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Cardiovascular system > Lecture 13- Arrhythmia drugs > Flashcards

Lecture 13- Arrhythmia drugs Flashcards

1
Q

Abnormalities of heart rate or rhythm

A
  • Bradycardia
  • Atrial flutter
  • Atrial fibrillation
  • Tachycardia
    • Ventricular tachycardia
    • Supraventricular tachycardia (atrial)
  • Ventricular fibrillation
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2
Q

Causes of arrhythmias: 1) Tachycardia

A
  • Ectopic pacemaker activity
    • Damaged area of myocardium becomes depolarised and spontaneously active
    • Latent pacemaker region activated due to ischaemia
      • Dominates over SA node
  • Afterdepolarisations
    • Abnormal depolarisation following the action potential
    • Atrial flutter/fibrillation
  • Re-entry loop
    • Conduction delay
    • Accessory pathway
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3
Q

2) Bradycardia

A
  • Sinus bradycardia
    • Sick sinus syndrome (intrinsic SA node dysfunction, some calcium blockers)
    • Extrinsic factors such as drugs
  • Conduction block
    • Problems at AV node or bundle of His
    • Slow conduction at VC node due to extrinsic factors (e.g. beta blockers, some calcium blockers)
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4
Q

delayed afterdepolarisations (triggered activity)

A
  • Delayed after-depolarisation
  • More likely to happen if intracellular calcium high
  • Ventricular tachycardia
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5
Q

Early-after depolarisations (triggered activity)

A
  • Can lead to oscillations
  • More likely to happen if AP prolonged e.g. by calcium
  • Longer AP= longer QT interval
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6
Q

Re-entrant mechanism for generating arrhythmias

what normally happens

A

Two impulses meet and cancel each other out

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7
Q

Re-entrant mechanism for generating arrhythmias

block of conduction through damaged regions

A

Conduction blocked

All okay

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8
Q

Re-entrant mechanism for generating arrhythmias

Incomplete conduction (unidirectional block)

A

Excitation can take long route to spread the wrong way through the damaged area, setting up a circuit of excitation

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9
Q

Multiple re-entrant circuits in the atrial fibrillation

A

Possible to get several small re-entry loops in the atriaà atrial fibrillation

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10
Q

AV Nodal re-entry

A
  • Fast and slow pathway in AV node creates a re-entry loop
  • Continued depolarisation of the ventricles
  • Sets up tachycardia
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11
Q

Ventricular pre-excitation

A

Ventricular pre-excitation is a condition in which some or all of the ventricular muscle of the heart undergoes electrical activation (or depolarization) earlier in relation to atrial events than would be expected had the electrical impulses travelled normally by way of the atrioventricular (AV) conduction system.

An accessory pathway between atria and ventricles creates a re-entry

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12
Q

Example of ventiruclar pre-excitation

A

Wolff- Parkinson- White syndrome

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13
Q

4 basic classes of anti-arrhythmic drugs

A
  1. Drugs that block voltage sensitive sodium channels
  2. Antagonists of B-adrenoreceptors
  3. Drugs that block potassium channels
  4. Drugs that block calcium channels
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14
Q

Drugs that block voltage sensitive sodium channels example

A

lidocaine- local anaesthetic

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15
Q

how do voltage sensitive sodium channels work

A

use-dependent block

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16
Q

use-dependent block

A

Only blocks voltage gated sodium channels in open or inactive state- therefore preferentially blocks damaged depolarised tissue

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17
Q

benefit of use-dependent block

A
  • Little effect in normal cardiac tissue because it dissociates rapidly
  • Block during depolarisation but dissociates in time for next AP
    • Keeps refractory period longer to prevent the next AP in damaged myocardium
    • E.g. could be used in ventricular tachycardia
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18
Q
A
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19
Q

lidocaine is used following

A

MI

  • only if paitents show signs of VT
  • given intravenously
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20
Q

Lidocaine affect on: Damaged areas of myocardium

A

damaged myocardium may be depolarised and fire automatically

  • More na+ channes are open in depolarised tissue
  • Lidocaine block these sodium channels
  • Preventing automatic firing of depolarised ventricular tissue
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21
Q

lidocaine is not used

A

used prophylactically following MI (even in patients showing VT – generally use other drugs)

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22
Q
  1. Antagonists of B-adrenoreceptors (beta blockers)
A
  • Block sympathetic action
  • Act on B1 adrenoreceptors in the heart
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23
Q

effect of B blocker on the pacemaker potentials of the ehart

A

Decrease slope of pacemaker potential in SA and slow conduction at AV node

E.g. propranolol, atenolol

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24
Q

when are B blockers used

A
  • Prevent supraventricular tachycardia
  • Used following MI
  • Also reduces O2 demand
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25
Q

B blockers in the prevention of supraventricular tachycardia

A
  • Slow conduction at AV node
  • Slows ventricular rate in patients
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26
Q

B blockers used following MI

A
  • MI often causes increased sympathetic activity (damaged myocardium firing more AP- autofires)
  • Arrhythmias may be partly due to increased sympathetic activity
  • B-blockers prevent ventricular arrhythmia
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27
Q

beta blockers used to reduce O2 demand

A
  • Reduces myocardial ischaemia
  • Beneficial following MI
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28
Q
  1. Drugs that block potassium channels (type III anti-arrhythmic)
A
  • Not very good anti-arrhythmic
  • Prolong action potential by blocking potassium channels- potassium cant flow out causing repolarisation
  • Lengthens the absolute refractory period (when no AP can occur)
  • In theory would prevent another AP occurring too soon but in reality proarrythmic
    • ​prolong QT intervals
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29
Q

which drugs that block potassium channels, is an exception to the rule (that they are not very good anti-arrhythmics)

A

amiodarone

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30
Q

amiodarone

A
  • Other actions in addition to blocking K+ channels
  • Used to treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop to due an accessory/extra conduction pathway)
  • Successful for supressing ventricular arrhythmias post MI
    *
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31
Q
  1. Drugs that block calcium channels
A
  • decreases slope of AP at SA node
  • decreases AV nodal conduction
  • decreases force of contraction (negative Inotropy)
  • also some coronary and peripheral vasodilation
32
Q

types of calcium channel blockers

A

non-dihydropyridine types

dihydropyridine types

33
Q

non-dihydropyridine types

A

Verapamil and diltiazem

34
Q

Dihydroxypyridine Ca2+ blockers are

A

not effective in preventing arrhythmias- but do act on vascular smooth muscle e.g. nifedipine, amlodipine act on vasculature

35
Q

name another anti-arrhythmic drug

A

Adenosine

36
Q

Adenosine

A
  • Produced endogenously at physiological levels
  • can also be administered IV
  • acts on A1 receptors at AV node but has a very short half life
  • enhances K+ conductance
37
Q

adenosine enhances k+ conductance

A

hyperpolarises cells of conducing tissue (Gi- decreases cAMP- decrease pacemaker potential)

38
Q

what is adenosine useful in treating

A

Anti- arrhythmic

  • great for supraventricular tachycardia
  • useful for terminating re-entrant SVT
39
Q

other drugs acting on the CVS

A
  1. ACE-inhibitors
  2. ANgiotensin II receptor blockers (ARBs)
  3. Diuretics
  4. Ca2+ blockers
  5. positive inotropes
  6. B-adrenoreceptor agonists
  7. Nitrates in treatment of angina
  8. Antithrombotic drugs
40
Q

ACE- inhibitors e.g. perinodopril

A
  • inhibits action of angiotensin converting enzyme (ACE)
  • reducing amount of angiotensin II
  • a strong vasoconstrictor
    • stimulates sodium reabsorption
    • increased aldosterone (increase number of aquaporins)
    • increase blood volume
  • important treatment of hypertension and heart failure
41
Q

side effect of ACE-inhibitors

A
  • dry cough (excess bradykinin- vasodilator)
  • can lead to both peripheral and pulmonary oedema
42
Q

ACEi and heart failure

A
  • ACEi decrease vasomotor tone decreasing blood pressure
    • Reduces afterload of the heart- how much the heart has to pump against i.e. the higher the TPR in the periphery the more force needed to expel from the heart
  • Also reduces fluid retention
    • Reduce preload of the heart (how much the heart has to pump out)
    • Reducing workload of the heart
43
Q

Angiotensin II receptor blockers (ARBs)

A

In patients who cart tolerate ACEi can use AT1 receptor blocker e.g. Losartan

  • Used to treat heart failure and hypertension
44
Q

diuretics used to treat

A

Heart failure and hypertension

45
Q

loop diuretics useful in

A

congestive heart failure e..g furosemid

46
Q
A
47
Q

Congestive heart failure (CHF)

A

is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently

48
Q

diuretics reduce

A

Reduces pulmonary and peripheral oedema

49
Q

thiazide diuretics more useful in

A

less serious cases

50
Q

Dihydropyridine Ca2+ channel blockers not effective in preventing arrhythmias- but can….

A

act on vascular smooth muscle

51
Q

what can dihydropyridine Ca2+ channel blockers be used to do

A

decrease peripheral resistance

decreased arterial BP

reduced workload of the heart by reducing afterload

Amlodipine, Nicardipine

52
Q

which calcium blockers reduce workload of the heart by reducing afterload

A

Other types calcium blockers e.g. verapamil and diltiazem act on the heart

verapamil also reduces force of contraction

53
Q

Positive inotropes

A

Increase contractility and thus Cardiac Output

  • E.g. cardiac glycosides e.g. digoxin
  • E.g. B adrenoreceptors agonists e.g. dobutamine
54
Q

Cardiac glycosidesI

A

improve symptoms but not long term outcome

  • Extracted from foxglove digitalis
  • Primary mode of action is to block sodium / potassium ATPase
    • Calcium is extruded via the Na-Ca exchanger
    • Driven by sodium moving down conc gradient
    • Cardiac glycosides block Na/K ATPase
    • Leads to rise in sodium
    • Reduces activity of Na-Ca exchanger
    • Causes intracellular calcium to increase (more stored in SR)Increased force of contraction
55
Q

digoxin also

A

Also increase vagal activity

  • Slows AV conduction
  • Slows heart rate
  • May be used in heart failure when there is an arrhythmia
56
Q

B- adrenoreceptors agonists

A
  • Dobutamine
    • Selective b1- adrenoreceptors agonist
    • Stimulate b1 receptor present at SA node and AV node and on ventricular myocytes
57
Q

uses of B-adrenoreceptor agonists

A

Cardiogenic shock

Acute but reversible heart failure (e.g. following cardiac surgery)

58
Q
A
59
Q

Treating heart failure

A
  • Cardiac glycosides will relieve symptoms by making heart contract harder
  • But there is no long-term benefit
  • Don’t flog a dying horse
  • Making the heart work harder is not good in the long run
  • Better to reduce workload
  • ACEinhibitors or ARBs and diuretics better for heart failure
  • Beta blockers can also reduce workload of the heart
60
Q

angina occurs when

A
  • Angina occurs when O2 supply to the heart does not meet its need- but of limited duration and does not result in death of myocytes
  • Ischaemia of heart tissue- chest pain
  • Usually pain with exertion
61
Q

organic nitrates

A
  • Reaction of organic nitrates with thiols (-SH groups) in vascular smooth muscle causes relaxation- NO released endogenously from endothelial cells
  • NO2- reduced to nitric oxide
62
Q

examples of organic nitrate medications

A
  • NO GTN spray (quick, short acting)
  • Isosorbide dinitrate (longer acting)
63
Q

NO are powerful …… especially on

A

vasodilators

veins

64
Q

why is exogenous NO more effective on veins

A

Less endogenous NO in veins

  • less effect on arteries (more endogenous NO)
  • Very little effect on arterioles
65
Q

pathway NO works by

A
  1. NO activates guanylate cyclase
  2. Increases cGMP which increases PKG
  3. Lowers intracellular [Ca2+]
  4. Causes relaxation of vascular smooth muscle
66
Q

primary action of NO

A
  • Venodilations
  • Reduces venous pressure and the return of blood to the heart
  • Lowers preload
    • Reduces work load of the heart
    • Heart fills less therefore force of contraction reduced (Starlings law)
    • Lowers O2 demand
67
Q

secondary action of NO

A
  • Action on coronary collateral arteries improves O2 delivery to the ischaemic myocardium
    • Acts on collateral arteries not arterioles
68
Q
A
69
Q

to treat agina we want to

A

reduce work load of the heart

improfve the blood supply to the heart

70
Q

reduce work load of the heart

A
  • Organic nitrates (venodilation)
  • B-adrenoreceptor blocker
  • Ca2+ channel antagonist
71
Q

improve blood supply to the heart

A
  • Ca2+ channel antagonist
  • Minor effect of organic nitrates
72
Q

Antithrombotic drugs

A

Certain heart conditions carry an increased risk of thrombus formation

  • Atrial fibrillation
  • Acute myocardial infarction
  • Mechanical heart valves
73
Q

Anticoagulation’s prevent venous thromboembolism

A

heparin

fractionated heparin

warfarin

antiplatelet drugs

74
Q

Heparin (given via IV)

A
  • Inhibits thrombin
  • Used acutely for short term action
75
Q

fractionated heparin is a

A

subcutenous injection

76
Q

Warfarin (given orally)

A

Antagonised action of Vit K

77
Q

Antiplatelet drugs

A

Aspirin

Clopidogrel

  • Following acute MI or high risk MI

Cardiovascular system (30 decks)

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