Anti-Arrhythmic (General) Flashcards

1
Q

Arrhythmia

A

Electrical impulses that coordinate the heart no longer function properly
–> Fast, Slow, Irregular patterns

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2
Q

Heart Rate

A

Number of times the heart beats per minute
- BPM

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3
Q

Heart Rhythm

A

Pattern of heart beat
- Fast, Slow, Irregular

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4
Q

Rate Control

A

Drugs that reduce rapid ventricular rate
- Negatively chronotropic drugs
- electrophysical interventions

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5
Q

Rhythm Control

A

Restore normal sinus rhythm by:
- Antiarrhythmic Medication
- Cardioversion
- Surgery

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6
Q

Electrical Activity of Pacemaker Cell
- Pacemaker Potential (Initial)

A

Initial spontaneous (Slow) depolarization
- Funny Channels open
–> Na+ Moves in

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7
Q

Electrical Activity of Pacemaker Cell
- Pacemaker Potential (Latter)

A

Latter spontaneous depolarization
- T-Type Ca2+ Channels open
–> Ca2+ Moves in

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8
Q

Electrical Activity of Pacemaker Cell
- Rapid Depolarization

A

L-Type Fast Ca2+ Channels Open
- Ca2+ Moves in

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9
Q

Electrical Activity of Pacemaker Cell
- Rapid Repolarization

A

K+ Channels open
- K+ moves out of cell

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10
Q

Sympathetic Activity effect on Heart

A

NE/EP act on Beta1 receptors on SA node
–> Increased open state of funny calcium channels
–> Increased rate of spontaneous depolarization
–> Increased Heart Rate

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11
Q

Parasympathetic Activity effect on Heart

A

Vagus Nerve acts on Muscarinic Cholinergic Receptors on SA node
- Increased open state of K+ Channels
- Increased closed state of Ca2+ Channels
–> Decrease rate of spontaneous depolarization and Hyperpolarizes cell
–> Decrease Heart Rate

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12
Q

Electrical Activity of Contractile Cell
- 0 Stage

A

Rapid Depolarization
- Na+ Channels Open
–> Na+ moves in

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13
Q

Electrical Activity of Contractile Cell
- 1 Stage

A

Small Repolarization
- Na+ Channels Inactivated
–> Na+ decreases in cell

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14
Q

Electrical Activity of Contractile Cell
- 2 Stage

A

Plateau
- K+ Channels Close
–> Small K+ out of cell
- Ca2+ L-Type Channels Open
–> Ca2+ into cell

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15
Q

Electrical Activity of Contractile Cell
- 3 Stage

A

Repolarization
- Delayed K+ Channels Open
–> K+ out of cell
- Ca2+ L-Type Channels Close
–> Less Ca2+ into cell

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16
Q

Electrical Activity of Contractile Cell
- 4 Stage

A

Resting Potential
- Both types of K+ open
–> K+ out of cell
Na+ and Ca2+ stay close

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17
Q

Refractory Period

A

Time when cell is incapable of repeating an action

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18
Q

Define ERP

A

Effective Refractory Period:
- Longest interval when a cell can not respond to stimuli

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19
Q

What is worse Atricular or Ventricular Fibrillation

A

Ventricular Fibrillation is worse as blood is not being pumped across the body

  • Articular Fibrillation just increases chances of a stroke
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20
Q

P Wave

A

Atrial Depolarization

21
Q

QRS Complex

A

Ventricular Depolarization
(Atrial Repolarization is mixed in)

22
Q

T Wave

A

Ventricular Repolarization

23
Q

PQ Segment

A

AV Nodal Delay
(Atrial Depolarization)
- Time for ventricle to fill

24
Q

QT Segment

A

Ventricular Systole

25
Q

TQ Interval

A

Ventricular Diastole

26
Q

RR Interval

A

Heart Rate

27
Q

Atrial Fibrilation

A

Blood in atrium is pumping irregularly to the ventricles

28
Q

Ventricular Fibrillation

A

Cardiac Arrest
- Signal is occurring but ventricle is not contracting and pushing blood to body

29
Q

Heart Block

A

Signal from atrial fails to transfer to ventricle

30
Q

Long QT Syndrome

A

Disorders that delay repolarization of ventricle
- Causes prolonged ventricular AP
–> Long pauses on ECG

31
Q

Causes of Arrhythmias

A
  1. Impulse Formations
  2. Impulse Conduction/Propagation
32
Q

Arrhythmia Causes
(Impulse Formations)

A

Altered Automaticity
- Increased (Sympathetic)
- Decreased (Parasympathetic)
- Escape Rhythm
–> (AV node is firing quicker than SA node)
- Enhanced latent pacemakers
–> (SA node is firing quicker than AV node)

Abnormal Automaticity

Triggered Activity
- Early afterdepolarization
–> Prolonged AP, enough to trigger another depolarization
- Delayed afterdepolarization
–> Excess intracellular Ca2+

33
Q

Arrhythmia Causes
(Altered Impulse Conduction)

A

Conduction Block
- Impulse is blocked
Unidirectional Block (Reentry)
- Electrical signal repeatedly circles around
–> Occurs in cells with heterogenous refractory periods

34
Q

Altered Impulse Conduction
(Re-entry)

A

One side is fast pathway
- Fast conduction, long refractory period
One side is slow pathway
- Slow conduction, short refractory period

Signal goes down the slow path and up the fast path.
- By the time the fast signal reaches the start the slow path is ready for another AP
- Signal goes through cycle again
–> Constant recycle leading to tachycardia

35
Q

Class I Anti-Arryhthmics

A

Sodium Channel Blockers

MOA:
- Bind to alpha subunit of Na+ Channels and blocks Na+ Channel
–> Blocks phase 0 depolarization
–> Slows conduction velocity

Works better at High HR - Terminates Afib

36
Q

Class IA

A

Moderate Effect Phase 0 (Prolong AP)
- Associate/Dissociate Midway

  • Treat large variety of Arrhythmia
37
Q

Class IB

A

Weak Effect Phase 0
- Associate/Dissociate Rapidly
- Treat Ventricular Arrhythmia

38
Q

Class IC

A

Strong Effect Phase 0
- Associate/Dissociate Slowly
- Treat Ventricular Arrhythmia

39
Q

Class 1(Three States of Sodium Channels)

A

Open: Ions flow
Close: Ions do not flow
- Channel can be depolarized

Inactivated: Ions do not flow
- Channel is repolarizing and can not be activated

To ensure that Class I drugs do not influence normal heart activity
–> Only target open/inactivated states
–> Only prolongs repolarization, does not cause random depolarization

40
Q

Class II Anti-Arryhthmics

A

Beta-Adrenoceptors Antagonists
- Decrease Heart Rate and Contractility
- Indirectly impacts calcium channels

41
Q

Class II - Anti-Arryhthmics
(Pacemaker Cells)

A

Targets Na+ and Ca2+ currents
- Slows pacemaker potential
- Decrease repolarization
- Slows conduction of AV node

42
Q

Class II - Anti-Arryhthmics
(Contractile Cells)

A

Lowers Calcium:
- Regulates intracellular Ca2+
- Decrease contraction force, rate
- Inhibits afterdepolarization

–> Decrease Heart Rate

43
Q

Class III - Anti-Arryhthmics

A

Potassium Channel Blockers

  • Delays repolarization, increases refractory period

Works better at Low HR - Prevents Afib

44
Q

Class IV - Anti-Arrhythmic

A

Calcium Channel Blockers
- Blocks L-Type Calcium Channels

  • Decreases Contractility
  • Decreases Heart Rate
  • Decreases Conduction Velocity
45
Q

L-Type Calcium Channels

A

Long Type
- Pacemaker Cells, Myocytes, Vasculature

46
Q

T-Type Calcium Channels

A

Transient (Short) Type
- Pacemaker Cells

47
Q

Non-Dihydropines

A

Calcium Channel Blockers
- Focuses on Contractile Cells (Heart)
–> Binds to high frequency L-Type Channels that undergo constant depolarization
(Pacemaker, Myocyte)

MOA:
- Decreases Cardiac Contractility
- Decreases Heart Rate

48
Q

Dihydropine

A

Calcium Channel Blockers
- Focuses on Arterial Blood Vessels (Vasculature)
- Favours the inactivated state

MOA:
- Vasodilation
- Reduce Peripheral Vascular Resistance

49
Q

Contraindications of Class IV

A

Do not combine calcium channel blockers with beta blockers