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CVS > L14 - Electrocardiogram > Flashcards

L14 - Electrocardiogram Flashcards

1
Q

What produces an ECG?

A

Summation of cells depolarisation/repolarisation gives resultant vectors
Measurement of vectors produces an ECG

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2
Q

Where can electrical potentials be recorded?

A

When cardiac impulse passes through the heart, the electrical current spreads to adjacent tissues
- Small amount even reaches the surface of the skin
If electrodes are placed on the skin around the heart, electrical potentials can be recorded

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3
Q

What are the two different ways to record electrical activity?

A

Surface electrodes - placed on to the skin and connected by cables to the ECG
Standard limb leads – tracing of voltage difference and what is actually produced by the ECG recorder
o

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4
Q

How does use of standard limb leads work?

A 
Right arm, left arm, left leg 
Einthovens triangle - 
- Lead 1 – RA and LA
- Lead 2 – RA and LL
- Lead 3 – LA and LL
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5
Q

What causes an upward deflection on an ECG?

A

Net current flow towards an electrode causes an upward deflection on ECG

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6
Q

What does an ECG show?

A

The ECG is the spread of electrical excitation through the heart
Electrical excitation causes muscle contraction its progression through the heart

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7
Q

What are the 6 different stages of an ECG?

A
  1. P wave - atria depolarisation
    o Small muscle mass so deflection is small
  2. Atria depolarisation complete
  3. QRS wave – ventricular depolarization begins at apex
    o Big muscle mass so deflection is big
    o Repolarisation of atria happens at the same time but this electrical activity is swamped by ventricular depolarisation
  4. Ventricular depolarisation complete and blood ejected to the lungs/body
  5. T wave – ventricular repolarisation begins at apex
    o Progresses superiorly
    o It occurs in the same direction as depolarisation so it also produced an upward deflection
  6. Ventricular repolarisation complete
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8
Q

How long is PR typically?

A

0.12-0.20 s

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9
Q

How long is QRS typically?

A

0.8-0.10 s

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10
Q

How long is QT typically?

A

0.40-0.43 s

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11
Q

How long is ST typically?

A

0.32 s

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12
Q

What is atrial hypertrophy?

A

High P wave amplitude

More muscle mass, more to depolarise, bigger deflection

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13
Q

What is ventricular hypoxia?

A

Low T wave amplitude

Not enough oxygen

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14
Q

What is acute myocardial infarction?

A

Longer ST interval

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15
Q

What is arrhythmia?

A

A lack of rhythm

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16
Q

What is it known as when the heart rate naturally varies?

A

Bradycardia and tachycardia
E.g. exercise from 65-180 bpm
E.g. sinus arrhythmia – 15% increase on inspiration, 15% decrease on expiration

17
Q

What are some examples of when heart rate varies abnormally?

A

E.g. non-exercise tachycardia 150-200 bpm
E.g. flutter – 200-300 bpm
E.g. ventricular fibrillation – 300+ bpm
Often caused by interruptions in the hearts conduction pathway

18
Q

What can cause heart blocks?

A

Myocardial infarction

Artery disease

19
Q

What is a first degree heart block?

A

Interruption between the SA and AV nodes
Slowing SA-AV conduction
This leads to an increased PR interval

20
Q

What are the two stages of a second degree heart block?

A

Mobitz 1

Mobitz 2

21
Q

What occurs during Mobitz 1?

A

Some SA impulses fail to evoke QRS
Progressive prolongation of PR interval culminating in a non-conducted P wave
- PR interval longest immediately before dropped beat
- PR interval shortest immediately after dropped beat
Progressive fatigue of the AV nodal cells

22
Q

What occurs during Mobitz 2?

A

Intermittent non-conducted P wave without progressive prolongation of PR interval
- PR interval in conducted beats remains constant
- PR interval surrounding the dropped beat is an exact multiple of the preceding PR interval
All or nothing - his-purkinje cells suddenly fail to conduct a supraventricular impulse

23
Q

What are the characteristics seen in Mobitz 2 due to?

A

Failure of conduction at the level of the his-purkinje system
Structural damage to conducting system
- Infarction, fibrosis

24
Q

Patient with Mobitz 2 usually have a pre-exsiting?

A

Patients typically have a pre-existing LBBB or block

- 2nd degree AV block is produced by intermittent failure of remaining fascicle

25
Q

What occurs during a third degree heart block?

A

Complete absence of AV conduction – no supraventricular impulses
Perfusing rhythm is maintained by a junctional or ventricular escape rhythm

26
Q

Patients with a third degree heart block may suffer with?

A

Ventricular standstill leading to fainting or sudden cardiac death
Severe bradycardia with independent atrial and ventricular rates

27
Q

What are the consequences of a first degree heart block?

A

Benign – often seen in athletes

28
Q

What are the consequences of a second degree heart block?

A

Benign (type1)

May require pace maker (type 2)

29
Q

What are the consequences of a third degree heart block?

A

Chamber contraction out of synchrony
Atrial contraction against closed tricuspid
- Cannon wave in jugular vein
- R atria contract at the same times as R ventricle so pressure wave is sent back up the jugular vein
Reduced perfusion of tissue
- Dizziness and syncope

30
Q

What is atrial fibrillation?

A

Most common arrhythmia
Starts with brief abnormal rhythm of atria which becomes longer (sometimes constant)
May be perceived as palpitations or exercise intolerance

31
Q

Symptoms of atrial fibrillation?

A

Usually asymptomatic

  • Accompanied by symptoms related to rapid heart rate
  • May produce angina
  • Shortness of breath
  • Oedema of ankles
32
Q

What are the treatments for atrial fibrillation?

A

Flecainide
Beta blockers
Amiodarone/dronedarone
Warfarin/anticoagulants

33
Q

What are circus movements?

A

Electrical signal not completing normal circuit but alternative circuit looping back upon itself rapidly
Refractory muscle normally prevents re-excitation
If wave of excitation meets non-refractory tissue it will carry on

34
Q

How can circus movements be non-refractory?

A

Unidirectional block

Transient bidirectional block

CVS (15 decks)

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