L13: Interpreting ECGs, when things go wrong... Flashcards Preview

Semester 2 Cardiovascular System > L13: Interpreting ECGs, when things go wrong... > Flashcards

Flashcards in L13: Interpreting ECGs, when things go wrong... Deck (31)
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1
Q

What does normal sinus rhythm look like on ECG?

A

Lead 2 rhythm strip

  • Regular rhythm
  • Heart rate 60-100bpm
  • P waves present
  • P waves normal and upright
  • PR interval normal (3-5 little squares)
  • QRS complex follow P wave
  • QRS normal (3 small boxes)
  • QT interval corrected prolonged if >44small boxes
2
Q

What do we mean by atrioventricular conduction block?

A

Delay/ distrubtion of signals from atria to ventricles

3
Q

What are the different types of AV conduction block?

A

Three types

  • First degree
  • Second degree –> Mobitz Type 1 and 2
  • Third degree
4
Q

What causes heart block?

A

Degeneration with age
Acute myocardial ischemia
Medication
Valvular heart disease

5
Q

What is first degree heart block?

A

Conduction is slowed without skipping a beat

Prolonged PR interval (>0.20s) but always followed by QRS complex

6
Q

What is second degree heart block?

A

Two types
Mobitz Type 1 (Wenkebach)
- Sucessively prolonged PR interval followed by sudden drop in QRS complex
- Electrical signal not conducted through ventricles

Mobitz Type 2

  • PR interval always same normal length (0.12-0.20s) sudden drop in QRS complex
  • Atrial rhythm is regular
  • Ventricle rhythm is irregular
7
Q

What is third degree heart block?

A

AKA complete heart block
Atria and ventricles depolarise independently
Complete failure of AV conduction
Ventricle pacemaker takes over–> escape rhythm–> slow 20-40bpm
Too slow to maintain BP
Pacemaker required
No evidence of atrial impulse getting to ventricles

8
Q

What is bundle branch block?

A

Delayed conduction in the bundle branches
Can be right or left
Wider QRS complex–> ventricle depolarisation takes longer

9
Q

What are the different types of arrythmias that are possible?

A

Atria–> above the ventricles so are called supraventricular arrythmias
Can be in sinus node, atrium itself or AV node
Normal narrow QRS complex as depolarisation stays the same across the ventricle, usually increased HR

Ventricles–> Ventricular arrythmias
Wider QRS complex as ectopic pacemaker cells fire randomly –> risk of tipping into ventricular fibrillation

10
Q

What is atrial fibrillation?

A

Multiple areas in the atria fire at the same time–> multiple foci
Rapid chaotic impulses
Reach AV node but not all go through–> irregular rate
No P waves, just wavy or flat baseline–> depends on number of foci
Atria ‘quiver’ but don’t contract
When conducted ventricles contract normally so normal QRS complex

11
Q

What does atrial fibrillation look like on ECG?

A
Slow--> ventricle response <60bpm 
Fast--> ventricle response >100bpm
Normal--> 61-99bpm
Coarse fibrillation with amplitude >0.5mm
Fine fibrillation with amplitude <0.5mm
Irregularly iregular HR and pulse
12
Q

What does loss of contraction in atrial fibrillation lead to?

A

Increase blood stasis–> pooling–> blood clots

Stasis most evident in LA–> risk of stroke

13
Q

What is premature ventricular ectopic beats (contraction) PVCs?

A

Ectopic focus in ventricle muscles
Impulse does not spread via fast His- Purkinje fibres
Slower depolaristaion –> Wider QRS complex
Premature–> earlier than expected for next sinus impulse
Assymptomatic or can feel palpitation with out haemodynamic consequence
Risk–> develop into ventricular tachycardia

14
Q

What is ventricular tachycardia?

A

Run of more then 3 consecutive premature ventricular ectopic beats (contractions)
Complex tachycardia
Dangerous rhythm require urgent treatment
High risk progression to ventricular fibrillation

15
Q

What is ventricular fibrillation?

A

Abnormal, chaotic fast ventricular depolarisation
Ectopic sites
No coordinated contraction
Ventricle ‘quiver’ but no contraction
No cardiac output if sustained–> cardiac arrest

16
Q

What is the general classification of arrythmias?

A

Brachycardia (slows heart down) or tachycardia (speeds heart up)
AF can fall into either category

17
Q

What are the ECG changes in ischaemia and myocardial infarction?

A

Depends on location of occlusion

And area supplied by that BV

18
Q

What is ischemia?

A

Lack of O2 but no necrosis

Blood test negative for markers of necrosis

19
Q

What is myocardial infarction?

A

Occlusion of blood supply
Results in area of necrosis
Markers of necrosis will be present

20
Q

What is STEMI?

A
ST elevated myocardial infarction 
Occlusion of coronary artery 
Full thickness of myocardium involved
ST elevation (reason unknown)
Behaves as if current coming towards electrode resulting in upward deflection (abnormal)
Indication for intervention
21
Q

What is the ECG like a few weeks after STEMI?

A

Fibrous tissue–> doesn’t conduct electrical impulse
ST and T wave normal
Q wave persists –> remains deep

22
Q

What does the pathological deep Q wave persist after STEMI?

A

Myocardium can’t conduct electricity–> fibrous
Living cells needed for depolarisation
ECG looks ‘through’ dead tissue and picks up signal from the other side of the heart
(Q waves not always pathological–> normal L-R depolarisation)

23
Q

Are all Q waves a sign of old infarct or depolarisation of septum?

A
Pulmonary embolism can causes Q wave in Lead III
Along with:
--> S wave in Lead I
--> Q wave Lead III
--> Inverted T wave in Lead III
24
Q

What are the difference between non-STEMI and ischemia?

A

No myocardial damage in angina (ischaemia)
Non-STEMI–> acute myocardial damage but not full thickness
Differentiated by blood test for necrosis–> troponin

25
Q

What changes occur in non-STEMI and ischemia?

A

Same ECG for Non-STEMI and Ishcemia
ST segment depression and T wave inversion
Abnormal current traversing damage tissue goes away from the electrode

26
Q

How can you tell T wave inversion is pathological?

A

Normally upright in all ECG Leads (except aVR and V1)
Inversion usually symmetrical and deep
T wave inversion is consistent with anatomical region supplied by the occluded coronary artery
e.g. occlusion in RCA–> T wave inversion in Leads II, III, and aVF

27
Q

What ECG changes are seen in stable angina?

A

ST depression during exercise
Changes go away with rest
Exercise: treadmill (exercise stress test) or chemically induced (Dobutamine stress test)

28
Q

What is hypokalaemia? What are the signs and symptoms?

A
Potassium level <3.5mmol/L
Moderate <3.0mmol/L
Severe <2.5mmol/L
Decreased extracellular K+--> myocardial hyperexcitability 
Generalised muscle weakness
Respiratory depression 
Ascending paralysis
Ileus, constipation
Palpitations, arrhythmia and cardiac arrest
29
Q

What does an ECG of hypokalaemia look like?

A

Peaked P waves
T waves flattening and inversion
U waves–> downwards deflection on ECG after QRS complex

30
Q

What is hyperkalaemia? What happens? What are the signs and symptoms?

A
K+ above >5mmol/L
Problems arise at 6.5- 7mmol/L
Resting membrane potential becomes less negative
Some Na+ channels inactivated
Heart becomes less excitable
Conduction problems occur
Generalise muscle weakness
Respiratory depression 
Ascending paralysis
Palpitations, Arrhythmia and cardiac arrest
31
Q

What does an ECG of someone with hyperkalaemia look like?

A

5.5-6.5–> Tall tented T waves
6.5-7.5–> Loss of P waves
7.5-8.5–> Widening QRS complex–> not conducting normally through the ventricles
>8.5–> QRS continues to widen, sine wave appearance–> not depolarising and repolarising properly