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Cardiovascular > Session 7 > Flashcards

Session 7 Flashcards

1
Q

What is tension in myocardial cells proportional to?

A

The concentration of calcium in.

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2
Q

What changes occur to the calcium concentration to cause systole and diastole?

A

Systole - calcium concentration increases

Diastole - calcium concentration decreases

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3
Q

What is the equilibrium potential?

A

The hypothetical membrane potential that would develop if it was the only ion that could cross the membrane.

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4
Q

Myocardial cells have which voltage gated channels.

A

Sodium, potassium and calcium.

These are to present in the pacemaker cells!

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5
Q

What is the cell membrane mostly permeable to in diastole?

A

Potassium.

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6
Q

What is the membrane voltage during diastole?

Extra point - Why?

A

-80mV

Because it is only permeable to potassium, it is close to the equilibrium potential for potassium.

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7
Q

What happens when the initial depolarisation reaches the threshold?

A

Fast voltage gated sodium channels open.

The membrane potential goes closer to the sodium equilibrium potential and depolarises further.

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8
Q

Once the fast voltage gated sodium channels are open, the close fast too. What stops the membrane from repolarising quickly?

A

Calcium voltage gated channels.

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9
Q

What does calcium entering the cell stimulate?

A

Intracellular stores to release calcium, causes contraction.

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10
Q

How long do the calcium channels stay open for?

A

250ms

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11
Q

What channel opens while the calcium channels are open to cause depolarisation to occur faster?

A

Potassium voltage gated channels.

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12
Q

Do pacemaker cells have fast sodium channels?

A

No.

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13
Q

What causes the upstroke (once threshold is reached) in pacemaker cells?

A

Slow calcium channels.

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14
Q

Why is the action potential short in pacemaker cells?

A

Because calcium channels close quickly.

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15
Q

Once the action potential has finishes, what causes it to depolarise slowly?

A

The membrane potential is not stable so the ion permeability alters.

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16
Q

What is the significance of pacemaker cells having no fast sodium channels?

A

They are not sensitive to the membrane potential.

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17
Q

What does the interval between beats depend on?

A

How fast the pacemaker cells depolarise.

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18
Q

What speeds up pacemaker depolarisation?

A

Sympathetic innovation.

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19
Q

What slows down the pacemaker potential?

A

Parasympathetic innovation.

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20
Q

How does noradrenaline speed up the heart rate?

A

Makes the pacemaker potential steeper.

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21
Q

How do acetylcholine slow the heart rate?

A

Makes the pacemaker potential shallower.

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22
Q

What can CVS drugs treat?

A

Arrhythmias, heart failure, angina and hypertension.

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23
Q

What can CVS drugs alter?

A

Rate and rhythm of the heart, the force of contraction, blood flow and blood volume.

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24
Q

What can cause disorders of rhythms?

A

Ectopic pacemaker activity.

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25
Q

What is ectopic pacemaker activity?

A

Where a damaged area (can be from MI) becomes active.

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26
Q

What can allow after depolarisations?

A

Anything that prolongs the action potential.

27
Q

What are the 4 classes of anti arrhythmia drugs?

A

Drugs that block voltage sensitive sodium channels.
Antagonists of beta adrenoreceptors.
Drugs that block potassium channels.
Drugs that block calcium channels.

28
Q

Give an example of a drug that blocks the voltage sensitive sodium channels.

A

Local anaesthetics such as lidocaine.

29
Q

Give an example of an antagonist of beta adrenoreceptors.

A

Propranolol
Atenolol
-called beta blockers.

30
Q

Give an example of a drug that blocks calcium channels.

A

Verapamil.

31
Q

How do drugs that block voltage sensitive sodium channels work?

A

It blocks sodium channels in their open or inactive state.
It dissociates rapidly in time for the next action potential.
It prevents automatic firing of damaged tissues.

32
Q

When can lidocaine be used?

A

After an MI if there are signs of ventricular tachycardia.

33
Q

How do antagonists of beta adrenoreceptors work?

A

They block the sympathetic action of beta 1 adrenoreceptors in the heart and decrease the pacemaker potential slope in the sinoatrial node.

34
Q

Give an example of a drug that blocks the potassium channels.

A

amiodarone.

35
Q

When are antagonists of beta adrenoreceptors used?

A

Can be used after an MI.
Reduces myocardial ischaemia by reducing oxygen demand.
Can prevent supra ventricular (originates from the atria) tachycardia by slowing conduction in the atrioventricular node.

36
Q

How do drugs that block the potassium channel work?

A

They prolong the action potential by blocking the potassium channels, lengthening the absolute refractory period.

37
Q

What is the risk when using drugs that block potassium channels?
Extra point - What drug is the exception?

A

They are for likely to cause arrhythmias because they increase the absolute refractory period.
Extra point - amiodarone is the only exception.

38
Q

How do drugs that block the calcium channels work?

A

They decrease the slope of the pacemaker action potential at the sino atrial node.
They decrease the atrioventricular node conduction.
They decrease the force of contraction.
Can cause vasodilation.

39
Q

What is adenosine?

A

A substance produced endogenously that prevents re entry arrhythmias with a very short half life.

40
Q

What does adenosine act on?

A

Alpha 1 receptors.

41
Q

How does adenosine work?

A

It increases potassium conductance which slows conduction.

It hyper polarises conducting tissue cells.

42
Q

How do you give adenosine?

A

Intra venously.

43
Q

We is heart failure?

A

The chronic failure of the heart to provide sufficient output to meet the body’s requirements.

44
Q

What is associated with heart failure?

A

A reduced force of contraction.
A reduced cardiac output.
A reduced tissue proliferation.
Oedemas.

45
Q

What are the 2 approaches to treating heart failure?

A

Drugs which reduce the work load of the heart by reducing the preload and after load.
Drugs which increase the cardiac output as they are positive inotropes.

46
Q

What drugs used after a cardiac failure have a positive inotrophic effect?

A

Cardiac glycosides. Eg Digoxin.

Beta adrenoreceptor agonists. Eg Dobutamine.

47
Q

How do cardiac glycoside drugs work?

A

Block the sodium/calcium exchanger. So the intracellular concentration of sodium increases, causing inhibition of the exchanger. Increased concentration of calcium in the myocytes.
**They improve symptoms, but not the long term outcome.

48
Q

How does beta adrenoreceptor agonists work?

A

They increase the concentration of cAMP, so calcium increases and contraction increases.
**They are not often used.

49
Q

What drugs used to treat cardiac failure reduce the workload of the heart?

A

ACE inhibitors - Angiotnsin Converting Enzyme.

Beta adrenoceptor antagonists. (Beta blockers) eg Diuretics.

50
Q

How do ACE inhibitors work?

A

They prevent the conversion of angiotensin 1 –> Angiotensin 2 (acts in the kidneys by increasing sodium and water reabsorption.)
Vasoconstrictor.
Decrease vasomotor tone and BP
Reduce the after load of the heart and fluid retention
So reduce the preload of the heart - starlings law means reduced work of the heart.

51
Q

How do beta adrenoreceptor antagonists work?

A

They reduce the blood volume by promoting the loss of sodium and water at the kidneys.

52
Q

What is angina?

A

Myocardial ischaemia - not enough O2.
Chest pain ONLY with exertion.
There may be narrowing of the coronary arteries.

53
Q

How can angina be treated?

A

Reduce the workload of the heart by using beta adrenoreceptor blockers or calcium channel antagonists.
Improve the blood supply to the heart - using organic nitrates. These work by -SH groups in vascular smooth muscle cause NO2- to be released. This is reduced to NO which is a vasodilator.

54
Q

NO is a powerful vasodilator. How does it work?

A

It activated guanylate cyclase which increases cGMP. This lowers incracellular calcium stores and causes relaxation of the vascular smooth muscle.

55
Q

How does NO alleviate symptoms?

A

Primary - on the venous system is lowers the preload so heart workload reduces, lowering the O2 demand.
Secondary - on coronary arteries. Increases the O2 delivery to the ischaemic myocardium by dilating collateral arteries so there is another route for the blood flow.

56
Q

What are the two types of anti thrombotic drugs?

A

Anticoagulants eg heparin and warfarin.

Anti platelet eg aspirin.

57
Q

What is hypertension associated with?

A

An increase in blood volume due to sodium and water retention by the kidneys.
OR
An increase in total peripheral resistance.

58
Q

How can you treat hypertension?

A 
Diuretics
ACE inhibitors
Beta blockers (not usually used)
Calcium channel blockers
Alpha 1 adrenoreceptor antagonists
59
Q

How do diuretics work in treating hypertension?

A

They decrease the sodium and water retention by the kidneys.

So there is a decreased blood volume.

60
Q

How do ACE inhibitors work in treating hypertension?

A

They decrease the sodium and water retention by the kidneys.

Decrease the total peripheral resistance with vasodilation.

61
Q

How do beta blockers reduce hypertension?

A

They decrease the cardiac output.

62
Q

How do calcium channel blockers decrease hypertension?

A

They act on vascular smooth muscle and cause vasodilation and reduced Total peripheral resistance.

63
Q

How do alpha 1 adrenoceptor antagonists reduce hypertension?

A

They act on vascular smooth muscle by causing vasodilation.

Cardiovascular (15 decks)

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