ECG interpretations Flashcards
1
Q
what is the QT interval and why is it corrected for?
A
- QT interval is the time taken for depolarisation and repolarisation of ventricle.
- varies with heart rate so needs to be observed in relation to HR.
2
Q
what does prolonged QT indicate?
A
- usually 0.44-0.45 secs so, if longer than that suggests prolonged ventricular repolarisations associated with arrhythmias.
3
Q
name some characteristics of normal sinus rhythms.
A
- HR 60-100bpm.
- QRS preceded by normal P wave.
- PR constant.
- QRS < 100ms unless delay at interventricular spread.
4
Q
what is an atrioventricular conduction block?
A
- delay/failure of conduction of impulses from A–>V via ANV and BOH.
- first degree, second degree ( mobitz type 1,2 ), third degree heart block.
5
Q
what causes heart block?
A
- degeneration of electrical conduction system w/ age. ( sclerosis, fibrosis ) - acute myocardial ischaemia. - medication. - valvular heart disease.
6
Q
what is a first degree AV block?
A
- depolarisation from SAN spreads to ventricles, but delay in conduction resulting in lengthened PR.
- may be a sign of coronary artery disease etc.
7
Q
what is second degree block : mobitz type 1?
A
- lengthening of the PR intervals and then failure of conduction through to ventricles, resulting in lack of QRS and cycle starts again.
8
Q
what is second degree block : mobitz type 2?
A
- PR remains fairly constant with a sudden atrial depolarisation without subsequent ventricular depolarisation so no QRS.
- irregular ventricular rhythm which may progress to complete heart block.
9
Q
what is a third degree block?
URGENT PACEMAKER REQUIRED.
A
- complete failure of spread of conduction to ventricles causing ‘escape mechanism’ (ventricular pacemaker) to take over.
- 20 to 40bpm which is too slow to maintain BP.
- wide QRS.
10
Q
describe the effects of a bundle branch block.
A
- delay in conduction within bundle branches : RBBB or LBBB.
- P, PR normal.
- wide QRS as ventricular depolarisation delayed.
11
Q
what is a supra-ventricular arrhythmia?
A
- involves the atria.
- problem in SAN, AVN or atrium itself.
- usually concerns tachycardia and narrow QRS complexes.
12
Q
what can you see in atrial fibrillation?
A
- no distinct P waves just a wavy baseline.
- irregular R-R intervals.
- AVN receives impulses fast and irregularly from cardiac tissue.
- not all conducted.
- when conducted normal QRS.
13
Q
what are the ECG variations seen in Afib?
A
- HR can be fast (>100), slow (<60) or normal.
- irregularly irregular.
- coarse fibrillation or fine fibrillation.
14
Q
what are the haemodynamic effects of Afib?
A
- atria quiver, ventricle contraction normal.
- HR and pulse ‘irregularly irregular’
- increased blood stasis in atria as loss pf contraction.
- LA clots so risk of ischaemic stroke secondary to emboli as it may enter LV and systemic.
15
Q
what is PVC? ( premature ventricular ectopic contractions)
A
- impulse doesn’t spread via fast His-purkinje, so slower depolarisation of ventricle so wide QRS.
- abnormal contraction begins at ventricle premature to expected.
16
Q
what is ventricular Tachycardia?
A
- more than 3 consecutive PVC may cause.
- VTACH if persistent may progress to ventricular fibrillation.
- no adequate cardiac output.
17
Q
what is ventricular fibrillation?
A
- abnormal, chaotic ventricular depolarisation.
- impulses from numerous ectopic sited in ventricle.
- ventricles quiver, no cardiac output as no coordinated contraction.
- if sustained cardiac arrest!!
18
Q
define ischaemia.
A
- lack of perfusion but no muscle necrosis (infarction)
- blood tests negative for markers of myocyte necrosis like cardiac troponins.
19
Q
define myocardial infarction.
A
- muscle necrosis present, so blood test positive for cardiac troponins.
- STEMI or non-STEMI.
20
Q
what is a STEMI?
ST segment elevation myocardial infarction.
A
- complete occlusion of coronary artery causing ST elevation as impulse spread abnormal.
- depending on area of damage ECG from that view affected accordingly.
21
Q
in anterior cardiac wall necrosis what artery is affected?
A
- left anterior descending artery which carries almost 50% of blood for coronary circulation. ‘widow maker’
- V3 and V4 sees changes in ECG the most. V2 if septum involved.
22
Q
what does a normal Q wave suggest?
with that in mind, what would a pathological Q wave suggest?
A
- small Q waves show normal spread of left to right depolarisation on septum.
- deeper Q seen in leads 3, aVR and none from V1-V3.
- myocardial necrosis means no electrical activity in dead tissue, so no AP.
- In anterior wall MI a Q wave seen in V1-V2 abnormally.
23
Q
what other conditions may cause prominent Q waves?
A
- pulmonary embolism causes Q in lead 3.
24
Q
what is unstable angina?
A
- ST segment depression while the patient has pain caused by severe ischaemia.
25
what is non- STEMI?
- actual cardiac muscle damage occured but not of entire heart muscle wall.
26
what happens to ST segment at ischaemia/ non-STEMI?
- depression of ST as impulse transversing damaged tissue and moving away from recording electrode.
27
what happens to t wave at ischaemia/ non-STEMI?
- inversion of T wave due to Myocardial ischaemia or non-STEMI damage to area supplied by the coronary artery.
28
what is stable angina?
- ST depression during exercise due to coranary disease; atherosclerotic plaque focising on narrowing.
29
what are the cardiac implications in hypokalaemia?
- palpitations.
- arrhythmia.
- cardiac arrest.
30
what ECG changes can be observed in hypokalaemia?
- greater PR.
- T wave flattening and inversion.
- ST depression.
- U waves (repolarisation of purkinje)
31
what are the cardiac implications in hyperkaelemia?
- heart less excitable.
- palpitations.
- arrhythmias.
- cardiac arrest.
32
what ECG changes can be observed in hyperkaelemia?
- tall T waves.
- loss of p waves.
- wide QRS.
