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2 - Sarah's CVS > Action of Drugs on the CVS -- 7.2 > Flashcards

Action of Drugs on the CVS -- 7.2 Flashcards

1
Q

What do drugs for the CVS have an effect on?

A
    • rate and rhythm of heart
    • force on contraction
    • peripheral resistance and blood flow
    • blood volume
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2
Q

Define arrhythmia

A

an abnormality of heart rate or rhythm

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3
Q

Give 5 types of arrythmia

A
  1. Bradycardia
  2. Atrial flutter
  3. Atrial fibrillation
  4. Tachycardia (ventricular and supraventricular)
  5. Ventricular fibrillation – no coordinated electrical activity so no coordinated contraction
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4
Q

What are the 3 causes of arrhythmias?

A
  1. Ectopic pacemaker activity – pacemaker activity not where it is meant to be
  2. Afterdepolarizations
  3. Re-entry loop – problem with conduction
  4. Sarah’s Doctor Who Uno
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5
Q

Define afterdepolarisations

A
    • anything that prolongs the duration of the AP
    • can trigger a premature action potential
    • longer AP so longer QT interval
    • could be due to increased intracellular calcium
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6
Q

GIve an example of re-entry loop and describe it

A

problem with conduction e.g. conduction delay
There is a block of a branch of purkinje fibre
Incomplete conduction damage

– unidirectional block

– excitation takes the long route to spread the wrong way setting up a circus of excitation

– can get several small re-entry loops in the atria which can cause atrial fibrilation

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7
Q

Describe ectopic pacemaker activity

A

Damaged area of myocardium because depolarised and spontaneously active.
Latent pacemaker region activated due to ischaemia
Dominate over SA node

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8
Q

What are the 4 basic classes of anti-arrhythmic drugs?

A
  1. Drugs that block voltage gated Na+ channels
  2. Antagonists of β-adrenoceptors
  3. Drugs that block K+ channels
  4. Drugs that block Ca2+channels
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9
Q

Give an example of a drug that blocks voltage-gated Na channels and what they do

A

lidocaine
They block channels in open or inactive state
– are able to dissociate rapidly before the next AP
– Prevents firing of AP too close to each other

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10
Q

When are class I drugs used and why?

A

After MI w/ ventricular tachycardia

– prevents the automatic firing of the depolarised, damaged area of the myocardium

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11
Q

Give an example if antagonists of B-adrenoceptors and what they do

A

Propranolol, atenolol

– block sympathetic action (B-1 adrenoceptors in heart) and decrease slope of pacemaker potential in the SA

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12
Q

When are class II drugs used?

A

Used after MI –> decreased sympathetic activity which prevent ventricular arrhythmias.

– reduces O2 demand to reduce the risk of myocardial ischaemia

– slows AV node conduction (prevents supraventricular tachycardias)

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13
Q

What do drugs that block K+ channels do?

A

– prolong the AP to lengthen the absolute refractory period
– should prevent and AP from occurring too soon, but can be proarrhythmic
Are not generally used

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14
Q

What class III drug is used regularly?

A

Amiodarone
– used to treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop due to extra conduction pathway)

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15
Q

GIve an example of a drug which blocks calcium channels and what they do

A

Verapamil

    • Decreases the slope of pacemaker action potential at SA node and decreases AV node conduction.
    • This causes a decrease in the force of contraction (negative ionotropy)
    • Can cause coronary and peripheral vasodilation
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16
Q

What is adenosine?

A

Acts on A2 receptors at AV node to enhance K+ conductance (prevents conduction through the AV node)
– inhibits adenylyl cyclase
Does not fit into the classes
– short half life of ~ 10 seconds
– Allows heart to get back to a synchronous rhythm h

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17
Q

What are the features of heart failure that have to be combatted?

A

– Reduced force of contraction – Reduced cardiac output
– Reduced tissue perfusion
– Oedema

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18
Q

What are positive ionotropes used for?

Give an example of a positive ionotrope

A

Increase the cardiac output

Cardiac glycosides

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19
Q

What are the general actions of cardiac glycosides?

A

Improve the symptoms of heart failure

Are not good in the long term

20
Q

What is the molecular action of cardiac glycosides?

A
  • -> blocks Na+/K+ ATPase so increases intracellular Na conc as well as intracellular Ca as the Na/Ca exchanger is inhibited
  • -> increase vagal activity via CNS (slows AV conduction and heart rate
21
Q

Give an example if antagonists of B-adrenoceptors and what they do

A

Propranolol, atenolol

– block sympathetic action (B-1 adrenoceptors in heart) and decrease slope of pacemaker potential in the SA

22
Q

What is the effect of cardiac glycosides?

A
  • -> blocks Na+/K+ ATPase
  • -> Na/Ca exchanger still works so [Na] increases
  • -> increased [Na] causes Na/Ca to exchange less, so [Ca] increases
  • -> increase [Ca] increases the force on contraction (positive ionotropic effect)

INCREASE CARDIAC OUTPUT

Also cause increase vagal activity
(slows AV conduction and HR)

23
Q

What class of drugs increase myocardial activity and give an example

A

Beta-adrenoceptor agonist

Dobutamine

24
Q

When are drugs which increase myocardial activity used?

A
  1. Cardiogenic shock

2. Acute but reversible heart failure, for example after heart surgery

25
Q

What are ACE-inhibitors?

A

drugs which inhibit the action of angiotensin converting enzyme

26
Q

What do ACE-inhibitors do?

A

They prevent the conversion of angiotensin I to angiotensin II
– angiotensin II acts on the kidneys to increase Na+ and H20 reabsorption. It is also a vasoconstrictor.
– decrease Na+ and water retention by kidney (decrease blood volume)
– decrease total peripheral resistance due to vasodilation
- decrease blood pressure by decreasing vasomotor tone, reducing afterload

27
Q

What does angiotensin II stimulate the release of?

A

Aldosterone from the adrenal cortex

28
Q

Define angina

A

Occurs when O2 supply to the heart does not meet its need
Causes Ischaemia of heart tissue
Usually causes chest pain upon exertion which is due to narrowing of the coronary arteries

29
Q

What are the general ways of treating angina

A

Reduce the work load of the heart
and
Improve the blood supply to the heart

30
Q

What drugs reduce the work load of the heart?

A

– β-adrenoreceptor blockers
– Ca2+ channel antagonists
– organic nitrates

31
Q

What drugs improve the blood supply of the heart?

A

– organic nitrates

– Ca2+ channel antagonists

32
Q

What is the general action of organic nitrates?

A

Reduce venous pressure due to venodilation and dilate the coronary arteries

33
Q

Describe the molecular action of organic nitrates

A

The react with -SH groups in vascular smooth muscle causing the release of NO (powerful vasodilator)
NO activates guanylate cyclase. This converts GTP to cGMP to lower [Ca].
Lower [Ca] relaxes the vascular smooth muscle –> venodilation

34
Q

What is the primary action of organic nitrates?

A

Cause venodilation which lowers preload

– reduces work load, lowers force on contraction and lowers O2 demand

35
Q

What is the secondary action of organic nitrates?

A

Acts to dilate the coronary arteries so improves O2 supply to ischaemic myocardium
– usually collateral arteries rather than arterioles to bypass atheromatous plaque

36
Q

Which conditions carry an increased risk of a thrombus forming?

A

– Atrial fibrillation
– Acute myocardial infarction
– Mechanical prosthetic heart valves

37
Q

What are the two classes of drugs that are antithrombitic drugs?

A

Anticoagulants and anti-platelet drugs

38
Q

Give three anticoagulants and what they do

A
  1. Heparin (given intravenously)
    - - inhibits thrombin and is used acutely (short term action)
  2. Fractionated heparin (subcutaneous injection)
  3. Warfarin (given orally)
    - - antagonises action of vitamin K so can be used long term
39
Q

Give an antiplatelet drug

A

Aspirin

– taken following an acute MI of if someone has a high risk of an MI

40
Q

What are possible treatments for hypertension?

A 
– diuretics
– ACE-inhibitors
– β-blockers
– Ca2+ channel blockers which act at vascular smooth muscle
– α1-adrenoceptor antagonists
41
Q

What characteristics are associated with hypertension?

A

Increased blood volume

Increased TPR

42
Q

What do diuretics do?

A

decrease Na+ and water retention by kidney therefore decrease blood volume

43
Q

What do beta-blockers do?

A

Decrease the cardiac output

44
Q

What do drugs that are Ca2+ channel blockers selective for vascular smooth muscle do?

A

Cause vasodilatation

45
Q

What do alpha-one adrenoceptor antagonists do?

A

Cause vasodilation

46
Q

What is the equation the links BP, TPR and CO?

A

BP = CO x TPR

47
Q

What do organic nitrates not dilate?

A

Arterioles

2 - Sarah's CVS (13 decks)

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