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CVS > 10. Arrythmias & drug actions > Flashcards

10. Arrythmias & drug actions Flashcards

1
Q

What are some causes of tachycardia?

A

Afterdepolarisations
Atrial flutter/ fibrillation
Re-entry loop
Ectopic pacemaker activity

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2
Q

What are some causes of bradycardia?

A
  • Sinus bradycardia- drugs, sick sinus syndrome

- Conduction block

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3
Q

When are delayed after-depolarisations most likely to occur?

A

When [Ca2+] is high - DIGOXIN overdose

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4
Q

When are early after-depolarisations most likely to occur?

A

Prolonged action potential with lengthened QT inverval- hypokalaemia

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5
Q

What is AV node re-entry?

A

Fast and slow pathways in the AV node create a re-entry loop for continuous depolarisation

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6
Q

What is ventricular pre-excitation?

A

Accessory pathway between atria and ventricles creates a re-entry loop
- Wolf parkinson White syndrome

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7
Q

What are the 4 classes of drugs that affect CV rate and rhythm?

A
  1. Block V-gated Na+ channels
  2. B-adrenoceptor antagonists
  3. K+ channel blockers
  4. Ca2+ channel blockers
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8
Q

What is an example of a voltage-gated sodium channel blocker?

A

Lidocaine

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9
Q

What effect does lidocaine have on normal cardiac tissue?

A

Little effect as blocks during depolarisation, which is followed by a refractory period anyway.
Dissociates quickly before following action potential is generated.

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10
Q

When is lidocaine used?

A

Following MI if the patient has signs of ventricular tachycardia when damaged areas of myocardium may be depolarised and fire automatically.

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11
Q

What effects do B1 antagonists have?

A

Slow conduction at AV node

Reduces O2 demand

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12
Q

Why are B1-antagonists used following MI?

A

MI causes increased sympathetic activity with increases risk of arrythmia.Beta blockers prevent ventricular arrythmias.
Reduces oxygen demand, reducing myocardial ischaemia.

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13
Q

Othen than following an MI, when else are beta-blockers used?

A
  • Prevent supraventricular tachycardias

- Patients with AF - slow ventricular rate

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14
Q

What effect to K+ channel blockers have?

A

Prolong the action potential by lengthening the absolute refractory period.

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15
Q

Why are K+ blockers rarely used?

A

Pro-arrythmic, likely to lead to after depolarisations.

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16
Q

Which is the only K+ blocker that is used, how does this differ to the others?

A

Amiodarone

Lacks specificity, also blocks B1 receptors and calcium channels.

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17
Q

What is amiodarone used to treat?

A

Tachycardia associated with wolf-parkinson-white syndrome (re-entry)
Suppressing ventricular arrythmias following MI

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18
Q

How do Ca2+ blockers affect the action potential?

A

Decrease the slope of the AP at the SA node.

Decreases AV node conduction and force of contraction

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19
Q

What are dihydropyridines?

A

CCB that is not effective in preventing arrythmias but act on vascular smooth muscle to cause vasodilation.
E.g Amlodipine

20
Q

What is the MOA of adenosine?

A

Acts on A1 receptors at AV node to enhance K+ conductance, hyper polarising cells of conducting tissue.
Very short half life

21
Q

What is adenosine used to treat?

A

Anti-arrythmic - terminating re-entrant SVT

22
Q

What approach is taken when treating HF?

A

Aiming to reduce the workload of the heart rather than increase its contractility as better outcomes in the long run. Positive inotropes not routinely used.

23
Q

What drugs increase myocardial contractility?

A

Cardiac glycosides - improve symptoms but not long term outcome
B-adrenoceptor agonists

24
Q

What is an example of a cardiac glycoside?

A

Digoxin

25
Q

What is the MOA of digoxin?

A

Inhibits Na+/K+ ATPase which leads to a rise in intracellular [Na+] and decreases the activity of NCX. This increases intracellular [Ca2+] and increases inotropy.

26
Q

How can cardiac glycosides affect heart rate?

A

Increase vagal activity:

  • Slow AV conduction
  • Slows HR
27
Q

When are cardiac glycosides used?

A

In HF when there is an arrhythmia - e.g AF

28
Q

What is an example of a B1 adrenoceptor agonist?

A

Dobutamine

29
Q

When is dobutamine used?

A

Cardiogenic shock

Acute but reversible HF (following surgery)

30
Q

What drugs function to reduce the workload of the heart?

A

ACE Inhibitors
B-adrenoceptor antagonists
Diuretics

31
Q

How do ACE inhibitors reduce the cardiac workload?

A

Inhibiting AngII formation:
Decrease fluid retention - reduce preload
Decrease vasomotor tone - reduce after load

32
Q

What drug is often used if ACE inhibitors are not tolerated?

A

Angiotensin II receptor antagonists

33
Q

What are the aims of angina treatment?

A
  1. Reduce workload of the heart (oxygen demand)

2. Improve blood supply of the heart

34
Q

What drugs are used in angina to reduce the workload?

A

beta blockers
CCBs
Organic nitrates

35
Q

What drugs are used to treat angina by improving the blood supply to the heart?

A

Organic nitrates

CCBs (vasodilation)

36
Q

What is an example of an organic nitrate?

A

Glyceryl trinitrate (GTN)

37
Q

What is the MOA of organic nitrates?

A

Organic nitrates react with tools in VSMCs to cause NO2- to be released.
NO2- is reduced to NO, a potent vasodilator.

38
Q

How does NO lead to vasodilation?

A

Stimulates guanylate cyclase, which converts GTP to cGMP, which activates PKG, PKG decreases intracellular calcium conc, causing relaxation of the VSMC.

39
Q

What is the primary action of organic nitrates?

A

Acts on venous system primarily - venodilation lowers preload
Less filling therefore contractility reduced (Starling) which lowers oxygen demand.

40
Q

What is the secondary action of organic nitrates?

A

Acts on coronary collateral arteries to improve oxygen delivery to the ischaemic myocardium (minor contribution).
Note: there are not many coronary collateral arteries, end arteries.

41
Q

What blood vessels do organic nitrates NOT affect?

A

Arterioles

42
Q

Why do organic nitrates preferentially act on veins?

A

Less endogenous NO present, so most marked effect,

Little effect on arteries but no effect on arterioles.

43
Q

When might anti-thrombotic drugs be given?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic valves

44
Q

What is heparin, when is it used?

A

Anticoagulant that inhibits thrombin.

Used acutely for short term action - given IV

45
Q

How does warfarin act as anticoagulant, when is it used?

A

Antagonises the action of vitamin K

Given orally

46
Q

Give an example of an anti-platelet drug?

A

Aspirin

47
Q

When is aspirin given?

A

Following acute MI or high risk of MI

CVS (16 decks)

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