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Pharmacology > Antiarrhythmatics part 2 > Flashcards

Antiarrhythmatics part 2 Flashcards

1
Q

What is the resting membrane potential of pacemaking cells?

A

-40 to -65

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2
Q

What is the resting membrane potential of non-pacemaking cells?

A

-80 to -95

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3
Q

What is an arrhythmia?

A

any rhythm that is not a normal sinus rhythm with normal atrioventricular (AV) conduction

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4
Q

What are the different arrhythmia patterns?

A
  • irregular
  • tachycardia
  • bradycardia
  • problems related to abnormal conduction and/or muscle depolarization
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5
Q

What is considered bradycardia?

A

HR < 50-60 bpm

  • sinus sick syndrome
  • atrio-ventricular conduction block
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6
Q

What is considered a tachycardia?

A

HR > 100 bpm

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7
Q

What is considered a paroxysmal tachycardia?

A

HR of 150-250 bpm

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8
Q

What is considered an atrial flutter?

A

atria beat at 250-350 bp, regular heart rhythm

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9
Q

What is considered atrial fibrillation?

A

atria beat up to 500 bpm, irregular rhythm, uncoordinated contraction

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10
Q

What is considered a ventricular tachycardia?

A

over 120 bpm, regular heart rhythm

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11
Q

What is considered a ventricular fibrillation?

A

irregular rhythm with uncoordinated contraction, immediate cause of death

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12
Q

What is a tornado de points?

A

Long QT syndrome

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13
Q

What is an arrhythmia caused by?

A
  • alteration in the movement of ions responsible for the action potentials int he pacemaker calls, conduction system and/or muscle
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14
Q

What are the 2 important ions in the action potential?

A
  1. pacemaking (slow) cells (SA node, AV node)
    - Ca and K are most important
    - this is in the atria
  2. Conduction and muscle (fast) cells (atria, parking fibres, ventricles)
    - Na, Ca and K are the most important
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15
Q

What are some common causes of cardiac arrhythmias?

A
  • insufficient oxygen to myocardial cells
  • acidosis or accumulation of waste products
  • electrolyte disturbances
  • structural damage of the conduction pathway (can be patients with heart failure and patients with the previous MI)
  • drugs (antipsychotic and anti-arrythmias. Drugs can also participate an MI)
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16
Q

What are the 2 mechanisms of cardiac arrhythmias?

A
  1. Abnormal impulse formation
    (abnormal automaticity and triggered activity)
  2. Abnormal conduction
    (impaired AV node leads to bradyarrhythmias, re-entry conduction leads to tachyarrhythmias)
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17
Q

What is triggered activity?

A

slow and poorly conducted action potential in the atria or the ventricles

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18
Q

Describe abnormal automaticity

A
  • altered SA node firing rate through changes in autonomic activity
  • enhanced activity of spontaneous pacemakers (ie. AV node, purkinje fibres) - ectopic pacemakers
  • — decrease in phase 4 K conductance (hypokalemia) - increases spontaneous depolarization
  • —- inactivation of Na channels in depolarized cells (schema)- converts fast cells into ectopic pacemakers
  • — localized supersensitivity to catecholamines following ischemia
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19
Q

What happens when you increase the rate of depolarization? When you decrease the rate of depolarization?

A

Increase: increased HR
Decrease: decreased HR

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20
Q

What happens when you make the RMP more depolarized? More hyper polarized?

A

depolarized: increased HR

more hyperpolarized: decreased HR

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21
Q

What happens when there is a more negative threshold? What happens with a more positive threshold?

A

negative: inreased HR

more positive threshold: decreased HR

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22
Q

What is the action of the NT acetylcholine?

A
  • released from parasympathetic nerve
  • acts on the muscarininc receptors
  • phase 4- slows depolarization rate
  • decreases automaticity (SA node), slowed conduction (AV node)
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23
Q

What is the action NT norepinephrine and epinephrine?

A
  • released from the sympathetic nerves
  • acts on B-adrenergic receptors
  • phase 4 - increases depolarization rate and reduces AP firing threshold
  • increases automaticity (SA node), increased conduction (AV node)
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24
Q

What is the triggered activity?

A
  • cells depolarize before complete depolarization has occurred
  • non-automatic myocardial cells (atria, ventricles)
  • – repolarization is required to change Na channels from inactive to resting
  • – Ca channel availability is based on time
  • – may be caused by prolonged duration of the action potential- prolonged QT interval? (i.e.. blockade of K channels by class 1 and 3 anti arrhythmic drugs)
  • – with increased action potential duration (QT interval) calcium channels may be ready before the sodium channels
25
Q

What happens when EAD is sub threshold?

A

prolonged action potential leads to early after depolarization

26
Q

What happens when EAD reaches threshold?

A

prolonged action potential leads to a run of spontaneous activity

27
Q

What can EADs trigger?

A

Torsade de pointes

28
Q

Conditions/drugs which prolong the QT interval may precipitate _____

A

Torsades de Pointes

29
Q

What is a torsades de pointes?

A
  • it is characterized by twisting of isoelectric points on ECG and prolonged QT interval
  • inherited and/or drug induced (increased QT interval)
  • can lead to ventricular fibrillation and sudden death
  • responds to magnesium
30
Q

What drugs can increase the QT interval?

A
  • antiarrhythmics
  • antihistamines
  • anti-psychotics
  • antibiotics (e.g. erythromycin)
  • can cause sudden death - hERG assays now routine during drug development
31
Q

What is the mechanism of cardiac arrythmias that lead to abnormal conduction reentry?

A
  • local differences in conduction velocity and membrane characteristics lead to development of electrical circuits (circus conduction)
  • re-reouting of the normal electrical circuitry results in multiple beats before the next sinus beat is generated, resulting in tachycardia
32
Q

What does normal conduction reentry involve?

A
  • reentry requires an available circuit (closed conduction loop)
  • unidirectional block
  • different conduction speed in limbs of circuit: conduction time (CT) > effective refractory period (ERP)
33
Q

What does unidirectional block re-entry involve?

A
  • available circuit (closed conduction loop)
  • unidirectional block
  • different conduction speed in limbs of circuit: conduction time (CT) > effective refractory period (ERP)
34
Q

What are the main causes of re-entry?

A
  • ischemia
  • congenital
  • hyperkalemia
35
Q

What parts of the heart can re-entry occur in?

A
  • AV node
  • between the SA node and the atria
  • between atria and ventricles
  • accounts for most tachyarrhythmias in cardiac patients
36
Q

How can re-entry be stopped?

A 
can be stopped by converting the unidirectional block tissue to bi-directional block 
- in non-pacemaker (fast) cells, this can be done with drugs that block Na channels directly (class 1 drugs )
37
Q

What is paroxysmal supra ventricular tachycardia?

A
  • its a special case of reentry in the AV node

- the cause is not clear and is often short lasting

38
Q

What can a paroxysmal supra ventricular tachycardia?

A
  • controlled by drugs that depress AV conduction, causing bidirectional block
  • calcium channel blockers (Class 4)
  • B-adrenergic receptor blockers (class 2)
  • adenosine (class 5)
39
Q

What is it called when there is an an abnormal electrical pathway in the paroxysmal supra ventricular tachycardia?

A

Wolff-Parkinson-White syndrome (conducts from the ventricles to atria - bundle of Kent)

40
Q

What is the treatment options of Wolff-Parkinson-White syndrome?

A
  • treated by catheter ablation of abnormal electrical pathway
  • amiodarone first choice agent used to stabilize heart rate
41
Q

Should void AV node blockers if _________ or _______. What drugs do these include?

A

atrial fibrillation
flutter

B-adrenergic receptor blocker, calcium antagonist, adenosine or digoxin

42
Q

What are the three mechanisms of action of anti-arrhythmic drugs?

A
  1. reducing automaticity
  2. blocking re-entry mechanisms
  3. normalize ventricular rate (supra-ventriular tachycardia)
43
Q

Blocking inactivated Na+ or Ca++ channels depolarizing tissues (preventing conversion to “resting” state) lead stop reduced ________

A

triggered activity

44
Q

Hyperpolarizing resting membrane potential (more negative RMP) leads to reduced _______ activity

A

pacemaker

45
Q

When you have an increasing membrane threshold potential for activation of Na+ (fast cells) or Ca++ channels (slow cells) leads to what?

A

reduced pacemaker activity

46
Q

What is 1 way that you can block re-rentry mechanisms via anti-arrythmic drugs?

A

reduce phase 0 depolarization -> slows conduction in ischemia area -> converts region of unidirectional block of bidirectional block

47
Q

What is another mechanism of blocking re-entry mechanisms?

A

prolong the action potential depolarization -> increases the effective refractory period (ERP) -> conduction time < ERP = re-entry blocked

48
Q

How to antiarrhythmic drugs work to normalize ventricular rates in supra-ventricular tachycardia?

A

slowing AV nodal conduction (beta blockers, calcium channel blockers and digoxin) -> reduces ventricular rate -> increasing time for ventricular filling from atrium -> improves stroke volume -> increase cardiac output (CO =HRx increases SV) -> improved hemodynamics

49
Q

What are examples of class 1 antiarrhythmic drugs and what is their action in the cell?

A
  • procainamide, lidocaine, flecainide

- primarily block Na channels

50
Q

What are the examples of class 2 antiarrythmic drugs and what is their action inside the cell?

A
  • propanolol, metoprolol, esmolol

- primarily blocks B-adrenergic receptors

51
Q

What are the examples of class 3 antiarrythmic drugs and what is their action inside of the cell?

A
  • amiodarone, sotalol

- primarily blocks K channels

52
Q

What are the example of class 4 antiarrythmic drugs and what is their action inside of the cell?

A
  • verapamil

- primarily blocks Ca channels

53
Q

What are the examples of class 5 antiarrythmic drugs and what is their action inside of the cell?

A
  • magnesium, adenosine and digoxin

- block calcium gated channels - K blockers target on pacemaking cells

54
Q

Describe IA sodium channel blockers. What is an example of this?

A
  • moderate phase 0 depression and slow conduction; usually prolong repolarization
  • procainamide
55
Q

Describe IB sodium channel blockers. What is an example of this?

A
  • minimal phase 0 depression and slow conduction; usually shorten repolarization (lidocaine)
56
Q

Describe IC sodium channel blockers. What is an example of this?

A
  • shows marked depression and slow conduction; little effect on repolarization
    (flecainide)
57
Q

Class 1A Na channel blockers primarily block _______, especially in depolarized cells

A

Na channels

58
Q

What are the two things that cane seen on an ECG after giving a class 1A drug that corresponds to the bloc?

A

slowing of the phase 0 depolarization

- slowing conduction velocity (widening of the QRD complex of the ECG)

Pharmacology (23 decks)

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