Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular physiology > Pharmacological control of contractility > Flashcards

Pharmacological control of contractility Flashcards

1
Q

What are 2 main uses of positive inotropes?

A

Cardiac failure (chronic/ischaemic and acute)

Hypovolaemia (actual and functional e.g. vasodilation so lose effective circulating volume)

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

What 3 main factors affect cardiac output?

A

Cardiac input (i.e. venous return) and thus SV
Contractility
Peripheral resistance

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

What are the priorities for inotropes treating ischaemic heart disease?

A

Increase contractility but not oxygen demand
Vasodilation to reduce afterload
Increase cardiac output

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

What are the focuses of inotropes in treating cardiogenic shock?

A

Vasoconstriction (avoid vasodilation)

Must increase cardiac output

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

What is a risk of using inotropes to treat acute cardiac failure?

A

Increasing contractility may enhance ischaemia due to reduced coronary perfusion

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

What are 2 main types of positive inotropes?

A

Sympathomiemetics

Non sympathomimetic positive inotropes

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

What are the 3 types of inotropes needed for exams?

A

Sympathomimetics
Cardiac glycosides
Calcium sensitising agents

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

When are sympathomimetics used?

A

Acute shock/hypotension to increase cardiac contractility

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

What is the risk of sympathomimetics?

A

Myocardial ischaemia (due to increased oxygen supply) and arrhythmias

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

What are the direct and indirect effects of sympathomimetics?

A

Direct: affect symp receptors
Indirect: effect intracellular messengers

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

What are 2 broad examples of sympathomimetics?

A

Phosphodiesterase inhibitor

Catecholamines

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

What are examples of PDE inhibitors?

A

Milrinone, methyl xanthines

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

What are the actions of indirect sympathomimetics?

A

Inhibit phosphodiesterase 3 so amplify effects of beta adrenergic stimulation, prolong effects of cAMP

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

When are phosphodiesterase inhibitors not effective?

A

When beta blockers taken

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

What are examples of catehcolamines?

A

Noradrenaline, adrenaline, dopamine, dobutamine

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

What are the effects of catecholamines (+ve and -ve), what do they act on?

A

Beta 1 receptors
Increase heart rate and contractility
Increased myocardial oxygen consumption

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

What is the benefit of catecholamines increasing vascular tone?

A

Reduce blood supply to vascular beds of gut, kidney etc so more fluid available in circulating volume

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

What is the effect of high levels of adrenaline on bp, why is this useful?

A

Increased blood pressure so can be used for hypotension

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

Why does moderate adrenaline cause vasodilation in skeletal muscle but elevated amounts cause vasoconstriction?

A

At moderate levels: mostly bound to beta receptor

Higher doses: beta receptors saturated so adrenaline binds alpha receptors

20
Q

How can adrenaline and dopamine cause myocardial ischaemia?

A

Increase cardiac workload, insufficient perfusion to cornary arteries so not enough oxygen.

21
Q

What are the solutions to the problems of dopamine and adrenaline, how come?

A

Dobutamine (b1 agonist):
reduces risk from myocardial infarction but increases cardiac output.
Does not act on dopamine receptors so less prone to hypertension

22
Q

What is a problem with dobutamine?

A

Not as effective as dopamine at vasoconstriction and also causes mesenteric vasodilation so lose blood volume to gut

23
Q

Why is dobutamine not used for ischaemic heart disease?

A

Increases heart rate and thus myocardial oxygen demand, though note, better than adrenaline

24
Q

Describe action of propanolol

A

Adrenoceptor antagonist so have negative effect on contractility and inotropy

25
Q

Examples of calcium sensitisers?

A

Levosimendan, omecamtiv

26
Q

What do calcium sensitisers do, why are they good?

A

Increase sensetivity of contractile mechanism to calcium so increase force of contraction without extra ion pumping (i.e. doesn’t increase oxygen demand much)

27
Q

What does omecamtiv do?

A

Myosin activator: prolong contractile phase of actin myosin cycling so increase contractility

28
Q

What are examples of cardiac glycosides?

A

Digoxin, ouabain and digitoxin

29
Q

What are the benefits of cardiac glycosides?

A

Increase contractility
Little increase in oxygen demand
Have diuretic effect so reduce effect of circulating volume so reduced ventricular dilation

30
Q

What are some side effects of cardiac glycosides?

A

Risk of arrhythmia as delayed after depolarisations

31
Q

How come cardiac glycosides don’t increase oxygen demand?

A

Heart does not have to exert as much force to pump the blood, or they directly increasing the heart’s contractile force, so that the heart can overcome the higher blood pressure.

32
Q

What are good treatments for ischaemic heart failure?

A

Calcium sensitiser

Cardiac glycosides

33
Q

What is a possible mechaism for cardiac glycosides?

A

Inhibition of Na+ K+ ATPase
So build up of sodium within cell
This reduces Na+ gradient to drive NCX
So less Ca2+ extruded, Ca builds up and increase contractility.

34
Q

How do after depolarisations arise?

A

Excessive increase in Ca2+ inside cells during depolarisation causes delayed after depolarisations due to activation of Na+ Ca2+ exchange (which brings in more Na+ so cell depolarises) and opening of Ca2+ sensitive non selective ion channels

35
Q

Why can after depolarisations be problematic?

A

As heart rate increases, after depolaristation increases until it is high enough to trigger an AP - self perpertuating effect leading to tachycardia.

36
Q

What is the initial therapy you would give?

A

NICE
Beta blockers
ACE inhibitors
Diuretics

37
Q

Why do ACE inhibitors treat cardiac failure?

A

ACE inhibitors
Reduce reabsorption of sodium and water at the kidneys
Reduces after-load

38
Q

What are some examples of ACE inhibitors?

A

Ramipril
Enalapril
Captopril

39
Q

What use do beta blockers give in treating heart disease?

A

Reduce risk of arrythmias
Reduce the oxygen demand of tissue proportionally more than they reduce contraction – tissue more efficient
Reduce heart rate, improved mortality

40
Q

What is an example of a negative inotrope?

A

Beta blocker

41
Q

Why are beta blockers good for treating ischaemic heart disease?

A

Reduce oxygen demand of tissue

42
Q

Why are diuretics effective at treating heart disease?

A

Reduce after load by lowering blood volume (normal starling range), lowers oedema

43
Q

How does NO act as a good first line treatment for CHD?

A

Causes smooth muscle relaxation

Improves blood flow to cardiac tissue itself (e.g. used for angina)

Reduces the pressure against which the heart has to work

44
Q

When is ivabradine used?

A

As a second line of treatment (if beta blockers ineffective), reduce heart rate (CHD)

45
Q

What does ivabradine act on and what is its effect?

A

HCN4 (If) inhibitor, reduces the rate of pacemaker potential decay and slows heart rate

46
Q

After blockade of both sympathetic and parasympathetic neural influence on the heart, the heart rate would typically be…

A

Higher than the control rate

Cardiovascular physiology (11 decks)

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