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Cardiovascular System > Session 6 Interpreting ECGs > Flashcards

Session 6 Interpreting ECGs Flashcards

1
Q

How to determine if it’s a normal sinus rhythm?

A
  • Regular rhythm?
  • HR 60-100 bpm?
  • P waves upright in leads I and II?
  • Normal PR interval? (3-5 small boxes)
  • Every P wave followed by QRS?
  • QRS normal? (< 3 small boxes)
  • Corrected QT interval normal?
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2
Q

What happens in atrioventricular conduction blocks?

A

Delay or failure of conduction of impulses from atria to ventricles via AVN and bundle of His.

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3
Q

What are the 3 types of heart block?

A
  • First degree heart block
  • Second degree heart block (Mobitz type I and II)
  • Third degree heart block
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4
Q

What causes heart block?

A
  • Degeneration/fibrosis of electrical conducting system with age
  • Acute MI
  • Medication
  • Valvular heart disease
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5
Q

How to spot a first degree heart block?*

A
  • Regular rhythm and QRS
  • All normal P waves followed by QRS
  • Prolonged PR interval (> 0.2 seconds)
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6
Q

How to spot a second degree Wenkebach heart block (Mobitz type I)?*

A
  • Successively longer PR intervals until one QRS is dropped
  • Signifies that electrical signal is not conducted to ventricles
  • Cycle starts again
  • Not typically pathological
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7
Q

How to spot a Mobitz type II second degree heart block?*

A
  • PR intervals do not lengthen
  • QRS dropped suddenly (must look if QRS present every p wave)
  • Regular atrial rhythm
  • Irregular ventricular rhythm
  • High risk progression to complete heart block
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8
Q

What is third degree heart block and how to spot it?*

A

Atria and ventricles are depolarising independently and there is no AV conduction
- Ventricular pacemaker takes over and pumps at 20-40 bpm (slow ventricular rate)
- Atrial rate at approx. 100bpm (fast, narrow P wave)
- Wide QRS complex
- Bizarre shape QRS
URGENT PACEMAKER REQUIRED

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9
Q

What is bundle branch block and how to spot it?*

A

Delayed conduction within the bundle branches - can either be left or right.

  • P wave and PR intervals are normal
  • Wide QRS as ventricular depolarisation takes longer
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10
Q

Where may supraventricular arrhythmias arise from?

A
  • Atrium itself
  • Sinoatrial node
  • Atrioventricular node
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11
Q

Where may ventricular arrhythmias arise from?

A

Ventricles

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12
Q

How do supraventricular arrhythmias present?*

A
  • Normal QRS (narrow)

- Issues with P wave

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13
Q

How do ventricular arrhythmias present?*

A
  • Wide and bizarre QRS
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14
Q

What is atrial fibrillation?*

A
  • Most common supraventricular arrhythmia
  • Arises from MULTIPLE ATRIAL FOCI
  • Atria do not contract, just quiver
  • Rapid, chaotic
  • NO P WAVES, JUST WAVY BASELINE
  • Irregular R-R intervals as not all impulses conducted and reach AVN at different rates
  • When conducted, normal - normal QRS
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15
Q

What are the variations of atrial fibrillation?

A
  • Slow: ventricular response <60 bpm
  • Fast: ventricular response > 100 bpm
  • Normal: 61-99 bpm
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16
Q

What is coarse fibrillation?*

A

Amplitude >0.5 mm. Can appear as if there are some P waves

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17
Q

What is fine fibrillation?*

A

Amplitude < 0.5 mm. Closer to isoelectric baseline in appearance than coarse.

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18
Q

Why are individuals with AFib at a higher risk of ischaemic strokes?

A
  • Loss of atrial contraction leads to increased blood stasis (mainly left atrium)
  • Leads to small clots in LA
  • Clots can travel through aorta to the brain
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19
Q

What are ventricular ectopic contractions?*

A
  • Occur due to ectopic foci in the ventricles that provide abnormal conduction pathways
  • Impulse does not spread via the His-Purkinje system
  • Slower depolarisation = wide QRS
  • May be asymptomatic
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20
Q

What is ventricular tachycardia?*

A
  • 3 or more consecutive premature ventricular contractions
  • Broad complex tachycardia
  • High risk progression to Vfib
  • Requires urgent treatment
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21
Q

What is ventricular fibrillation?*

A

MEDICAL EMERGENCY

  • Abnormal. chaotic and fast ventricular depolarisation
  • Impulses from many ventricular ectopic sites
  • No coordinated contraction
  • Ventricles quiver
  • No cardiac output
  • May lead to cardiac arrest if untreated
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22
Q

How are arrhythmias classified?*

A

SLIDE 20!

23
Q

How to look at ECG changes when ischaemia and myocardial infarction are present?

A
  • Must look at the PQRST of all 12 leads
  • Changes will be seen in leads facing the affected area
  • Must know which leads look at which part of the heart
24
Q

What leads face the inferior surface of ventricles?

A

II
III
aVF

25
Q

What leads face the septum and anterior surface of ventricles?

A

V1
V2
V3
V4

26
Q

What leads face the right ventricle and septum?

A

V1
V2
aVR

27
Q

What leads face the apex and anterior surface of the ventricles?

A

V3

V4

28
Q

What leads face the lateral surface of the ventricle?*

A

I
aVL
V5
V6

29
Q

What is ischaemia?

A

Lack of oxygen without muscle necrosis (blood tests will be negative for markers of necrosis, such as cardiac troponins)

30
Q

What are differences in myocardial infarction?

A
  • Muscle necrosis present (cardiac troponins in blood)
  • STEMI - ST elevation myocardial infarction that affects the full thickness of the cardiac wall
  • Non-STEMI - no ST elevation
31
Q

What is a ST Elevation Myocardial Infarction (STEMI)?*

A
  • Injury causing ST elevation in leads facing the affected area
  • Complete occlusion of coronary artery
  • Full thickness of myocardium involved
32
Q

What ECG changes are seen on a STEMI?*

A
  • ST elevation

- Positive deflection as abnormal current going through damaged tissue and coming towards the electrode

33
Q

What are the EVOLVING ECG changes in a STEMI?*

A

Acute: ST elevation
Hours: smaller R wave, Q wave begins
Day 1-2: T wave inversion, deeper Q wave
Weeks later: ST & T normal but Q wave persists

34
Q

What causes big pathological Q waves?

A
  • No electrical activity, action potential or current present in the dead tissue
  • ECG looks through the dead tissue and will pick up electrical forces from the OPPOSITE SIDE of the infarcted heart
  • Small Q waves represent normal left-to-right depolarisation in LATERAL leads
35
Q

What else can lead to q waves?*

A

PULMONARY EMBOLISM

  • S wave in lead 1
  • Q wave in lead 3
  • Inverted T wave in lead 3
36
Q

What defines a pathological Q wave?*

A
  • More than 1 small square wide
  • More than 2 small squares deep
  • Deeper than 1/4 of height of R wave
37
Q

How do you differentiate from acute angina from non-STEMI?

A

Do blood tests for myocyte necrosis (Troponin I + T)

38
Q

What changes are seen in non-STEMIs and ischaemia?*

A
  • ST segment depression
  • T wave inversion
  • Damage tissue AWAY from electrode
39
Q

What is a non-STEMI?

A
  • Supply to the heart NOT completely blocked
  • Smaller part of heart damaged
  • May progress to STEMI if not treated
40
Q

Where is T wave inversion present?

A
  • Unstable angina

- non-STEMI

41
Q

What is the definition of pathologic T wave?

A
  • Symmetrical

- Deep (>3mm)

42
Q

What artery supplies the inferior heart wall?

A
  • Right coronary artery

- via Posterior descending artery

43
Q

Where would ischaemia secondary to atherosclerosis in RCA lead to changes?*

A

Leads facing inferior heart (II, III, aVF)

44
Q

What changes are seen on the ECG in stable angina?

A
  • ST depression and down-sloping during exercise due to atherosclerotic plaque causing narrowing
  • Changes will REVERSE at rest
45
Q

What is stable angina?

A

Pain that develops when the vessel is unable to dilate enough to meet myocardial demand due to an atherosclerotic plaque

46
Q

What is unstable angina?

A

Atherosclerotic plaque rupture causes thrombus formation around the plaque, causing partial occlusion of vessels and causing pain even at rest

47
Q

Describe changes in anginas, STEMI and Non-STEMI.*

A

SLIDE 34!

48
Q

What is hypokalaemia and what are the signs and symptoms of it?

A

Potassium level below 3.5 mmol/L

  • Decreased potassium = myocardial hyperexcitability
  • Generalised muscle weakness
  • Respiratory depression
  • Ascending paralysis
  • Arrhythmia/cardiac arrest
  • Constipation
49
Q

How does hypokalaemia present on an ECG?*

A
  • Peaked P waves
  • T wave flattening and inversion
  • U wave
50
Q

What is hyperkalaemia and what are the problems with it?

A

Potassium level above 5 mmol/L (problems usually develop at levels of 6.5 and above)

  • Resting membrane potential becomes less negative
  • Inactivates some voltage gated Na+ channels
  • Heart less excitable therefore conduction problems
51
Q

What can hyperkalaemia lead to?

A
  • Generalised muscle weakness
  • Respiratory depression
  • Ascending paralysis
  • Palpitations
  • Arrhythmia/cardiac arrest
52
Q

What is hyperkalaemia an indication for?

A

Emergency dialysis

53
Q

How can hyperkalaemia present?*

A
  • Tall, tented T waves (loss of atrial depolarisation)
  • Loss of P wave
  • Widening QRS
  • QRS widening to look like a sine wave

Cardiovascular System (11 decks)

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