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Cardiovascular System > CVS10 Arrhythmias and CVS drugs-Evita > Flashcards

CVS10 Arrhythmias and CVS drugs-Evita Flashcards

1
Q

define bradycardia

A

Heart rate lower than 60 beats per minute

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2
Q

define tachycardia

A

Heart rate greater than 100 beats per minute

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3
Q

List the different types of heart arrhythmias

A
  • bradycardia
  • atrial flutter
  • atrial fibrillation
  • tachycardia
  • ventricular fibrillation
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4
Q

What is ventricular tachycardia?

A

Overly fast heart rate originating from the ventricles

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5
Q

What can ventricular tachycardia lead to?

A

Ventricular fibrillation

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6
Q

define supraventricular tachycardia

A

tachycardia originating above the ventricles, i.e. in the atria or the conduction system between the atria and ventricles

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7
Q

list the four causes of tachycardia

A
  • ectopic pacemaker activity
  • afterdepolarisations
  • atrial flutter/atrial fibrillation
  • re-entry loop
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8
Q

list the 2 causes of bradycardia

A
  1. sinus bradicardia
    • sick sinus syndrome
    • drugs
  2. conduction block
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9
Q

why may an ectopic pacemaker potential occur?

A
  1. damaged area of the myocardium becomes depolarised and spontaneously active
  2. latent pacemaker region is activated due to ischaemia and dominates over the SAN
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10
Q

what are afterdepolarisations?

A

abnormal depolarisations following an action potential

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11
Q

what type of tachycardia does atrial fibrillation cause?

A

supraventricular tachycardia

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12
Q

what is sick sinus syndrome?

A

intrinsic sinoatrial node dysfunction (it’s a group of disorders)

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13
Q

what can sick sinus syndrome lead to?

A

sinus bradycardia

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14
Q

what can drugs such as beta blockers cause?

A

sinus bradycardia

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15
Q

what can cause a conduction block?

A
  1. problems at AVN or bundle of His

2. slow conduction at AVN due to extrinsic factors (drugs)

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16
Q

what can conduction block cause?

A

bradycardia

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17
Q

what are delayed afterdepolarisations?

A

depolarisation of cardiomyocytes during phase 4, before another action potential would normally occur

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18
Q

what causes delayed afterdepolarisations?

A

high intracellular Ca concentration

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19
Q

what are early afterdepolarisations?

A

deepolarisation of cardiomyocytes in phase 2 or 3 (plateau or repolarisation phases)

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20
Q

what can cause early afterdepolarisations?

A

prolonged action potential (longer QT interval)

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21
Q

what is the QT interval equal to?

A

the amount of time that ventricles are depolarised for

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22
Q

what is a re-entry loop?

A

electrical activation occurs via an abnormal circuit which loops back on itself

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23
Q

what are the requirements for establishing a re-entry loop?

A
  1. a circuit of tissue around which waves of depolarisation can travel
  2. an area within this circuit which allows conduction to only travel in one direction
  3. conduction is slow enough to allow distal myocytes to depolarise but fast enough to ensure distal myocytes are depolarised before the next normal beat
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24
Q

what causes atrial fibrillation?

A

multiple re-entrant loops, caused by damaged myocardium setting off ectopic foci

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25
Q

what is AV nodal re-entry?

A

two electrical pathways connect in the AVN and then travel back up one of the pathways, forming a re-entrant loop

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26
Q

what does AV nodal reentry cause?

A

AV nodal reentry tachycardia

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27
Q

what is ventricular pre-excitation?

A

an accessory pathway is present between the atria and ventricles, allowing conduction to by-pass the AVN

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28
Q

what is Wolff-Parkinson-White syndrome?

A

heart condition in which there is an accessory pathway between the atria and ventricles, by-passing the AVN, causing ventricular pre-excitation

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29
Q

what are the four basic classes of anti-arrhythmic drugs?

A
  1. Drugs that block voltage-sensitive sodium channels
  2. Antagonists of β-adrenoreceptors
  3. Drugs that block potassium channels
  4. Drugs that block calcium channels
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30
Q

describe how drugs that block voltage-dependant Na channels work to reduce arrhythmias

A

block voltage-gated Na channels in the open or inactive state, therefore blocking depolarised tissue

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31
Q

how do drugs which block Na channels act on normal cardiac tissue?

A

little effect on normal cardiac tissue because the drug dissociates rapidly from normal cells

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32
Q

how do drugs which block Na channels affect action potential generation?

A

no effect on action potential generation in normal cardiac tissue
block action potentials caused by damaged myocardium which is setting up ectopic foci

33
Q

how does the drug lidocaine function?

A

block Na channels

34
Q

what are the indications for lidocaine use?

A

ventricular tachycardia following MI
intravenous regional anaesthesia
nerve block
cardiopulmonary resuscitation (if amiodarone isn’t available)

35
Q

what is the mechanism of beta blockers?

A

slow ventricular rate by blocking beta-1 adrenoreceptors in the heart.
decrease the slope of the pacemaker potential in SAN and slow conduction at AVN

36
Q

name some beta blockers

A

propranolol

atenolol

37
Q

what can propranolol be used for?

A 
angina
hypertension
atrial fibrillation
heart failure 
ventricular tachycardia
38
Q

other than the decrease in ventricular rate, how else do beta blockers help heart problems?

A

reduce oxygen demand (by decreasing heart rate)

- reduced myocardial ischaemia (beneficial after MI)

39
Q

how do drugs which block K channels prevent arrhythmias?

A

block K channels, prolong the action potential and lengthen the absolute refractory period, preventing another action potential from occurring too soon

40
Q

why can drugs which block K channels be problematic when treating arrhythmias?

A

because they lengthen the cation potential, can actually be pro-arhythmic as more likely to develop early after-depolarisations

41
Q

give an example of a K channel blocker

A

amiodarone

42
Q

what are drugs that block K channels used for?

A

arrhythmias

ventricular fibrillation

43
Q

how do drugs that block Ca channels work to treat arrhythmias?

A

decrease slope of action potential at SAN (due to Ca entry)
decrease AVN conduction
decrease force of contraction

44
Q

give an example of a Ca channel blocker

A

verapamil

45
Q

what can verapamil be used to treat?

A

hypertension
supraventricular arrhythmias
paroxysmal tachyarrhythmias
angina

46
Q

what is the mechanism of action of IV adenosine?

A

acts on A1 receptors, GiPCRs.

causes hyperopolarisation of cells in AVN and SAN. lengthens the refractory period, interrupting reentry pathways.

47
Q

to which class of anti-arrhythmics do beta adrenoreceptors belong?

A

class 2

48
Q

to which class of anti-arrhythmics do Na channel blockers belong to?

A

class 1

49
Q

to which class of anti-arrhythmics do K channel blockers belong to?

A

class 3

50
Q

to which class of anti-arrhythmics do Ca channel blockers belong to?

A

class 4

51
Q

to which class of anti-arrhythmics does adenosine belong to?

A

class 5

52
Q

what are cardiac glycosides?

A

a class of organic compounds that increase the output force of the heart and decrease its rate of contractions by acting on the sodium-potassium ATPase pump

53
Q

name a type of cardiac glycoside

A

digoxin

54
Q

how do cardiac glycosides carry out their function?

A

block sodium-potassium ATPase

55
Q

describe the mechanism of action of cardiac glycosides, to increase inotropy

A 
block Na-K ATPase
rise in intracellular Na conc
causes decreases in NCX
increases intracellular Ca conc as less being extruded
increased force of contraction
56
Q

how do cardiac glycosides decrease heart rate?

A

increase vagal activity (activity of vagus nerve-parasympathetic)
slows AV conduction
slows heart rate

57
Q

why are drugs, such as cardiac glycosides and beta-adrenergic agonists, which increase cardiac output not routinely used to treat heart failure?

A

they don’t improve long-term survival as they make the heart work harder to increase cardiac output

58
Q

which drugs are typically used to treat heart failure?

A

ACE-inhibitors
Beta-adrenoceptor antagonists
Diuretics

59
Q

why are ACE inhibitors used to treat heart failure?

A

reduce preload by reducing blood volume

-> reduce workload of the heart

60
Q

what is the mechanism of action of ACE inhibitors?

A

prevent conversion of angiotensin 1 into angiotensin 2

  • > leads to decreased Na and water resorption, lowering blood volume and therefore lowering preload
  • > leads to vasodilation, lowering BP, so lowering afterload
61
Q

what are the two general ways in which angina is treated?

A
  1. reduce workload of the heart

2. improve blood supply to the heart

62
Q

which drugs are used to reduce work load of the heart to treat angina?

A
  1. Beta blockers
  2. Ca channel antagonists
  3. organic nitrates
63
Q

how do organic nitrates reduce the work load of the heart?

A

cause venous dilation
reduces venous pressure
reduces ventricular preload

64
Q

how do beta adrenoreceptor antagonists and Ca channel antagonists reduce work load of the heart?

A

reduce heart rate

65
Q

which drugs are used to improve the blood supply to the heart when treating angina?

A 
organic nitrates (coronary artery dilation)
Ca channel antagonists (cause vascular smooth muscle relaxation, so coronary artery vasodilation)
66
Q

describe the mechanism of action organic nitrates

A

organic nitrates react with thiols in vascular smooth muscle, causing NO2- to be released. NO2- is reduced to NO which is a powerful vasodilator

67
Q

how do nitric oxides cause vasodilation?

A

No activates granulate cyclase
Guanylacte cyclase converts GTP into cGMP
cGMP activate PKG
PKG causes a decrease in intracellular Ca concentration

68
Q

why do nitric oxides help to alleviate angina symptoms?

A

venodilation lowers venous pressure, lowering preload
-> reduces workload of the heart
-> reduces oxygen demand of the heart
coronary artery dilation increases blood flow to myocardium

69
Q

is nitric oxide more effective on veins or arteries?

A

veins more affected by NO

70
Q

what is the action of No on collateral arteries?

A

dilates collateral arteries, increasing blood flow to ischaemic areas a little

71
Q

what is the action of NO on arterioles?

A

no action on arterioles

72
Q

which heart conditions increase the risk of thrombus formation?

A
  1. atrial fibrillation
  2. acute MI
  3. mechanical prosthetic heart valves
73
Q

what are the two groups of antithrombotic drugs?

A

anticoagulants

antiplatelet drugs

74
Q

list the different anticoagulant drugs

A
  1. heparin
  2. fractioned heparin (subcutaneous injection)
  3. warfarin
  4. oral thrombin inhibitors
75
Q

name an anti platelet drug

A

aspirin

76
Q

describe the action of warfarin

A

antagonises the action of vitamin K which is needed to synthesise some calcium-dependent clotting factors

77
Q

describe the action of heparin

A

inhibits thrombin, preventing blood clotting

78
Q

list the drugs used to treat hypertension

A
  1. ACE inhibitors
  2. Ca channel blockers selective for vascular smooth muscle
  3. diuretics
  4. beta blockers
  5. alpha-1 adrenoceptor antagonist

Cardiovascular System (22 decks)

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