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Drugs: from molecules to man > Antidysrhythmic Drugs > Flashcards

Antidysrhythmic Drugs Flashcards

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1
Q

What is a dysrhythmia?

A

an abnormal heart rhythm. It may result in the heart beating too fast, slow or irregularly

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2
Q

What does any disturbance of the heart’s rhythm have the potential to cause?

A

Any disturbance of the rhythm has the potential to cause ill health, either by compromising the heart’s ability to supply blood to the rest of the body or by increasing the risk of other serious conditions such as heart attack or stroke

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3
Q

What can the most serious forms of dysrhythmia result in?

A

the heart ceasing to pump blood

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4
Q

What does the risk of developing a dysrhythmia increase with?

A

Age

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5
Q

What are the risk factors for dysrhythmias?

A
  • Excessive alcohol consumption
  • Smoking
  • Genetics
  • Congenital abnormalities
  • Obesity
  • Existing damage to the heart e.g. myocardial infarction
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6
Q

What can dysrhythmias be triggered or precipitated by?

A

medications, caffeine, stress, exercise, posture and recreational drugs

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7
Q

What is the most common form of dysrhythmia in Europe?

A

Atrial fibrillation

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8
Q

What do dysrhythmias arise due to?

A

faults in the electrical control circuits of the heart

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9
Q

What is the order of flow of the cardiac conducting system?

A

Heart beats are initiated in pacemaker cells in SA node -> bring about atrial contraction -> AV node (slows down impulse conduction to allow ventricles to contract slightly after the atria) -> bundle of His -> left and right branches take signal to the base of the muscle via the purkinjie muscles

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10
Q

What is an ECG and what is it useful for?

A

• ECG – sum of electrical activity across the whole heart

  • Pattern tells us whether the heart is healthy or not
  • One of the main tools in diagnosing dysrhythmias
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11
Q

Where do cardiac action potentials differ?

A

In different sections of the heart

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12
Q

What is the action potential of ventricular muscle?

A
  • Sharp upward strike: voltage gated Na+ channels (activate and then very quickly after inactivate)
  • Voltage gated Ca2+ channels open – responsible for plateau
  • Then K+ channels open and repolarisation takes place bringing membrane potential back to baseline
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13
Q

What is the action potential of the SA node?

A
  • Upward rising baseline – ‘funny current’ due to HCN channel bringing membrane potential slowly up the threshold
  • Action potential bought about mostly by Ca2+ channels opening
  • At peak Ca2+ channels close and K+ channels open repolarising
  • ‘funny current’ potential responsible for pacemaker activity
  • Changing the slope of the pacemaker potential changes how quickly an action potential is fired – therefore how quickly the heart beats
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14
Q

How do you set up an ECG and what does it measure?

A

• ECG (EKG) – 12 lead electrocardiogram

  • ‘leads’ refer to connection combinations
  • Actually 10 electrodes placed on the body
  • 6 on the chest
  • 1 on each limb
  • Measure the connections between different electrodes
  • Deviations from standard rhythm tells us what is going on in the heart
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15
Q

What are the origins of the ECG wave?

A
  • P wave – atrial activation
  • QRS complex – ventricular activation
  • T wave – recovery wave (ventricles repolarise)
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16
Q

What does a disrupted electrical rhythm lead to?

A

Disrupted electrical rhythm -> disrupted cardiac mechanical cycle -> impaired cardiac output

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17
Q

What are the different sites of origins of dysrhythmias?

A
  • Atrial (supraventricular)
  • Junctional (AV node)
  • Ventricular
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18
Q

What is a fibrillation/flutter?

A

Disorganised rhythm

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19
Q

What is tachycardia?

A

Heartbeat is too fast

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20
Q

What is bradycardia?

A

Heartbeat is too slow

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21
Q

What are the different dysrhythmic mechanisms?

A
  • Ectopic pacemakers
  • Delayed after depolarisation
  • Re-entry circuits
  • Congenital abnormalities
  • Heart block
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22
Q

What is an ectopic pacemaker?

A

Cardiac tissue other than SA node initiates heart beat

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23
Q

What is delayed after-depolarisation?

A

Build up of Ca2+ in cells lead to a train of action potentials

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24
Q

What are re-entry circuits?

A
  • Electrical signals go round and round in circles ‘circus movement’
  • Occur due to damage or abnormalities in conduction
  • Local, nodal, global (whole heart – Wolff Parkinson White)
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25
Q

What are congenital abnormalities?

A

Additional conducting pathways between atria and ventricles

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26
Q

What is heart block?

A

Damage to conducting pathways disrupts atrial-ventricular signalling

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27
Q

What are local re-entry circuits?

A
  • Need a piece of tissue where electrical activity is separated by non-conducting tissue
  • Usually there is mutual annihilation of action potential where they meet
  • In this condition we have an area of damage specific to one branch of the pathway – stops signals being conducted in the normal direction. Allows signal to be conducted the other way
  • Normograde transmission blocked through damaged area
  • But signal can go down the other way and then go back up through the damaged area (creates a never ending circuit)
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28
Q

What is an AV node re-entry circuit?

A
  • Two conducting pathways separated by non-conductive tissue
  • One pathways conducts quickly with slow refractive period
  • Other pathway conducts slowly with quick refractive period
  • In normal cycle get a wave of depolarisation from atria into AV node and get conduction primarily through quick pathway
  • If we have an extra wave of atrial activity, if it enters the AV node while the fast pathway is still in it’s refractory period
     We get conduction to the rest of the heart via our slow pathway
     If fast pathway recovers before the signal reaches the point where the pathways meet the slow pathway will excite the fast pathway in retrograde fashion causing a cycle of depolarisation
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29
Q

What are after-depolarisations?

A
  • Split into early and delayed
  • Early happens when the action potential is prolonged and leads to reactivation of voltage sensitive Ca+ currents and Na+ currents
  • Delayed after-depolarisations occur because of calcium depolarisations – calcium pumped out through sodium calcium exchanger (3 sodiums enter the cell for every calcium pumped out). This means we will depolarise the membrane slightly triggering another action potential
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30
Q

What is atrial fibrillation?

A
  • Re-entry circuits or ectopic pacemakers
  • Most common dysrhythmia 14% of over 80s
  • Atrial rate up to 600 bpm
  • Occasional conduction to ventricles – irregular
  • Fatigue, ‘palpitations’/racing heart sensation
  • Increases risk of stroke
  • Characterised by an uneven baseline, do discernible P waves and occasional QRS complexes
  • Risk factors for AF: heart disease, high BP, congenital heart disorders, genetics
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31
Q

What is paroxysmal supraventricular tachycardia (PSTV)?

A
  • Most commonly a re-entry circuit through AV node
  • Paroxysmal – happens in attacks
  • About 0.2% of population: starts at a young age (teens – 40s)
  • Ventricular rate 250 bpm
  • Palpitations, shortness of breath, chest pain
  • Attacks can be halted (sometimes) by Calsalva Manoeuvre (increases BP so triggers baroreceptors)
  • Cause unknown but triggered by anxiety, stress, caffeine and smoking
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32
Q

What is ventricular fibrillation?

A
  • Ventricular re-entry circuits or ectopic foci
  • Ventricles cease beating in co-ordinated way
  • No QRS waves on ECG
  • Rapidly fatal
  • DC shock (defibrillation) may be only way of restoring contraction
  • Common as a complication following a heart attack
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33
Q

What is heart block?

A
  • A form of bradycardia
  • Damage to AV node impairs atrial to ventricular conduction
  • Three ‘degrees’
  • First degree: slowed conduction, PQ increased by you get a QRS for every P wave
  • Second degree (several different types): miss QRS complexes (QRST complexes)
  • Third degree block: impulses do not get from atria to ventricles
     Ventricles or AV node can take over as pacemaker so may get some ventricular contractions (rate will be slower)
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34
Q

What is Wolff-Parkinson-White syndrome?

A
  • Congenital abnormality: accessory AV pathway
     Kent bundle
  • Global re-entry circuit: re-entry AV tachycardia
  • No rate-limiter in Kent bundle, so AF -> very fast ventricular rate -> ventricular fibrillation (AV node usually has a rate block – Kent bundle doesn’t have this limit)
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35
Q

In what three ways can dysrhythmias be treated?

A
  • Pharmacological approaches
  • Surgical approaches
  • Electrical approaches
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36
Q

What are the different classes in the Vaughn-Williams system of classification?

A

I (a,b,c), II, III, IV, unclassified

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37
Q

What do class I drugs target and give examples

A
  • Sodium channels
  • Ia Disopryamide
  • Ib Lidocaine
  • Ic Flecainide
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38
Q

What do class II drugs target and give examples

A
  • Beta 1 adrenoceptor
  • Atenolol
  • Bisoprolol
  • Propranolol
  • Metoprolol
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39
Q

What do class III drugs target and give examples

A
  • potassium channels
  • Amiodarone
  • Sotalol
  • Dronedarone
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40
Q

What do class IV drugs target and give examples

A
  • calcium channels
  • Verapamil
  • Dilitiazem
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41
Q

Give examples ofunclassified drugs

A

Adenosine
Atropine
Digoxin

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42
Q

What does the sympathetic nervous system influence in an ECG?

A

Sympathetic nervous system influences slope of pacemaker potential and plateau of action potential due to calcium channels

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43
Q

What are the effects of antidysrhythmic drugs on the cardiac action potential?

A
  • Class 1: Na+ channel blockers block sodium channels important in action potentials in cardiac muscle
  • Class 2: beta blockers block sympathetic nervous system influences over the pacemaker potential and plateau phase
  • Class 3: K+ channel blockers prolong AP
  • Class 4: Ca2+ blocker: map onto plateau phase and influence upwards phase of action potential in SA node
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44
Q

What class drug is disopyramide and what does it do?

A
  • class Ia
  • Moderate Na+ channel block
  • Increased effective refractory period (ERP)
  • Increase action potential duration (ADP)
  • Supresses re-entry circuits but can increase TDP (dysrhythmia) risk
45
Q

What class drug is lidocaine and what does it do?

A
  • Ib

- Weak Na+ channel block (stronger in ischaemic tissue)

46
Q

What class drug is flecainide and what does it do?

A
  • Class IC
  • Strong Na+ channel block
  • No change in ERP or APD
47
Q

What is the effect of sodium channel blockers on the cardiac action potential?

A
  • All have an effect on Sodium channels
  • However, also seem to have an effect on potassium channels – weakness of the VA system:
  • 1a blocks K+ efflux
  • 1b promotes K+ efflux
  • 1c no effect on K+ efflux
48
Q

What is disopyramide useful for and when is it used?

A
  • Useful for preventing ventricular and supraventricular dysrhythmias, WPW
  • Can be used after heart attack and after defibrillation
49
Q

What are the side effects of disopyramide and when is it contradicted?

A
  • Side effects: GI tract problems, arrhythmias, cognitive problems, visual problems, urinary disorders, hypotension, depresses force of contraction
  • Contraindicated in heart block and severe heart failure
50
Q

What is the sodium channel mechanism?

A
  • Three main states: resting state, open state, inactivated state
  • Resting to open state as membrane depolarises
  • More depolarised and we end up in inactive state
  • As membrane depolarises voltage sensor moves, pulls the channel gate open and we get sodium influx, becomes more depolarised (channel in open state)
  • As we get into very depolarised state the block blocks the mouth of the channel (inactive)
51
Q

What does lidocaine do and when is it given?

A
  • Binds to inactivated sodium channels
  • Use dependent: fast dissociation
  • When sodium is at it’s normal rate sodium has no effect
  • If we have a tachycardia, lidocaine stays bound long enough to suppress the extra heart beat we see in tachycardia
  • Given intravenously to supress ventricular dysrhythmias – alternative to amiodarone
  • Given after defibrillation
  • No longer given routinely after heart attack
52
Q

What are the adverse effects of lidocaine and what is it contradicted in?

A

 CNS excitation – anxiety, agitation, dizziness, seizures
 CNS depression (at high doses) lethargy, coma, respiratory depression
 Bradycardia, hypotension, dysrhythmias
- Lots of drug interactions
- Contraindicated in WPW, severe heart block

53
Q

When if Flecainide used and what does it do?

A
  • Blocks sodium channel but much slower dissociation than lidocaine (much stronger blocker)
  • Used for supraventricular, ventricular arrhythmias
     Only under supervision of specialist
54
Q

What are the side effects of flecainide and when is it contradicted?

A
  • Side effects include dysrhythmias, oedema, visual disturbances
  • Narrow therapeutic window
  • Contraindicated after heart attack
     Was hypothesised that it would be beneficial
     Actually increased risk of sudden death (CAST trial)
  • Many interactions
55
Q

What is the structure of the B1 adrenoceptor?

A
  • Member of family A of g protein coupled receptor
  • Has 7 transmembrane structure
  • Binding site for adrenaline and noradrenaline located along the tops of the TM domains
56
Q

What effects does the sympathetic nervous system have on cardiac conduction?

A
  • Controls slope of pacemaker potentials – chronotropic effects
  • Increases rate of conduction through the AV node
  • Modulates the plateau phase (amount of calcium in cell – controls contraction) – inotropic effect
57
Q

What do B1 antagonists do?

A

reduce slope of pacemaker potential, force of contraction and blocks increase of conduction through AV node

58
Q

What happens if we increase the slope of the pacemaker potential?

A

If we increase the slope of the pacemaker we get to threshold quicker and fire action potentials quicker

59
Q

what does atenolol do?

A
  • Reduces automaticity, slows SA node, AV node conduction

- Many other beta blockers also used: bisoprolol, metoprolol

60
Q

When are atenolol or other beta blockers useful?

A
  • Useful in dysrhythmias where sympathetic activation is a trigger:
     Atrial fibrillation
     Supraventricular tachycardias
  • Useful in preventing dysrhythmias after heart attack
  • Used when increased catecholaime release, thyrotoxicosis
  • Also used in angina, anxiety, (hypertension), (heart failure)
61
Q

what are the adverse effects and contraindications of atenolol and other class II drugs?

A
  • Bronchoconstriction (non-selective BB)
     Asthma, bronchitis, emphysema
  • Precipitation of heart failure, block
     Start low, go slow
  • Diabetes
     T1DM: masks sympathetic signs of hypoglycaemia
     Decreases mobilization of glucose from glycogen (non-selective BB)
     T2DM: May decrease insulin sensitivities
  • cold extremities, Raynaud’s phenomenon
62
Q

What is the structure of a voltage sensitive potassium channel?

A

Tetramer of subunits with ion channel in the centre

63
Q

What is the structure of amiodarone (potassium channel blocker)?

A
  • Lipophilic

- Analogue thyroid hormone due to two iodine residues

64
Q

Apart from being a potassium channel blocker what else does Amiodarone do?

A
  • Inhibits beta adrenoceptors (Class II)
  • Blocks calcium channels (class IV)
  • Inhibits sodium channels (Class Ia)
65
Q

What does blocking potassium channels do?

A
  • Blocking potassium channels delays repolarisation -> prolonged action potential and refractory period
  • Decreased AV node conduction velocity
  • Decreases re-entry tendency
66
Q

What are the indications or amiodarone?

A
  • Useful in a wide range of dysrhythmias:
     Atrial fibrillation/flutter
     Ventricular and supraventricular tachycardias
     Wolff-Parkinson-White syndrome
67
Q

How can amiodarone be administered?

A
  • Can be administered orally or IV

- Oral has variable bioavailability

68
Q

What are teh contraindications, adverse effects, interactions and pharmacokinetics of amiodarone?

A
  • Can make bradycardias or AV node block worse
  • Can cause TDP as it prolongs action potential duration
  • It is an analogue of thyroxine – can interfere with thyroid function
  • Very lipophilic and so is deposited in tissues:
  • Causes lung fibrosis
  • Is deposited in the eye (can sometimes cause visual problems)
  • Liver toxicity (serious cases rare)
  • Deposited in the skin: blue-gray colouration on exposure to UV light
  • Metabolised by CYP3A4 so many interactions with drugs (and grapefruit juice)
  • Very long plasma half-life (up to 100 days)
  • Takes a long time to reach steady state – binds to tissues
  • Uses IV into central vein for CV emergencies (refractory VF)
69
Q

What is Verapamil?

A

L type calcium channel blocker

70
Q

What is the structure of Ca2+ alpha-subunit?

A
  • Alpha subunit has 24 membrane spanning domains
  • Fold together into four subunit like structures (pseudo subunits) which cluster around the central ion channel
  • Membrane dipping domain from each of the four pseudo-subunits that help form the lining of the channel
71
Q

What 3 states does a voltage gated calcium channel exist in?

A
  • Resting
  • Open
  • Inactivated
72
Q

What are the ligands that act on L type calcium channels, what tissue are L type calcium channels found in and what are their alpha subunit genes?

A
  • Ligands: verapamil, diltiazem, dihydropyridines (act primarily in vascular smooth muscle)
  • Tissue: heart, smooth skeletal muscle
  • A-subunit gene: CaV 1.1-1.4
73
Q

What are the two main classes of calcium channel blockers?

A

dihydropyridines and non-dihydropyridines

74
Q

What do Dihydropyridines do?

A
  • All end in ‘dipine’ e.g. amlodipine
  • Binds to inactivated state of calcium channel
  • See inactivated state a lot more in tissues that are depolarised
  • Vascular smooth muscle is more depolarised than cardiac tissue
75
Q

What does Verapamil do?

A
  • binds to open state of calcium channels: cardiac selective
  • Ca2+ channels important in tail end of pacemaker potential
  • Verapamil blocks Ca2+ in tail end of pacemaker potential and in the main part of the action potential
  • We see reduced automaticity (not as many ectopic pacemakers produced), reduced re-entry tendency, reduced AV node conduction velocity.
  • Also see effects in cardiac muscle: effects plateau phase of cardiac muscle action potentials
76
Q

What are Verapamil indications?

A
  • Oral, IV formulations
  • Used to prevent PSVT (or terminate)
  • Helps keep ventricular rate under control in AF
  • Angina, hypertension, cluster headaches
77
Q

What are Verapamil contraindications, side effects and interactions?

A
  • Contraindicated in Wolff-Parkinson-White, bradycardia, heart block (exacerbates)
  • Side effects: headache, constipation, flushing, hypotension
  • Many drug interactions. Metabolism partially via CYP3A4 so avoid grapefruit
78
Q

What does grapefruit contain?

A

Citrus furanocoumarins (Bergmottin)

79
Q

What is CYP3A4?

A
  • Cyt P450 enzyme
  • Intestinal and liver expression
  • Responsible for >30% of drug metabolism
  • Oxidizes foreign molecules
  • Irreversibly inhibited by furanocoumarins
  • Effects can occur >3 days after consuming druit
  • Can cause overdose of prescription drugs (reduces metabolism)
  • As little as one fruit, or a glass of juice can cause effect
80
Q

What are the adenosine receptors and how does A1 work?

A

• Four GPCR subtypes: A1, A2A , A2B, A3

- A1: Gi coupled. Beta gamma subunits interact with potassium channel KACh (member of GIRK family of potassium channels)

81
Q

How does adenosine produce antidysrhythmic effects?

A

When adenosine activates Gi, the beta and gamma subunits go off into the membrane and activate KACh channel and this leads to potassium efflux and hyperpolarisation. This inhibits voltage sensitive calcium channels in the cell membrane. This is how we produce the antidysrhythmic effects – indirect inhibition of voltage gated calcium channels

82
Q

How does acetylcholine produce a slowing effect on the SA node?

A

The M2 muscarinic receptor also couples to this potassium channel through the same mechanism as adenosine

83
Q

What does atropine do?

A

Atropine is a non-selective muscarinic receptor antagonist. If we inhibit the muscarinic receptors with atropine we will diminish the activation of our KACh channels making our cell less hyperpolarised, this will promote activation of voltage gated calcium channels – atropine leads to speeding up of the heart rate (can be used to treat bradycardias)

84
Q

What are the indications of adenosine?

A
  • Very short plasma half-life (10s)
  • Rapid uptake by red blood cells and metabolism
  • Given as rapid IV bolus: effects last 20-30s
  • Suppression of:
     PSVT
     Ventricular tachycardia with WPW syndrome
     Supraventricular tachycardias during surgery
  • Has largely replaced verapamil for these purposes: short duration of action is an advantaged
85
Q

What are the adverse effects, contraindications and interactions of adenosine?

A
  • Can cause bradycardia (but short duration)
     Avoid in heart block, heart failure
     Facial flushing
  • Chest pain
  • Bronchospasm and dyspnoea
     Avoid in asthma
    -Dangerous interaction with some local anaesthetics (theoretical risk?)
  • Caffeine and theophylline are adenosine antagonists
86
Q

What does Digoxin do?

A
  • Blocks sodium pump directly
  • Indirectly blocks sodium/calcium exchange
  • Increases calcium in stores (via CIRCA): more contraction force (force of contraction directly related to the amount of calcium)
87
Q

What are the antidysrhythmic actions of Digoxin?

A
  • Stimulates parasympathetic nervous system (mechanism less certain)
     AV node conduction, SA node firing rates decreases
  • Increases AV node refractory period but decreases it in myocytes
  • Increases force of contraction, slows ventricles -> better filling
88
Q

What does Digoxin do at higher doses?

A

 Digoxin CAUSES dysrhythmias at higher doses

 Increases automaticity (tendency to become ectopic pacemakers)

89
Q

What are the adverse effects, contraindications and interactions of Digoxin?

A
  • Very narrow therapeutic window
     Nausea and vomiting
     Visual disturbances; acuity and colour (xanthopsia)
     Ventricular tachyarrhythmias
  • May need to monitor plasma levels (not done routinely)
  • Digoxin binds to K+ site on sodium pump so toxicity increased by hypokalaemia
  • Contraindicated in ventricular dysthymias, Wolff Parkinson White, heart block
  • Interacts with a lot of other drugs
  • Overdose treatment: stop digoxin, correct hypokalaemia, give beta blockers to control dysrhythmias, give Digibind Ab fragment IV
90
Q

When is atropine used and what does it do in low doses?

A
  • Used IV in bradycardia, some forms of heart block

 Low doses: causes bradycardia via central effect

91
Q

What are atropines contraindications, side effects and interactions?

A
  • Contraindicated in glaucoma, certain GI tract disorders, urinary retention
  • Causes dizziness, drowsiness, photophobia (as it dilates the pupil), constipation, headache, nausea, palpitations, tachycardia
  • Severe interaction with phenylephrine (hypertension), interacts with any drug with muscarinic actions
92
Q

What is ablation surgery and when is it used?

A
  • In many of the dysrhythmias we’ve met the root of the problem is a small piece of tissue that is abnormal – either it is damaged, or it is a congenital abnormality.
  • If it is possible to identify the location of the abnormality, it may be possible to correct the problem by destroying it (ablation surgery) – it can be a relatively minor procedure
  • Ablation surgery can be used to correct a range of dysrhythmias but most commonly supraventricular tachycardias
  • Wolff Parkinson White syndrome also responds well to this treatment
93
Q

Why is ablation not usually the first line of treatment for dysrhythmias?

A

Because of the risks

94
Q

What is cardioversion?

A
  • Cardioversion is a procedure that is used to ‘jolt’ a heart out of its abnormal rhythm and back into a pattern under the control of the SA node
  • It can be done pharmacologically – and many of the agents that we have met in this module can be used for this purpose
95
Q

What are the two types of electrical cardioversion?

A
  • defibrillation

- synchronised electrical cardioversion

96
Q

What is defibrillation and when is it used?

A
  • Defibrillation is the use of a non-synchronised pulse of electricity when the patient is in pulseless ventricular tachycardia or ventricular fibrillation
  • Because defibrillation is a potentially life-saving procedure, automated devices have been developed that can be used by members of the public
  • An automated external defibrillator (AED) is designed so that it will not deliver a defibrillation shock unless the patient actually needs it
97
Q

What is synchronised electrical cardioversion and when is it used?

A
  • Synchronised electrical cardioversion can be used when a pulse is present e.g. in a supraventricular tachycardia
  • In this type of cardioversion, the shock is synchronised with the cardiac cycle so that it is given during the R wave. This minimises the chance that the electric shock will trigger a worse dysrhythmia e.g. ventricular fibrillation
  • Medications e.g. amiodarone may be given after cardioversion to help maintain the patient in sinus rhythm. If the procedure is planned, then drugs can be given before cardioversion to help maximise the chance of success
98
Q

What is the basic principle in both defibrillation and synchronised electrical cardioversion?

A

To depolarise a large block of cardiac muscle

99
Q

What is an implantable cardioverter-defibrillator and when is it used?

A

For patients who are at high risk of going into life threatening dysrhythmias such as ventricular fibrillation, an implantable cardioverter defibrillator (ICD) can be placed inside the patient’s body. These devices constantly check cardiac electrical activity and if a dysrhythmia is detected, electrodes in the heart administer a shock in a similar way to an external device

100
Q

What are pacemakers commonly used for?

A

Bradycardias

101
Q

If a patient has heart block what does an artificial pacemaker do?

A

the pacemaker can detect atrial impulses and then, after an appropriate delay, it stimulates the ventricles – this overcomes the problem posed by the defective AV node

102
Q

If a patient has undergone a procedure to ablate the AV node what will an implanted pacemaker do?

A

take over stimulation of the ventricles

103
Q

How are modern pacemakers put in the body?

A

The electrode for modern pacemakers can be put in place using a catheter inserted in the femoral or pectoral vein. The main circuitry is placed in the chest just below the collar bone. Modern batteries can last up to 10 years

104
Q

What do hERG channels code for and what do mutations do?

A

codes for a cardiac potassium channel. This channel is important in cardiac action potentials and mutations can cause the QT interval to lengthen

105
Q

What can Long QT syndrome lead to?

A

a dangerous dysrhythmia called torsafes de pointes

106
Q

What can also interfere with the function of the hERG channel?

A

Drugs

107
Q

What has drug induced long QT syndrome caused

A

several drugs to be withdrawn from the market

108
Q

What is long QT syndrome commonly caused by?

A

Long QT syndrome is commonly caused by drug side effects and more rarely caused by gene mutations

109
Q

What can antidysrhythmic drugs that prolong the action potential do?

A

Antidysrhythmic drugs that prolong the action potential can also lengthen QT and hence increase the risk of torsades. Examples include amiodarone and disopyridamide

Drugs: from molecules to man (22 decks)

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