ECG2 Flashcards
What is AV conduction blocks and what are the causes and types?
• 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)
What is 1st degree heart block?
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
What is 2nd degree heart block –
Mobitz type 1
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
What is 2nd degree heart block –
Mobitz type II
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
What is 3rd degree heart block?
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
What are the characteristics seen in a 3rd degree heart block ECG
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)
Where may abnormal rhythms arise from?
Sinus node, atrium, av node, these are also called supraventricular rhythms - arise above the ventricle
What is the difference between supraventricular rhythms and ventricular rhythms
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
What is atrial fibrilation?
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
What are the haemodynamic effects of atrial fibrillation?
- Atrial contraction lost, (they just quiver)
- Ventricles contract normally (but irregular rate)
- Heart rate and pulse irregular
What are ventricular ectopic beats?
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
What is ventricular tachycardia?
• 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
What is ventricular fibrillation?
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
What are the ECG changes of ischaemia and MI?
- 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
What does partial narrowing/complete occlusion of the lumen cause?
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
What is STEMI?
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
What is ST elevation?
-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
In which leads is ST elevation seen in?
ST elevation in II, III, AVF, and a little bit in V6
What are the evolving changes seen in STEMI?
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
What are the ECG hangers seen in non-STEMI and ischaemia?
- ECG changes due to Sub endocardial injury:
* ST segment depression & T wave inversion
What are the changes seen in severe ischaemia?
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)
What are the ECG changes in hyperkalaemia?
• 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
What are the ECG changes in hypokalaemia?
With decreasing level….
3.5 - Low T wave
3 - High U wave
2.5 - Low ST segment
What should be noted when reporting an ECG
- Rhythm
- Rate
- PR interval
- QRS interval
- QT interval
- P wave (LA or RA enlargement)
- Description of QRS complex
- ST segment
- T wave
- Axis
What is sinus tachycardia
Sinus Tachycardia: sinus rhythm with rate > 100 bpm
What is sinus bradycardia
Sinus Bradycardia: sinus rhythm with rate < 60 bpm
What is bundle branch block
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
