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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
What are Early Afterdepolarizations (EAD's)?
* Phase 2 or 3 "premature" depolarization * **Some** Na⁺ or Ca⁺⁺ channels have repolarized and can be depolarized again.
26
What are Delayed Afterdepolarizations? (DAD's)? What is the usual cause of these?
* Depolarizations occurring during Phase 4. * Usually caused by ↑ serum Ca⁺⁺ (needs verification)
27
Is an EAD or a DAD depicted by A on the figure below?
Early Afterdepolarization (EAD)
28
Is an EAD or a DAD depicted by B on the figure below?
Delayed Afterdepolarization (DAD)
29
Regarding disturbances in impulse conduction, differentiate blocks from circus movement arrhythmias,
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
What is the usual cause of reentry tachycardias and "circus movement"?
scar tissue formation (from ischemia, injury, etc.)
31
What characterizes 1° heart block?
* PR > .20sec * Usually asymptomatic * all P-waves conduct
32
What characterizes 2° Type I heart block?
* Slower, slower, slower, drop (Wenkebach) * Progressive prolongation of PR interval until QRS is dropped.
33
What characterizes 2° Type II heart block?
Consistent PR interval w/ dropped QRS complexes
34
What characterizes 3° heart blocks?
Complete AV dissociation (needs pacemaker)
35
How are reentrant tachycardias typically treated?
By slowing down circular current to re-sync next action potential. - Na⁺ and Ca⁺⁺ channel blockers to ↑ or ↓ refractory period.
36
What are the classes of the Vaughn Williams Classification of antiarrhythmic Agents and their respective mechanism of actions?
* Class I - Na⁺ channel blockade * Class II - Sympatholytic * Class III - ↑ AP duration (usually by slowing K⁺ efflux) * Class IV - Block Cardiac Ca⁺⁺ channels
37
What class of antiarrhythmic is causing the action potentials depicted below for: * Red? * Blue? * Green?
* Red = Class 1A * Blue = Class 1B * Green = Class 1C
38
What is the prototypical Class 1A antiarrythmic? What are the action potential characteristics of this drug?
- Quinidine * ↑ Action Potential Duration * ↑ Effective Refractory Period
39
What is the prototypical Class 1B antiarrhythmic? What are the action potential characteristics of this drug?
- Lidocaine - ↓ Action Potential Duration - ↓ Effective Refractory Period
40
What is the prototypical Class 1C antiarrhythmic? What are the action potential characteristics of this drug?
- Flecainide - Essentially just blocks Na⁺ channels - No changes to APD or ERP.
41
Which class 1A anti-arrhythmic has a PO form? Why might this drug not be utilized much anymore?
Quinidine * ↑ QT interval (2-8% Torsades rate)
42
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?
Lidocaine (3% bioavailability orally) Acts exclusively on Na⁺ channels w/ low toxicity and high effectiveness making it safe.
43
Which drug is the old ICU "drug of choice" for V-tach?
Lidocaine
44
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?
* Flecainide & Propafenone * Slow Na⁺ channel dissociation, suppressing erroneous Na⁺ channels. * Minimal effects on APD and ERP * Some β-blocking properties
45
What class of drugs are Class 2 Anti-arrhythmics? Which of this category actually is both a class 2 and a class 3?
β-blockers Satolol
46
What drug is prototypical of Class 3 Anti-arrhythmics? What is the mechanism of action for this class?
Amiodarone Blockade of K⁺ efflux channels to slow repolarization.
47
Which drug is the new "drug of choice" for V-tach?
Amiodarone
48
What makes Amiodarone's mechanism of action unique among all anti-arrhythmics?
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
Which drug can produce iodine stains on sun-exposed tissues (ex. face)?
Amiodarone
50
What extracardiac effects does amiodarone have? What 3 main toxicity symptoms exist for amiodarone?
Extracardiac Vasodilation * ↓ HR or heart block * Heart Failure * Fatal pulmonary fibrosis
51
What is the T½ of amiodarone? How about if a loading dose is given?
T½: 13-100 days T½ w/ LD: 15 - 30 days
52
Why would Dronedarone be a good alternative to Amiodarone?
* Lacks iodine * 24 hours T½ * No Thyroid or Pulm toxicity * Excellent for Afib
53
Why would Amiodarone be chosen for administration over Dronedarone?
V-Tach
54
What is Verapamil's class of Anti-arrhythmic? What is Verapamil's mechanism of action?
Class IV. Ca⁺⁺ Channel Blockade and negative dromotropy of nodal tissues ( ↓ AV & SA node conduction).
55
What are Verapamil's uses?
* SVT (post-adenosine administration) * ↓ Ventricular rate in Afib and Aflutter
56
Which 4 drugs mentioned in lecture were stated as anti-arrhythmics that don't fit into classes 1-4?
* Digoxin * Adenosine * Mg⁺⁺ * K⁺
57
What is Mg⁺⁺ usage as an antiarrhythmic? What is K⁺ usage as an antiarrhythmic?
Mg⁺⁺ used for digoxin toxicity K⁺ used for normalizing serum levels
58
What is adenosine's mechanism of action? What is adenosines T½?
* ↑ K⁺ conductance * ↓ cAMP = ↓ Ca⁺⁺ influx * T½: 10 seconds
59
What is adenosine's mechanism of action? What is adenosines T½?
* ↑ K⁺ conductance * ↓ cAMP = ↓ Ca⁺⁺ influx * T½: 10 seconds
60
What ion, when administered as a drug, counteracts digoxin toxicity?
Mg⁺⁺ sulfate

Pharm (Fall 2022) (23 decks)

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