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Clinical Pharmacology, Therapeutics & Intro to Prescribing > Lecture 11– Cardiac arrhythmia drugs > Flashcards

Lecture 11– Cardiac arrhythmia drugs Flashcards

1
Q

for the heart to function efficiently it needs to

A
  • contract sequentially (atria, then ventricles) and in synchronicity
  • Relaxation must occur between contractions
  • Coordination of heartbeat is a result of complex, coordinated sequence of changes in mem. potential and electrical discharges in various heart tissue
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2
Q

normal heart beat

A
  • Triggered in pacemaker cells in SAN
  • Depolarise atrial tissue
  • Then AVN
  • Down purkinje system
  • Ventricle contraction
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3
Q

Atrial arrhythmia

A
  • Chaotic electrical activity of atrial tissue
    • AP fire off from different places in the atria in a disorganised way
  • Causes atria to quiver or twitch fibrillation
  • Ventricles respond to extra, chaotic. Signals by beating faster than normal
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4
Q

the ECG

A

P wave= atrial depolarisation(SAN)

QRS complex= ventricular depolarisation (AVN)

T wave= repolarisation of ventricles

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5
Q

Arrhythmias

*

A
  • Heart conditions where there are disturbances in
    • Pacemaker impulse formation
    • Contraction impulse conduction
    • Combination of the two
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6
Q

arrhytmias result in

A
  • Results in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal CO- syncope
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7
Q

resting potential electrophysiology

A
  • Transmembrane electrical gradient (potential is maintained (by K+ channels), with the interior of the cell negative with respect to the outside cell
  • Caused by unequal distribution of ions inside vs outside
    • Na higher outside than inside
    • Calcium much higher outside than inside
    • K+ higher inside cell than outside
  • Maintained by ion selective channels, active pumps and exchangers
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8
Q

the fast cardiac action potential is found in

A

cardiac myoctes (atrial and ventricular) and purkinje tissue

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9
Q

resting membrane potential and depolarised potential of fast cardiac action potential

A
  • Resting membrane potential = -90 mV
  • Depolarised = +55mV
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10
Q

outline the fast cardaic action potential

A
  1. Rapid influx of sodium inside the cell – rapid depolarisation(0)
  2. Efflux of potassium (1)- causing slight repolarisation
  3. Influx of calcium into cell causing prolonged plateau phase (2)
  4. Repolarisation caused by potassium efflux (3)
  5. Na/K ATPase brings cell back to resting potential (4)
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11
Q

slow action potnetial is found in

A

SAN and AVN

  • automatic spontaensou depolarisation (pacemakers)
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12
Q

difference between slow and fast cardiac AP

A
  • funny current (spontaenous depolarisation)
  • Short Action Potential Duration
  • No phase 1 or 2
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13
Q

outline the slow action potnetial

A
  1. Spontaneous depolarisation (4) is characterised by If (funny current) which is created by slow Na channels
  2. Depolarisation is triggered by influx of calcium into the cell (0)
  3. Repolarisation is characterised by potassium leaving the cell (3)
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14
Q

spontaneous depolarisation found in. slow cardiac AP is characterised by

A
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15
Q

drugs used to alter the fast cardiac action potential

A
  • Class 1 – Sodium channels blockers
  • Class 2- Beta blockers
  • Class 3- Potassium channel blockers
  • Class 4- Calcium channel blockers
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16
Q

drugs used to alter the slow cardiac action potential

A
  • Calcium channel blockers
  • Drugs affecting automaticity
    • ​Beta agonists- adrenaline
    • Muscarinic agonists
    • Adenosine
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17
Q

Mechanisms of arrhythmia generation

A

Abnormal impulse generation

  1. Automatic rhythms
  2. triggered rhythms

Abnormal conduction

  1. Conduction block
  2. Reentry
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18
Q

Automatic rhythms

A
  • Enhanced normal automaticity- sinus tachycardia (physiological) e.g. if stressed for results
  • Ectopic focus- AP arises from site other than SA node (from atria or ventricles)
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19
Q

Triggered rhythms​

A
  • Delayed afterdepolarisations- begin during phase 4, after repolarisation is completed but before another AP would normally occur via the normal conduction system
  • Early depolarisation- occur with abnormal depolarisation during phase 2 or phase 3, and are caused by an increase in frequency of abortive action potentials before normal repolarisations completed
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20
Q

Conduction block

A

degenerative disease of conducting tissue

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21
Q

Abnormal anatomic conduction

A

Some people are born with extra piece of tissue which conducts electricity from atrium to the ventricles (other than AVN) e.g Wolf- Parkinson white syndrome

  • causes reentry loop due to extra conduction pathway
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22
Q

Wolff- Parkinson- white syndrome

A

faster conduction pathway between atria and ventricles created by:

  • Accessory pathway- connecting atrium to ventricle
    • Allows conduction going back down the AV node and back up the pathway to re-enter the atrium (re-entry rhythm)
    • Or can go down the pathway back up the AV node to re-enter the atrium that way
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23
Q

Wolf- Parkinson- White syndrome ECG

A
  • Short PR interval
  • Delta wave- slurring of the upstroke of the QRS complex
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24
Q

Re-entrant mechanism for generating arrhythmias

A
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25
Q

Localised conduction block

A
  • Due to scar tissue created by MI
  • Wave of depolarisation goes into scar and hangs around and comes back out and causes ventricular tachycardia (because AP arising in ventricles)
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26
Q

Pharmacologic rationale and goal

*

A
  • Restore normal sinus rhythm and conduction
  • Prevent more serious and possibly lethal arrhythmias from occurring
  • Antiarrhythmic drugs used to:
    • Decrease conduction velocity
    • Change duration of the effective refractory period (ERP)
    • Supress abnormal automaticity
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27
Q

classification system of antiarrhythmic drugs

A
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28
Q

Class 1 antiarryhythmics are

A

sodium channel blockers

  • can be classified as 1a, 1b, 1c
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29
Q

effect of Class 1 drugs (Sodium channel blockers) on the Action potential

A
  • Block sodium channels
  • Decreases rapid depolarisation (0)
    • Flattens and shifts curve to the right
  • Marked slowing conduction in tissue
  • Minor effects on AP duration (APD)
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30
Q

Name some class 1 drug (sodium channel blockers)

A

Class 1a- Quinidine

Class 1b- Lidocaine and mexiletine

Class 1c- Flecainide

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31
Q

main difference ebtween class 1b and 1c drugs

A
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32
Q

name a Class 1B drug (sodium channel blocker)

A

Lidocaine (IV only)

Mexiletine (oral only)

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33
Q

Class 1B drugs uses

A
  • Ventricular tachycardia (in relation to a scar in the heart- ischaemia)
  • Not used in atrial arrhythmias or AV junctional arrhythmias
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34
Q

Class 1B drugs mode of action

A
  • Use-dependent block
    • Only blocks voltage gates sodium channels in open or inactive state- therefore preferentially blocks damaged depolarised tissue- preventing automatic firing of depolarised ventricular tissue
      • i.e. dmaaged areas of the myocardium may be depolarised and fire autonatically
      • more sodium channels are open in depolarised tissue
  • Little effect in normal cardiac tissue because it dissociates rapidly
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35
Q

Class 1B (lidocaine and mexiletine) effect on cardiac acrtivity

A
  • Fast binding offset kinetics
  • In normal tissue
    • No change in phase 0 (no tonic block)
    • ADP slightly decreased
  • Fast beating or Ischaemic tissue
    • Increase threshold for Na
    • Decrease phase 0 conduction
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36
Q

Class 1b effect on ECF

A
  • Effect on ECG
    • None in normal tissue
    • In fast beating or ischaemic tissue= increase QRS
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37
Q

adverse drug response: class 1B agents

A
  • CNS effect: dizziness, drowsiness
  • Abdominal upsets
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38
Q

Contraindications :Class 1B agents (Sodium channel blockers)

A

Sinus bradycardia.

Heart block greater than first degree.

Cardiogenic shock & overt cardiac failure

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39
Q

name the Class 1c drug

A

Flecainide (IV or oral)

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40
Q

Class 1c drug use

A
  • Wide spectrum
    • Supraventricular arrhythmias
      • Atrial fibrillation
      • Atrial flutter
    • Premature ventricular contractions
    • Wolff- Parkinson-White syndrome (ectopic beats)
41
Q

class 1c drug mode of action

A
  • Na+ channel blocker
  • Effect on cardiac activity
    • Very slow binding offset kinetics (>10s)
    • In normal tissue
      • Decreased phase 0 (Na+)
      • Decreased automaticity
    • In rapidly depolarising atrial tissue
      • Increased APD (K+) and increased refractory period
42
Q

class 1c drug effect on ECG

A
  • beware of Torsades de Pointe
    • Increase PR
    • Increase QRS
    • Increase refractory
43
Q

adverse drug response Class 1C drugs (Flecainide)

A
  • Pro-arrhythmia and sudden death especially with chronic use and ins structural hear disease
  • Increase ventricular response to supraventricular arrhythmias (flutter)
  • CNS and GI effects like other local anaesthetics
44
Q

Contraindications: Class 1c drugs

A
  • Coronary heart disease
  • Structural heart disease e.g. previous MI
45
Q
A
46
Q

Class 2 Antiarrhythmics are

A

Beta blockers (Beta antagonists)

47
Q

How do Beta blockers work in general?

A
  • reduced sympathetic activity
  • reduction in calcium influx
    • Shift to the right of the AP
      • Increase AP duration (APD)
    • Diminishes (4) depolarisation and automaticity
48
Q

name some Class 2 agents (B blockers) and mention how they are delivered

A

Propranolol (oral, IV)

Bisoprolol (oral- most common)

Metoprolol (IV and oral)

Esmolol (IV only- very short acting))

49
Q

uses of B blockers (Class 2 agents)

A
  • Treating sinus and catecholamine dependent tachycardia
  • Converting repentant arrythmias at AV node
  • Protecting the ventricles from high atrial rates (slow AV conduction) in atrial flutter or atria fibrillation
50
Q

mode of action of B blockers (Class 2 agents) as antiarrhythmics

A
  • Inhibition of sympathetic influences on cardiac electrical activity i.e. B1 antagonists- blocking NA binding (also reduce sympathetic stimulation of aberrant pacemaker activity- ectopic foci)
  • Reduction in influx of calcium
    • Effect on cardiac activity
    • Increase Action Potential Duration and refractory period
    • Decrease phase 4 depolarisation (catecholamine dependent)
    • Blocking arrhythmias caused by re-entry
51
Q

B blockers (Class 2 agents) effect on ECG

A
  • Increase PR
  • Decrease HR
52
Q

Adverse drug response: B blockers

A
  • Bronchospasm
  • Hypotension
53
Q

contraindication of B blockers

A

ASTHMAAA

54
Q

how do class 3 drugs work in general

A
  • Block potassium efflux during repolarisation
  • Therefore APD shifts to the right (increase APD duration)
  • Refractory period prolonged
  • Difficult for another AP to start during refractory period
  • Reduces conduction of electrical signals
55
Q

name 2 class 3 agents

A

amiodarone and sotalol

56
Q

how is amiodarone delievered and indicate half life

A

oral or IV

  • long half life (3 months)- need loading dose
57
Q

uses of amiodarone (class 3 drug)

A
  • Very wide spectrum- effective for most arrhythmias
58
Q

Mode of action of amiodarone (Class 3 agent)

A
  • Block potassium channels
    • Class effects of 1,2,3 and 4
  • Reduction in influx of calcium
  • Effect on cardiac activity
    • Increase APD and refractory period and increase APD (K+)
    • Decrease phase 0 and conduction (Na)
    • Increase threshold for AP
    • Decrease phase 4 depolarisation (B block and Ca2+ block)
    • Decrease speed of AV conduction
59
Q

effect of amiodarone on ECG

A
  • Increase PR
  • Increase QRS
  • Increase QT
  • Decrease HR
60
Q

adverse drug response: Amiodarone

A
  • Pulmonary fibrosis
  • Hepatic injury
  • Thyroid disease
  • Photosensitivity (factor 50)
  • Optic neuritis (transient blindness)
61
Q

contraindications of amiodarone

A
  • May need to reduce the dose of digoxin and monitor warfarin more closely
    • amiodarone can inhibits CYP needed for digoxin and warfarin metabolism leading to higher plasma levels
62
Q

Sotalol (oral) (class 3 drug) use

A
  • Wide spectrum: Supraventricular and ventricular tachycardia
63
Q

MOA of Sotalol (class 3)

A
  • Block potassium channels
    • Class effects of 1,2,3 and 4
  • Effect on cardiac activity
    • Increase APD and refractory period in atrial and ventricular tissue
    • Slow phase 4 (B blockers)
    • Slow AV conduction
64
Q

Sotalol (class 3) effect on ECG

A
  • Increase QT
  • Decrease HR
65
Q
A
66
Q

Adverse drug response: Sotalol

A
  • Proarrhythmic
  • Fatigue
  • insomnia
67
Q

class 4 agents mode of action

A

Calcium channel blockers

  • Block calcium channels decreasing inward ca2+ currents resulting in decrease of phase 4 spontaneous depolarisation
  • Effects plateau phase of AP(2)
  • Shift in AP curve to right
68
Q

name 2 class 4 drugs

A

Verapamil (oral or IV) and diltiazem (oral)

69
Q

use of class 4 agents

A
  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia (re-entry around AV)
  • Used with people who have asthma (cant use B blockers)
70
Q

mode of action of verapamil (class 4)

A
  • Calcium channel blockers
  • Effect on cardiac activity
    • Slow conduction through Av (Ca2+)
    • Increase refractory period in AV node
    • Increase slope of phase 4 in SA to slow HR
71
Q

class4 agents effect on ECG

A
  • Increase PR
  • Decrease HR (or increase depending on baroreceptor reflex)
72
Q

Adverse drug response: Verapamil (class 4)

A

GI problems (constipation)

73
Q

Contraindications: Verapamil (class 4)

A
  • AV block- can get asystole if B blocker is on board
    • Don’t give B blockers and CBB together
  • Hypotension
74
Q

class 5 durgs=

A

additional antiarrhythmic agents

75
Q

name some additional antiarrhythmic agents (class 5)

A
  • adenosine
  • ivabradine
  • digoxin
  • atropine
76
Q

uses of adenosine

A
  • Supraventricular tachycardia
  • Terminating re-entrant SVT
  • Diagnosis of coronary artery disease
77
Q

how is adenosine delivered

A

rapid IV bolus - very short half life

*stops the heart temporarily- feels like dying*

78
Q

Mode of action of 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
    • hyperpolarises cells of conducing tissue (Gi- decreases cAMP- decrease pacemaker potential)
79
Q

cardiac effects of adenosine

A
  • leads to decreased calcium currents and increased refractory period in AV node
  • slowing AV conduction
  • reduced heart rate
80
Q

contraindicatons of adenosine

A

asthmatics

81
Q

ivabradine is given

A

orally

82
Q

uses of ivabradine

A
  • Reduce inappropriate sinus tachycardia
  • Reduce heart rate in heart failure and angina (avoiding blood pressure drops)
83
Q

Mode of actions: adenosine

A
  • Blocks If ion current highly expressed in sinus node (funny current- blocks sodium channel)
  • Cardiac effect
    • Slows sinus node but does not affect blood pressure
84
Q

Adverse drug reaction: Ivabradine

A
  • Flashing lights
  • Teratogenicity not known (avoid in pregnancy)
85
Q

Contraindication: Ivabradine

A

Pregnancy

86
Q

digoxin (cardiac glycoside) uses

A

Treatment to reduce ventricular rates in AF and flutter

87
Q

Mode of actions: Digoxin

A
88
Q

atropine uses

A

vagal bradycardia

89
Q

Mode of actions: Atropine

A
  • Selective muscarinic antagonist
  • Blocks vagal activity to speed AV conduction and increase HR
90
Q

which antiarrhythmic is the most efficacious

A

amiodarone

91
Q

which antiarrhythmic is the most tolerable

A

most- B blockers

least- amiodarone (sunburn and breathless)

92
Q

Which drugs could be used in AF?

A

Rate control= chronic

Rhythm control= if it comes and goes

93
Q
  1. Which IV drug would you use first for VT
A

Depends on which drugs that are already on

  • Intravenous metoprolol/bisoprolol
    • If BP low- cardiovert electrically
    • If BP okay just metoprolol
  • If already on B blocker
    • IV lignocaine or oral mexiletine
  • Or Amiodarone (IV central line)
94
Q

Best drug for Wolf- PW?

A
  • Flecainide or amiodarone
  • Avoid AV nodal blocking drugs (B blockers) due to risk of pre-excited AF and therefore VF
95
Q

List drugs used in re-entrant SVT?

A
96
Q

Which drugs would be used for ectopic atrial tachycardia?

A
  • First line- bisoprolol (safest
  • Next line- CCB
  • Lastly: Flecainide, sotalol, amiodarone
97
Q
A
98
Q

Which drugs for sinus tachycardia?

A
  • Ivabradine (no drop in BP)
  • Bisoprolol, verapamil

Clinical Pharmacology, Therapeutics & Intro to Prescribing (39 decks)

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