ECG2 Flashcards

1
Q

What is AV conduction blocks and what are the causes and types?

A

• Delay /Failure of conduction of impulses from atrium to ventricles
via AV node and bundle of His

  • Causes
  • Acute myocardial infarction - can be transient
  • Degenerative changes - as people age
• 3 types:
• First degree heart block
• Second degree heart block
  - Mobitz type 1 
  - Mobitz type 2
• Third degree heart block (Complete Heart Block)
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2
Q

What is 1st degree heart block?

A

PR interval prolonged >0.2 seconds (5 small boxes)
On it own - not going to cause any haemodynamic upset - pulse rate the same - but can be picked up on ECG -
May occur after someone who didnt have it had MI - may develop 2nd/3rd degree later

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3
Q

What is 2nd degree heart block –

Mobitz type 1

A

Also called Wenkebach type
Successively longer PR intervals until one QRS dropped - av node has time to recover
Then cycle starts again
On its own relatively benign
But may go on to get 3rd degree after MI - not high risk otherwise though

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4
Q

What is 2nd degree heart block –

Mobitz type II

A

PR intervals do not lengthen, but suddenly dropped QRS complex
High risk of progression to complete heart block
Would feel gap between pulse - realise miss beat
Dangerous - high risk onto progression onto 3rd degree

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5
Q

What is 3rd degree heart block?

A

Complete failure of atrioventricular conduction
Atria ad ventricles depolarising independently
SAN depolarising at usual rate - atria contraction and p wave the same
P waves at regular intervals - put they are not being conducted
Then after a while…
• Ventricular pacemaker takes over (Ventricular escape rhythm)
• Usually wide QRS complexes
• Ventricular Rate is very slow (~30 - 40 bpm), often too slow to maintain BP
• Urgent pacemaker insertion usually required
Ventricular beat arising from ventricular muscle - finding its way in an abnormal pathway - slower than his-purkynje system

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6
Q

What are the characteristics seen in a 3rd degree heart block ECG

A

P – P intervals constant and about about 93 pbm
R – R intervals constant but much slower (about 37 bpm)
No relationship between P waves and QRS complexes (the P-R interval completely variable from beat to beat)

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7
Q

Where may abnormal rhythms arise from?

A

Sinus node, atrium, av node, these are also called supraventricular rhythms - arise above the ventricle

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8
Q

What is the difference between supraventricular rhythms and ventricular rhythms

A

Supra - narrow qrs complexes
No matter where a neat arises feom (SAN, AVN or ectopic atrial foci) it will in each case follow the same normal pathway across the ventricles - normal QRS

Ventricular - wide and bizarre qrs complexes
Rhythms originating in ventricle - ventricular pathway abnormal and the ventricular complex is wide and bizarre

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9
Q

What is atrial fibrilation?

A

Is a Supra ventricular rhythm
• Rhythm arises from multiple atrial foci - random depolarisation
• rapid, chaotic impulses
• no p waves, just wavy baseline bc no orderly conduction
• Impulses reach AV node at rapid irregular rate - 300/min
• Not all are conducted (because of AV node refractory period)
• When conducted, ventricles depolarise normally
• Therefore, narrow (normal shape) QRS complexes with irregular R-R intervals

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10
Q

What are the haemodynamic effects of atrial fibrillation?

A
  • Atrial contraction lost, (they just quiver)
  • Ventricles contract normally (but irregular rate)
  • Heart rate and pulse irregular
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11
Q

What are ventricular ectopic beats?

A

Sudden venricular beat coming through in the middle of sinus rhythm
No p wave but wide QRS
• Ectopic focus in ventricle muscle
• Impulse does not spread via the fast His -purkinje system
Therefore much slower depolarisation of ventricular muscle
See slide for ecg

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12
Q

What is ventricular tachycardia?

A

• Run of ≥ 3 consecutive ventricular ectopics is defined as Ventricular Tachycardia (VT)
• VT is a broad complex tachycardia
• Persistent VT is a dangerous rhythm – needs urgent treatment
• High risk of Ventricular fibrillation - causes cardiac arrest
See slide for ecg

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13
Q

What is ventricular fibrillation?

A

Multiple foci - spontaneously depolarising
• Abnormal, chaotic, fast, ventricular depolarisation
• impulses from numerous ectopic sites in ventricular muscle
• No co-ordinated contraction
• Ventricles quiver
• No cardiac output
• Cardiac arrest
Irregular pattern on ecg - see slide

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14
Q

What are the ECG changes of ischaemia and MI?

A
  • Coronary artery occlusion -> ischaemia or infarction (necrosis) in area supplied by artery.
  • Changes seen in leads facing affected area of ventricle
  • Need to look at P-QRST in all 12 leads
  • Need to know which groups of leads look at different parts of the heart
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15
Q

What does partial narrowing/complete occlusion of the lumen cause?

A

Myocardial ischaemia & Infarction
• Reduced perfusion
• due to narrowed coronary artery/ies

Partial narrowing of lumen causes:
• Sub endocardial ischaemia /injury
- this area is furthest away from coronary arteries which lie on the surface of heart (Part affected first = myocardium under endocardium = last part to get supplied
– hence most vulnerable region, involved first

Complete occlusion of lumen causes:
• full thickness (trans mural) injury
• including sub-epicardial region

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16
Q

What is STEMI?

A

ST segment Elevation Myocardial Infarction (STEMI)
• Due to complete occlusion of coronary artery by thrombus
• ‘full thickness’ of myocardium involved
• Sub epicardial injury causes ST segment elevation in leads facing affected area - Electrodes facing the damaged myocardium usually show elevation of ST segment

17
Q

What is ST elevation?

A

-Behaves as if abnormal current coming towards injured epicardium during repolarisation
• ST elevation is the earliest sign of a STEMI
• Diagnostic of STEMI (some criteria need to be fulfilled)
• Indication for urgent re-perfusion (to prevent/minimise muscle necrosis)
Open arteries q/ stent/balloons - prevent from necrosis by restoring perfusion a

18
Q

In which leads is ST elevation seen in?

A

ST elevation in II, III, AVF, and a little bit in V6

19
Q

What are the evolving changes seen in STEMI?

A

Acute - ST elevation
Hours - ST elevation, low R wave, Q wave begins
Day 1-2 - T wave inversion, Q wave deeper
Days later - ST normalises, T wave inverted
Weeks - ST and T normal, Q wave persists

20
Q

What are the ECG hangers seen in non-STEMI and ischaemia?

A
  • ECG changes due to Sub endocardial injury:

* ST segment depression & T wave inversion

21
Q

What are the changes seen in severe ischaemia?

A

Severe ischaemia: changes present in resting ECG Same ECG changes seen in both:
• Unstable Angina (UA) &
• Non ST elevation Myocardial infarction (NSTEMI)

T wave inversion or ST depression - weeks later - STand T normal, no Q waves

UA & NSTEMI are
Differentiated by a blood test
for evidence of myocyte
necrosis  (e.g. cardiac
troponin)
22
Q

What are the ECG changes in hyperkalaemia?

A

• Resting Membrane Potential is less negative,
• This inactivates some voltage gated Na+ channels
• Heart becomes less excitable
• Conduction problems occur
Normal

With increasing potassium level.....
Tall, peaked T wave – earliest sign
Tall, peaked T wave Flattened p wave; prolonged PR interval
Tall, peaked T wave Absent p waves – atrial standstill widened QRS
widened QRS
ST segment merges with T wave
To give “sine wave pattern”
SEE SLIDE FOR ECG
23
Q

What are the ECG changes in hypokalaemia?

A

With decreasing level….
3.5 - Low T wave
3 - High U wave
2.5 - Low ST segment

24
Q

What should be noted when reporting an ECG

A
  • Rhythm
  • Rate
  • PR interval
  • QRS interval
  • QT interval
  • P wave (LA or RA enlargement)
  • Description of QRS complex
  • ST segment
  • T wave
  • Axis
26
Q

What is sinus tachycardia

A

Sinus Tachycardia: sinus rhythm with rate > 100 bpm

27
Q

What is sinus bradycardia

A

Sinus Bradycardia: sinus rhythm with rate < 60 bpm

28
Q

What is bundle branch block

A

Delayed conduction in the branches of the bundle of HIs
P wave and PR interval normal
Wide QRS couples >3 small squares since depolarisation takes longer
Whichever bundle branch blocked - impulse travels through muscle which is slower than HIs-purkyje system