CVS Session 10 - CVS Drugs Flashcards Preview

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Flashcards in CVS Session 10 - CVS Drugs Deck (32):
1

Outline, briefly, the action of drugs in the cardiovascular system.

- Drugs can alter:

I. The rate and rhythm of the heart

II. The force of myocardial contraction

III. Peripheral resistance and blood flow

IV. Blood volume 

- Some drugs can act at more than one site.

2

What are some disturbances of the cardiac rhythm (arrhythmia or dysrhythmias)?

Abnormality of heart rate or rhythm

- Bradycardia

- Atrial flutter

- Atrial fibrillation

- Tachycardia

I. Ventricular Tachycardia

II. Supraventricular tachycardias

- Ventricular fibrillation 

3

What are some causes of arrhythmia?

4

Outline delayed after-polarisations.

5

Outline early after-polarisations.

6

Describe the re-entrant mechanism for generating arrhythmias.

7

Outline atrial fibrillation in terms of the multiple re-entrant circuits in the atria

8

Describe AV nodal re-entry and ventricular pre-excitation.

9

There are 4 basic classes of anti-arrhythmic drugs. What are the drugs affecting the rate and rhythm of the heart?

 

- Drugs that block voltage-sensitive sodium channels

- Antagonists of β-adrenoreceptors

- Drugs that block potassium channels

- Drugs that block calcium channels

Don’t need to know the classification – just understand the way some types of anti-arrhythmic drugs work 

10

Outline the action of drugs which block voltage-dependant Na+ channels (Class I) 

- A typical example is the local anaesthetic lidocaine 

- Use-dependent block. Only blocks voltage gated Na+ channels in open or inactive state – therefore preferentially blocks damaged depolarised tissue

- Little effect in normal cardiac tissue because it dissociates rapidly

- Blocks during depolarisation but dissociates in time for next AP 

11

Outline the action of β-adrenoreceptor antagonists (class II) 

- Examples: propranolol, atenolol (Beta blockers)

- Block sympathetic action – act at β1-adrenoreceptors in the heart

- Decrease slope of pacemaker potential in SA and slows conduction at AV node 

12

Describe, in detail, the effects of beta blockers.

- β-blockers slow conduction in AV node

I. Can prevent supraventricular tachycardias - arrhythmias may be partly due to increased sympathetic activity

II. Slows ventricular rate in patients with AF

- Used following myocardial infarction

I. MI causes increased sympathetic activity

II. β-blockers reduces O2 demand - hence reduces myocardial ischaemia

III. Beneficial following MI 

13

Outline the action of drugs that block K+ channels (class III)

- Class III anti-arrhythmics

- Prolong the action potential – mainly by blocking K+ channels

- This lengthens the absolute refractory period

- In theory prevents another AP occurring too soon

- In reality can be pro-arrhythmic 

14

Outline the actions of drugs that block Ca2+ channels (class IV)

- Example: verapamil

- Decreases slope of action potential at SA node

- Decreases AV nodal conduction

- Decreases force of contraction (negative inotropy) • Also some coronary and peripheral vasodilation

- Dihydropyridine Ca2+ channel blockers are not effective in preventing arrhythmias, but do act on vascular smooth muscle - examples: amlopidine, felopidine, nicardipine etc 

15

What are the drugs used in the treatment of heart failure? 

- Positive inotropes to increase cardiac output (not routinely used)

I. Cardiac glycosides

II. β-adrenergic agonists - dobutamine

- Drugs which reduce work load of the heart – reduce afterload and preload 

16

Outline drugs which increase myocardial contractility. 

- Cardiac glycosides
I. Have been used to treat heart failure for over 200 years

II. Improves symptoms but not long term outcome

- Digoxin is the prototype

I. Extracted from leaves of the foxglove digitalis purpurea or digitalis lanata

II. Blocks Na+/K+ ATPase 

17

Outline the action of cardiac glycosides on heart rate.

- Cardiac glycosides also cause increased vagal activity

I. Action via central nervous system to increase vagal activity

II. Slows AV conduction

III. Slows the heart rate

- Cardiac glycosides may be used in heart failure when there is an arrhythmia such as AF 

18

Outline the use of β – adrenoreceptor agonists 

- E.g. dobutamine

- Acts on β1 receptors

- Uses

I. Cardiogenic shock

II. Acute but reversible heart failure (eg following cardiac surgery) 

19

Outline drugs which reduce the workload of the heart: ACE-inhibitors 

- Drugs which inhibit the action of angiotensin converting enzyme are important in the treatment of heart failure

- Prevent the conversion of angiotensin I to angiotensin II

- Angiotensin II acts on the kidneys to increase Na+ and water reabsorption

- Angiotensin II is also a vasoconstrictor

- Or use Ang II receptor blocker if ACEi not tolerated 

20

Outline the use of Ace inhibitors

- Very valuable in treatment of heart failure

- Decrease vasomotor tone (blood pressure)

- Reduce afterload of the heart

- Decrease fluid retention (blood volume)

- Reduce preload of the heart

- Reduce work load of the heart 

21

What are other drugs which reduce the workload of the heart?

- β–adrenoceptor antagonists (β-blockers)

- Diuretics – reduce blood volume

22

How does one treat angina?

- Reduce the work load of the heart

I. β-adrenoreceptor blockers

II. Ca2+ channel antagonists

III. Organic nitrates

- Improve the blood supply to the heart

I. Organic nitrates

II. Ca2+ channel antagonists 

23

Outline the action of organic nitrates.

- Reaction of organic nitrates with thiols (-SH groups) in vascular smooth muscle causes NO2- to be released

- NO2- is reduced to NO (Nitric Oxide)

- NO is a powerful vasodilator 

- Examples: 

I. Glyceryl trinitrate (GTN spray)

II. Isosorbide dinitrate 

24

Describe how NO causes vasodilation. 

25

How does NO vasodilation help alleviate symptoms?

26

Why do organic nitrates preferentially act on veins?

- Probably because there is less endogenous nitric oxide in veins

- Most effective on veins > arteries

- Little effect on arterioles 

27

Organic nitrates don’t work by dilating arterioles (may help to dilate collaterals – minor contribution). Explain this 

28

Explain how the main action of organic nitrates is by venodilation.

29

Why do we need antithrombotic drugs?

Certain heart conditions carry an increased risk of thrombus formation:

- Atrial fibrillation

-  Acute myocardial infarction

- Mechanical prosthetic heart valves 

30

Outline antithrombotic drugs (examples and uses).

- Anticoagulants 

I. Heparin (given intravenously)

  • Inhibits thrombin
  • Used acutely for short term action

II. Fractionated heparin (subcutaneous injection)

III. Warfarin (given orally) - antagonises action of vitamin K
IV.  Direct acting oral thrombin inhibitors such as digabatran

 

- Antiplatelet drugs – Aspirin

I. Following acute MI

II. In the case of high risk of MI 

31

Outline hypertension.

32

Outline drugs used to treat hypertension

- ACE-inhibitors
I. Decrease Na+ and water retention by kidney
II. Decrease total peripheral resistance - vasodilation

- Ca2+ channel blockers selective for vascular smooth muscle – vasodilation

- Diuretics

I. Decrease Na+ and water retention by kidney

II. Decrease blood volume

- β-blockers – not routinely used – decrease cardiac output

- α1 – adrenoceptor antagonist – not routinely used – vasodilation