Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3.23 > Lecture 16 > Flashcards

Lecture 16 Flashcards

1
Q

What is resting membrane potential?

A

The electrical potential across a plasma membrane is determined by two main factors:
- The distribution of ions across the membrane.
- The selective permeability of the cell membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the major determinant of resting membrane potential?

A

Potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a fast depolarizing cell?

A

Cardiac myocyte - has a quick action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is part of the intrinsic conduction system?

A
  • Fast depolarizing cell
  • Slow depolarizing cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What drives cell excitation?

A

Autonomic sympathetic drive combined with intrinsin pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are slow depolarizing cells found?

A

SA/AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are slow depolarizing cells?

A

Pacemaker cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes an increase in membrane potential?

A

Influx of sodium, efflux of potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is refractory period?

A

The cell has been activated, it cant be reactivated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the absolute refactory period?

A

No response to excitary stimuli - cant be further activated. Good situation for cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the relative refractory period?

A

Cell can be triggered to activate early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to arythmia drugs affect the refractory period?

A

Dugs that extend refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Thinking about sympathetic/ parasympathetic control of heart function. What would vagal nerve stimulation do to the resting membrane potential?

A

Make it become more negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Tachyarrhythmia

A

> 100 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bradyarrhythmia

A

<60 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Supraventricular?

A

Originating in the atrium or atrioventricular node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is ventricular?

A

Originating in the ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the narrow complex (QRS part)?

A

describes supraventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is broad complex?

A

Describes ventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is heart block?

A

Impulse origininating in the SA node is impeaded partially or completely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is persisitant or paroxysmal?

A

Intermittent attacks - they come and go

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the mechism of arrhythmias?

A
  • Heart rate faster or slower
  • Site of origin: supraventricular/ ventricular
  • Complexxes on ECG: narrow/ broad
  • Cardiac rhythm: regular/ irregular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do we get an arrhythmias?

A
  • Abnormal conduction: becomes slow or blocked - may be due to ischemia
  • Abnormal automaticty: ischemic tissue becomes damaged and fires
  • Re-enrty: circle of cells go round and fire off in addition to normal pacemaker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What must happen to the refractory period or the conduction velocity for re-entry to occur?

A

Refractory period must shorten. Conduction velocity must decrease. The conduction velocity is reduced due to depolarization. Cells are within refractory period.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is conduction velocity?

A

Speed at which it moves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is phase 0 of action potential of cardiac cells?

A

rapid depolarisation (inflow of Na+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is phase 1 of action potential of cardiac cells?

A

partial repolarisation (inward Na+ current deactivated, outflow of K+)

28
Q

What is phase 2 of action potential of cardiac cells?

A

plateau (slow inward calcium current) - calcium interacts with myosin resulting in contraction

29
Q

What is phase 3 of action potential of cardiac cells?

A

repolarisation (calcium current inactivates, K+ outflow)

30
Q

What is phase 4 of action potential of cardiac cells?

A

pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) ‘autorhythmicity’

31
Q

What are class I antiarrhythmic drugs?

A

block sodium channels
- Ia (quinidine, procainamide, disopyramide) increaes AP
- Ib (lignocaine) decrease AP
- Ic (flecainide) elongates AP duration

32
Q

Where do class II drugs have thier effect?

A

On nodal tissues (SA node)

33
Q

How do the class II drugs work?

A

Rhythm control drugs - reduce rate of firing and sensitivity to noradrenaline

34
Q

What are class II antiarrhythmic drugs?

A

ß-adrenoceptor antagonists (atenolol, sotalol)
- Important in the resting membrane potential

35
Q

What are class III antiarrhythmic drugs?

A

prolong action potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol)

36
Q

What are class IV antiarrhythmic drugs?

A

Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil)

37
Q

Are beta blockers rate or rhythm controling drugs?

A

Rate control drugs

38
Q

Give an example of a class IA sodium channel blocker?

A

Qunidine

39
Q

Give an example of a class IB sodium channel blocker?

A

Lidocaine

40
Q

Give an example of a class IC sodium channel blocker?

A

Flecanide

41
Q

How do sodium channel blockers work?

A

The principal effect of reducing the rate and magnitude of depolarization by blocking sodium channels is a decrease in conduction velocity

42
Q

How do beta blockers (Class II antiarrhythmic) drugs work?

A
  • Inhibit sympathetic driven electrical activity
  • Sympathetic drive increases conduction velocity
  • Increases aberrant pacemaker activity (ectopic beats).
  • Decrease sinus rate
  • Decrease conduction velocity
    -Increase APD and the ERP
43
Q

What is the primary role of potassium channels in cardiac action potentials?

A

Cell repolarization

44
Q

How do potassium channel blockers (Class III Antiarrhythmics) work?

A
  • Block the potassium channels that are responsible for phase 3 repolarization
  • Since these agents do not affect the sodium channel, conduction velocity is not decreased
  • Prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias
45
Q

Name three potassium channel blockers

A

-Amiodarone
- Sotalol
- Dronedarone

46
Q

What are the therapeutic uses for amiodarone?

A

Supraventrular and ventricular arrhythmias

47
Q

What are the therapeutic uses for sotalol?

A

Ventriclar arrhythmias; atrial flutter and fibrilation

48
Q

What are the therapeutic uses for dronedarone?

A

Atrial flutter and fibrillation conversion, occasionally SVGT

49
Q

What drives cell excitation?

A

Autonomic sympathetic drive combined with intrinsin pacemaker

50
Q

What controls heart rate?

A

Sympathetic and parasympathetic influences

51
Q

What controls heart rate at rest?

A

Parasympathetic

52
Q

What are the sympathetic fibres?

A

Noradrenaline

53
Q

Where does sympathetic fibre noradrenaline act?

A

B1 receptors

54
Q

What happens when noradrenaline binds to B1 receptors?

A

Increase the permeability of the nodal cell plasma membrane to Na and Ca - increase the heart rate

55
Q

What is the parasaympathtic fibre?

A

Aceytylecholine

56
Q

Where does acytylcholine bind?

A

Muscarinic 2 receptors

57
Q

What happens when acetylecholine binds to M2 recepyors

A

Increases the permeability to K and decreases the Na and Ca permeability so reduced heart rate

58
Q

What affects pacemaker rate?

A

Tempertaure and Ph

59
Q

What is vagal stimulation?

A

Parasympathetic innervation - acetylecholine acting on M2 receptors

60
Q

What is the neuro-hormonal influences of parasympatehetic stimulation?

A
  • Makes the resting potential more negative
  • Pacemaker current slower
  • Raise the threshold
61
Q

What is the neuro-hormonal influences of the sympathetic stimulation?

A

Catecolamines make the resting potential more excited and speed up the pacemaker current and lower the threshold for discharge.

62
Q

How does adenosine work?

A
  • Negative inotrpic
  • Reduce rate of firing
  • Reduce conduction velocity
63
Q

How does atropine work?

A
  • Muscarininc receptor antagonist
  • Reduce the effect of excessive vagal activation on the heart
  • Negative inotrpic
  • Redcuce rate of firing
  • Reduce conduction velocity
64
Q

What affect does digoxin have in heart failure patients?

A
  • Increase inotropy
  • Increase ejection fraction
  • Decrease preload
  • Decrease pulmonary congestion/ oedema
65
Q

What affect does digoxin have in arrythmia patients?

A
  • Decrease AV nodal conduction
  • Decrease ventricular rate in atrial flutter and fibrillation
  • Increased intracellular calcium lengthens phase 4 and phase 0 of the cardiac action potential, which leads to a decrease in heart rate

3.23 (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions