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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
how are anti arrhythmic drugs classified
based on their effectd upon the cardiac action potential (vaughn williams classification) (four classes I to IV (I subdivided into Ia to Ic)
26
many arrhythmic agents are not what?
entirely selective blockers of Na+, K+, or Ca2+ channels, and may block more than one channel type
27
different classes of anti arrhythmic drugs act of different what
phases of the action potential in nodes and myocardium
28
what do class 1 drugs act on
block v activated sodium channels, therefore controlling the upstroke of the action potential
29
what separates Ia from Ib from Ic
their rate of association and dissociation with channels
30
describe Ib drugs
rapidly associates and dissociates. Prevents premature beats. 1B help to stop one action potential arising too quickly after another action potential
31
describe Ia drugs
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
32
describe Ic drugs
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
33
describe class II drugs
Beta antagonists. Good in stress induced arrhythmias as decrease effect as symp system on nodes, supress AV and SA conduction
34
describe class III drugs
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
describe IV class drugs
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
what do the relative proportions of time spent by calcium channels in different states (resting, open, inactivated)depend upon
depend upon firing fequency
37
during high frequency firing more time is spent by v activated calcium channels in what states
in the open and inactivated states
38
describe the use dependant manner of class 1 drugs
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
what is the resting to open state of v activated channels in response to
depolarisation
40
after being inactivated by depolarisation what takes the v activated sodium channels into resting state
restoration of membrane potential via repolarisation
41
when do class 1 agents dissociate from the sodium channel
when it is in the resting state
42
describe the role of heart rate in steady state block (class 1 agents)
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
how can class 1 agents act preferentially on ischaemic myocardium
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
how are arrhythmias classified
on their site of origin (supraventricular; atria, AV node- or ventricular) and their affect in heart rate (tachycardia or bradycardia)
45
give three examples of drugs used in supra ventricular arrhythmias
adenosine, digoxin (stimulates vagal activity) and verapamil
46
give an example of a drug used in ventricular arrhythmias and how it works
lignocaine- rapid block of voltage activated Na+ channels
47
give three examples of drugs used in atrial AND ventricular arrhythmias
disopyramide and procainamide (moderate rate), flecainide (slow rate), propranolol and atenolol (beta blockers), amiodarone and sotolol
48
what does mitral stenosis cause in an ECG
atrial hypertrophy and bi-p waves
49
what does a prolonged PR interval suggest
atrial ventricular block
50
what part of AP does QRS represent
upstroke
51
how wide is a QRS normally
less than 1 big square
52
what does the QT interval represent
from start of ventricular depolarisation to end of ventricular repolarisation
53
what does the U wave represent
at end of t wave, part of ventricular repolarisation
54
what is a short PR interval and what can it lead to
pre excitation, wolff-parkinson-white syndrome lends itself to re-entry/ SV tachycardia
55
what is sinus arrhythmia
normal changes in heart rate due to breathing
56
what can cause left axis deviation in an ECG
left ventricular hypertrophy, inferior MI
57
what can cause right axis deviation
RVH, cor pulmonale, PE, lupus
58
a PR interval longer than what means first degree heart block
200ms
59
what can cause first degree heart block
digoxin, beta blockers, excessive vagal tone, ischaemia, intrinsic disease in AV junction/ bundle branch system
60
how is bundle branch block shown on an ECG
wiLLiam maRRow if V1 looks like a W then LBBB if V6 looks like M then RBBB broad QRS
61
what is used to treat sinus bradycardia
atropine, adrenaline/ isoprenaline
62
what does sick sinus syndrome require
pacing
63
what is wenckebach
mobitz type 1
64
what is the treatment for SVT
valsava maneouver/ carotid massage (to increase vagal tone)
65
how do you slow conduction
adenosine, verapamil
66
what is atrial flutter
form of SVT
67
how is atrial flutter treated
cardiovert or amiodarone
68
what is amiodarone used for
atrial and ventricular tachycardias
69
how is atrial fibrillation treated
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
how is paroxysmal VT treated
with amiodarone or lidocaine
71
what does LVH look like on an ECG
high R's, deep S's, sinus rhythm, left axis deviation
72
how is heart failure treated
beta blockers, ACEI's, aldosterone antagonists (spironlactone), diuretics
73
what can cause heart failure
CHD, HT, DCM, valve disease, tachycardiac arrhythmias, heart failure with preserved ejection fraction
74
what is ascites and what is it a sign of
accumulation of fluid in the abdominal (peritoneal) cavity HF
75
what is the gold standard for investigating HF
echocardiography
76
what is ANP
atrial hormone
77
what is BNP
ventricular hormone
78
what does ivabrodine do
sinus node blocker, specifically binds to the funny channel, influencing the pacemaker potential, reduces HR
79
what drugs prolong survival in heart failure
RAS inhibitors (ACEI's, ARII antagonists) Beta blokckers aldosterone antagonists (spironolactone and epierenone) vasodilators (hydralazine and nitrates combined) sinus node blocker (ivabrodine)
80
what drugs improve symptoms in HF
digoxin and frusemide
81
what is normally found in a clinical exam of a patient with HF
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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