Lecture 11 Flashcards
Fibrous ring
Dose connective tissue
4 - between atria and ventricles
Function:
Allows ventricles and atria to contract separately
Anchors the valves
Electrical insulator - bundle of His acts as passageway
Interventricular septum depolarisation
Left to right (left thicker)
P wave
Atrial depolarisation
PR interval
Start of P wave to start of Q wave
Beginning of atrial depolarisation to beginning of ventricular depolarisation
3-5 small boxes 0.12 - 0.2 seconds
Delay at AV node - isoelectric line
Bundle of His spread from atria to ventricles - isoelectric line
q wave
Depolarisation of the intervertebral septum (left to right)
Small downwards depolarisation - move obliquely away
R wave
Depolarisation of the free ventricular walls and apex
Large upwards deflection
S wave
Depolarisation spreads to ventricular bases
Downwards deflection
T wave
Ventricular repolarisation
From base to apex to positive electrode
Upwards deflection
No QRS complex
AV block - Heart block
QRS complex
Depolarisation of ventricles
ECG
10 electrodes - 4 limb 6 chest 12 views (leads)
C1 electrode
Right of sternum - Ruth intercostal space
C2 electrode
Midclavicular line - 4th intercostal space
C3 electrode
Halfway between V2 and V4
C4 electrode
Midclavicular line - 5th intercostal space
C5 electrode
Level with C4 at left anterior axillary line
C6 electrode
Level with C5 at left mid axillary line
V1 - V4
Antero-septal leads
LAD
V5-V6
Lateral leads
Circumflex
Leads for lateral left side of heart
Lead 1
V5-V6
AVL
Circumflex artery
Leads for inferior surface of heart
Lead II
Lead III
AVF
Right coronary artery
Right ventricle and septum
V1
V2
Apex and anterior surface of ventricles
V3 and V4
V1 relationship to v6
Inverse
Lead II relationship with AVR
Inverse
5 large squares
1 second
300 large squares
1 minute
1 small square
1/25
0.04 seconds
1 large square
1/5 - 0.2 seconds
1 cardiac cycle
P wave to p wave
QRS interval
Start of Q wave to end of S wave
Time takes for ventricular depolarisation
3 small boxes - 0.12 seconds
Widened QRS - depolarisation not via His-Perkinje fibres
QT interval
Time taken for depolarisation and repolarisation of ventricles
Beginning of Q wave to end of T wave
9- 11 small boxes - 0.44 seconds
ST interval
End of S to start of T
Isoelectric line
If raised or depressed - MI or ischaemia
Sinus rhythm
Regular rhythm HR = 60 - 100bpm P wave present PR interval - 3 - 5 small boxes QRS complex - 3 small boxes Every P wave followed by QRS complex
First degree heart block
Prolonged PR interval - 5+ small boxes
Delay in conductance between atria and ventricles via AV node and Bundle of His
Causes:
- acute MI (transient)
- fibrosis (permanent)
Second degree heart block mobitz type 1 (Wenkebach)
Successfully longer PR interval until 1 QRS complex dropped
Second degree heart block type 2
Sudden drop of QRS complex without PR interval elongation
High risk of progression to complete heart block
Prophylaxis pace maker
Third degree heart block
Complete failure of AV conduction
Atria and ventricles contract independently
Regular P waves
No steady PR interval
Ventricular escape rythmn - ventricular pacemaker takes over
Wide QRS complex - myocytes to myocytes spread
P-P interval and R-R interval have different rates
Urgent pacemaker required
Bundle branch block
Delayed conduction in the branches of the bundle of His
P wave and PR interval normal
Widened QRS complex as ventricular depolarisation takes longer
atrial Fibrillation
Supraventricular rhythms normal QRS complex - ventricle depolarisation intact. R-R interval intact Atrium - multiple atrial foci Rapid and Chaotic Wavy baseline - no P waves
Caused by multiple re-entrant circuits
Ventricular arrythmia
Arise from ventricles
Widened QRS
Ventricle tachycardia
Atrial fibrillation effect on haemodynamics
Atrial contraction lost - quiver
Ventricular contraction intact but irregular
Therefore:
Irregular heart rate
Irregular pulse
Ventricular tachycardia
3 + consecutive ventricular ectopics
Broad complex
Persistent VT is dangerous as can lead to ventricular fibrillation and cardiac arrest
Ventricular fibrillation
Fast, chaotic abnormal ventricular depolarisation
No coordinated contraction - quiver
No cardiac output
Cardiac arrest
Narrow QRS complex tachycardia
Sinus tachycardia
AF
Supraventricular tachycardia
Broad complex tachycardia
VF
VT
Bradycardia can lead to what?
Heart block
Simple bradycardia
STEMI
ST segment elevation - behaves as if abnormal current towards lead during repolarisation
Complete occlusion of coronary artery
complete myocardial thickness involved
Sub epicardium injury
Urgent reperfusion required
STEMI progression
- Ischaemia- ST elevation
- Injury - smaller R wave and deeper Q wave
- Necrosis - T wave inversion and Q wave deeper (2+ small squares)
Recovery - ST and T wave normalised
Q wave persists
Why is Q wave permanent
Necrosis of muscle causes no AP propagation so ECG leads look ‘through’ damaged area therefore more electrical forces from opposite side of lead
Non - STEMI
ST depression
T wave inversion
Sub endocardial injury
Differentiated by blood test
Differences between STEMI and Non - STEMI
ST depression
No pathological Q wave as no muscle necrosis
Similarities between STEMI and Non - STEMI
T wave inversion
Unstable angina
Stable angina
Pain during exercise - ST depression
Normal at rest
Hyperkalaemia ECG
Early:
Tall peaked T wave - stronger repolarisation
Flattened p wave - less excitable
Longer PR - atrial depolarisation decreases
Later:
Widened QRS
ST segment merges with T wave
Sine wave
Hypokalaemia
Low T waves - harder to repolarise
U wave
Low ST segment or depression
