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Cardiovascular System > CVS Drugs > Flashcards

CVS Drugs Flashcards

1
Q

List some conditions that cardiovascular drugs treat

A

– Arrhythmias

– Heart failure

– Angina

– Hypertension

– Risk of thrombus formation

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2
Q

How can drugs affect the CVS?

A

– The rate and rhythm of the heart

– The force of myocardial contraction

– Peripheral resistance and blood flow

– Blood volume

Some drugs can act on multiple sites

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3
Q

What are some causes of arrhythmias?

A

Ectopic pacemaker activity:

– damaged area of myocardium becomes depolarised and spontaneously active

– latent pacemaker region activated due to ischaemia and dominates over SA node

Afterdepolarisations:

– abnormal depolarisations following the action potential (triggered activity)

Re-entry loop:

– conduction delay

– accessory pathway

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4
Q

What are delayed after-depolarisations?

A
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5
Q

What are early after-depolarisations?

A
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6
Q

What is the re-entrant mechanism for generating arrhythmias?

A

It is possible to get several small re-entry loops in the atria, leading to atrial fibrillation

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7
Q

What classes of drugs affect the rate and rhythm of the heart?

A
  • Drugs that block voltage-sensitive sodium channels
  • Antagonists of β-adrenoreceptors
  • Drugs that block potassium channels
  • Drugs that block calcium channels
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8
Q

What class of drug is lidocaine and how does it work?

A

It is a drug which blocks voltage-dependant Na+ channels (class I)

  • Typical example is the local anaesthetic lidocaine (class Ib)
  • Only blocks voltage gated Na+ channels in open or inactive state
  • Dissociates rapidly in time for next AP
  • Little effect in normal cardiac tissue
  • Use-dependent block
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9
Q

When is lidocaine used in relation to heart pathology?

A

Sometimes used following MI:
– only if patient shows signs of ventricular tachycardia – given intravenously

Damaged areas of myocardium may be depolarised and fire automatically

More Na+ channels are open in depolarised tissue – lidocaine blocks these Na+ channels (use-dependent)
– prevents automatic firing of depolarised ventricular tissue

Not used prophylactically following MI
– Even in patients showing VT may use other drugs

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10
Q

What are beta-adrenoceptor antagonists?

A

Examples: propranolol, atenolol (Beta blockers)

  • Block sympathetic action by acting at β1-adrenoreceptors in the heart
  • Decrease slope of pacemaker potential in SA
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11
Q

How do beta-blockers work?

A

Used following myocardial infarction
– MI causes increased sympathetic activity
– β-blockers prevent ventricular arrhythmias
– Arrhythmias may be partly due to increased sympathetic activity

Also reduces O2 demand:
– Reduces myocardial ischaemia

– Beneficial following MI

β-blockers slow conduction in AV node

– Can prevent supraventricular tachycardias

– Slows ventricular rate in patients with AF

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12
Q

How do drugs that block K+ channels work

A
  • 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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13
Q

Drugs that block K+ channels aren’t generally used as anti-arrythmic. What is the exception?

A

One exception – amiodarone

Included as a type III anti-arrhythmic, but has other actions in addition to blocking K+ channels

Used to treat tachycardia associated with Wolff- Parkinson-White syndrome (re-entry loop due to an extra conduction pathway)

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14
Q

How do drugs that block Ca2+ channels work?

A

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

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15
Q

How does adenosine work?

A

Produced endogenously:

  • Can also be administered pharmacologically
  • Acts on A1 receptors at AV node

• Enhances K+ conductance
– hyperpolarises cells of conducting tissue

• Anti-arrhythmic
– administered intravenously
– doesn’t belong in any of the classes mentioned

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16
Q

What is heart failure and its features?

A

– Chronic failure of the heart to provide sufficient output to meet the body’s requirements

Features:

– Reduced force of contraction

– Reduced cardiac output
– Reduced tissue perfusion
– Oedema

17
Q

What drugs are used in the treatment of heart failure?

A

Positive inotropes increase cardiac output:

– cardiac glycosides
– β-adrenergic agonists

  • dobutamine
  • Drugs which reduce work load of the heart – reduce afterload and preload
18
Q

What are cardiac glycosides?

A

Have been used to treat heart failure for over 200 years. They improve symptoms but not long term outcome

Digoxin is the prototype. Extracted from leaves of the foxglove digitalis purpurea or digitalis lanata

– Blocks Na+/K+ ATPase

19
Q

How do cardiac glycosides work?

A

Ca2+ is extruded via the Na+-Ca2+ exchanger which is driven by Na+ moving down concentration gradient.

Cardiac glycosides block Na+/K+ ATPase so there is a rise in [Na+] intracellularly.

Rise in intracellular Na+ leads to decrease in activity of Na+-Ca2+ exchanger which causes increase in [Ca2+] intracellularly.

There is more Ca2+ stored in SR and an increased force of contraction

Cardiac glycosides also cause increased vagal activity: – action via central nervous system to increase vagal activity
– slows AV conduction
– slows the heart rate

20
Q

What kind of drug increases myocardial contractility?

A

β–adrenoreceptor agonists – eg dobutamine

– act on β1 receptors

Uses:

  • cardiogenic shock
  • acute but reversible heart failure (eg following cardiac surgery)
21
Q

How do ACE inhibitors work?

A
  • 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
  • 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
22
Q

What types of drugs can reduce the workload of the heart?

A

β–adrenoceptor antagonists (β-blockers)

Diuretics:
– reduce blood volume
– more to follow in Urinary module

ACE inhibitors

23
Q

How is angina treated?

A

• Reduce the work load of the heart

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

• Improve the blood supply to the heart – organic nitrates
– Ca2+ channel antagonists

24
Q

How does NO exert its vasodilatory effects?

A

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 activates guanylate cyclase
  • Increases cGMP
  • Lowers intracellular [Ca2+]
  • Causes relaxation of vascular smooth muscle

Examples of Organic Nitrates;

  • glyceryl trinitrate
  • isosorbide dinitrate
25
Q

How does NO affect the heart?

A

PRIMARY ACTION:

action on venous system venodilation lowers preload

– reduces work load of the heart

– heart fills less therefore force of contraction reduced (Starling’s Law)

– this lowers O2 demand

SECONDARY ACTION:

action on coronary arteries improves O2 delivery to the ischaemic myocardium

– acts on collateral arteries rather than arterioles

26
Q

Which heart conditions can lead to thrombus formation?

A
  • Atrial fibrillation
  • Acute myocardial infarction
  • Mechanical prosthetic heart valves
27
Q

What are some anti-thrombotic drugs?

A

Anticoagulants:

  • Heparin (given intravenously) inhibits thrombin. It is used acutely for short term action.
  • Fractionated heparin (subcutaneous injection).
  • Warfarin (given orally) antagonises action of vitamin K and can be used long term.

Antiplatelet drugs:

– Aspirin following acute MI or high risk of MI

28
Q

What are the potential consequences of hypertension?

A

Associated with increases in blood volume – Na+ and water retention by the kidneys or an increase in total peripheral resistance (TPR).

29
Q

How can hypertension be treated?

A
  • Diuretics decrease Na+ and water retention by kidney and therefore decrease bloodv olume
  • ACE-inhibitors decrease Na+ and water retention by kidney, decrease total peripheral resistance- causing vasodilation
  • β-blockers– decrease cardiac output
  • Ca2+ channel blockers selective for vascular smooth muscle cause vasodilation
  • α1 – adrenoceptor antagonist – vasodilation

Cardiovascular System (12 decks)

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