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Cardiovascular > Pharmacology- Arrhythmias and Heart Failure > Flashcards

Pharmacology- Arrhythmias and Heart Failure Flashcards

1
Q

what 2 pathophysiological events can cause arrhythmias

A

defects in impulse formation, defects in impulse conduction

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2
Q

give two examples of arrhythmias caused by a defect in impulse formation

A

missed beats, eptopic beats

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3
Q

explain what is meant by a defect in impulse formation

A

SA-node automaticity is interrupted or altered

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4
Q

what are the two types of defects in impulse formation

A

altered automaticity, triggered activity

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5
Q

describe physiological altered automaticity

A

modulation of SA node activity by the ANS

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6
Q

give 2 examples of physiological altered autoimmunity

A

sinus tachycardia, sinus arrhythmia

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7
Q

describe pathological altered automaticity

A

latent pacemaker subverts the SA node’s function as the normal pacemaker of the heart (overdrive suppression is lost)

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8
Q

what might cause a pathological altered automaticity

A

SA node firing at low frequency

conduction of impulse impaired

a latent pacemaker firing at a rate faster than the SA node

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9
Q

give 2 examples of arrhythmias caused bu SA node firing frequency is pathologically low (or when conduction of the impulse from the SA node is impaired is impaired)

A

escape beat, escape rhythm

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10
Q

give 2 examples of arrhythmias caused by a latent pacemaker firing at a rate faster than the SA node

A

ectopic beat and ectopic rhythm

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11
Q

what is triggered activity

A

afterdepolarisations triggered by a normal action potential

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12
Q

what is an EAD

A

early afterdepolarisation, occurs during the inciting action potential between phase 2 (plateau) and 3

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13
Q

what is a DAD

A

delayed afterdepolarisation, occurs after complete repolarisation

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14
Q

what are the three types of defect in impulse conduction

A

re-entry, conduction block, accessory tracts

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15
Q

describe re entry

A

self sustaining electrical circuit stimulates an area of the myocardium repeatedly/ rapidly

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16
Q

what does the re-entrant circuit require

A

unidirectional block, slowed retrograde conduction velocity

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17
Q

what causes a partial conduction block and give an example

A

slowed conduction, first degree AV block

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18
Q

what is an intermittent conduction block and give an example

A

second degree AV block

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19
Q

what are the two types of second degree AV block

A

mobitz type 1, mobitz type 2

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20
Q

describe mobitz type 1

A

PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed

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21
Q

describe mobitz type 2

A

PR interval is constant but every ninth ventricular depolarization is missing

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22
Q

describe complete conduction block and give an example

A

no impulses,Atria and ventricles beat independently, governed by their own pacemakers
Ventricular pacemaker is now the Purkinje fibres – fire relatively slowly and unreliably – manifest as bradycardia and low cardiac output, third degree AV block

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23
Q

describe accessory tract pathways

A

Some individuals possess electrical pathways that bypass the AV node
A common pathway is the bundle of Kent
Impulse through bundle of Kent is conducted more quickly that that through the AV node
Ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias

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24
Q

what do anti arrhythmic drugs do

A

inhibit specific ion channels with the intention of suppressing abnormal electrical activity

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25
Q

how are anti arrhythmic drugs classified

A

based on their effectd upon the cardiac action potential (vaughn williams classification) (four classes I to IV (I subdivided into Ia to Ic)

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26
Q

many arrhythmic agents are not what?

A

entirely selective blockers of Na+, K+, or Ca2+ channels, and may block more than one channel type

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27
Q

different classes of anti arrhythmic drugs act of different what

A

phases of the action potential in nodes and myocardium

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28
Q

what do class 1 drugs act on

A

block v activated sodium channels, therefore controlling the upstroke of the action potential

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29
Q

what separates Ia from Ib from Ic

A

their rate of association and dissociation with channels

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30
Q

describe Ib drugs

A

rapidly associates and dissociates. Prevents premature beats. 1B help to stop one action potential arising too quickly after another action potential

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31
Q

describe Ia drugs

A

bind to and from channel at a slower rate (moderate kinetics) as a result slow rate of rising AP and prolong duration of AP. Increase amount of time in refractory (inactive) state

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32
Q

describe Ic drugs

A

associate and dissociate with very slow kinetics- greatly depresses rise of AP, but has little effect on duration. These drugs strongly suppress conduction within the heart

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33
Q

describe class II drugs

A

Beta antagonists. Good in stress induced arrhythmias as decrease effect as symp system on nodes, supress AV and SA conduction

34
Q

describe class III drugs

A

act to block v activated potassium channels work on repolarising phase by blocking channels responsible for repolarisation increase duration of AP and refractory period

35
Q

describe IV class drugs

A

block v activate ca channels, suppress upstroke of AP in normal tissue and decrease amount on calcium, entering cell during plateau, neg inotropic effect and slow conduction within the nodes

36
Q

what do the relative proportions of time spent by calcium channels in different states (resting, open, inactivated)depend upon

A

depend upon firing fequency

37
Q

during high frequency firing more time is spent by v activated calcium channels in what states

A

in the open and inactivated states

38
Q

describe the use dependant manner of class 1 drugs

A

targeting areas of the myocardium in which firing frequency is highest in a use-dependent manner without preventing the heart from beating at normal frequencies (block open state, stabilise inactivated state)

39
Q

what is the resting to open state of v activated channels in response to

A

depolarisation

40
Q

after being inactivated by depolarisation what takes the v activated sodium channels into resting state

A

restoration of membrane potential via repolarisation

41
Q

when do class 1 agents dissociate from the sodium channel

A

when it is in the resting state

42
Q

describe the role of heart rate in steady state block (class 1 agents)

A

if heart rate increases, less time is available for unblocking (dissociation) and more time available for blocking (association). Steady state block increases, particularly for agents with slow dissociation rates

43
Q

how can class 1 agents act preferentially on ischaemic myocardium

A

In ischaemic myocardium, myocytes are partially depolarized and the action potential is of longer duration thus:
The inactivated state of the Na+ channel is available to Na+ channel blockers for a greater period of time
The rate of channel recovery from block is decreased

Collectively the higher affinity of Na+ channel blockers for the open and inactivated states of the channel allows them to act preferentially on ischaemic tissue and block an arrhythmogenic focus at it source

44
Q

how are arrhythmias classified

A

on their site of origin (supraventricular; atria, AV node- or ventricular) and their affect in heart rate (tachycardia or bradycardia)

45
Q

give three examples of drugs used in supra ventricular arrhythmias

A

adenosine, digoxin (stimulates vagal activity) and verapamil

46
Q

give an example of a drug used in ventricular arrhythmias and how it works

A

lignocaine- rapid block of voltage activated Na+ channels

47
Q

give three examples of drugs used in atrial AND ventricular arrhythmias

A

disopyramide and procainamide (moderate rate),

flecainide (slow rate),

propranolol and atenolol (beta blockers),

amiodarone and sotolol

48
Q

what does mitral stenosis cause in an ECG

A

atrial hypertrophy and bi-p waves

49
Q

what does a prolonged PR interval suggest

A

atrial ventricular block

50
Q

what part of AP does QRS represent

A

upstroke

51
Q

how wide is a QRS normally

A

less than 1 big square

52
Q

what does the QT interval represent

A

from start of ventricular depolarisation to end of ventricular repolarisation

53
Q

what does the U wave represent

A

at end of t wave, part of ventricular repolarisation

54
Q

what is a short PR interval and what can it lead to

A

pre excitation, wolff-parkinson-white syndrome

lends itself to re-entry/ SV tachycardia

55
Q

what is sinus arrhythmia

A

normal changes in heart rate due to breathing

56
Q

what can cause left axis deviation in an ECG

A

left ventricular hypertrophy, inferior MI

57
Q

what can cause right axis deviation

A

RVH, cor pulmonale, PE, lupus

58
Q

a PR interval longer than what means first degree heart block

A

200ms

59
Q

what can cause first degree heart block

A

digoxin, beta blockers, excessive vagal tone, ischaemia, intrinsic disease in AV junction/ bundle branch system

60
Q

how is bundle branch block shown on an ECG

A

wiLLiam maRRow

if V1 looks like a W then LBBB
if V6 looks like M then RBBB

broad QRS

61
Q

what is used to treat sinus bradycardia

A

atropine, adrenaline/ isoprenaline

62
Q

what does sick sinus syndrome require

A

pacing

63
Q

what is wenckebach

A

mobitz type 1

64
Q

what is the treatment for SVT

A

valsava maneouver/ carotid massage (to increase vagal tone)

65
Q

how do you slow conduction

A

adenosine, verapamil

66
Q

what is atrial flutter

A

form of SVT

67
Q

how is atrial flutter treated

A

cardiovert or amiodarone

68
Q

what is amiodarone used for

A

atrial and ventricular tachycardias

69
Q

how is atrial fibrillation treated

A

if lasting more than 48 hours; anticoagulate with warfarin and slow HR (beta blocker, digoxin, verapmil, CCB)

if less than 48 hours can cardiovert

70
Q

how is paroxysmal VT treated

A

with amiodarone or lidocaine

71
Q

what does LVH look like on an ECG

A

high R’s, deep S’s, sinus rhythm, left axis deviation

72
Q

how is heart failure treated

A

beta blockers, ACEI’s, aldosterone antagonists (spironlactone), diuretics

73
Q

what can cause heart failure

A

CHD, HT, DCM, valve disease, tachycardiac arrhythmias, heart failure with preserved ejection fraction

74
Q

what is ascites and what is it a sign of

A

accumulation of fluid in the abdominal (peritoneal) cavity

HF

75
Q

what is the gold standard for investigating HF

A

echocardiography

76
Q

what is ANP

A

atrial hormone

77
Q

what is BNP

A

ventricular hormone

78
Q

what does ivabrodine do

A

sinus node blocker, specifically binds to the funny channel, influencing the pacemaker potential, reduces HR

79
Q

what drugs prolong survival in heart failure

A

RAS inhibitors (ACEI’s, ARII antagonists)

Beta blokckers

aldosterone antagonists (spironolactone and epierenone)

vasodilators (hydralazine and nitrates combined)

sinus node blocker (ivabrodine)

80
Q

what drugs improve symptoms in HF

A

digoxin and frusemide

81
Q

what is normally found in a clinical exam of a patient with HF

A

crackles or decreased breath sounds in lung bases, S3 gallop, cool pale cyanotic extremities, elevated JVP, peripheral oedema, ascites, hepatomegaly, splenomegaly, displaced PMI (apical impulse displaced)

Cardiovascular (34 decks)

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