ECG Pathologies Flashcards
What are the 2 ways by which arrhythmias can arise?
Re-entry loops
Ectopic pacemaker
How can you tell if the depolarisation is travelling via the normal conducting pathway or if it is a ventricular ectopic?
The width of the QRS complex
Broad = ventricular ectopic
What are re-entry loops?
Damage to the conducting myocardium causes a unidirectional conduction block
Impulses can only travel via the 1 way and end up not cancelling out so the impulse travels retrogradely back through the damaged tissue forming a continuous loop
What can AV node re entry loops cause?
Supra-ventricular tachycardia
What can atrioventricular re-entry lead to?
An accessory pathway between atria and ventricles leading to a re-entry loop like in Wolff-Parkinson-White syndrome
What can causes atrial tachycardia?
How does it appear on ECG?
Digoxin
Ischaemic heart disease
Rheumatic heart disease
Tachycardia and P and T waves can merge together
What causes atrial flutter?
Re-entry loop in Atria
What is an example of a type of Atrial Flutter?
How does it appear on an ECG?
2:1 AV block
2 atrial contractions per 1 ventricular contraction
2 p waves before a QRS complex
What is Atrial Fibrillation?
How does it appear on ECG?
What problem is commonly associated with AFib?
Irregularly irregular impulses in atria
Causes irregular R-R intervals but normal shaped QRS complexes
Stasis of blood in atria, leading to formation of thrombus leading to embolism (high risk in left atrium due to structure of left oracle)
What can ventricular tachycardia degenerate into?
Ventricular fibrillation
What causes ventricular fibrillation?
What is bad about VF?
Multiple (3) ectopic foci in ventricles
Severely reduced Cardiac Output leading to cardiac arrest
What is Torsades de Pointes?
How is it treated?
Polymorphic ventricular tachycardia meaning the QRS complex’s are all very different in the Ventricular fibrillation
There’s twisting around the axis
Treated with Mg
What is First Degree AV block (heart block)?
How does it appear on ECG?
Delayed conduction through the AV node causing a consistently prolonged PR interval (>5small boxes)
What are the 2 types of Second Degree AV block?
Mobitz type I
Mobitz type II
What is Mobitz type I second degree AV block?
PR interval gets progressively longer until one of the QRS complexes gets dropped
Then PR interval back to normal then cycle continues
What is Mobitz type II second degree AV block?
PR interval is normal and constant but occasionally P wave not conducted so a QRS gets dropped
What is Third Degree AV block?
When no impulses are transmitted between the atria and ventricles so they work independently to each other (no relationship between P waves and QRS complexes)
In Third degree heart block how is blood pressure and heart rate affected and why?
They are both reduced
The escape rhythm produced by the ventricular pacemaker depolarises much slower
What is a pathological Q wave?
Where are pathological Q waves seen?
When the Q wave is more than 1 small box wide, more than 2 small boxes depp and more than a quarter of the depth of the R wave
A couple of hours after a STEMI
What is a STEMI?
Full thickness myocardial infarction caused by a full occlusion of a coronary artery
What ECG changes and investigations are seen with a STEMI?
ST elevation (acutely)
Pathological Q waves (after a few hours)
Raised Troponin I and T
T wave inversion after 1-2 days
What is a NSTEMI?
Partial thickness MI as a result of a coronary artery being almost completely occluded
What ECG changes and investigations are seen with a NSTEMI?
ST depression or T wave inversion
Raised Troponin I and T
What affects does Hyperkalaemia have on the heart?
How does it appear on an ECG?
RMP now less negative
So always partially depolarised
This inactivates some voltage gated Na+ channels so slower upstroke of ventricular AP and so slower heart rate
First tall peaked T waves
Tall peaked T wave, flattened P wave anad prolonged PR interval
Tall peaked T wave, absent P wave and a widened QRS
Widened QRS. The ST segment merges with the T wave causing a sine-wave pattern.
What affect does Hypokalaemia have on the heart?
How does it appear on an ECG?
Causes lengthen ventricular action potential (PR interval) delaying repolarisation
This can lead to early after depolarisations causing oscillations in membrane potential which can result in VF
First low T-wave
Then low T-wave and high U-wave
Then low T-wave, high U-wave and a low ST segment
What is Delayed afterdepolarisations?
What causes it?
When membrane spontaneously depolarises quickly after it repolarised
Usually happens when there’s a high intracellular calcium level
What is Early Afterdepolarisations?
What makes it more likely?
What can it lead to?
When membrane depolarises while it is repolarising
More likely with longer QT intervals
Consecutive EADs can result in VF
