Brainscape's Knowledge GenomeTM

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


See full index

Human Diseases > Drugs used in management of heart failure and cardiac arrhythmias > Flashcards

Drugs used in management of heart failure and cardiac arrhythmias Flashcards

1
Q

Mechanism of action of inotropes?

A

Increase force of contraction of heart

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

Mechanism of action of diuretics?

A

Increase in passage of urine - excrete Na and water

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

Mechanism of action of beta blockers?

A

Stabilise heart rhythm by inhibiting action of adrenaline

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

Effect of ACE inhibitors and angiotensin receptor blockers?

A

Dilation of BV and reduce work of contraction of the heart

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

Name 2 types of inotropes and its effect?

A

Adrenoreceptor agonist
Mimic effects of adrenaline
+ve inotropic effects = increase contractility of heart

Cardiac glycosides
antiarrythmic and inotrpic effects

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

Why do adrenoreceptor agonists (inotropes) have to be given by continuous iv drip?

A

Very short half life (30 secs)

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

Consequences of adrenoreceptor agonists?

A

Arrythmias and increase myocardial oxygen demand

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

Action of cardiac glycosides?

A 
Antiarrythmic = vagolytic effects = reduce rate and conduction in sinus and AV node
Inotropic = increase intracellular Ca+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Indications for cardiac glycosides

A

Supraventricular arrythmias
Chronic atrial fibrillation
Heart failure (improve symptoms)

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

Describe pharmacology of cardiac glycosides?

a) elimination
b) effect of this on certain patients
c) therapeutic index
d) when plasma concentrations should be monitored?

A

a) hepatic
b) impaired renal function = lower doses
c) narrow TI = easily toxic
d) monitor when possible toxic symptoms showing or lack of efficacy of drug

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

How do cardiac glycosides cause inotropic effects?

A

Inhibti Na K pump - so Sodium accumulates in the cell
This prevents Na Ca exchanger which normally pumps Na in and Ca out
So Ca accumulates int he cell = inotropic

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

Possible effect of increased Na in the cell due to to cardiac glycoside treatment?

A

Arrhythmias

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

Adverse effects of cardiac glycosides?

A 
Cardiac = heart block, supra-ventricular and ventricular arrhythmias
Non-cardiac = nausea, vomiting, constipation, confusion, visual disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can diuretics be catergarised?

A

Causing potassium loss (K+ loosing)

Causing potassium retention (K+ sparing)

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

Effect of K+ loosing and K+ sparing diuretics?

A

K+ lost with water

K= retention despite loss of water

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

Adverse effects of loop diuretics result from …

A

Profound diuresis

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

Why do loop diuretics cause profound diuresis?

A

Stronger diuretics

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

What kind of adverse effects are caused by thiazide diuretics?

A

Metabolic effects e.g. impaired glucose intolerance

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

Generally what are common adverse effects of K+ loosing diuretics like loop and thiazide diuretics?

A

Hypokalaemia
Gout
Pancreatits

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

How do K+ sparing diuretics like spirolactone work?

A

Inhibit aldosterone

21
Q

Adverse effects of spironolactone (K+ sparing diuretic)

A

Gynaecomastia
Hyperkalaemia
GI disturbances

22
Q

Effect of ACE inhbitors?

A

Vasodilation, reduce aldosterone secretion, decrease Bp, reduced sympathetic NS activity

23
Q

Adverse effects of ACE inhbitors?

A

Renal failure
Cough
Hyperkalamia
Angioedema

24
Q

Effects of angiotensin receptor blockers?

A

Vasodilation, redcued SNS activity

25
Q

Benefits of angiotensin receptor blockers vs ace inhibitor?

26
Q

Describe cardiac action potential?

A

Fast sodium entry

inactivation of sodium channels

Slow calcium influx

Efflux of K+ = repolarisation

Spontaneous diastolic drift towards threshold potential

27
Q

What is atropine?

A

Antimuscarinic anticholinergic drug

Blocks vagal inhibition of sinus and AV node

28
Q

adverse effects of atropine?

A

Dry mouth
Postural hypotension
Anticholingeric

29
Q

What is heart block?

A

Bradycardia due to impulses not being conducted through AV node or to ventricles

30
Q

What is atropine used for?

A

Treat heart block

31
Q

Adverse effects of atropine and reason for these?

A

Dry mouth
Postural hypotension
Due to it being an anticholinergic drug

32
Q

Name another drug aside from atropine that can be used to treat bradycardia arrythymias?

A

Isoproterenol

33
Q

Describe isoproterenol mechanism of action?

A

B1 and B2 adrenoreceptor agonist = positive chronotropic effect on the sinus node = increase heart rate

34
Q

Adverse effects of isoproterenol?

A

tachycardia and arrythmias due to it being sympathomimetic

35
Q

Name the 2 categories of tachyarrhthymias?

A

Supraventricular tachycardia - somewhere above the bundle of His (sinus node, atria)
Ventricular tachycardia = bundle of His or ventricular tissue

36
Q

What type of tachyarrhythmias are more serious?

A

Ventricualr tachycardias are more life threatening than supraventricular tachycardia

37
Q 
What is the mechanism of action of these antiarrhythmic drugs:
class I
Class II
Class III
Class IV
A

Class I = inhibit phase 0 depolarisation = block fast entry of Na = sodium channel blockers

Class II = antisympathetic drugs (beta blockers) = inhibit phase 4 diastolic drift = slow HR

Class III = potassium channel blockers = inhibit phase III depolarisation = prolong refractory period

Class IV = inhibit Ca-dependent depolarisation = calcium channel blockers = block AV node

38
Q

Generally how do anti-arrhythmic drugs prevent arrhythmias?

A

Altering conduction velocity - interfering with re-entry
Reduce intrinsic pace maker rate
Prolong effective refractory period

39
Q

What are the general adverse effects of antiarrhythmic drugs?

A

Can precipitate arrhythmias

Negative inotropic effects = hypotension and heart failure

40
Q

Lidocaine is a class I drug. Describe its action

A

Blocks fast sodium channels and slows phase 0 depolarisation = shortens action potential duration

41
Q

When is lidocaine prescribed for arrhythmias?

A

Ventricular arrhythmias

42
Q

Adverse effects of lidocaine as an antiarrhythmic drug?

A

Hypotension, heart block, neurotoxicity = fits

43
Q

Amiodarone is a class III antiarrhythmic drug, describe its action.

A

Prolongs action potential duration and refractory period = lengthened QT interval

44
Q

Indications of class III drugs?

A

Ventricular and supra-ventricular arrhythmias

45
Q

Amiodarone (class III) adverse effects?

A 
Thyroid disturbances
Pulmonary fibrosis
Pro-arrhythmia
Hepatitis 
Blue/grey skin discolouration
46
Q

Verapamil is a class IV drug. Describe its action?

A

Calcium channel blocker - reduces rate and conduction in sinus and AV node

47
Q

Indications for class IV drugs?

A

Supraventricular arrhythmias

48
Q

Adverse effects of class IV drugs?

A

Heart failure, hypotension, constipation, vasodilation, oedema

Human Diseases (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions