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pharmacology BM322 > antiarrhythmics > Flashcards

antiarrhythmics Flashcards

1
Q

what are arrhythmias?

A

theyre a group of condidtions in which the heaart beats irregularly, too fast or too slow

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2
Q

what are arrythmias a result of?

A

theyre as a result of abnormal activity

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3
Q

what is the abnormality of cardiac rhythm called?

A

cardiac arrythmia

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4
Q

what may arrythmias arise from?

A

ischemia, infarction, fibrosis or drugs

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5
Q

what are the two main types of arrythmias?

A

irregular bradycardia and tachycardia

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6
Q

what is irregular bradycardia?

A

itw where the heart beats too slowly (<60bpm)

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7
Q

what is irregular tachycardia?

A

its where the heart beats too quickly (>100bpm)

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8
Q

what are the symptoms of cardiac arrhythmias?

A
  • Palpitations
  • Heart failure symptoms (e.g. edema)
  • Fatigue
  • Dyspnea (breathing difficulties)
  • Dizziness
  • Angina
  • Syncope (fainting)
  • No symptoms at all
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9
Q

what do cardiac arrythmias arise form?

A

the formation of impulses or altered conduction of the impulse through the heart

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10
Q

what are ectopic beats?

A

theyre beats arising from fibres or a group of fibres outside normal pacemaker (SA node)

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11
Q

what is the role of the SA node?

A

the sinoatrial node is the pacemaker region of the heart

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12
Q

what is the treatment of cardiac arrythmias?

A
  • Pharmacological therapy.
  • DC Cardioversion.
  • Pacemaker therapy.
  • Surgical therapy e.g. aneurysmal excision.
  • Interventional therapy “ablation”.
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13
Q

what is ‘excitability’?

A

its the ability to respond to stimuli by producing and conducting action potentials

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14
Q

what is the refractory period?

A

its the time following excitation during which a second action potential cant be excited and conducted

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15
Q

what is membrane responsiveness?

A

its the relationship between membrane activation voltage and the maximal rate of the rise of the action potential

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16
Q

how do antiarrythmic drugs work?

A

they increase the refractory period or slow the upstroke of action potentials or both

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17
Q

what does ‘gating’ mean in ion channels?

A

Channel gating regulates the passage of current through the ion-conducting pore, and thereby enables the generation of action potentials

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18
Q

what are the two important features of ion channels?

A

gating and ion selectivity

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19
Q

what is ion selectivity?

A

it means that some channels only allow Na+ ions to cross while others only allow K+ ions or Ca2+ ions

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20
Q

what types of ion channels are there?

A

Ca2+ channels
Na+ channels
K+ channels

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21
Q

are the concentrations of sodium and calcium high inside or outside of the cell?

A

outside

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22
Q

what is the membrane potential?

A

its where the charge is neutral as the positive and negative charges are balanced on each side of the neuron

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23
Q

how are the changes of the ions the same if theres a large concentration gradient?

A

as the potassium is at high concentrations inside the cell and there are an equal number of negative ions inside the cell

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24
Q

what is the electrochemical gradient?

A

its the stable membrane concentration gradient and a stable electrochemical gradient

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25
Q

how does the lethal injection stop the heart beating?

A

the injection of potassium chloride causes cardiac arrest and this disturbs the resting membrane potential and its dependance on the external potassium concentration

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26
Q

what is the contraction process of the heart preeceded by?

A

electrical excitation

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27
Q

what are the two main classifications of cells in the heart?

A

cardiomyocytes and pacemaker cells

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28
Q

what are some of the cell types that make up the heart?

A

cardiomyocytes, fibroblasts, endothelial cells and perivascular cells

29
Q

what are pacemaker cells?

A

they’re highly specialised myocardial cells with an intrinsic ability to depolarise rhythmically and initiate action potentials

30
Q

where are pacemaker cells found in the heart?

A

they can be found primarilt in the sinoatrial node and in the atrioventricular node, some of the cells are also found in the bundle of His and purkinje fibres

31
Q

what does it mean by ‘pacemaker cells possess a characteristic known as automaticity’?

A

it means that they can initiate action potentials on their own, this is then conducted down the cardiac conduction system as an electrical impulse and also between one cardiomyocyte to another through gap junctions, helping the heart contract in a synchronised fashion

32
Q

what is the conduction system?

A

its the pathway the electrical impulse takes through the heart

33
Q

what pathway do the electrical impluses take through the heart?

A

the SA node is located above the right atrium near the opening of the vena cava. from here, the depolarisation current spreads through the right atrium gap junctions then to the left atrium via bachman’s bundle.
the impulse then goes to the AV node, to ensure the blood has emptied from the atria into the ventricals.
then the depolarisation wave passes via the bundle of His branches and purkinje fibres, eventually reaching the ventricular cardiomyocytes

34
Q

what is the fucntion of cardiac action potentials and their associated repolarisations?

A

theyre essential for maintaining profusion to the vital organs of the body

35
Q

are the action potentials of cardiomyocytes and pacemaker cells the same?

A

no, the action potential of cardiomyocytes has 5 phases and the action potential of pacemaker cells only has 3

36
Q

what are the phases of cardiomyocyte action potentials? (just an outline of each of the steps)

A

phase 0- phase of rapid depolarisation
phase 1- the inactovation of the perviously activated channels
phase 2 - plateau phase
phase 3- repolarisation

37
Q

what happens in phase 0 in cardiomyocyte action potentials?

A

its the phase of rapid depolarisation where the voltage gated Na+ channels open, resulting in the rapid influx of Na+ ions
because of the influx of these cations, the membrane potential changes form -70mV to +50mV.
the voltage-gated sodium channels are faster channels than calcium channels, so theres a steep upstroke in the action potential

38
Q

what happens in phase 1 of cardiomyocyte action potential?

A

the previously activated voltage-gated Na+ channels are inactivated and the outward potassium current is activated, leading to a slight drop in the membrane electrochemical potential, beginning phase 2

39
Q

what happens in phase 2 of the cardiomyocyte action potential?

A

this is the plateau phase, voltage-gated Ca2+ channels open, causing a calcium influx, and balancing the K+ influx, creating a plateau around +50mV, this is part of the effective refractory period.

40
Q

what happens in phase 3 of the cardiomyocyte action potential?

A

this is the repolarisation phase where the K+ channels allow K+ ions flow out of the cell and the Ca2+ channels close, to return the membrane potential to -90mV

41
Q

what is the absolute refractory period?

A

this is when the Na+ channels are inactivated and no matter what stimulus is applied, the channels wont reopen to allow Na+ in to allow the membrane to depolarise to the threshold level of an action potential

42
Q

what is the relative refractory period?

A

this is when some of the Na+ channels have reopened from being inactivated but the threshold is higher than normal, making it harder for the activated Na+ channels to raise the membrane potential to the threshold to get an action potential

43
Q

what are the phases of action potentials in pacemaker cells? (just an outline)

A

theres only 3 phases
phase 0- the phase of depolarisation
phase 3 - repolarisation
phase 4 - phase of gradual depolarisation

44
Q

what happens in phase 0 of action potentials of pacemaker cells?

A

this is the phase of depolarisation
it starts when the membrane potential reaches -40mV, the threshold potential in pacemaker cells
theres an opening of voltage-gated Ca2+ channels and on reaching threshold, it causes an influx of Ca2+ ions, this influx of cations results in an upstroke in membrane potential from -40mV > +10mV (not as steep as cardiomyocytes) because calcium channels are slow channels Vs Na channels

45
Q

what happens in phase 3 of the action potential in pacemaker cells?

A

phase of repolarisation, in this phase, the closing of Ca2+ channels blocks the flow of Ca2+ channels.
voltage gated K+ channels open, allowing K+ ions out of the cell, rapidly decreasing the membrane potential from +10mV > - 60mV

46
Q

what happens in phase 4 of action potentials in pacemaker cells?

A

this is a phase of gradual depolarisation and is unique to pacemaker cells.
its mainly via a depolarisation current, causing the membrane potential to change from -60mV to the threshold potential of -40mV. the slope of this phase determines heart rate and is different for pacemaker cells in different regions.

47
Q

what is the rate that pacemaker cells in the SA node depolarise at?

A

60-100 per min

48
Q

what is the rate that pacemaker cells in the AV node depolarise at?

A

40-60 per min

49
Q

is it the AV or SA node that is the primary pacemaker?

A

its whatever one has the highest rate of depolarisation is the primary pacemaker, in healthy people this is the SA node

50
Q

what type of cells are blocked by verapamil?

A

it would be cells in the sinoatrial node as theyre slow conductors which mainly use calcium channels in their action potentials and verapamil is a calcium channel blocker

51
Q

what type of cells would be blocked by drugs such as lidocane?

A

lidocane is a sodium channel blocker so it would block fast conducting cells such as cells in the atrium, ones part of the bundle of His and ventricular cells as they mainly use sodium channels in their action potentials

52
Q

what do effective antiarrythmic drugs do?

A

they either increase the refractory period or slow the upstroke of action potentials or both

53
Q

how are antiarrythmic drugs classified?

A

theyre classified according to their effects

54
Q

what are some examples of class 1 antiarrythmic drugs and what do they block?

A

they block Na+ channels
class 1A– quinidne, procainamide and disopyramide
class 1B - lidocane and mexiletine
class 1C- Flecainide, Propafenone

55
Q

what is the difference between the class 1 A, B and C drugs?

A

class 1A- causes moderate degree blockage of Na+ channels and a prolonged QTc interval
class 1B - causes mild degree blockage of Na+ channels and shorten the QTc interval
class 1C - causes a marked degree of Na+ blockage and no effect on QTc intervals

56
Q

what are class II antiarrhythmic drugs?

A
  • theyre beta-blockers and are useful to reduce recurrent arrhythmias and improve symptoms.
  • they reduce the sinoatrial node and atrioventricular node conduction.
  • they also decrease cardiac automacity and contractiltiy, partly by blocking beta-adrenergic receptors and partly by direct effects on cardiac cell membranes
  • they can antagonise the effects of catecholamines on Ca2+ channels and slow conduction in partially depolarised cells and decrease myocardial contractility
57
Q

how do class 3 antiarrhythmias work?

A

they block K+ channels

58
Q

what are some examples of class 3 antiarrhythmics?

A

amiodarone and sotalol

59
Q

what are some examples of class 4 antiarrhythmics?

A

verapamil and diltiazem

60
Q

what is class 5 of antiarrhythmics?

A

its the group of drugs made up of the drugs that dont fit in the traditional groups

61
Q

what class is digoxin in?

A

class 5

62
Q

how does digoxin work?

A

its a cardiac glycoside and reduces heart rate and improves the filling of the ventricles
the two mechanisms of action are positive inonotrophic and AV node inhibition

63
Q

how does the inhibition of the AV node work by digoxin?

A

it has vagomimetric effects on the AV node and by stimulating the parasympathetic nervous systen, it slows electrical conduction in the AV node, deceasing HR. the rise in calcium levels leads to the prolongation of phase 4 and phase 0 in the cardiac action potential thus increasing the AV nodes refractory period

64
Q

what does slower conduction through the AV node carry?

A

a decreased ventricular response

65
Q

how do class 4 drugs work?

A

the block mainly L-type lectin calcium channels and decrease sinoatrial node and purkinje fibre automacity, and slows contraction through increasing the refractory period of the AV node

66
Q

how do inonotrophic drugs work and state an example of one?

A

digoxin - is a cardiac glycoside
it increases the contractile force and inhibits the sodium-potassium-ATPase, which is responsible for Na+/K+ exchange accross the muscle cell membrane, increasing Na+ inside the cell, which causes an increase of Ca2+ in the cell with increases the force of myocardial contraction

67
Q

what are the indirect effects of digotoxin?

A

it increases vagal activity and facilitates muscarininc transmission to the heart, this slows HR, atrioventricular conductance and prolongs the refractory period of the AV node

68
Q
A

pharmacology BM322 (7 decks)

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