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Electrocardiogram (ECG) Flashcards

(52 cards)

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1
Q

Why are there 3 parts to the QRS complex?

A
  • Different parts of the ventricles depolarise at slightly different times.
    1. Interventricular Septum depolarises from left to right (Q wave)
    2. R wave: bulk of ventricle depolarises from endocardial to epicardial surface
    3. Upper part of interventricular septum depolarises.
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2
Q

What is the PR interval?

A

Start of P wave to start of QRS complex
Its the time from the start of atrial depolarisation to the start of ventricular depolarisation, mainly transmission in the AV node.

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3
Q

What is the QT interval?

A

Time from the start of the QRS complex to the end of the T wave.
Essentially the time the ventricle spends depolarised.

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4
Q

How long is the QT interval?

A

It varies with HR.

The standard is 0.42 seconds at 60 BPM.

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5
Q

How do you calculate rate from ECG?
Regular rhythm
Irregular rhythm

A

Regular rhythm - 300/no of R waves

Irregular rhythm - No of R waves in 10s rhythm strip x 6

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6
Q

Complete the sequence:

300, ___, ___, ___, 60.

A

300, 150, 100, 75, 60

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7
Q

Intervals
How long should the PR interval last?
How long should the QRS complex last?

A

PR interval
0.12-0.2 seconds
3-5 small squares

QRS complex
~0.08 seconds
<3 small squares

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8
Q

Systemic approach to ECG

A 
Rate
Rhythm
Axis
Intervals
Everything else
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9
Q 
Prolonged PR interval? Think Heart Blocks
List the features of:
1) First Degree [1]
2) Mobitz Type 1 [2]
3) Mobitz Type 2 [2]
4) Third Degree [3]
A

1) First Degree - constantly prolonged PR
2) Mobitz Type 1 - progressively prolonged PR, dropped beat
3) Mobitz Type 2 - constantly prolonged PR, dropped beat every couple of beats
4) Third Degree - no relationship between atrial and ventricular depolarization, bradycardia

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10
Q

BBB: WIDE QRS
Describe the 3 features of RBBB
Whats the mnemonic?

A

Broad QRS >0.12
RSR’ in V1 [m]
Slurred S wave in V6 [w]
Normal Axis

MARROW

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11
Q

BBB: WIDE QRS

Describe the features of LBBB

A

Broad QRS >0.12
Dominant S wave in V1 [w]
RSR’ in V6 [m]
Left axis deviation

WILLIAM

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12
Q

Myocardial infarction/Acute Coronary Syndrome
Localisation: state which leads the changes are most likely to be seen and what artery is most commonly involved
Anterior
Septal
Inferior
Lateral

A

Anterior
V1-V4, LAD

Septal
V2-V4, Septal branches of LAD

Inferior
III, AVF, II
80% RCA, 20% LCA

Lateral
V5, V6, AVL, I
Left Circumflex Artery

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13
Q

AXIS
Which leads to look for net deflection
What should we see in the leads if axis is normal
Right axis deviation - what should we see in the leads
Left axis deviation - what should we see in the leads

A

I, AVF > II

If lead 1 is positive, lead II negative> LAD
If Lead 1 is negative, AVF is positive > RAD

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14
Q

How to spot an RV infarction?
Suspect in patients with _______ in the presence of:
1)
2)

A

Suspect RV infarction in patients with inferior STEMI picture
ST elevation in V1
ST elevation in lead III > lead I

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15
Q

WPW syndrome
What is the problem in WPW? [2]
ECG features [3]

A

In WPW the accessory pathway is often referred to as theBundle of Kent [1] which bypasses the AV node causing early activation of ventricles [1]

Delta wave
QRS prolongation
Sinus tachycardia ~ 100 bpm

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16
Q

What ECG changes in a dyspneic patient would suggest COR pulmonale due to massive PE?
However these ECG changes are not specific to PE and may be seen in other conditions of RV dilation and pulmonary HTN eg COPD

A

Sinus tachycardia
RV strain pattern in V1-V4
= T wave inversion in right precordial leads (V1-V4)

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17
Q

3 ECG features that would make massive pericardial effusion highly suspect

A
  1. Tachycardia
  2. Low QRS voltages
  3. Electrical alternans
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18
Q

ECG pattern characteristic of raised ICP (classically seen in context of massive intracranial hemorrhage)

A
  1. Giant T wave inversion

2. Marked QT prolongation

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19
Q

Posterior infarction ECG features [4]

Which set of infarct patients should you look for evidence of posterior infarction [1]

How to confirm that it is a posterior infarction if in doubt [1]

A

Look at V2 for:
Horizontal ST depression
Tall broad R wave
Upright T wave

Look for evidence of posterior involvement in any patient with aninferiororlateral STEMI.

Confirm with recording posterior lead ECG V7-9

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20
Q

ST elevation in MI [3]

A

○ >1mm in height
○ New: hyperacute T waves, ST elevation
○ Old: pathological Q waves

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21
Q

Causes of ST elevation other than MI [9]

Study These Flashcards
A 
Pericarditis
Benign early repolarization
Left bundle branch block
Left ventricular hypertrophy
Ventricular aneurysm
=Brugada syndrome
Ventricular paced rhythm
Raised intracranial pressure
Takotsubo Cardiomyopathy
22
Q

ST depression MI (NSTEMI) [2]

Study These Flashcards
A

ST depression

T wave inversions

23
Q

What are the features of ST depression that [3]

Three types of ST depression

Study These Flashcards
A
  • ST depression ≥ 0.5 mm at the J-point
  • in ≥ 2 contiguous leads
  1. Upsloping
  2. Downsloping
  3. Horizontal
24
Q

ST segment depression - what do these mean?

  1. Upsloping
  2. Horizontal
Study These Flashcards
A
  1. Upsloping
    - LAD occlusion
  2. Horizontal
    - Posterior MI in V1-V3 + upright T waves and tall R waves
25
Other causes of ST depression [8]
``` Reciprocal change in STEMI Posterior MI Digoxin effect Hypokalaemia SVT LBBB, RBBB LVH, RCH Ventricular paced rhythm ```
26
Conduction disease and arrhythmias: overview
- AV node disease - Bundle branch disease or fascicle disease - Escape rhythms i.e. tachyarrhythmias (when no impulse arise...)
27
Describe what axis you may see in single fascicle blocks
Left anterior fascicular block causes LEFT AXIS DEV | Left posterior fascicular block causes RIGHT AXIS DEV
28
Bifascicular blocks: 1. RBBB + LAFB 2. RBBB + RAFB
1. RBBB + LAFB: Left axis deviation | 2. RBBB + LPFB: Right axis deviation
29
Trifascicular block
Bifascicular block + PR interval up i.e. there is heart block
30
Bradycardia algorithm: | What will cause bradycardia + narrow complex QRS [5]
``` Sinus bradycardia 1st degree HB 2nd degree HB 3rd degree HB Junctional rhythm ```
31
What differentiates junctional rhythm from HB or sinus bradycardia? [3]
Junctional Rhythm: - QRS narrow and regular rhythm - BUT there are no P waves or they are buried in QRS/T - HR 40-60 bpm Heart block, p waves will be seen
32
What can cause bradycardia + wide QRS complex + regular rhythms
``` Sinus brady with BBB First degree HB with BBB Mobitz type 2 AV block Complete HB AF with complete HB ```
33
What can cause bradycardia + wide QRS complex + IRREGULAR rhythms
AF with slow response | BBB pattern
34
Tachyarrhythmias algorithm: | What can cause QRS narrow + regular rhythms [5]
``` Atrial flutter Ectopic atrial tachycardia Sinus tachycardia AVNRT AVRT ```
35
What tachyarrhythmia cause QRS narrow + irregular rhythms + no P waves? ``` How to distinguish Atrial flutter Ectopic atrial tachycardia Sinus tachycardia AVNRT AVRT ```
Tachyarrhythmia, QRS narrow + irregular rhythms + no P waves = Atrial fibrillation Atrial flutter: continuous and fluttery P waves 'sawtooth' Ectopic atrial tachycardia and Sinus tachycardia = discrete P waves AVNRT and AVRT = No p waves
36
What tachyarrhythmias have BROAD QRS + regular rhythms [7]
``` SVT with BBB SVT with aberrancy WPW antidromic Ventricular tachycardia AF with BBB or AF with aberrancy Torsades des pointes, other polymorphic VTs Ventricular fibrillation ```
37
Tachyarrhythmias: BROAD QRS + regular rhythm | How are they distinguished from each other? [3]
Typical BBB pattern > SVT + BBB/Aberrancy Delta wave > WPW antidromic Unlike BBB pattern, fusion and capture beats > VT
38
Tachyarrhythmias: BROAD QRS + irregular rhythm | How are they distinguished from each other? [2]
Tachyarrhythmias: BROAD QRS + irregular rhythm: Tall QRS Flat wavy QRS = Ventricular fibrillation
39
If you suspect that it is VT and the patient has a wide complex tachycardia, do you wait for investigation before treating?
No, any wide complex Tachycardia is VT until proven otherwise
40
What is VT characterized by? [3] | Types of VT [2]
``` Regular rhythm P waves absent 3 or more ventricular beats Capture or fusion beats Types: 1. Monomorphic 2. Polymorphic ```
41
Explain Torsades des Pointes - it is a type of polymorphic VT
Twisting of the points Changing in amplitudes of ventricular impulses Several escape beats are happening and they take turns
42
SVT with aberrancy [3]
Narrow complex tachycardia + other conduction defect e.g. BBB (regular + broad QRS) so it has a WIDE QRS complex AV dissociation Extreme axis deviation
43
Causes of right axis deviation [2] | acute, chronic, congenital, normal variants.
* right ventricular hypertrophy * left posterior hemiblock * lateral myocardial infarction * chronic lung disease → cor pulmonale * pulmonary embolism * ostium secundum ASD * Wolff-Parkinson-White syndrome - left-sided accessory pathway * normal in infant < 1 years old * minor RAD in tall people
44
Causes of LAD
* left anterior hemiblock * left bundle branch block * inferior myocardial infarction * Wolff-Parkinson-White syndrome - right-sided accessory pathway * hyperkalaemia * congenital: ostium primum ASD, tricuspid atresia * minor LAD in obese people
45
Describe how digoxin toxicity can manifest as ECG changes [4]
down-sloping ST depression ('reverse tick', 'scooped out') flattened/inverted T waves short QT interval arrhythmias e.g. AV block, bradycardia
46
Hypokalemia in ECG [5]
* U waves * small or absent T waves (occasionally inversion) * prolong PR interval * ST depression * long QT | In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT
47
When would bradycardia and a J wave be seen?
ECG: hypothermia The following ECG changes may be seen in hypothermia * bradycardia * 'J' wave (Osborne waves) - small hump at the end of the QRS complex * first degree heart block * long QT interval * atrial and ventricular arrhythmias
48
Causes of LBBB | New LBBB is always pathological
* myocardial infarction * diagnosing a myocardial infarction for patients with existing LBBB is difficult * rhe Sgarbossa criteria can help with this - please see the link for more details * hypertension * aortic stenosis * cardiomyopathy * rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
49
Causes of ST elevation [7]
Causes of ST elevation * myocardial infarction * pericarditis/myocarditis * normal variant - 'high take-off' * left ventricular aneurysm * Prinzmetal's angina (coronary artery spasm) * Takotsubo cardiomyopathy * rare: subarachnoid haemorrhage
50
Name normal variants in athletes that can be misinterpreted as pathological on an ECG
The following ECG changes are considered normal variants in an athlete: * sinus bradycardia * junctional rhythm * first degree heart block * Mobitz type 1 (Wenckebach phenomenon)
51
Causes of a prolonged PR interval
* idiopathic * ischaemic heart disease * digoxin toxicity * hypokalaemia * rheumatic fever * aortic root pathology e.g. abscess secondary to endocarditis * Lyme disease * sarcoidosis * myotonic dystrophy
52
Prolonged ECG monitoring | methods
* Holter- 24h to 7d * External recorders: patient places monitor on chest at onset of symptoms * Wearable loop recorder: continuous monitoring, patient activates recorder when symptoms occur, records minutes before, during after event * Implantable loop recorders: records when there is pre-specified alarm criteria, implanted for 3y.

Cardiology (29 decks)

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