CVS Session 7 - Interpreting the ECG Flashcards Preview

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Flashcards in CVS Session 7 - Interpreting the ECG Deck (25):

What are the causes for abnormal rhythms?

- Abnormal impulse formation 

- Abnormal conduction (e.g. AV conduction blocks)


What are the two types of rhythms?

- Supraventricular rhythms; arise from:

I. Sinus node


III. AV node

- Ventricular rhythms 


Outline supraventricular rhythms. 

- Conducted into and within ventricles by His-Purkinje system

- Normal ventricular depolarisation

- Normal (narrow) QRS complexes


Outline ventricular rhythms.

- From a focus/foci in ventricle

- Conduction not via usual His-Purkinje system

- Depolarisation takes longer

- Wide (> 3 small boxes) & bizarre QRS complexes

- Rhythms from different foci will have different shapes

- Could be:

I.Ventricular premature beats

II.Ventricular tachycardia

III. Ventricular fibrillation


What is the significance of the variation in the P wave and QRS complex according to the origin of the impulse. 

It allows us to diagnose the arrhythmia.


Outline Ventricular tachycardia.

- Run of ≥ 3 consecutive ventricular ectopics is defined as VT

- VT is a broad complex tachycardia

- Persistent VT is a dangerous rhythm – needs urgent treatment

- High risk of Ventricular fibrillation


Outline Atrial fibrillation 

- Multiple atrial foci impulses chaotic

- Atrial depolarisation chaotic – no p waves, just wavy baseline

- Atria quiver rather than contract

- Impulses arrive at AVN at rapid irregular rate

- Only some conducted to ventricles (at regular intervals)

- When AVN not refractory

- Ventricles depolarise and contract normally

- Pulse and heart rate irregularly irregular


Outline Ventricular fibrillation. 

- Abnormal, chaotic, fast, ventricular depolarisation

- Impulses from numerous ectopic sites in ventricular muscle

- No co-ordinated contraction

- Ventricles quiver

- No cardiac output

- Cardiac arrest


What are AV conduction blocks? 

- Delay/ Failure of conduction impulses atrium to ventricles via AVN and bundle of His.


- Causes:

I. Acute myocardial infarction – commonest

II. Degenerative changes


- Three types:

I. First degree heart block

II. Second degree heart block (Mobitz type 1 and Mobitz type 2)

III. Third degree heart block aka Complete Heart Block (CHB)


- In CHB, a pacemaker in the ventricle will take over (Ventricular Escape rhythm)



Outline first degree heart block (10 HB)

- P wave normal

- Slow conduction in AVN and His bundle

- PR interval prolong > 5 small squares

- QRS normal


Outline second degree heart block (20 HB)

- Mobitz type 1 (aka Wenkebach phenomenon)

I. Progressive lengthening of PR interval

II. Until one P is not conducted (this allows time for AVN to recover),

III. Then cycle begins again


- Mobitz type 2 

I. PR interval normal 
II. Sudden non-conduction of a beat 
III. Dropped QRS
IV. High risk of progression to complete heart block


Outline third degree heart block (CHB)

- Atrial depolarisation normal

- But, impulses not conducted to ventricle

- Ventricular pacemaker takes over (ventricular escape rhythm)

- Rate is very slow (~30 -40 bpm)

- Usually wide QRS complexes

- HR often too slow to maintain BP and perfusion

- Urgent pacemaker insertion required


Describe the ECG changes of ischaemia and myocardial infarction 

- Due to reduced perfusion of myocardium

- Does not affect all parts of the heart

- Changes seen in leads facing affected area

- Need to look at P-QRST in all 12 leads

- Need to know which groups of leads look at different parts of the heart?


In ECG changes associated with ischaemia and myocardial infarction, what is the problem? 

- Reduced  myocardial perfusion due to coronary atherosclerosis

- Major coronary arteries lie on epicardial surface

- Sub endocardial muscle is furthest away & most vulnerable

- Flow is during diastole

- If diastole is short (at rapid HR) less time for blood flow (eg exercise)


- Sub endocardial region is most vulnerable

- Leads facing affected area show:

I. ST segment depression

II. T wave inversion

- Due to abnormal current during repolarisation

- Many theories (do not need to know)

- Ischaemic ECG changes may only be seen during exercise, but, if severe reduction of lumen:  ischaemic changes at rest


Outline STEMI.

- ST segment elevation Myocardial infarction (STEMI)

- Due to complete occlusion of lumen by thrombus

- Muscle injury extends ‘full thickness’ from endocardium to epicardium

- Epicardial injury: ST segment elevation in leads facing area

- Abnormal current during repolarisation

- If perfusion not re-established, muscle necrosis will follow



Outline the evolving changes in an ST segment elevation MI


Outline Acute STEMI

- Earliest change: ST elevation in leads facing MI

- Marked ST segment elevation in V2 – V4, less marked in I, aVL, V5 & V6

- Elevated ST segment merges with tall broad T waves


How do we identify pathological Q waves?

- > 1 small square (> 0.04 seconds)

- > 2 small squares (> 2mm) deep

- Depth more than 1/4 of the height of subsequent R wave  


Outline the ECG changes due to potassium abnormalities 

- ECF Potassium level affects the resting membrane potential

- Hyperkalaemia: RMP less negative (more depolarised)

- Hypokalaemia: RMP more negative (hyper polarised)


Outline the ECG changes with hyperkalaemia.


Outline the ECG changes with hypokalaemia.


How does one attempt to interpret the rhythm?

- Look at the ‘rhythm strip’ at the bottom of 12 lead ECG

- A long (approx. 10 second) recording of limb lead II

- Lead II – usually best for looking at ‘p’ waves

- Some machines record Lead II, V1 and V5 rhythm strips.


What are ventricular ectopic beats?

- Ectopic focus in ventricle muscle

- Impulse not spread via the fast His-purkinje system

- Therefore, much slower depolarisation of ventricle

- Therefore, the QRS complex, different in shape to usual QRS


Compare and contrast Ventricular and Atrial Fibrillation.


Outline the localisation of MI using the ECG