ECG memory stuff Flashcards
What does the measured potential difference depend on?
1) magnitude of the charges/dipole
2) orientation of dipole and electrodes
3) distance between dipole and electrode
What is the origin of the T wave?
epicardial myocyte AP’s are shorter, so the wave of depolarization is inside to out, causing a posotve deflection( think of drawing)
Leads 1, 2 and 3
1- RA(-) to LA(+)
2- RA (-) to LL(+)
3- LA (-) to LL (+)
What is the QT interval a reflection of? what s the ST segment?
QT-AP duration reflection
ST- plateau of AP
How can WPW syndrome present on ecg?
For a pre excitation, short PR, wide QRS and delta wave, due to the other entryway of depolarisation, QRS occurs earlier.
Re-entrant- one way gives a narrow complex. one gives a wide complex (due to slower conducting myocytes when it conducts in a particular rotation)
Long QT syndrome
QT interval gives an indication as of the AP duration, so a long QT syndrome means there is a delay between depolaristion and repolarisation.
What are some causes of long QT syndrome
Drug induced- e.g. amidarone to prevent one type of arrythmia
Genetic- ion channel change, so the iK is affected as the iKs is abnormal, meaning take longer for repolarization to occur
AV blocks
1st degree: prolonged PR interval
Second degree AV block:
1)Wenckebach:
2)missed beats one, mobitz 2
vent hypertropy
mean QRS axis shifted towards side of hypertrophy. Enlarged QRS on leads on right side (aVr, V1, V2 maybe V3.) lead 3 most? down up up)
Left would be V4, V5, V6, lead 2? aVL QRS axis left shift (which is up up down on leads 1, 2, 3)
Hyperkalaemia and hypokalaemia
hyperkalaemia: some K channels conduct faster, higher T waves (sensitve to extracellular)
hypokalaemia: flat T waves
Hypercalcaemia and hypocalcaemia
hypercalcaemia: increased ext. calcium leads to more intracellular calcium. this leads to inactivation of L-type calcium channels, which reduces the duration of calcium current during plateau, so shorter QT interval
hypocalcaemia- long QT interval
What can digitalis do?
cause ST segment depression (may mimic ischaemia), or T wave inversion or PR prolongation (AV bundle block)
What happens to an AP in ischaemia?
T wave is typically altered (ST in injnury and QRS in MI)
shorter AP due to lowered Na/K ATPase activity. Hyperkalaemia means repolarisation occurs faster.
Also iK,ATP activtate at low ATP to shorten AP for energy consumption.
Explain T wave changes specific to MI?
are focalised to area of ischaemia, mechanism similar to that of hyperkalaemia
What is the mechansim of ST elevation (2 types)
Diastolic: Due to damaged tissue having altered RMP. (less negative). AP will still reach plateau, the same but whole ecg is below baseline.
As NO current flow in plateau, moves up to the isoelectric line, elevated.
Systolic: RMP is okay but the injury current occurs during the plateau phase