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pharm II exam 2 > arrhythmias > Flashcards

arrhythmias Flashcards

1
Q

how many phases are in the action potential of a purkinje cell

A

5

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2
Q

What happens during phase 0 in the action potential of a purkinje cell

A
  • opening of the sodium channels, rapid depolarization, inactivation of the sodium channels
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3
Q

what happens during phase 1 of action potential of purkinje fibers

A

– rapid partial repolarization due to the inactivation of fast sodium channels and increased K+ channel permeability.

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4
Q

what happens during phase 2 of action potential of purkinje fibers

A

plateau phase, Ca2+ (main effector, L-type) and some Na+ (aka: “window” or late current) channels are open

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5
Q

what happens during phase 3 of action potential of purkinje fibers

A

repolarization, Ca2+ channels inactivated, K+ channels open, Na+ channels turning to rested state

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6
Q

what happens during phase 4 of action potential of purkinje fibers

A

– resting membrane potential

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7
Q

Effective Refractory Period (ERP)

A
  • ERP is the shortest interval at which a premature stimulus results in a propagated response. The ERP usually includes phase 0, 1, 2 and most of 3.
  • it is due to the availability of resting Na+ channels
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8
Q

What phases are present in action potential of SA node cell

A
  • 0, 3, 4
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9
Q

What is happening during phase 0 in SA node cell action potential

A
  • opening of the Ca2+ channels (T-type depolarize early, but are not responsible for action potential, but L-type channels are) causing a slow depolarization.
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10
Q

What is happening during phase 3 in SA node cell action potential

A

repolarization, Ca2+ channels inactivated, K+ channels open

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11
Q

what is happening during phase 4 in SA node action potential

A
  • resting membrane potential never static like in the Purkinje cell, rather a spontaneous depolarization occurs because of a slow Na+ current (If, or “funny” current), at a more depolarized potential, T- and L-type Ca 2+ channels also open and cause phase 0
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12
Q

is there ever a static resting potential in the SA node

A

resting membrane potential never static like in the Purkinje cell, rather a spontaneous depolarization occurs because of a slow Na+ current (If, or “funny” current),

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13
Q

The fraction of Na+ channels available for opening in a purkinje fiber in response to a stimulus is determined by

A

the membrane potential immediately preceding the stimulus.

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14
Q

Action Potential Duration (APD)

A

Action potential duration is the time interval between the point of depolarization and repolarization. Normally, the ERP and APD are closely linked with the ERP being roughly 85% of APD.

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15
Q

what are the basic causes of cardiac arrhythmias

A
  • disturbances in impulse formation
  • disturbances in impulse conduction
  • both
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16
Q

SA node reaches threshold at what potential

A

-40 mV

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17
Q

SA node is at resting membrane potential at what value

A

-65 mV

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18
Q

List the 4 factors that determine rate of pacemaker cells

A
  1. maximum diastolic potential
  2. slope of phase 4 depolarization
  3. threshold potential
  4. duration of action potential
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19
Q

list the two causes of simple block disturbance of impulse conduction

A
  • AV nodal block
  • bundle branch block
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20
Q

list the two causes of reentry mechanism disturbance of impulse conduction

A

*major mechanism

  • obstacle to homogenous condution
  • unidirectional block at some point
  • condution time along the circuit is long enough to find excitable tissues
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21
Q

Explain what happens in normal electircal impulse condution

A
  • two impulses meet and extinguish eachother due to trying to activate cells in the effective refractory period
  • all electrical activity stops and allows for resetting of the channels
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22
Q

explain what occurs during unidirectional block and reentry

A
  • the impulse traveling through the unidirectional block is extinguished in the anterograde direction
  • the conduction pathway can now re-enter in the retrograde direction and will cause a reentry arrhythmia circuit
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23
Q

Remember the Gaussian distribution of patient responses! Antiarrhythmic agents can precipitate what

A

lethal arrhythmias

  • at higher doses, antiarrhythmic agents can depress conduction in normal tissues and produce drug induced arrhthymias
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24
Q

list the drugs in class 1A of sodium channel blockers

A
  • Quinidine (Quinora)
  • Procainamide (Pronestyl)
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25
Q

list the drugs in class 1B of sodium channel blockers

A

Lidocaine

26
Q

MOA of drugs in class 1A of sodium channel blockers

A
  • preferentially block open or activated Na+ channels
    • slows rate of rise of action potential
  • Blocks K+ channels
    • lengthen the duration of action potential and ERP
  • **will completely block damaged cells
27
Q

MOA of drugs in class 1B of sodium channel blockers

A
  • Block inactivated sodium channels
    • preferentially affects damaged tissue; blocks “window” current
    • shorten the duration of action potential and ERP
28
Q

MOA of drugs in class 1C of sodium channel blockers

A
  • Binds to ALL sodium channels; no effect on the duration of action potential (ERP stays the same)
29
Q

List the drugs in class 1C of sodium channel blockers

A

Flecainide

30
Q

what are the class II antiarrhythmic drugs

A
  • beta blockers
  • reduce adrenergic activity on the heart
31
Q

MOA of drugs in class III antiarrhythmic agents

A
  • inhibit K+ channels and Prolong repolarization (ERP increases)
32
Q

list drugs in class III antiarrhythmic agents

A
  • Amiodarone
  • Sotalol
33
Q

list drugs in class IV antiarrhythmic agents

A
  • verapamil
  • diltiazem
34
Q

MOA of drugs in class IV antiarrhythmic agents

A
  • calcium channel blockers
    • block slow L-type cardiac Ca2+ channels
  • decrease HR and contractility
35
Q

When is Quinidine used

A
  • broad spectrum
  • acute or chronic tx of atrial and ventricular arrhythmias
36
Q

adverse effects of Quinidine

A
  • low theraputic index
  • cardiac toxicity
  • blocks alpha receptors -> severe hypotension and reflex tachycardia
  • paradoxical tachycardia
  • increase QT interval -> Torsade de pointes -> Quinidine syncope
  • Diarrhea (top 5 drug to cause this)
  • Cinchonism: loss of hearing, angioedema, tinnitus, visual disturbances
37
Q

What is different about Procainamide from Quinidine even though they are both in Class 1A drugs

A

procainamide can cause lupus erythematosus in slow acetylators

38
Q

DOC for acute ventricular arrhythmias

A

Lidocaine

39
Q

route of administration of Lidocaine

A

IV

40
Q

adverse effects of Lidocaine

A
  • least negative inotropic
  • convulsions
41
Q

when is Flecainide used

A
  • last ditch effort drug
    • atrial arrhythmias
    • life threatening ventricular arrhythmias
42
Q

adverse effects of Flecainide

A

strong pro-arrhythmic effect

43
Q

which beta blocker is B1 specific, given IV, and has a short half life

A

Esmolol

44
Q

use of Esmolol

A

acute treatment of PSVTs-2nd line

  • Paroxysmal supraventricular tachycardia (PSVT)
45
Q

DOC for ventricular arrhythmias -> ACLS

A

Amiodarone

46
Q

when is Amiodarone used

A
  • effective against both atrial and ventricular arrhythmias
47
Q

even though Amiodarone prolongs QT, what stands out about it

A

Does not cause Torsade de pointes

48
Q

adverse effects of Amiodarone

A
  • pulmonary fibrosis
  • deposited in tissues, cornea (yellow-brown), skin (grayish blue)
  • thyroid disfunction
49
Q

MOA of Sotalol

A
  • class III
    • K+ blocker -> prolongs APD
  • also non-selective beta blocker
50
Q

when is Sotalol used

A
  • in tx of ventricular and atrial arrhythmias
51
Q

adverse effects of Sotalol

A

Torsade de pointes

52
Q

When is Verapamil and Diltiazem used

A
  • Reentrant supraventricular tachycardia
  • PSVT
  • Atrial fibrillation and flutter
    • marked effects on SA and AV nodes
53
Q

which drug class is only effective in the atria

A

CCB

54
Q

MOA of adenosine

A
  • enhance K+ conductance and inhibition of cAMP-induced Ca2+ influx
    • hyperpolarizes everything and resets the heart
55
Q

when is adenosine used

A
  • reentry arrhytmias
  • acute PSVT
  • WPW syndrome
56
Q

DOC for acute PSVT and WPW syndrome

A

adenosine

57
Q

acute PSVT treatment order

A
  1. adenosine
  2. Esmolol
  3. CCB
58
Q

chronic PSVT treatment order

A
  1. B-blocker
  2. CCBs
59
Q

DOC for torsade de pointes

A

Magnesium

60
Q

MOA of potassium in treatment of arrhythmias

A
  • increased serum K has membrane potential stabilizing action by increasing K+ permeability (hyperpolarizes)
    • decreases ADP
    • decreases conduction
    • decreases pacemaker rate
61
Q

which drug class only works for ventricular arrhythmias

A

class 1B: lidocaine

  • because that’s the only place where there is a plateau phase where the “window” current is functioning.
62
Q

Lidocaine, adenosine and magnesium are administered

A

IV only

  • are useful only in acute therapy.

pharm II exam 2 (9 decks)

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