* **left axis deviation**
83
1. where are q waves seen normally?
2. What do q waves signify?
1. left ventricular leads i.e. lateral leads
* i.e. V5, V6
2. depolarization of the septum from left to right
84
Describe an abnormal q wave
q wave \> 1 small square in _width_ (representing 40 ms)
q wave \> 2 mm in _depth_
**when seen in any leads other than _V5_ or _V6_**
***_(_**see image - q waves seen earlt in V4 in pt 2)*
85
When are abnormal (ly present) q waves seen?
MIs
* leads in which they are seen indicate the type of MI e.g. anterior, lateral, inferior, etc
86
What is the electrical basis for seeing abnormal q waves?
If an MI causes **complete death of muscle from inside surface to outside surface** of heart
* --\> an electrical ‘window’ is created
* and an electrode looking at the heart over that window will record a **cavity potential** i.e. a Q wave.
*(in the image, if the electrode was slightly superior or inferior, a flast line would be seen)*
87
Do q waves every disappear?
once present, they are always present
* hence require other signs to show whether MI is an old or acute
88
What signs on an ECG show that the q waves present are due to an old MI i.e. ischaemia?
* **flat** ST segments +
* **inverted T waves**
89
What signs on an ECG show that the q waves are due to an acute MI?
ST elevation
90
Which artery is associated with an anterior MI?
left anterior descending artery (LAD)
91
Which artery is associated with an inferior MI?
Inferior STEMI _can_ result from occlusion of all **three coronary arteries**:
* The vast majority (~80%) of inferior STEMIs are due to occlusion
* dominant **right coronary artery (RCA).**
* Less commonly (around 18% of the time), the culprit vessel
* dominant **left circumflex artery (LCx).**
* *Occasionally, inferior STEMI may result from occlusion of a “type III” or “wraparound” left anterior descending artery (LAD). This produces the unusual pattern of concomitant inferior and anterior ST elevation.*
92
Which artery is associated with an lateral MI?
* The lateral wall of the LV is supplied by branches of:
* **left anterior descending (LAD**) AND
* **left circumflex (LCx) arteries.**
* Infarction of the lateral wall usually occurs as part of a larger territory infarction, e.g. anterolateral STEMI.
* **_Isolated_** _lateral STEMI_ is less common, but may be produced by occlusion of smaller branch arteries that supply the lateral wall
* e.g. the **_first diagonal branch (D1) of the LAD_**,
* **_obtuse marginal branch (OM) of the LCx_**, OR
* **_ramus intermedius._**
93
Which leads show abnormal(ly present) q waves in an anterior MI (of the left ventricle)?
leads w an anterior view of left ventricle
* anterior lead: **V2**
* septal leads: **V3, V4**
* or lateral lead: **V5**
94
Which leads show abnormal(ly present) q waves in an anterio-lateral MI?
* septal: **V3, V4** AND
* lateral leads: **I, VL, V5, V6**
95
Which leads show abnormal(ly present) q waves in an inferior MI?
* inferior leads: **III, VF**
96
How is a posterior MI identified on an ECG?
lead V1: dominant R wave
97
Why is a dominant R wave seen in V1 in a posterior MI?
_Normally_:
* right ventricle occupies the front of the heart anatomically,
* depolarization of the right ventricle (moving towards the recording electrode V1) is overshadowed by depolarization of the left ventricle (moving away from V1).
* --\> result is a dominant S wave in lead V1.
_With infarction of posterior wall of left ventricle:_
* depolarization of right ventricle is less opposed by left ventricular forces
* and so becomes more obvious,
* --\> a dominant R wave develops in lead V1
98
What do flattened t waves indicate?
ischaemia (in the anatomical area represented by the leads w flattened t waves)
t waves return to normal post-resolution of ischaemia
99
What is the normal appearance of the ST segment?
**isoelectric**’ – that is, at the same level as the part between the T wave and the next P wave
100
What 2 abnormalities of the ST segment may be seen?
* elevation
* depression
101
What does ST elevation indicate?
**_acute_ myocardial injury** usually due either to:
* **recent myocardial infarction** OR
* **pericarditis**
102
How do you differentiate between pericarditis and a recent MI on an ECG?
_pericarditis_
* ST elevation in **most/all leads**
_recent MI_
* **localised** to the leads representing the area of infarct
103
What does horizontal depression of the ST segment, associated with an upright T wave indicate?
ischaemia (as opposed to infarction)
* t waves will still be flattened
* when the ECG at rest is normal, ST segment depression may appear during exercise, particularly when effort induces angina*
104
What does downward-sloping (vs horizontally depressed) ST segments indicate?
treatment w digoxin
105
In which leads is the t wave normally inverted?
* aVR, V1
* ~ III, V2
* some black people: V3
106
Other than in normal leads, when might t waves be inverted?
* Ischaemia
* Ventricular hypertrophy
* Bundle branch block
* Digoxin treatment.
107
Name the abnormalities seen on an ECG during an MI, in order of appearance
1. very early stage: hyperacute t waves
2. elevation of the ST segment
3. Q waves appear
4. T waves become inverted.
108
What happens to the ECG post-resolution of an MI?
* ST segment returns to the baseline
* whole process taking a variable time but within 24–48 h
* T wave inversion is often permanent.
109
What are the differences seen on an ECG between STEMIs and NSTEMIs?
STEMI:
* T wave inversion
* Q waves
* ST elevation
NSTEMI:
* T wave inversion BUT
* **no** Q waves
* **no** ST elevation
110
What is the physiological difference between a STEMI and an NSTEMI?
_NSTEMI_:
infarction is not full thickness
_STEMI_:
infarction is full thickness (confined to inner layer of heart)
111
Abnormalities in which electrolytes cause ECG changes?
plasma levels of
* **potassium**
* **calcium**
* **magnesium**
_BUT NOT sodium levels_
112
Which parts of the ECG are most commonly affected in electrolyte abnormalities?
* **T wave**
* **QT interval**
* ***(**measured from the onset of the QRS complex to the end of the T wave)*
113
How is a low potassium level identified on an ECG?
* T wave flattening/inversion (in severe cases) +
* ‘U’ wave
* *appearance of a hump on the end of the T wave*
* *'biphasic t wave'*
114
How is a high potassium level identified on an ECG?
* peaked T waves
* 'tall tented t waves'
* disappearance of ST segment
* ~ QRS complex widened.
115
How is a low magnesium level identified on an ECG?
same as potassium
116
How is a high magnesium level identified on an ECG?
same as potassium
117
How is a low calcium level identified on an ECG?
prolongation of the QT interval
118
How is a high calcium level identified on an ECG?
shortened QT interval
119
Which pathologies cause hyperacute t waves?
* early stage of MI
* prinzmetal angina
* hyper- kalaemia/magnesia
120
What is Polymorphic ventricular tachycardia (PVT)?
* ventricular tachycardia in which there are multiple ventricular foci
* with the resultant QRS complexes varying in
* amplitude
* axis AND
* duration.
* The commonest cause of PVT is myocardial ischaemia
121
What is torsades de pointes?
specific form of polymorphic ventricular tachycardia occurring in the
* context of **QT prolongation**;
* characteristic morphology in which the **QRS complexes “twist” around the isoelectric line**
can occur secondary to hypokalaemia
