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Pharm (Fall 2022) > Arrhythmias (Exam III) > Flashcards

Arrhythmias (Exam III) Flashcards

1
Q

What is the prevalence of patients with arrhythmias if:
1. Being treated with digoxin.
2. Anesthetized
3. Acute MI

A
  1. 25%
  2. 50%
  3. 80%
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2
Q

What does the concept of automaticity refer to?

A

The ability of nodal tissue in the heart to automatically produce it’s own action potential at a certain interval.

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3
Q

Describe the 5 step conduction pathway for the heart, defined in lecture, starting with the SA node.

A
  1. SA node
  2. AV node
  3. Bundle of His
  4. Bundle Branches
  5. Purkinje Fibers
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4
Q

What structure links cardiac myocytes together to rapidly facilitate depolarization?

A

Gap Junctions

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5
Q

Which 3 ions are most important in determination of Vᵣₘ ?

A

Na⁺, K⁺, and Ca⁺⁺

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6
Q

During a normal action potential, which ion will always influx first?
Which one influxes second?

A

Na⁺ 1st
Ca⁺⁺ 2nd

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7
Q

Where does the myocardium’s ATP come from primarily?

A

Fatty Acid Oxidation (FOX)

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8
Q

What type of threshold is possessed by pacemaker cells (i.e. nodal tissue) in the heart?

A

Lower threshold (~ 60mV)

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9
Q

During a nodal tissue (pacemaker cell) action potential, which ion influxes first?
Is this a rapid depolarization like other action potentials?
Which ion produces rapid depolarization in this specialized cell?

A

Na⁺

No, Na⁺ influx is slow until the threshold is met.

Ca⁺⁺ produces rapid depolarization in nodal tissue.

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10
Q

What type of cell is producing the action potential depicted below?

A

Non-Pacemaker Cardiac Myocyte (i.e. Atrial, Ventricles, or Purkinje Fibers)

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11
Q

The upstroke noted in Phase 0 below (also denoted by D.) is a result of which ion going where?

A

Rapid Na⁺ influx inside the cell

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12
Q

What causes the “plateauing” of the action potential in Phase 2 noted in the figure below?

A

Opening of L-type Ca⁺⁺ channels to allow Ca⁺⁺ to influx into the cell.

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13
Q

What is occurring in Phase 1 that marks the peak of the action potential and the rapid downward slope thereafter?

A

At Peak: H-Gates for Na⁺ close, K⁺ starts rapid efflux
Downward slope: rapid K⁺ effluxing

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14
Q

What is occurring in Phase 3 of the figure below?

A

Continued efflux of K⁺ bringing the cellular membrane closer to Vᵣₘ

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15
Q

What is occurring in Phase 4 of the figure below?

A

Re-establishment of Vᵣₘ by Na⁺K⁺ATPase pump.

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16
Q

Regarding Voltage-Gated (V-G) Na⁺ channels, what gates are open at resting state vs closed at resting state?

A

Resting State:
M-Gates are closed
H-Gate is open

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17
Q

Regarding Voltage-Gated (V-G) Na⁺ channels, what gates are open at the activated state vs closed at activated state?

A

Activated State:
M-Gates are open
H-Gate is open

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18
Q

Regarding Voltage-Gated (V-G) Na⁺ channels, what gates are open at the inactivated state vs closed at inactivated state?

A

Inactivated State:
M-Gates are open
H-Gate is closed

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19
Q

Closure of what gate on a V-G Na⁺ Channel is indicative of the absolute refractory period?

A

H-Gate

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20
Q

What are the two main classifications of Arrythmias?

A
  1. Disturbances in Impulse Formation
  2. Disturbances in Impulse Conduction
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21
Q

What 3 factors can cause a disturbance in impulse formation?

A
  1. SA/AV Node abnormalities
  2. Ion changes (ex. ↑K⁺ )
  3. SNS stimulation
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22
Q

What two factors can cause a disturbance in impulse conduction?

A
  1. Block
  2. Reentry
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23
Q

What effects would Vagal discharge have on impulse formation?
Conversely, how would sympathetic stimulation affect impulse formation?

Answer specifically on the effects to the phase(s) of cardiac myocyte depolarization.

A
  • ↓ HR by ↓ Phase 4 slope
  • ↑ HR by ↑ Phase 4 slope
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24
Q

What are Afterdepolarizations?

A

Abnormal depolarizations occurring in Phases 2, 3, or 4 of the cardiac myocyte action potential cycle.

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25
Q

What are Early Afterdepolarizations (EAD’s)?

A
  • Phase 2 or 3 “premature” depolarization
  • Some Na⁺ or Ca⁺⁺ channels have repolarized and can be depolarized again.
26
Q

What are Delayed Afterdepolarizations? (DAD’s)?

What is the usual cause of these?

A
  • Depolarizations occurring during Phase 4.
  • Usually caused by ↑ serum Ca⁺⁺ (needs verification)
27
Q

Is an EAD or a DAD depicted by A on the figure below?

A

Early Afterdepolarization (EAD)

28
Q

Is an EAD or a DAD depicted by B on the figure below?

A

Delayed Afterdepolarization (DAD)

29
Q

Regarding disturbances in impulse conduction, differentiate blocks from circus movement arrhythmias,

A

Blocks occur when conduction is delayed or stopped entirely.

“Circus Movement” arrhythmias occur when scar tissue
prevents normal movement of impulse conduction and the signal “circles” around a certain portion of tissue, causing continuous depolarization in this one area. (obviously wordy)

(card needs work)

30
Q

What is the usual cause of reentry tachycardias and “circus movement”?

A

scar tissue formation (from ischemia, injury, etc.)

31
Q

What characterizes 1° heart block?

A
  • PR > .20sec
  • Usually asymptomatic
  • all P-waves conduct
32
Q

What characterizes 2° Type I heart block?

A
  • Slower, slower, slower, drop (Wenkebach)
  • Progressive prolongation of PR interval until QRS is dropped.
33
Q

What characterizes 2° Type II heart block?

A

Consistent PR interval w/ dropped QRS complexes

34
Q

What characterizes 3° heart blocks?

A

Complete AV dissociation (needs pacemaker)

35
Q

How are reentrant tachycardias typically treated?

A

By slowing down circular current to re-sync next action potential.
- Na⁺ and Ca⁺⁺ channel blockers to ↑ or ↓ refractory period.

36
Q

What are the classes of the Vaughn Williams Classification of antiarrhythmic Agents and their respective mechanism of actions?

A
  • Class I - Na⁺ channel blockade
  • Class II - Sympatholytic
  • Class III - ↑ AP duration (usually by slowing K⁺ efflux)
  • Class IV - Block Cardiac Ca⁺⁺ channels
37
Q

What class of antiarrhythmic is causing the action potentials depicted below for:
* Red?
* Blue?
* Green?

A
  • Red = Class 1A
  • Blue = Class 1B
  • Green = Class 1C
38
Q

What is the prototypical Class 1A antiarrythmic?
What are the action potential characteristics of this drug?

A
  • Quinidine
  • ↑ Action Potential Duration
  • ↑ Effective Refractory Period
39
Q

What is the prototypical Class 1B antiarrhythmic?
What are the action potential characteristics of this drug?

A
  • Lidocaine
  • ↓ Action Potential Duration
  • ↓ Effective Refractory Period
40
Q

What is the prototypical Class 1C antiarrhythmic?
What are the action potential characteristics of this drug?

A
  • Flecainide
  • Essentially just blocks Na⁺ channels
  • No changes to APD or ERP.
41
Q

Which class 1A anti-arrhythmic has a PO form?
Why might this drug not be utilized much anymore?

A

Quinidine
* ↑ QT interval (2-8% Torsades rate)

42
Q

Which class 1B anti-arrythmic can’t be given orally and thus must be given parenterally?

What does this drug act exclusively on? Does this make it relatively safe?

A

Lidocaine (3% bioavailability orally)

Acts exclusively on Na⁺ channels w/ low toxicity and high effectiveness making it safe.

43
Q

Which drug is the old ICU “drug of choice” for V-tach?

44
Q

What are the two Class 1C anti-arrhythmics?
What is the mechanism of action of this class of drugs?
What are class 1C’s effects on the action potential graph?
Do these drugs have any other properties?

A
  • Flecainide & Propafenone
  • Slow Na⁺ channel dissociation, suppressing erroneous Na⁺ channels.
  • Minimal effects on APD and ERP
  • Some β-blocking properties
45
Q

What class of drugs are Class 2 Anti-arrhythmics?

Which of this category actually is both a class 2 and a class 3?

A

β-blockers

Satolol

46
Q

What drug is prototypical of Class 3 Anti-arrhythmics?

What is the mechanism of action for this class?

A

Amiodarone

Blockade of K⁺ efflux channels to slow repolarization.

47
Q

Which drug is the new “drug of choice” for V-tach?

A

Amiodarone

48
Q

What makes Amiodarone’s mechanism of action unique among all anti-arrhythmics?

A

Amiodaonre has all 4 anti-arrhythmic class effects.
1. Na⁺ channel blockade
2. Slight α & β non-competitive inhibition
3. ↑ K⁺ channel blockade
4. Ca⁺⁺ channel blockade

49
Q

Which drug can produce iodine stains on sun-exposed tissues (ex. face)?

A

Amiodarone

50
Q

What extracardiac effects does amiodarone have?

What 3 main toxicity symptoms exist for amiodarone?

A

Extracardiac Vasodilation

  • ↓ HR or heart block
  • Heart Failure
  • Fatal pulmonary fibrosis
51
Q

What is the T½ of amiodarone?
How about if a loading dose is given?

A

T½: 13-100 days
T½ w/ LD: 15 - 30 days

52
Q

Why would Dronedarone be a good alternative to Amiodarone?

A
  • Lacks iodine
  • 24 hours T½
  • No Thyroid or Pulm toxicity
  • Excellent for Afib
53
Q

Why would Amiodarone be chosen for administration over Dronedarone?

54
Q

What is Verapamil’s class of Anti-arrhythmic?

What is Verapamil’s mechanism of action?

A

Class IV.

Ca⁺⁺ Channel Blockade and negative dromotropy of nodal tissues ( ↓ AV & SA node conduction).

55
Q

What are Verapamil’s uses?

A
  • SVT (post-adenosine administration)
  • ↓ Ventricular rate in Afib and Aflutter
56
Q

Which 4 drugs mentioned in lecture were stated as anti-arrhythmics that don’t fit into classes 1-4?

A
  • Digoxin
  • Adenosine
  • Mg⁺⁺
  • K⁺
57
Q

What is Mg⁺⁺ usage as an antiarrhythmic?
What is K⁺ usage as an antiarrhythmic?

A

Mg⁺⁺ used for digoxin toxicity
K⁺ used for normalizing serum levels

58
Q

What is adenosine’s mechanism of action?

What is adenosines T½?

A
  • ↑ K⁺ conductance
  • ↓ cAMP = ↓ Ca⁺⁺ influx
  • T½: 10 seconds
59
Q

What is adenosine’s mechanism of action?

What is adenosines T½?

A
  • ↑ K⁺ conductance
  • ↓ cAMP = ↓ Ca⁺⁺ influx
  • T½: 10 seconds
60
Q

What ion, when administered as a drug, counteracts digoxin toxicity?

A

Mg⁺⁺ sulfate

Pharm (Fall 2022) (23 decks)

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