ECGs Flashcards
Which leads is T wave inversion normal?
aVR and V1
Which condition is characterised by biphasic T waves in V2-3 (or inverted ones) with chest pain?
Wellen’s syndrome - LAD stenosis, high risk of anterior MI in coming days
U waves in V2-3 and QT prolongation = hypokalaemia
e.g. due to diarrhoea
In hypokalaemia, U have no pot (K+) and no T (small/absent T waves), but a long PR and a long QT
What is seen in hyperkalaemia?
tall, tented T waves,
flattened P waves,
PR prolongation,
broad QRS complexes
aVR - ST elevation - ?left main stem disease
V2-6 - T wave inversion
How can you check if ST depression in anterior leads is meaning posterior infarct?
Repeat ECG with the leads on the back
What is a bifascicular block?
Bifasicular block = RBBB + LAD
What is a trifascicular block?
Trifascicular block (Complete) = Bifasicular + 3rd degree Heart block
Trifascicular block (incomplete) = Bifasicular + 1st/2nd degree heart block
Incomplete trifascicular block = RBBB + LAD + 1st degree heart block
Apart from M pattern in V1 and W in V6, what else is seen in RBBB?
broad QRS > 120 ms
rSR’ pattern in V1-3 (‘M’ shaped QRS complex)
wide, slurred S wave in the lateral leads (aVL, V5-6)
RBBB
When do you TREAT hyperkalaemia?
If >6.5 alone OR
ECG changes
What is the management of hyperkalaemia?
10-20mls of 10% calcium gluconate by slow IV injection
10U actrapid in 50ml of 50% glucose over 10-15min
salbutamol nebs
sodium bicarbonate infusion to correct acidosis
An ECG performed shows ST depression in V1-V3 with tall, broad R waves and upright T waves.
What is the next appropriate course of action?
Posterior ECG - Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)
If fibrinolysis is given for an ACS, when is an ECG repeated?
an ECG should be repeated after 60-90 minutes - transfer urgently for PCI if not resolved
Which antibiotic requires you to check ECG first?
Azithromycin - to rule out prolonged QT and baseline liver function tests
II, III, aVF = inferior MI
anterior MI = V1-4 LAD
AND
pathological Q waves in II, III and aVF so previous inferior MI
Define pathological Q wave.
Old and simple definition:
Q-wave of >=0.04 s and an amplitude >=25% of the R-wave in that lead
New definition:
Any Q-wave in leads V2 - V3 >= 0.02 s or QS complex in leads V2 and V3
Q-wave >= 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4 - V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4 - V6; II, III, and aVF)
R-wave >= 0.04 s in V1 - V2 and R/S >= 1 with a concordant positive T-wave in the absence of a conduction defect
What investigation must be used before using flecainide to cardiovert AF?
Echocardiogram for structural heart disease or ischaemia
A CT shows a collection of blood in the subarachnoid space, midline shift, and hydrocephalus. Whilst the patient is being scheduled and prepared for surgery, he becomes haemodynamically unstable and drops his GCS further to 8 out of 15.
What is most likely to been seen on an ECG?
Torsades de pointes i.e. polymorphic ventricular tachycardia
The ECG shows Q-waves, ST elevation, and hyperacute T-waves in V2 and V3, diagnostic of myocardial infarction. This patient was later shown to have a left anterior descending (LAD) occlusion.
What is a sinusoidal pattern on ECG indicative of?
Severe hyperkalaemia - can also cause loss of P waves, tall tented T waves, broad QRS, VF
Hypokalaemia
The ECG findings are:
prominent U-waves, best seen in precordial leads - V2,4,5.
T waves have a ‘sine wave’ appearance
prolonged QTc > 600ms
borderline PR interval
rsr pattern - rSR’ pattern V1 or V2 can be a normal finding or variant in a younger person or athlete. It may also be called an incomplete right bundle branch block
Left ventricular hypertrophy - he ECG shows large R waves in the left-sided leads (V5, V6) and deep S-waves in the right-sided leads (V1, V2). There is also ST elevation in leads V2-3.
Hyperacute T waves in V2-3 - early sign of MI
Ventricular fibrillation - most common cardiac arrest rhythm, usually due to thromboembolic causes
Shows irregular waves with varying morphology and amplitude. No P, QRS or T waves can be seen.
CPR and defibrillation required - hyperkalaemia is a cause
ventricular tachycardia degenerating into VF
Asystole
Patient has no pulse but has this ECG:
Pulseless electrical activity - noticed when person loses consciousness; managed by CPR and treat underlying cause if known, and adrenaline IV. Defibrillation cannot be used as it is the myocardial tissue which is the problem not the electical impulses.
What are the reversible causes of cardiac arrest?
Atrial flutter with 2:1 block - rate is 144. In leads II and V1 you can see that there is more than 1 P wave per QRS complex
Hyperkalaemia - tall ‘tented’ T waves, progressive flattening of P waves, prolongation of the PR interval (PR interval > 200 ms) and eventually disappearance of P waves, and broad QRS complexes.
Then will change to sine pattern and VF
LBBB - look at V1 and V6, WiLLiam MaRRow
Widespread ST depression - likely an old STEMI
ST depression in anterior leads so posterior MI
Anterior lead ST depression so posterior MI
Widespread ST elevation – pericarditis
Brugada syndrome - cove shape in leads V1 and V2
What are the Sgarbossa criteria used for?
Used to help detect STEMI in the presence of a LBBB which often makes it difficult
ST depression
T inversion
Hypokalaemia - U waves seen, flattened T waves, long PR
This ECG is showing sinus tachycardia, the beginning of QRS widening (especially in V3-6), peaked T waves, and ST changes in V1-3, aVR and aVL. The symptoms of lethargy and palpitations are in line with a presentation of hyperkalaemia.
What are the causes of poor R wave progression?
Old MI
LVH
RVH
