Brainscape's Knowledge GenomeTM

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


See full index

BIOM3010 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

PSNS opens which channel to cause hyperpolarisation of the SA node?

A

K channels

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

Explain the mechanism allowing PSNS to hyperpolarise the SA node

A

Acetylcholine acts on muscarinic receptors to decrease cAMP activity, which slows the closure of K channels, lengthening time between pacemaker potentials

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

SNS acts via noradrenaline to increase HR by what mechanism?

A

NA acts on beta receptors to increase cAMP activity, causing increased closure of K channels and opening of sodium channels

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

Most common cause of arrhythmia?

A

Ischemic heart disease

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

Arrhythmias can be classified by rate or..?

A

Site of abnormality

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

Define sinus tachycardia

A

Fast heart rate, but the SA node is still the primary pacemaker so waveform would be normal

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

Appearance of atrial fibrillation on ECG?

A

Normal looking but irregular QRS + random and chaotic P waves

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

Explain the consequences of atrial fibrillation that can lead to emboli formation

A

Irregular atrial contractions cause blood to pool in the atria, which can form a clot. The clot can then dislodge and travel to brain

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

Compare atrial flutter and atrial fibrillation

A 
Flutter = regular ventricular contractions 
Fibrillation = irregular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

HR in atrial fibrillation?

A 
Atria = ~400 
Ventricles= 160-180
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 different options for atrial fibrillation?

A
  • rate control (e.g. BB or CCB) and anticoagulant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name the arrhythmia responsible for sudden cardiac death

A

Ventricular tachycardia

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

Drug + other Tx for treatment and prevention of ventricular tachycardia?

A

Amiodarone

Electric shock / defibrillation

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

Symptoms of bradycardia?

A

Palpitations, syncope, fatigue, dizziness, heart failure

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

Compare intrinsic and extrinsic causes of bradycardia

A 
Intrinsic = age, ischaemic heart disease, surgery 
Extrinsic = medications, electrolyte disturbances, metabolic rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define re-entry arrhythmias

A

Caused by an action potential that doesn’t die out like it is supposed to, but instead re-excites regions of myocardium right after the refractory period

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

Define heart block

A

Ventricular rate much slower than atria due to impairment of the AV node. Complete heart block = atria and ventricles beat independently of one another

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

Define pro-arrhythmic drugs

A

Drugs that prolong the QT interval

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

Drug used in bradycardia?

A

Atropine

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

Name 2 potential causes of dysrhymthias

A
  • hypo or hyperthyroidism
  • caffeine, sympathomimetic drugs
  • heart disease
  • electrolyte disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where do sodium channel blockers bind?

A

To the alpha subunit of the sodium channel, which prevents from being activated while at rest.

22
Q

Explain the MOA of sodium channel blockers

A

They prevent action potentials by blocking the activation of sodium channels, meaning the cell does not depolarise. This slows the HR down

23
Q

Name 3 sodium channel blockers (one from each class)

A

Disopyramide, lidocaine, flecainide

24
Q

Which sodium channel blocker has the shortest DOA?

A

Lidocaine

Preferentially binds to frequently activating channels. Means the drug is more active when the HR is high

25
Q

Compare lidocaine and flecainide

A

Flecainide has a longer duration of action

26
Q

Do disopyramide and quinidine lengthen the refractory period?

A

Yes

27
Q

Name 2 beta blockers that are selective for B1

A

Metoprolol and atenolol

28
Q

Which class is most commonly used for for atrial fibrillation?

A

Class 1C (e.g. flecainide)

29
Q

Which drug class is used to treat ventricular tachycardia?

A

Class 1B (lidocaine)

30
Q

How do beta blockers slow HR?

A

Prevents the binding of noradrenaline to the beta receptor, meaning it reduces the impact of the SNS

31
Q

Beta blockers reduce calcium influx. True or false?

A

True. Explains why they slow HR (authorhythmic AP) and are negative inotropes

32
Q

Class 3 drugs are..?

A

Drugs that prolong the cardiac action potential

33
Q

How do class 3 drugs work?

A

They block depolarisation by K channels which prolongs the action potential and lengthens the refractory period of the sodium channels

34
Q

Drug class that can prevent re-entrant tachycardia?

A

Class 3

35
Q

Name 1 class 3 drug

A

Amiodarone

36
Q

Define PR interval

A

Time between atrial depolarisation and beginning of ventricular depolarisation. Relates to delay at AV node

37
Q

Define QT interval

A

Depolarisation + contraction of ventricles

38
Q

Class 4 drugs are also known as?

A

Calcium channel blockers

39
Q

Name 2 calcium channel blockers

A

Verapamil and diltiazem

40
Q

CCBs increase after-depolarisation arrhythmias. True or false?

A

False. They reduce this type of arrhythmia

41
Q

MOA of adenosine?

A

Opens potassium channels, causing hyperpolarisation

42
Q

Which drug can be administered to terminate re-entry tachycardia?

A

Adenosine.

43
Q

MOA of digoxin?

A

Inhibits Na/K ATPase which increases intracellular sodium and calcium

44
Q

Is digoxin a positive or negative inotrope?

A

Positive. Due to increased calcium

45
Q

How is digoxin used for arrhythmias if it is a positive inotrope?

A

Slows conduction at AV node

46
Q

2 drugs used for bradycardia?

A

Atropine and isoprenaline

47
Q

MOA of atropine?

A

Muscarinic antagonist. Prevents PSNS activity

Prevents binding of acetylcholine

48
Q

Isoprenaline MOA?

A

Beta agonist - sympathomimetic

Increases contractility and heart rate

49
Q

Digoxin inhibition of Na/K ATPase pump causes what?

A

Increased intracellular calcium = increased contractile strength

50
Q

What activates the funny channel causing it to open?

A

Hyperpolarisation of the previous action potential

BIOM3010 (11 decks)

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