CVS Session 10 - CVS Drugs Flashcards Preview

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

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.


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 


What are some causes of arrhythmia?

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Outline delayed after-polarisations.

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Outline early after-polarisations.

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Describe the re-entrant mechanism for generating arrhythmias.

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

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

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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 


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 

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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 

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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 


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 

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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 


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 


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 


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 

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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) 


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 


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 


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

- β–adrenoceptor antagonists (β-blockers)

- Diuretics – reduce blood volume


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 


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 


Describe how NO causes vasodilation. 

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How does NO vasodilation help alleviate symptoms?

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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 


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

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

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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 


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 


Outline hypertension.

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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