ECG Flashcards
how is ECG recorded?
any pair of electrodes ( standard limb lead):
- SLL I = left arm from right arm
- SLL II = left leg from right arm
- SLL III = left leg from left arm
state the 3 basic principles (fast and slow events…):
- Fast events, e.g. depolarisation and repolarisation of the AP → transmitted well.
- Slow events, e.g. the plateau of the AP → not transmitted.
- A wave of approaching depolarisation causes an upward-going blip
describe the process of depolarisation and repolarisation in SLL II:
A wave of depolarisation approaching the left leg will cause a positive potential relative to the right arm.
a wave of depolarisation going away from the left leg will cause a negative potential relative to the right arm.
a wave of repolarisation approaching the left leg will cause a negative potential relative to the right arm.
a wave of repolarisation going away from the left leg will cause a positive potential relative to the right arm
state what the PR interval is and the conduction rate:
time from atrial depolarisation to ventricular depolarisation
- mainly due to transmission through the AV node
action potential transmitted very slowly = flat line
(delay box: 0.12 - 0.2 sec)
state what the QT interval is and the conduction rate:
the time for both ventricular depolarisation and repolarisation to occur
depends on the heart rate, but usually 0.42 sec at 60 bpm
state what the QRS complex is and the conduction rate:
time takes for the whole ventricle to depolarise
rapid conduction - Bundle of His & Purkinje Fibres
0.08 sec
describe the complexity of the QRS complex:
different parts of the ventricle depolarise at different times in different directions:
1st – the interventricular septum depolarises from left to right
2nd – the bulk of the ventricle depolarises from the endocardial to the epicardial surface
3rd – the upper part of the interventricular septum depolarises
why is atrial repolarisation not visible in an ECG?
atrial repolarisation coincides with ventricular depolarisation
ventricular depolarisation involves more tissue depolarising faster so it swamps any signal from atrial repolarisation
why is the T wave positive going?
the action potential is longer in endocardial cells than in epicardial cells, so the wave of repolarisation runs in the opposite direction to the wave of depolarisation
describe what augmented limb leads do:
they are amplified versions of the standard limb leads, providing better coverage of the heart’s electrical signals.
connecting two limbs together and measuring them against the other limb, gives you 3 other perspectives on events in the heart
why is the R wave bigger in SLL I than in SLL IIl?
the main vector of depolarisation is in line with the axis of recording from the left leg wrt the right arm
describe the role of precordial chest leads:
these leads are arranged in front of the heart and look at the same events but in the horizontal (or transverse) plane
define STEMI and NSTEMI:
STEMI = ST elevated myocardial infarction
NSTEMI = non-ST elevated myocardial infarction
STEMI is worse than NSTEMI
describe ventricular tachycardia:
this is when the electrical activity originates in the ventricles rather than the SA node
- broad QRS complex tachycardia.
- absence of any P-waves.
- heart rate will be fast as well.
the aVR reading in this lead is positive whereas in a normal ECG, it is always negative.
the patient could become haemodynamically unstable
describe ventricular fibrillation:
the patient will become haemodynamically unstable.
There are chaotic irregular deflections at a rate of up to 500 bpm.
The amplitude will decrease with time, all the way to asystole if defibrillation is not performed.
Can’t identify P, QRS, or T waves
describe atrial fibrillation:
irregularly irregular rhythm
this can be felt if you feel the patient’s pulse.
absence of any P-waves, just small fibrillations.
consider the risk of thromboembolism and consider giving warfarin
describe atrial flutter
different from atrial fibrillation:
- lots of P-waves in between each QRS complex.
- regularly spaced QRS complexes
These sawtooth P waves as opposed to atrial fibrillation:
- where there is a lack of P-waves
- small oscillations in the line between irregularly spaced QRS complexes.
describe first degree heart block
a delay in the depolarisation going through the AV node
elongated PR interval = longer than 200ms (5 small squares).
Sometimes if the PR elongation is longer than this, the P-wave can become buried in the T-wave of the previous beat
describe second degree AV heart block - mobitz 1 (wenkebach phenomenon)
cause: functional suppression of the AV node e.g. by drugs.
PR interval gets progressively longer until a QRS complex is actually skipped out.
describe second-degree heart block - mobitz 2
Here the block occurs below the AV node, in the His Purkinje system and is due to structural damage mostly e.g. infarction
The PR interval is constant but then one of the P waves will fail to conduct (indicated by the arrows).
Patients require pacemakers.
describe second-degree high grade/ 2:1 AV block
There are two p waves to every QRS.
Because we can only see one PR interval before there is a p wave that fails to conduct we cannot call it either Mobitz 1 or 2
and hence we don’t know if the block is at the AV node or below it.
describe third degree (complete) of heart block:
Here the impulses from the SA node are not being conducted through to the ventricles.
The AV node is firing slowly by itself causing the ventricles to contract. This is called escape rhythm.
There is no correlation between the P-waves and the QRS complexes and the rate of contraction of the ventricles is slow (roughly 40 bpm) but regular.
describe asystole:
there is a lack of any contraction in the ventricles and subsequently, there is a period of no electrical activity (flat line) on the ECG.
normally occurs from degeneration from ventricular fibrillation when the myocardium eventually runs out of energy and stops fibrillating altogether.
describe anterior myocardial infarction:
This happens due to occlusion of the left anterior descending coronary artery
This suggests that the MI has occurred in the anterolateral segment of the heart since the:
anterior leads V3 and 4 as well as the lateral leads V5 and 6 have the most marked elevation.
NOTE: there is also reciprocal ST depression in the inferior leads, mainly Ill and aVF.
describe lateral myocardial infarction:
Here branches of the left anterior descending and left circumflex arteries have been affected.
There is ST elevation in the lateral leads (I, avL, V5 and V6).
There is reciprocal ST depression in the inferior leads Ill and aVF
describe septal myocardial infarction:
ST elevation in leads V1 and V2 suggests a septal Ml.
However, there is also ST elevation in V3—6 so other areas of the heart are involved as well.
describe inferior myocardial infarction:
usually results from blockage of the right coronary artery.
Less commonly, it’s due to blockage of the left circumflex artery.
Because the SA node and AV nodes are supplied by the RCA, heart blocks are more common in inferior Mls.
There is ST elevation in the inferior leads (II, III, aVF) and there is reciprocal ST depression in lead I and aVL
