ECG memory stuff

Question 1

What does the measured potential difference depend on?

Answer 1

1) magnitude of the charges/dipole
2) orientation of dipole and electrodes
3) distance between dipole and electrode

Question 2

What is the origin of the T wave?

Answer 2

epicardial myocyte AP’s are shorter, so the wave of depolarization is inside to out, causing a posotve deflection( think of drawing)

Question 3

Leads 1, 2 and 3

Answer 3

1- RA(-) to LA(+)
2- RA (-) to LL(+)
3- LA (-) to LL (+)

Question 4

What is the QT interval a reflection of? what s the ST segment?

Answer 4

QT-AP duration reflection

ST- plateau of AP

Question 5

How can WPW syndrome present on ecg?

Answer 5

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)

Question 6

Long QT syndrome

Answer 6

QT interval gives an indication as of the AP duration, so a long QT syndrome means there is a delay between depolaristion and repolarisation.

Question 7

What are some causes of long QT syndrome

Answer 7

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

Question 8

AV blocks

Answer 8

1st degree: prolonged PR interval
Second degree AV block:
1)Wenckebach:
2)missed beats one, mobitz 2

Question 9

vent hypertropy

Answer 9

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)

Question 10

Hyperkalaemia and hypokalaemia

Answer 10

hyperkalaemia: some K channels conduct faster, higher T waves (sensitve to extracellular)
hypokalaemia: flat T waves

Question 11

Hypercalcaemia and hypocalcaemia

Answer 11

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

Question 12

What can digitalis do?

Answer 12

cause ST segment depression (may mimic ischaemia), or T wave inversion or PR prolongation (AV bundle block)

Question 13

What happens to an AP in ischaemia?

Answer 13

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.

Question 14

Explain T wave changes specific to MI?

Answer 14

are focalised to area of ischaemia, mechanism similar to that of hyperkalaemia

Question 15

What is the mechansim of ST elevation (2 types)

Answer 15

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

Question 16

Why is there low R wave in MI?

Answer 16

MI tissue is electrically inactive. Dipole is smaller around some V leads.
In trasnmural infarct, will see no r waves and only negative deflections.

Question 17

Second degree AV block

Answer 17

PR segment lenght increases, then no beat

Question 18

RV hypertrophy

Answer 18

RAD (so lead 1 down, 2 up, 3 up)
leads facing the right (aVr, V1, V2) have large R waves
depressed ST in tall R wave leads

Question 19

LBBB

Answer 19

`WIDER QRS, 
LAD
M shaped notch on leads 1??, aVL, V4,V5, V6!!! (left sided leads)
WILLIAM (V1-V6)
left axis shift

Question 20

LV hypertrophy

Answer 20

Deep S waves in V1 and V2
Tall R waves in LV leads so aVl, V4-6
Left QRS axis shift (up up down)

Question 21

RBBB

Answer 21

Wider QRS
MARROW (V1-V6)
right axis shift