ECG Signs and differentials Flashcards
Ecg changes in cor pulmonale?
Reminder: copd - reflex vasoconstriction/loss of pulmonary capillaries - pulmonary hypertension - right ventricular hypertrophy - right atrial enlargement
P. Pulmonale -Peaked p waves greater than 2.5mm amplitude (=right atrial enlargement)
PR and ST segments sagging - should normally be flat baseline between P-QRS-T (=Exaggerated atrial depolarisation)
Signs of severe hyperkalemia on an ecg?
No discernible p waves
Wide QRS complexes (>120ms)
Peaked t waves
Normal ECG: what needs to be normal? 8 things to look at
- Rate: 60-100bpm (300/no of large squares R-R)
- Rhythm: regular sinus rhythm, p waves starting 120-200ms before a QRS complex (see only 2 waves? Must be QRS and T, can’t have a lone P)
- Axis: QRS has positive deflection in leads 1 and 2 means normal axis
- QRS: less than 120ms
- Q: deeper in leads 3 and aVR is normal
- ST interval: should be isoelectric (flat/in line with) the baseline
- T: higher in chest leads, lower in limb leads, down turned in aVR and V1
- QT interval: varies depending on HR
Does a normal ECG exclude ACS?
No -
Two things required to diagnose STEMI?
ST elevation >/=1mm in leads 2 and 3
New left bundle branch block
(WiLLiaM: W in V1+V2, M in V3+V4, wide QRS, no Q waves in 1, V5 and V6)
Changes in ECG:
Initially = normal ecg in 20% of cases
Within hours = Tall tented T waves, new LBBB and ST elevation
Within days = T wave inversion and pathological Q waves
Causes of Left bundle branch block?
(“Where the left bundle Is blocked in the interventricular septum so the depolarisation starts in the right and moves to left, normal heart has left to right depolarisation”)
Aortic stenosis Ischemic heart disease HTN Dilated cardiomyopathy Anterior MI Hyperkalemia Digoxin poisoning
What event does the Q wave represent?
The normal left to right depolarisation of the interventricular septum
Hence we lose the Q waves in Lateral leads V5/V6 in left bundle branch block
Not normally seen in V1-3
Signs of MI in CAD (aka IHD/CHD) on ECG?
- pathological Q waves:
* > 40 ms (1 mm) wide
* > 2 mm deep
* > 25% of depth of QRS complex
* Seen in leads V1-3 - left bundle branch block
* Broad QRS (>3small square/0.12sec) and
* Deep S wave in V1 and
* No Q wave in V5/V6 - ST-segment and T wave abnormalities (for example, flattening or inversion).
(- indicate ischemia or previous MI)
Signs of left bundle branch block?
Broad QRS (>3small square/0.12sec)
Deep S wave in V1
No Q wave in V5/V6
What does ST elevation mean is happening in the heart?
Infarction of the myocardium
Or Transmural ischemia
What does ST depression mean is happening to the heart?
Ischemia of the endocardium
All to do with where the isoelectric baseline is:
Ischemic part of heart is ACTIVE, and generates its own currents before QRS, these move TOWARD the electrode.
Towards = positive deflection
Away = negative deflection
This makes the isoelectric baseline seem to be above 0mV [normally it is 0mV]
When total depolarisation occurs at ST interval, the baseline is finally at 0mV -> Depressed below baseline.
What are the ECG changes associated with pulmonary embolism?
Sinus tachycardia (HR >100)- most common change
Atrial fibrillation (caused by the PE)
S1Q3T3 - sign of acute cor pulmonale (pulmonary hypertension), so we have: S wave in lead 1, Q wave in lead 3 and T wave inversion in lead 3
RBBB - sign of delayed ventricular depolarisation, so we have: broad QRS, (MaRRoW) M-shaped QRS in V1-3 and W-shaped QRS in V5-6
(Reminder: the first part of the QRS is the left ventricle depolarising)
What are the differentials for a wide QRS complex?
LBBB
RBBB
Ventricular tachycardia
Ventricular fibrillation
Complete heart block (This is 3rd degree: impulses don’t reach from Atria to ventricles AT ALL)
Hyperkalemia
Tricyclics antidepressants
What is an early after depolarisation? (EAD)
A decrease in the efflux potassium currents in the heart, or an increase in the sodium channels. (Both of which will keep the cell depolarised for longer)
MOA:
- This slows the repolarisation of the myocyte when it is in phase 3 (depolarised - plateau).
- This can keep going long enough to reactivate L-type calcium channels.
- This will cause the release of calcium from the SR and cause a long depolarisation.
This is the cause of LONG-QT syndrome: too few potassium channels, since it takes longer for the heart to repolarise.
What is a delayed after depolarisation?
A very small action potential occurring just after a normal action potential, if they are big enough then they can trigger another contraction.
Classically caused by digoxin toxicity, but also MI
A normal cell releases calcium at the same time all over itself.
A DAD cell has spontaneous, chaotic release of calcium in random places on the call.
MOA:
- The SR of a myocyte is overloaded with calcium.
- Calcium is spontaneously released from the SR within the cell.
- This activates depolarising currents, if these currents are big enough then the impulse will be generated and the cell will contract.
