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Flashcards in Cardiac Electrical activity Deck (63):
1

3 types of cardiac electrical properties (Pg 38)

Excitability
Conductivity
Automaticity

2

Cells with fast response and their resting and threshold potentials (Pg 38)

Atria and Ventricles
RP = -90mV (Nearest to Nernst potential for K+)
TP = -70mV

3

Phase 0 (Pg 38)

Rapid depolarization:
-Na+ channels open
-Very rapid inward Na+ current due to both CHEMICAL and ELECTRICAL gradient
-20mV

4

Phase 1 (Pg38)

Early re-polarization:
- TRANSIENT outward potassium current
- 0mV

5

Phase 2 (Pg 39)

Plateau phase:
- Slow inward Ca2+ current from L-type calcium channels from SR (Ca induced Ca release) (depolarization)
- Na+/Ca2+ exchanger (3Na+ in for 1Ca2+ out)
(Depolarization)

BALANCED WITH

-Outward K+ potassium current (re-polarization)

6

Phase 3 (Pg 39)

Re-polarization:
1) Delayed rectifier/iK opens AFTER DELAY
- Triggered during depolarization but opens 200msec later
- Voltage and time dependent

2) Reactivation of iK1 INSTANTANEOUSLY after potential drops

7

Phase 4 (Pg 39)

Resting:
iK1 open therefore high conductance of potassium (-90mV)

8

Learn K+ channels that open depending on ATP or Ach (Pg39)

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9

Na+/Ca2+ exchanger - Pg 39

Phase 2
Exchanges 3Na+ in for 1Ca2+ out
Depolarizes

10

iK Pg 39

Phase 3
Delayed rectifier
Triggered on depolarization but opens about 200msec after
Causes re-polarization

11

iK1 - Pg 39

Outward flow of K+ (Re-polarization)

Phase 2 - Balances depolarization of L type Ca2+

Phase 3 - Causes re-polarization

Phase 4 - Defines resting membrane potential

12

i(to) - Pg 38

Phase 1 - Transient outflow of K+ causing early re-polarization

13

Learn "Timing's of main ionic pumps" (Pg 39)

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14

Cells with a slow AP response and their RP? (Pg 40)

Sinoatrial Node
Atrioventricular Node
-55mV

15

Main difference between Slow AP response and Fast AP response? (Pg 49)

Slow AP response:
-> Upstroke/Depolarization is much slower
- Due to Ca channels used instead of Na channels.

16

Why are there no Na+ channels in cells with Slow AP responses? (Pg 40)

1) Cells just don't have any
2) RP is -55mV which no Na+ channels are activated/required.

17

Refractoriness (Pg 40)

1) Absolute (Effective - group of cells) refractory period:
- Membrane cannot be re-excited during this time

2) Relative refractory period:
- Membrane needs stronger than normal stimuli to get propagated AP

3) Supernormal refractory period:
- Need weaker than normal stimuli to get AP

4) Full recovery time:
- May extend beyond return to RP

18

Interval (HR) - duration relationship (Pg 41)

Faster heart rate = Shorter AP
- Related to properties of ion channels

19

Word describing myocardial structure (Pg 41)

Laminar

20

Are cardiac muscle cells myogenic or neurogenic? (Pg 41)

Myogenic - They create their own electrical impulses from within heart itself.

21

How do electrical impulses spread through myocardium from cell to cell? (Pg 41)

Intercalated discs - They are sites of mechanical and electrical coupling

22

What is automaticity? (Pg 41)

The ability of cells to generate their own electrical impulse via pacemaker activity or diastolic depolarization.

23

Automaticity is found in which cells? (Pg 41)

SAN
Some cells around the AVN
His-Purkinje network

24

What outward currents decrease and what inward currents increase in automaticity? (Pg 41)

Outwards: iK decreases. Less positive ions leaving.

Inwards:
--> if (funny current)
- Inward sodium current activated by -ve potentials

--> iCa increases
- Slow inward current of Ca2+

25

Mechanisms for altering intrinsic rate of pacemaker discharge? (Pg 42)

1) Alter rate of depolarization (slope)

2) Change threshold potential

3) Alter maximum diastolic potential (Change the level of which the resting potential by opening or closing more K+ channels)

26

How does the Parasympathetic nervous system slow Heart rate? (Pg 42)

Release of Ach at vagal endings in heart
At SAN increases K+ permeability of cells
Therefore: - Hyper-polarized (Higher RP)
- Decreased pacemaker slope

27

How does SNS speed Heart rate? (Pg 42)

Release of Nor Adrenaline at SAN
Increases slope of pacemaker depolarization

28

Normal heart rate? (Pg 42)

60-100bpm

29

Bradychardia? (Pg 42)

<60bpm

30

Tachycardia (Pg 42)

>100bpm

31

Normal Cardiac activation sequence (Pg 43)

1 ) Sinoatrial Node - Small site of cells near SVC inlet continuous with atrial myocardial tissue about ~15mm long. Spontaneous depolarization at ~70bpm

2 ) Internodal tracts - cells aligned so impulse travels ALONG them, not ACROSS them which is slower.

3 ) Atria - AP travels from muscle cell to muscle cell via gap junctions

4 ) AV node - Delays impulse
- Very slow conduction velocity (~0.5m/s)
- Allows atria to "top up" ventricle before systole

5 ) Bundle of His - Pathway between atrium and ventricles as there is insulating fibrous skeleton separating the two.

6 ) Bundle branches - Split to left and right

7 ) Purkinje fibres - Branches off bundle branches which ramifies endocardial surface.
- Very rapid conduction velocity (~2-4m/s), due to large fibre radius.

8 ) Ventricular Myocardium - AP propagates from muscle cell to muscle cell via gap junctions
- From endocardium to epicardium because endocardial site of purkinje fibres.

32

Velocity is proportional to ? and therefore? (Pg 44)

Radius - Therefore AVN fibers with small radii are slower at conducting

33

Significance of rapid purkinje fibre conductance? (Pg 44)

So the the whole ventricle(s) contracts at once for a co-ordinated contraction

34

Disadvantage of Slow conducting AVN? (Pg 44)

The conduction can be so slow that it seems like it doesn't conduct at all. This means there is a higher chance of something going wrong leading to a AVN block.

35

What is an ECG? Pg 59

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36

Why do ECG's work on humans? Pg 59

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37

What does the P wave represent and why does it only have a small voltage "bump"? Pg 60

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38

P wave takes the same time as QRS complex despite being a smaller tissue mass. Why is this? Pg 60

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39

What does the PR segment represent? Why is there no bumps? Pg 60

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40

What does the QRS complex represent? Why is it greater magnitude than P wave? Pg 60

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41

What does the S-T segment represent? Pg 60

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42

What does the T wave represent? Why is it broader and flatter? Pg 60

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43

What is the QT interval? What does it represent? What is it's significance? Pg 61

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44

What does an ECG measure? Pg 61

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45

What does measured potential depend on? Pg 62

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46

How does the QRS form? Pg 63

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47

Why is the T wave still positive when it is repolarizing? Pg 64

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48

What are the two oversimplifications in ECG analysis? Pg 64

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49

What is a bipolar lead? Pg 64

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50

What are the 3 bipolar limb leads? What do they form? Pg 65

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51

What is Eithoven's law? Pg 65

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52

What are unipolar leads? Pg 66

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53

What are the unipolar chest leads? Pg 67

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54

How do you find the mean QRS vector? Pg 68

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55

What is Wolff-Parkinson White syndrome? Pg 76

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56

What does WPW present with in sinus rhythm? 76

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57

What are mechanisms that cause ventricular tachyarrhythmias? Pg 76

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58

What are treatment methods for WPW? Pg 76

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59

What is long QT syndrome? Pg 77

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60

What is long QT syndrome mainly caused by? Pg 77

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61

What can LQT syndrome cause? Why? Pg 77

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62

What are examples of other diagnostic capabilities of ECG's? Pg 77

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63

What is the sequence of ECG events in infarcted tissue? Pg 78

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