Session 6 Interpreting ECGs Flashcards

(53 cards)

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?*

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?

25
What leads face the septum and anterior surface of ventricles?
V1 V2 V3 V4
26
What leads face the right ventricle and septum?
V1 V2 aVR
27
What leads face the apex and anterior surface of the ventricles?
V3 | V4
28
What leads face the lateral surface of the ventricle?*
I aVL V5 V6
29
What is ischaemia?
Lack of oxygen without muscle necrosis (blood tests will be negative for markers of necrosis, such as cardiac troponins)
30
What are differences in myocardial infarction?
- 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
What is a ST Elevation Myocardial Infarction (STEMI)?*
- Injury causing ST elevation in leads facing the affected area - Complete occlusion of coronary artery - Full thickness of myocardium involved
32
What ECG changes are seen on a STEMI?*
- ST elevation | - Positive deflection as abnormal current going through damaged tissue and coming towards the electrode
33
What are the EVOLVING ECG changes in a STEMI?*
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
What causes big pathological Q waves?
- 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
What else can lead to q waves?*
PULMONARY EMBOLISM - S wave in lead 1 - Q wave in lead 3 - Inverted T wave in lead 3
36
What defines a pathological Q wave?*
- More than 1 small square wide - More than 2 small squares deep - Deeper than 1/4 of height of R wave
37
How do you differentiate from acute angina from non-STEMI?
Do blood tests for myocyte necrosis (Troponin I + T)
38
What changes are seen in non-STEMIs and ischaemia?*
- ST segment depression - T wave inversion - Damage tissue AWAY from electrode
39
What is a non-STEMI?
- Supply to the heart NOT completely blocked - Smaller part of heart damaged - May progress to STEMI if not treated
40
Where is T wave inversion present?
- Unstable angina | - non-STEMI
41
What is the definition of pathologic T wave?
- Symmetrical | - Deep (>3mm)
42
What artery supplies the inferior heart wall?
- Right coronary artery | - via Posterior descending artery
43
Where would ischaemia secondary to atherosclerosis in RCA lead to changes?*
Leads facing inferior heart (II, III, aVF)
44
What changes are seen on the ECG in stable angina?
- ST depression and down-sloping during exercise due to atherosclerotic plaque causing narrowing - Changes will REVERSE at rest
45
What is stable angina?
Pain that develops when the vessel is unable to dilate enough to meet myocardial demand due to an atherosclerotic plaque
46
What is unstable angina?
Atherosclerotic plaque rupture causes thrombus formation around the plaque, causing partial occlusion of vessels and causing pain even at rest
47
Describe changes in anginas, STEMI and Non-STEMI.*
SLIDE 34!
48
What is hypokalaemia and what are the signs and symptoms of it?
Potassium level below 3.5 mmol/L - Decreased potassium = myocardial hyperexcitability - Generalised muscle weakness - Respiratory depression - Ascending paralysis - Arrhythmia/cardiac arrest - Constipation
49
How does hypokalaemia present on an ECG?*
- Peaked P waves - T wave flattening and inversion - U wave
50
What is hyperkalaemia and what are the problems with it?
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
What can hyperkalaemia lead to?
- Generalised muscle weakness - Respiratory depression - Ascending paralysis - Palpitations - Arrhythmia/cardiac arrest
52
What is hyperkalaemia an indication for?
Emergency dialysis
53
How can hyperkalaemia present?*
- Tall, tented T waves (loss of atrial depolarisation) - Loss of P wave - Widening QRS - QRS widening to look like a sine wave