ECG Pathologies Flashcards

1
Q

What are the 2 ways by which arrhythmias can arise?

A

Re-entry loops
Ectopic pacemaker

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2
Q

How can you tell if the depolarisation is travelling via the normal conducting pathway or if it is a ventricular ectopic?

A

The width of the QRS complex

Broad = ventricular ectopic

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3
Q

What are re-entry loops?

A

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

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4
Q

What can AV node re entry loops cause?

A

Supra-ventricular tachycardia

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5
Q

What can atrioventricular re-entry lead to?

A

An accessory pathway between atria and ventricles leading to a re-entry loop like in Wolff-Parkinson-White syndrome

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6
Q

What can causes atrial tachycardia?
How does it appear on ECG?

A

Digoxin
Ischaemic heart disease
Rheumatic heart disease

Tachycardia and P and T waves can merge together

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7
Q

What causes atrial flutter?

A

Re-entry loop in Atria

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8
Q

What is an example of a type of Atrial Flutter?

How does it appear on an ECG?

A

2:1 AV block
2 atrial contractions per 1 ventricular contraction

2 p waves before a QRS complex

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9
Q

What is Atrial Fibrillation?

How does it appear on ECG?

What problem is commonly associated with AFib?

A

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)

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10
Q

What can ventricular tachycardia degenerate into?

A

Ventricular fibrillation

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11
Q

What causes ventricular fibrillation?

What is bad about VF?

A

Multiple (3) ectopic foci in ventricles

Severely reduced Cardiac Output leading to cardiac arrest

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12
Q

What is Torsades de Pointes?

How is it treated?

A

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

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13
Q

What is First Degree AV block (heart block)?

How does it appear on ECG?

A

Delayed conduction through the AV node causing a consistently prolonged PR interval (>5small boxes)

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14
Q

What are the 2 types of Second Degree AV block?

A

Mobitz type I

Mobitz type II

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15
Q

What is Mobitz type I second degree AV block?

A

PR interval gets progressively longer until one of the QRS complexes gets dropped
Then PR interval back to normal then cycle continues

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16
Q

What is Mobitz type II second degree AV block?

A

PR interval is normal and constant but occasionally P wave not conducted so a QRS gets dropped

17
Q

What is Third Degree AV block?

A

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)

18
Q

In Third degree heart block how is blood pressure and heart rate affected and why?

A

They are both reduced

The escape rhythm produced by the ventricular pacemaker depolarises much slower

19
Q

What is a pathological Q wave?

Where are pathological Q waves seen?

A

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

20
Q

What is a STEMI?

A

Full thickness myocardial infarction caused by a full occlusion of a coronary artery

21
Q

What ECG changes and investigations are seen with a STEMI?

A

ST elevation (acutely)
Pathological Q waves (after a few hours)
Raised Troponin I and T
T wave inversion after 1-2 days

22
Q

What is a NSTEMI?

A

Partial thickness MI as a result of a coronary artery being almost completely occluded

23
Q

What ECG changes and investigations are seen with a NSTEMI?

A

ST depression or T wave inversion
Raised Troponin I and T

24
Q

What affects does Hyperkalaemia have on the heart?

How does it appear on an ECG?

A

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.

25
Q

What affect does Hypokalaemia have on the heart?

How does it appear on an ECG?

A

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

26
Q

What is Delayed afterdepolarisations?

What causes it?

A

When membrane spontaneously depolarises quickly after it repolarised

Usually happens when there’s a high intracellular calcium level

27
Q

What is Early Afterdepolarisations?

What makes it more likely?

What can it lead to?

A

When membrane depolarises while it is repolarising

More likely with longer QT intervals

Consecutive EADs can result in VF