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Cardiovascular Week 1 & 2 2016/17 > 7: Drugs affecting cardiac rate and force > Flashcards

7: Drugs affecting cardiac rate and force Flashcards

1
Q

Cardiac rate and force are mainly regulated by the ___ nervous system.

A

autonomic

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2
Q

Sympathetic regulation of cardiac rate and force depends on a transmitter and a hormone - what are they called?

A

Adrenaline (hormone released from the adrenal medulla)

Noradrenaline (post-ganglionic transmitter)

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3
Q

Which type of receptor do adrenaline and noradrenaline activate?

A

ß1 adrenoceptors

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4
Q

In the context of cardiac rate and force, where are ß1 adrenoceptors found?

A

1) AV/SA nodal cells

2) Myocardial cells

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5
Q

ß1 are coupled to what kind of protein?

A

G protein

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6
Q

The activation of ß1 adrenoceptors by (nor)adrenaline triggers the activation of which enzyme?

A

Adenylyl cyclase

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7
Q

What does adenylyl cyclase do?

A

Increases the concentration of cAMP

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8
Q

What is the effect of sympathetic stimulation on heart rate, and what is another name for this effect?

A

Increases heart rate

‘Positive chronotropic effect’

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9
Q

What is the effect of sympathetic stimulation on force of contraction, and what is another name for this effect?

A

Increased force of contraction

‘Positive inotropic effect’

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10
Q

What effect does sympathetic stimulation have on the conduction velocity of the AV node?

A

Increased velocity of conduction

therefore increases heart rate

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11
Q

What is the name given to increasing mass of cardiac muscle caused by long-term sympathetic stimulation?

A

Cardiac hypertrophy

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12
Q

Which neurotransmitter is involved in parasympathetic regulation of cardiac rate and force?

A

Acetylcholine

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13
Q

What kinds of neurotransmitter are noradrenaline and acetylcholine? Which divisions of the nervous system are they part of?

A

Noradrenaline (post-ganglionic)

Acetylcholine (post-ganglionic, pre- too sometimes)

Noradrenaline - sympathetic

Acetylcholine - parasympathetic

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14
Q

In parasympathetic regulation of cardiac rate and force, which receptor is activated by acetylcholine?

A

M2 muscarinic receptors

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15
Q

Where are M2 muscarinic receptors usually found?

Which neurotransmitter binds to them?

On behalf of which nervous system does this neurotransmitter act?

A

Nodal cells

Acetylcholine

Parasympathetic

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16
Q

Which type of protein are M2 muscarinic receptors bound to?

A

G protein

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17
Q

Activated M2 muscarinic receptors reduce the activity of which enzyme?

A

Adenylyl cyclase

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18
Q

Adenylyl cyclase activity is reduced by the activation of which G-protein-coupled receptor?

A

M2 muscarinic receptors

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19
Q

What does adenylyl cyclase help synthesise?

What is the effect of sympathetic stimulation on the concentration of this chemical?

And parasympathetic stimulation’s effect?

A

cAMP

Increased [cAMP]

Decreased [cAMP]

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20
Q

Apart from decreasing [cAMP], the activation of M2 muscarinic receptors has another effect - what is it?

A

Opens potassium channels (GIRK) to hyperpolarise SA node cells (this reduces heart rate because the rate of action potentials decreases)

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21
Q

What effect does parasympathetic stimulation have on heart rate, and what is another name for this effect?

A

Decreases heart rate

Negative chronotropic effect

22
Q

What effect does parasympathetic stimulation have on force of contraction, and what is another name for this effect?

A

No effect

sry

23
Q

What effect does parasympathetic stimulation have on AV node conduction? Why?

A

Reduced AV node conduction

Opening of GIRK potassium contraction causes hyperpolarisation

24
Q

Parasympathetic stimulation may causes ___ to develop in the atria.

A

Arrythmias

25
Q

Which maneouvres increase parasympathetic output and may be employed in atrial tachycardia?

A

Vagal maneouvres

26
Q

Give an example of a vagal maneouvre which can be used to increase parasympathetic output.

A

Valsalva maneouvre - activates aortic baroreceptors

Massage of the bifurcation of the carotid artery - activates carotid baroreceptors

i.e massage of the baroreceptors found in aorta and carotid artery

27
Q

Blocking HCN channels ___ the slope of pacemaker potential and ___ heart rate.

A

decreases , reduces

28
Q

What increases the activation of HCN channels?

A

Cyclic AMP

29
Q

Name a drug which is a selective blocker of HCN channels and can be used to reduce O2 consumption in heart disease (reduced HR = reduced “).

A

Ivabradine

30
Q

During excitation of cardiac muscle, Ca2+ release from the sarcoplasmic reticulum is said to be what kind of release?

A

Calcium dependent/induced calcium release

31
Q

During relaxation of cardiac muscle, which channel is responsible for calcium efflux? What are the numbers of ions involved in this transport?

A

Na+ / Ca2+ exchanger 1 (NCX1)

1 calcium out, 3 sodiums in

32
Q

ß1 adrenoceptor activation increases heart rate and force of contraction. ___ acts on the enzyme ___ ___ _ to enhance contractility of muscle.

A

cAMP , Protein kinase A

33
Q

Cardiac muscle relaxation is dependent on Ca2+ being pumped out of the cell. Which enzyme performs which reaction on the protein that facilitates this?

A

Protein kinase A

Phosphorylation

Phospholamban

34
Q

Name two ß adrenoceptor agonists used in treatment of heart conditions.

A

Dobutamine

Adrenaline

35
Q

What are the pharmacodynamic effects of ß adrenoceptor agonists on the heart?

A

Increased force of contraction, heart rate and therefore cardiac output

Reduced cardiac efficiency (O2 consumption increases more than the cardiac work itself)

36
Q

ß adrenoceptors can cause disturbances in cardiac ___, also known as ___.

A

rhythm , arrythmias

37
Q

Adrenaline is commonly used clinically. Name two conditions in which it is used, and the route of administration.

A

Cardiac arrest - IV

Anaphylactic shock - IM

38
Q

Dobutamine is another ß adrenoceptor which is used clinically. When?

A

During acute heart failure which may be reversible (e.g cardiac surgery, shock)

39
Q

Name two ß adrenoceptor antagonists.

A

Propranolol (ß1 and ß2)

Atenolol, bisoprolol, metoprolol (ß1)

40
Q

Name a clinical effect of a non-selective ß adrenoceptor blocker such as atenolol, bisoprolol or metoprolol.

A

Reduces exercise tolerance

Reduces myocardial O2 requirement, allowing for better oxygenation of the myocardium

41
Q

What can ß adrenoceptor antagonists be used to treat clinically?

A

Arrhythmias (decrease excessive sympathetic drive and help to restore sinus rhythm)

Atrial fibrillation and superventricular tachycardia (delay conduction through AV node and help to restore sinus rhythm)

Angina

42
Q

Low dose ß blockers are used in compensated heart failure. Just remember this.

A

lol

43
Q

Name a couple of adverse effects of ß blockers as a class.

A

Bronchospasm

Aggravation of cardiac failure

Bradycardia

Hypoglycaemia (glucose release from liver is controlled by ß2 adrenoceptors in diabetics)

Fatigue and cold extremities

44
Q

Name a muscarinic ACh receptor antagonist.

A

Atropine

45
Q

Atropine blocks muscarinic ACh receptors. Which division of the nervous system are these receptors associated with?

What does increased parasympathetic discharge cause in a patient?

What will the effect of atropine administration be in a patient?

A

Parasympathetic

Bradycardia

Increased heart rate

46
Q

Give in low doses, atropine causes (increased / decreased) heart rate.

A

Decreased heart rate

(In higher doses it increases heart rate.)

47
Q

Name a cardiac glycoside which increases the contractility of the heart.

A

Digoxin

48
Q

What is heart failure?

A

A cardiac output insufficient to provide adequate tissue perfusion

49
Q

Name two inotropic drugs which enhance contractility.

A

Digoxin

Dobutamine

50
Q

Inotropic drugs increase stroke volume at any given __ __ __.

A

end diastolic volume

51
Q

Which membrane transporter does digoxin block?

A

Na+/K+ ATPase

(sodium-potassium pump)

Cardiovascular Week 1 & 2 2016/17 (19 decks)

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