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
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.
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
- 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