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Pharmacology > Exam2Lec6Anti-Arrhythmics > Flashcards

Exam2Lec6Anti-Arrhythmics Flashcards

1
Q
  1. What is an arrhythmia?
  2. What is are antiarrhymics
A
  1. abnormal heart beat
  2. class of drugs that able to treat arrthythmias
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2
Q

Why can the heart beat?

A

AP/electrial wave goes through the heart and causes calcium induced calcium release to then cause contraction

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3
Q
  • Where is the SA node located?
  • What is special about the nodal (SA and AV) cells?
A
  • located RA at jxn btw superior vena cava and RA roof-crista terminulus
  • Has automaticisty and generates AP, what allows this is the funny channel (Na+). Funny channel reaches the theshold so the Ca channals can open
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4
Q
  • What atrial and ventrical cells, what causes the AP?
  • Is it more or less hyperpol than the nodal cells?
A
  • Na channels
  • more hyper
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5
Q

What are the plateau regions caused from?

A

K and Ca currents

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6
Q

Compare ventricular and atrial AP wave

A

Vent: has rectangular shape
Atrial: has trianglar shape (plateau is less)
* Phase 0= d/t Ina channels
* Phase 2= d/t lca and k
* phase 3= k channels

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7
Q

Explain the phases in nodal action potential

A

phase 0 (depolar): ca channels d/t higher voltage which inactivates Na channels
Phase 3: Potassium
Phase 4: funny channel (na )

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8
Q

Explain the phases in nodal action potential

A

phase 0 (depolar): ca channels d/t higher voltage which inactivates Na channels
Phase 3: Potassium
Phase 4: funny channel (na )

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9
Q

Does the nodal action potentials have a resting potential? Explain

A

No resting potential, have maximum diastolic potential which is the most neg value of voltage of AP

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10
Q

When electrical excitation does not follow its normal paths…

A

an arrhythmia may occur

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11
Q
  • Failure of impulse initiation:
  • Failure of impulse propagation from atria to ventricles:
  • Enhanced automaticity, triggered automaticity, and reentry:
A
  • Failure of impulse initiation (something wrong with SA node-> cannot fire): slow heart rates (bradycardia bc no firing)
  • Failure of impulse propagation from atria to ventricles (if something is wrong at level of AV node or purkinje fiber): heart block
  • Enhanced automaticity, triggered automaticity, and reentry: rapid heart rates (Tachyarrhythmias-increase HR)
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12
Q

Explain the pathway of tachyarhythmia to impluse generation disorders and impulse conduction disorders and so on

A
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13
Q

Explain enhanced automaticity and when does this happen?

A
  • tissues/cells that use to not have automicity, now does fire on its own (ex. purkije cells will fire AP and cause ventricules to be fast)
  • Ischemia and reperfusion arrhythmias
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14
Q

What are the two types of triggered automaticity

A
  • delayed afterdepolarization
  • early afterdepolarization
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15
Q

What is delayed afterdepolarization? what happens?

A

Happens d/t pathology, NOT because of normal AP that has started in the atrium to venticle
* in venticles, atrium and purkinje (have a resting membrane)
* Ex with patho is CHF: causes causes ca overload which causes an increase chance of these cells to undergo triggered automaticity dt Na/Ca exchanger and bring Na in

Ca++ overload/ Digitalis toxicity

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16
Q

What is the early afterdepolarization? when does it happen?

A
  • Some drugs block the rapid delayed rectifier potassium current (Ikr or HERG) which prolong AP and it happens in the ventricular cells.
  • You can also inherted long QT syndromes dt mutations in the HERG channels-> decrease K currents
  • When you have long repol, you run the risk of initating EAD which is a depolarization b4 AP has repolarized
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17
Q

What are the two reentry

A

anatomical reentry and functional reentry

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18
Q

What is anatomical reentry?

A

Electrical impulse rotates around an anatomical obstacle
* ex. pt had an heart attack so there was an ischemia in part of the heart and tissue died-> fibrosis -> impulse will encounter this and cannot go through it so AP will start to go around in circles causing an increase in HR +Vfib

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19
Q

What is anatomical reentry?

A

Electrical impulse rotates around an anatomical obstacle
* ex. pt had an heart attack so there was an ischemia in part of the heart and tissue died-> fibrosis -> impulse will encounter this and cannot go through it so AP will start to go around in circles causing an increase in HR +Vfib

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20
Q

What is functional reentry?

A

Electrical impulse rotates around a functional obstacle
* diseased tissue (not died) will not be able to excite so AP will go around

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21
Q

For non-nodal cells, what are the phases

A
  • phase 0: Na (depolar)
  • 2: Ca + K (plateau)
  • 3: K (repolar)
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22
Q

For non-nodal cells, what are the phases

A
  • phase 0: Na (depolar)
  • 2: Ca + K (plateau)
  • 3: K (repolar)
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23
Q

What are the three states of Na channels and what is important about them?

A

Closed, open and inactivated
* Closed: activation gate is closed but inactivation gate is open
* Open: both open
* Inactived: activation gate open and inactivation gate closed to block ions

WHY WE NEED TO GIVE TIME BTW AP

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24
Q

What are the three states of Na channels and what is important about them?

A

Closed, open and inactivated
* Closed: activation gate is closed but inactivation gate is open
* Open: both open
* Inactived: activation gate open and inactivation gate closed to block ions

WHY WE NEED TO GIVE TIME BTW AP

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25
Q

What states of the Na channels need to be in for antiarrhymic drugs to bind and block?

A

open and inactive because their binding site is in vesibule

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26
Q

sodium channel blockade should do what?

A
  • Slow down the upstroke (phase 0) of the action potential, leading the slowing down of impulse conduction velocity
  • Increase the threshold for firing of the action potential
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27
Q

What should potassium channel blockade do:

A

Prolong the action potential duration, leading to an increase in refractoriness ( no effect on phase 0)

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28
Q

What should a calcium channel blockade do?

A
  • Inhibit excitability of nodal tissues (SA, and AV) since phase 0 is dependant on Ca
  • Depress abnormal automaticity dependent on Calcium channels
  • EADs depend on Ca channels so blocking calcium channels will stop this
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29
Q

What are the Vaughan Williams Classification of Antiarrhythmic Drugs

A
  • Sodium Channel Blockers (Class I)
  • Beta Blockers (Class II)-> do not black ion channels but can modulate rate
  • Potassium Channels Blockers (Class III)
  • Calcium Channels Blockers (Class IV)
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30
Q

What are the different subclasses of class 1

A
  • Class 1a
  • Class 1b
  • Class 1c

Sodium channel blockers

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31
Q
  • What does class 1a do?
  • When do we use it?
  • Side effects?
A

Decrease conduction velocity (bc slow dwn upstroke dt black of Na) and increase APD, and refractoriness.

Used most for trial fibrillation (AF), and atrial flutter, and maintenance of sinus rhythm.

Prolongs QT interval, and could be torsadogenic (fast vent rhym).

32
Q

What does class 1b do?
When it is not good to use and when it is good to use?

A

Decrease APD, and minimal effects on conduction velocity (b/c they block na channel in tissues that have depol cells).

Not good for atrial arrhythmias.

Best for ventricular arrhythmias associated with ischemic (ca build up after and have depol)/post MI depolarized Purkinje and ventricular tissue.

33
Q
  • What does class 1c do?
  • What is it used for?
  • When can we not use it?
A

Marked slow down of conduction velocity. (CLOSEST to perfect na channel blocker). No effects on APD in ventricular and Purkinje cells.

Used for AF/ atrial flutter in patients with structurally normal hearts.

Absolute NO NO in structural and ischemic heart disease. SO no fibrosis!

34
Q

When do we give beta blocker (class II)

A

given to someone has AFib but if they have structural issue (no class 1c) and other issues (no Class 1a)

Will not be used for rphymic contril and will not stop Afib but used for rate control

35
Q

How does the beta blocker work?

A

depress excitability of nodal tissue including AV node
* blocks beta adrengic pathway-> inhibit camp-> inhibt PKa activation (decres Ca) -> decrease exitability of nodal tissue because dercease of the Ca-> inhibit automaticity in nodal cells to protect venticles

36
Q

How does the beta blocker work?

A

depress excitability of nodal tissue including AV node
* blocks beta adrengic pathway-> inhibit camp-> inhibt PKa activation (decres Ca) -> decrease exitability of nodal tissue because dercease of the Ca-> inhibit automaticity in nodal cells to protect venticles

37
Q

What happens when you have atrial rhythm (what can the AV node do) ?

A

AV node protects the ventricles so not many fast beats hit the ventricles

38
Q

What happens when you have atrial rhythm (what can the AV node do) ?

A

AV node protects the ventricles so not many fast beats hit the ventricles

39
Q
  • What happens with potassium channels blockers (class 3)?
  • Used for?
  • SE?
A
  • Increase APD, increase the effective refractory period, and prolong the QT interval.
  • Used in atrial fibrillation, and flutter, ventricular tachycardia and fibrillation.
  • QT prolongation increases risk of Torsades de Pointes.
40
Q
  • What happens with calcium channel blockers (class IV)?
  • Used for?
  • SE?
A
  • Not effective in atrial or ventricular tissue (ONLY NODAL). Slows conduction velocity and depresses excitability in nodal tissue (dependent on Ca channels).
  • Used for nodal arrhythmias (’superventrical tachycardia (SVTs))
  • Can cause sinus node depression (bradycardia), and AV block
  • Use l- type ca channel blockers to control Afib-> rate control
41
Q

How does adenosine work?
What can it cause?

A
  • Very short acting, hyperpolarizes nodal tissues (through potassium channals), and depresses their excitability.
  • For abolishing and diagnosing SVT.
  • Effects blunted by caffeine, or theophylline. Can cause flushing, hypotension
42
Q

What are the two class 1a drugs we need to know?

A

Quinidine and procainamide

43
Q

QUINIDINE

  1. Class?
  2. MOA?
  3. How it works?
  4. Therapeutic uses?
  5. SE?
A
  1. Class 1A
  2. MOA: Binds to open & inactivated Na+ channels. Also blocks
    K+ channels.
  3. ↓ reentrant arrhythmias (fibrosis) by ↓ conduction velocity & ↑ APD and effective refractory period.
  4. Therapeutic Uses: Atrial fibrillation, Atrial flutter, Malaria (Plasmodium falciparium)
  5. Side Effects: Arrhythmias (Ventricular tachy, Torsade de Pointes), Cinchonism (blurred vision, tinnitus, disorientation, psychosis)
44
Q

PROCAINAMIDE

  1. Class
  2. MOA?
  3. Therapeutic uses?
  4. SE?
A
  1. Class 1a
  2. MOA: Binds to open & inactivated Na+ channels, also a K+
    channel blocker which prolongs Phase 3 repolarization.
  3. Therapeutic Uses: ventricular and atrial tachyarrhythmias
  4. Side Effects: Lupus erythematosus-like syndrome, Arrhythmias (VT, TdP), CNS (depression, hallucinations, psychosis)
45
Q

What are the two drugs for class 1b ?

A

Lidocaine and mexiletine

46
Q

LIDOCAINE

  1. Class?
  2. MOA?
  3. Therapeutic uses?
  4. SE?
A
  1. 1b
  2. Rapidly associate & dissociate from Na+ channels, Targets rapidly firing and depolarized cardiac myocytes
    (ischemia), Shortens repolarization & ↓ A.P. duration Suppresses abnormal automaticity arrhythmias ( if you have increase automicity dt ischemia
  3. Therapeutic Uses: Ventricular tachycardia, Ventricular fibrillation. Not useful in AF. -> ischemic or reperfusion injury
  4. Side Effects: Agitation, Confusion, Seizures, Arrhythmias
47
Q

MEXILETINE

  1. Class?
  2. MOA?
  3. Therapeutic uses?
  4. SE?
A
  1. Class 1b
  2. MOA: Rapidly associate & dissociate from Na+ channels. Equivalent to Lidocaine. Targets rapidly firing or depolarized
    cardiac cells. Shortens Phase 3 repolarization & ↓ A.P. duration. Suppresses abnormal automaticity arrhythmias similar to Lidocaine.
  3. Therapeutic Uses: Ventricular tachycardia
  4. Side Effects: Tremors and GI upset.

VENT ONLY

48
Q

MEXILETINE

  1. Class?
  2. MOA?
  3. Therapeutic uses?
  4. SE?
A
  1. Class 1b
  2. MOA: Rapidly associate & dissociate from Na+ channels. Equivalent to Lidocaine. Targets rapidly firing or depolarized
    cardiac cells. Shortens Phase 3 repolarization & ↓ A.P. duration. Suppresses abnormal automaticity arrhythmias similar to Lidocaine.
  3. Therapeutic Uses: Ventricular tachycardia
  4. Side Effects: Tremors and GI upset.

VENT ONLY

49
Q

What are the two drugs for class 1c

A

flecainide and propafenone

50
Q

FLECAINIDE

  1. Class?
  2. MOA?
  3. What does it do?
  4. Therapeutic uses
  5. SE?
A
  1. Ic
  2. MOA: Slowly associate & disassociate from resting Na+ channels & demonstrate prominent effects on normal heart rates.
  3. Suppresses Phase 0 upstroke, slows conduction. Minor effects on A.P. duration & refractoriness. Automaticity tissue ↓ by ↑ threshold potential (harder to fire)
  4. Therapeutic Uses: AF, Atrial flutter, VT, in the absence of structural heart disease.
  5. Side Effects: Arrhythmias, Blurred vision is most common extracardiac side effects. Increased mortality in CAST trial (Patients with MI). Prolongs PR, QRS, and QT (because you prolong QRS so much)
51
Q

PROPAFENONE

  1. Class?
  2. MOA?
  3. Therapeutic uses?
  4. SE?
A
  1. 1c
  2. MOA: Slowly associate & disassociate from resting Na+ channels & demonstrate prominent effects on normal heart
    rates, Suppresses Phase 0 upstroke, slows conduction. Minor effects on A.P. duration & refractoriness. Automaticity ↓ by ↑ threshold potential
  3. Therapeutic Uses: AF, Flutter
  4. Side Effects: Arrhythmias, Blurred vision
52
Q

PROPAFENONE

  1. Class?
  2. MOA?
  3. Therapeutic uses?
  4. SE?
A
  1. 1c
  2. MOA: Slowly associate & disassociate from resting Na+ channels & demonstrate prominent effects on normal heart
    rates, Suppresses Phase 0 upstroke, slows conduction. Minor effects on A.P. duration & refractoriness. Automaticity ↓ by ↑ threshold potential
  3. Therapeutic Uses: AF, Flutter
  4. Side Effects: Arrhythmias, Blurred vision
53
Q

What are the different class II drugs

A

beta blockers:
* Propranolol
* Acebutolol
* Esmolol
* Metoprolol
* Atenolol

54
Q

BETA BLOCKERS

  1. Class?
  2. MOA?
  3. How is works?
  4. Therapeutic uses?
  5. SE?
A
  1. Class 2
  2. MOA: ↓ Phase 4 depolarization
  3. ↓ automaticity, prolonging AV conduction, rate control in AF
  4. Therapeutic Uses: AF, Atrial flutter, SVT
  5. Side Effects: ↓ Sex ♂ (erectile dysfunction in men) , Bradycardia (dt depression of SA) , Fatigue (exercise intolerance)
55
Q

What are the class 3 drugs

A
  • Aminodarone
  • dronedarone
  • ibutilide
  • d,l sotalol
  • dofetilide
56
Q

Amiodarone’s MOA and how it works?

A
  • MOA: K+ channel blocker. Structurally similar to thyroid hormone. Highly lipophilic, concentrates in many tissues, and very slow onset
    of action, and very slow to eliminate. Adverse effects might be very slow to resolve.
  • ↑ AP duration, ↑ effective refractory period.
57
Q

What does amidodarone block?

A
  • Dirty drug: Blocks Na, K, Ca channels, and alpha and beta receptors.
58
Q

What are the therapeutic uses and side effects of amidodarone?

A
  • Therapeutic Uses: Very effective in maintenance of sinus rhythm in AF, Atrial flutter, and decreases risk of VT and VF. Safe to use in heart failure/ does not affect contractility. Safe to use in structural heart disease.
  • Side Effects: Hypo/Hyperthyroidism, Interstitial pulmonary fibrosis that can be irriversible and dangerous, Photosensitivity, Neuropathy,
    Tremor, Ataxia, Optic neuritis, Muscle weakness, bradycardia, however, despite QT prolongation, TdP is extremely rare.
59
Q

Dronedarone

  1. MOA?
  2. How does it work?
  3. Effects?
  4. Therapeutic uses?
  5. Side effects?
A
  • MOA: K+ channel blockers,
  • ↑ A.P. duration, without altering Phase 0
  • ↑ effective refractory period
  • Also has Class I, II & IV effects
  • Therapeutic uses: AF, Atrial Flutter
  • Side effects: ↑ mortality in patients w/ severe HF, Prolonged QTc interval, Bradycardia

CLASS 3

60
Q

Ibutilide

  1. MOA?
  2. How does it work
  3. Therapeutic uses
  4. SE?
A
  • MOA: K+ channel blocker
  • Prolongs APD, ↑ effective refractory period
  • Therapeutic Uses: Atrial fibrillation, Atrial flutter.
  • Side Effects: Arrhythmias (TdP)

Class 3

61
Q

d, l Sotalol

  • MOA?
  • how it works?
  • Therapeutic uses?
  • SE?
A
  • MOA: (d) K+ channel blocker, (L) non selective Beta blocker (BB and potassium)
  • Prolongs APD, ↑ effective refractory period
  • Therapeutic Uses: Atrial fibrillation, ventricular arrhythmias
  • Side Effects: Arrhythmias (TdP), fatigue, shortness of breath, increases mortality (SWORD trial- increase mortality in LV dysfunction after MI ).
62
Q

What class 3 drug can be used for siamond CHF and MI

A

Dofetilide

Use of this agent is reserved for physicians trained and certified in its use.

63
Q

When do you not use dofetilide?

A
  • Do not use if QTc >440 ms. Discontinue is QTc >500 ms
64
Q

DOFETILIDE

  • MOA?
  • How it works?
  • Therapeutic uses?
  • SE?
A
  • MOA: K+ channel blocker
  • Prolongs APD, ↑ effective refractory period
  • Therapeutic Uses: Atrial fibrillation, ventricular arrhythmias
  • Side Effects: Arrhythmias (TdP). Because it is so specific, extracardiac toxicity is very rare.
65
Q
  • Calcium channel blockers are not effective in what?
  • what does it do?
  • What is it used for?
  • What can it cause?
A
  • Not effective in atrial or ventricular tissue.
  • Slows conduction velocity and depresses excitability in nodal tissue (dependent on Ca channels).
  • Used for nodal arrhythmias (SVT’s)
  • Can cause sinus node depression, and AV block
66
Q

What are the class IV drugs?

A
  • Verapamil, Diltiazem
67
Q

Verapamil, Diltiazem

  • MOA?
  • How does it work?
  • Therapeutic use?
  • SE?
A
  • MOA: Bind to open, voltage gated Ca2+ channels
  • ↓ nodal tissue excitability, slows conduction & ↑ effective refractory period, e.g., AV node
  • Therapeutic Use: AF, Atrial Flutter, PSVT
  • Side Effects: (-) inotropic, Hypotension, arrhythmia
68
Q

Adenosine

  • MOA?
  • How does it work?
  • Therapeutic use?
  • Half life?
A
  • MOA: Adenosine receptor agonist, activates a specific
    potassium current through G-protein mediated mechanism.
  • hyperpolarizes nodal tissues, and depresses their excitability, ↓ AV node excitability
  • Therapeutic Use: For abolishing and diagnosing SVT
  • Very short t1/2 = < 10s
69
Q

What antirrhymaic drug is used for malaria?

A

Quinidine

70
Q

What class of drugs are used for ventricalar only, not nodal or atrial?

A

Mexiletine and lidocaine

71
Q

What Ib class has se of tremors and GI upset?

A

Mexiletine

72
Q

What class of drugs can we not use with structual defects?

A

1c

73
Q

What drug is K+ channel blocker that is structurally similar to thyroid hormone? Why is it dirty? What are the SE?

A

Amiodarone
Blacks Na, K, Ca channels and alpha and beta receptors
SE: hypo/hyperthyroidism, interstital pul fibrosis

74
Q

Which drug is a K+ and non selective beta blocker?

A

d,l, Sotalol

75
Q

What drug is used for PSVT, AF, Atrial flutter? it is a Ca channel blocker

A

Verapamil and diltiazem

76
Q

What drug is used for abolishing and diagnosing SVT

A

Adenosine

Pharmacology (26 decks)

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