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Cardiovascular System > Session 7 - Cardiac Arrhythmias And CVS Drugs > Flashcards

Session 7 - Cardiac Arrhythmias And CVS Drugs Flashcards

1
Q

What is ectopic pacemaker activity?

A

Damaged area of myocardium becomes depolarized and spontaneously active and dominates over SA node

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2
Q

What are afterdepolarisations?

A

Abnormal depolarisations following the action potential

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3
Q

What is sick sinus syndrome?

A

Intrinsic SA node dysfunction

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4
Q

When are early after depolarisations more likely to happen?

A

If AP is prolonged // if longer QT interval

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5
Q

When are delayed after depolarisations more like to happen?

A

High intracellular Ca2+

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6
Q

What is the re entrant mechanism for generating arrythmias?

A

When there is incomplete conduction damage, excitation can take a long route to spread the wrong way through damaged area, setting up a circus of excitation

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7
Q

How does re entrant circuits lead to atrial fibrillation?

A

Multiple re entrant circuits in atria causes many atrial fibrillation impulses and chaotic signals passes through AV node, causing rapid ventricular impulses

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8
Q

How does AV nodal re entry occur?

A

Fast and slow pathways in AV node creates a re entry loop

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9
Q

What is ventricular pre excitation?

A

Accessory pathway between atria and ventricles creates re entry loop

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10
Q

What are 4 basic classes of anti arrhythmic drugs?

A

Na+ channel blockers
Beta adrenoceptor antagonist
K+ channel blockers
Ca2+ channel blockers

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11
Q

What is an example of a voltage dependent-Na+ channel blocker?

A

Lidocaine

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12
Q

How does Na+ channel blocker work?

A

Only blocks in open or inactive state, hence preferentially blocks damaged depolarized tissue and not normal tissue as it dissociates rapidly

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13
Q

What is the effect of lidocaine?

A

Blocks Na+ channels, slows upstroke, shortens action potential and slows conduction velocity

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14
Q

What are 2 examples of beta blockers?

A

Propranolol

Atenolol

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15
Q

How do beta blockers work?

A

Block sympathetic action at beta 1 adrenoceptors in heart, decreases slope of pace,alter potential in sinoatrial node and slows conduction at AV anode

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16
Q

What can beta blockers used to prevent?

A

Supraventricular tachycardia as it slows conduction in AVnode and can slow ventricular rate in patients with atria fibrillation

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17
Q

What can beta blockers be used following?

A

MI as it often causes increased sympathetic activity, so beta blockers can prevent ventricular arrythmias

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18
Q

What can K+ channel blockers do?

A

Prolong action potential and lengthen absolute refractory period

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19
Q

What is an example of K+ channel blocker?

A

Amiodarone

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20
Q

What can amiodarone be used for?

A

Treat tachycardia associated with Wolff-Parkinson-White syndrome

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21
Q

What are 2 examples of non dihydropyridine Ca2+ channel blockers?

A

Verapamil

Diltiazem

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22
Q

What do non-dihydropyridine Ca2+ channel blockers do?

A

Decrease slope of action potential at SA node, decrease AV nodal conduction, hence slowing heart rate and decrease force of contraction

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23
Q

What does adenosine do?

A

Act on A1 receptors at AV node but has very short half-life, enhances K+ conductance hence hyper Polaris into cells of conducting tissue

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24
Q

What can adenosine be used for?

A

Termination re entrant supraventricular tachycardia

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25
Q

What are 2 conditions that ACE inhibitors can be used to treat?

A

Hypertension

Heart failure

26
Q

What is an example of ACE inhibitors?

A

Perindopril

27
Q

What is the mechanism of action of ACEi?

A

Angiotensin converting enzyme inhibitor, prevents conversion of angiotensin I to angiotensin II

28
Q

What does angiotensin II do?

A

Acts on kidney to increase Na+ and water reabsorption and causes vasoconstriction

29
Q

What is a side effect of ACEi?

A

Dry cough

30
Q

How does ACEi reduce blood pressure?

A

It is a vasoconstrictor so it decreases vasomotor tone, hence decreasing after load

31
Q

How does ACEi reduce blood volume?

A

Reduce fluid retention and preload

32
Q

When are angiotensin II receptor blockers used?

A

If patients cannot tolerate ACEi

33
Q

What is an example of a ARB?

A

Losartan

34
Q

What are 2 conditions that diuretics treat?

A

Heart failure

Hypertension

35
Q

What are loop diuretics used for?

A

Congestive heart failure

36
Q

What are 2 examples of diuretics?

A

Furosemide

Thiazide diuretics

37
Q

What do dihydropyridine Ca2+ channel blockers do?

A

Act on vascular smooth muscle, decreases peripheral resistance, decreases arterial BP and reduces afterload

38
Q

What are 3 examples of dihydropyridine Ca2+ channel blockers?

A

Amlodipine
Nicardipine
Nifedipine

39
Q

What do positive inotropes do?

A

Increase contractility and thus cardiac output

40
Q

What are 2 types of positive inotropes?

A

Cardiac glycosides

Beta-adrenergic agonists

41
Q

What is an example of cardiac glycosides?

A

Digoxin

42
Q

What is an example of a beta-adrenergic agonist?

A

Dobutamine

43
Q

What is cardiac glycosides primary mode of action?

A

Block Na K ATPase, leads to rise in intracellular Na+, so NCX doesn’t work as well so intracellular Ca2+ increases and more is stored in SR, hence increasing force of contraction

44
Q

How does cardiac glycosides affect heart rate?

A

Increased vagal activity, slowing AV conduction, slowing heart rate

45
Q

What is an example of beta adrenoceptor agonist?

A

Dobutamine

46
Q

What do beat adrenoceptor agonists do?

A

Stimulate beta 1 receptors on SA AV node and ventricular myocytes

47
Q

What are 2 uses of beta adrenoceptor agonists?

A

Cardiogenic shock

Acute but reversible heart failure

48
Q

Are cardiac glycosides good treatment of heart failure?

A

It will relieve symptoms by making heart contract harder but no long term benefit, it’s better to reduce workload

49
Q

How does angina occur?

A

When O2 supply doesn’t meet its demand, causing ischaemia and hence chest pain

50
Q

How does nitrates work to treat angina?

A

Reaction of organic nitrates with thiols in vascular smooth muscle causes NO2- to be released and reduced to NO which is a powerful vasodilator particularly effective on veins

51
Q

What are 2 examples of organic nitrates and the difference between them?

A

GTN spray short acting

Isosorbide dinitrate longer acting

52
Q

How does NO cause vasodilation?

A

Activates guanylate cyclase, increase cGMP, lowers intracellular Ca2+ and hence relaxation of vascular smooth muscle

53
Q

Why do organic nitrates preferentially act on veins?

A

Less endogenous nitric oxide in veins

54
Q

What is the primary action of nitrates that help alleviate symptoms?

A

Venodilation reduces venous pressure, return of blood to heart, lowers preload, reducing workload of heart, heart fills less, reducing force of contraction, reducing O2 demand

55
Q

What is the secondary action of organic nitrates that help alleviate symptoms?

A

Dilate coronary collateral arteries improved O2 delivery to ischaemic myocardium

56
Q

What are 2 types of anti thrombotic drugs?

A

Anticoagulants

Antiplatelet

57
Q

What are 4 types of anticoagulants?

A

Heparin
Fractionated heparin
Warfarin
Direct acting oral thrombin inhibitors

58
Q

How does heparin work as a anticoagulant?

A

Inhibits thrombin, used acutely for short term action

59
Q

What do antiplatelet drugs do?

A

Prevent platelet rich arterial thrombus formation

60
Q

What are 2 examples of antiplatelet drugs?

A

Aspirin

Clopidogrel

Cardiovascular System (11 decks)

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