ECG Flashcards
How does each component of the ECG trace form (lead II view?)?
P wave: atrial depolarisation
- small (little muscle)
- upwards (moving towards electrode)
Q wave: septal depolarisation
- small (not moving directly away from electrode)
- downwards (moving away from electrode)
R wave: main ventricular depolarisation
- large (lots of muscle & moving directly away from electrode)
- upwards (moving towards electrode)
S wave: end ventricular depolarisation
- small compared to baseline (not moving directly away from electrode)
- downwards (moving away)
T wave: ventricular repolarisation
- medium (timing of repolarisation of different cells is dispersed)
- upwards (moving away from electrode but repolarisation)
note: atrial repolarisation is lost in the QRS complex
What does the amplitude of a signal depend on? What does the direction of the signal depend on?
Amplitude of signal:
How much the muscle is depolarising and how directly towards the electrode the excitation is moving (vector angle)
Direction of signal:
DEPOLARISATION: towards an electrode (upwards) & away from an electrode (downwards)
REPOLARISATION: towards an electrode (downwards) & away from an electrode (upwards)
What do amplifiers do?
Input from one positive electrode & one negative electrode
Negative input inverted (effectively moves electrode to the opposite side of the heart) and added to positive input, then amplified
Allows small electrical potentials to be visualised
How does each lead view the heart?
LEAD I = views left side
LEAD II = views towards apex
LEAD III = views bottom of the heart
What do augmented leads do?
2 negative electrodes connected
Convert two negative inputs into one and then invert
Combine with positive input
2:1 ratio favours negative electrodes so that the negative electrodes have a greater effect on single electrode view than positive
What are the components of a 12-lead ECG?
- leads I, II, & III
- augmented leads: aVR, aVL, aVF (+ one ground neutral)
- chest leads: V1-V6
Where are the different chest leads positioned?
V1 = 4th ICS, right sternal edge V2 = 4th ICS, left sternal edge V3 = halfway between V2 & V4 V4 = 5th ICS, mid-clavicular line V5 = horizontal to V4, anterior axillary line V6 = horizontal to V4, mid-axillary line
What are some important qualities to look for in an ECG?
Rate: use lead II (“rhythm strip”) (calculate by 300/no. of squares)
Rhythm: choose lead with relevant components
- is rhythm regular or irregular?
- is rhythm regularly irregular or irregularly irregular?
- relationship between atrial & ventricular depolarisation?
P wave: absent in AF
PR interval:
- prolonged in 1st degree heart block
- erratic in 2nd degree heart block
- no relationship between P wave and QRS complex in 3rd degree heart block
QRS complex:
- look at lead with smallest, most eqiphasic deflection
- lengthened in bundle branch block
Describe the features of atrial fibrillation on an ECG. Why do the ventricles contract irregularly?
Irregular rhythm (non-functioning SAN so AVN takes over)
—-> chaotic atrial depolarisation
Absent P wave
Increased frequency between QRS complexes
Irregular rhythm of QRS complexes
++++???? (shallow T wave?)
Ventricles contract irregularly due to AVN being bombarded by depolarisation waves of varying strength
Describe the features of first degree heart block on an ECG. What can it be caused by?
Delay somewhere along conduction pathway between SAN and AVN
—-> prolonged P-R interval
- IHD
- electrolyte imbalances
- digoxin toxicity
Describe the features of second degree heart block. What can it be caused by?
Intermittent failure of conduction through AVN or bundle of His (erratic P-R interval)
- progressive lengthening of P-R interval until failure of conduction of an atrial beat —> conducted beat with shorter P-R interval (repeated cycle)
OR: - most beats conducted have a constant P-R interval, but sometimes there is atrial depolarisation without subsequent ventricular depolarisation (Mobitz Type II)
OR: - alternate conducted and non-conducted beats in ratios 2:1, 3:1, or 4:1 conduction velocities
Same causes as 1st degree heart block
Describe the features of third degree heart block. What causes this?
Not all of the SAN signals are conducted to the ventricles e.g. after MI, fibrosis around bundle of His
Ventricles depolarised by ventricular nodes (which are slower than the SAN)
P waves not followed by the QRS complex; QRS complexes have extra P waves in them (depolarisation has a ventricular focus instead of SAN & AVN)
Describe the features of bundle branch block.
Damage to conducting pathways in ventricles alters the route of spread/timing of conduction
Changes shape of QRS complex (usually lengthens due to delay in depolarisation)
Describe the features of MI on an ECG.
Ischaemic injury -> injury currents generated (extra signals in ST segment/ST depression???)
Infarction injury -> injury currents generated (ST elevation)
- ST elevation (acute injury)
- pathological Q waves (fibrotic tissue cannot conduct - remain long term) (necrosis)
- inverted T waves (ischaemia)
What causes the delay between the P wave and the QRS complex?
Delay of 120ms at AVN
