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Pharmacology Test 3 > CHAPTER 14 ARRYTHMIAS > Flashcards

CHAPTER 14 ARRYTHMIAS Flashcards

1
Q

What is a Block?

A

Conduction in the heart where transmission is not in the correct order. Deviations from the SA node, AV node, Bundle Branch, Purkinje Fibers.

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2
Q

Describe the conduction system of the heart?

A

SA node - left and right atrium will contract at same time
AV node - has own pacemaker in case SA node takes a dump
Atrioventricular Bundle/ Bundle of His
Bundle Branches
Purkinje Fibers- has own automaticity can also fire on their own

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3
Q

At resting sodium channels are ________.
What is the concentration and charge of Na+ outside?
What is the concentration and charge of Na+ inside?

A

Closed
Outside concentration and charge: 140 mmol/L and 0 mV
Inside concentration and charge: 10-14 mmol/L and -90 mV

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4
Q

At resting potassium channels are ________.
What is the concentration and charge of K+ outside?
What is the concentration and charge of K+ inside?

A

Open
Outside concentration and charge: 4 mmol/L and 0 mV
Inside concentration and charge: 140 mmol/L and -90 mV

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5
Q

What is the activation gate on the sodium channel?
What is the inactivation gate of the sodium channel?

A

M-gate (activation gate)
H-gate (inactivation gate)

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6
Q

What establishes the charge gradient and rectifying current inside the cell membrane?

A

The potassium channel staying open at rest

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7
Q

Where is our pacemaker cells?

A

SA Node

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8
Q

Site of spontaneous depolarization that occurs during diastole.

A

Pacemaker cells have their own automaticity.

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9
Q

Describe the action potential of a pacemaker cell.

A
  1. Vrm is -60mV, during prepotential phase there is a slow influx of Na+
  2. Threshold is reached at -40mV
  3. During depolarization, rapid influx of Ca2+
  4. During repolarization, outflux of K+
  5. Na/K/ATPase will re-establish gradient of the membrane
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10
Q

Describe the action potential of the atria, ventricular, and purkinje fiber cells.

A
  1. Vrm is -100 mV, once threshold potential is met there is an action potential upstroke (phase 0) dependent on sodium current. Massive influx of Na+ (m-gate open).
  2. Phase 1, H-gate inactivates sodium channel, providing the overshoot. K+ channels open and will provide the phase1 slope.
  3. Phase 2, plateau period d/t K+ being up and Ca2+ channels opening. Ca2+ and K+ balanced.
  4. Phase 3, Ca2+ channels have shut off. K+ is still leaving the cell.
  5. Before phase 4, N/K Pump is re-establishing the gradient.
  6. Phase 4 slow depolarization for the next action potential
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11
Q

What are the three states of sodium channels?

A

Resting - m-gate closed/ h-gate open
Activated - m-gate open/ h-gate open, massive Na+ influx
Inactivated- m-gate open/ h-gate closed

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12
Q

How does the sodium channel recovery to resting state?

A

During Effective Refractory Period:
m-gate close first
h-gate opens second

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13
Q

What is the Effective Recovery Period?

A

Sodium channels are inactivated and not able to fire another AP, until sodium returns to resting state. m-gate closed, h-gate open.

Genetic defects or medications can cause clusters of sodium channels to recovery faster, this can result in arrhythmias.

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14
Q

What are the two main classification of arrhythmias?

A

Disturbances in Impulse Formation
Disturbances in Impuse Conductance

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15
Q

What is Disturbances in Impulse Formation

A

Formation is where the current starts. SA/AV node abnormalities.
Ion Changes
SNS Stimulation

This will increase or decrease the pacemaker rate

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16
Q

What is Disturbances in Impulse Conduction

A

Typically we talk about blocks in the heart. Interruption in transmission.

Reentry is a type of block with one way current (circus movement)

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17
Q

Give examples of disturbance in impulse formation.

A

Vagal Discharge will slow pacemaker rate and cause a reduction in the phase 4 slope.

Acceleration of pacemaker maker rate will increase phase 4 slope (beta agonist, fiber stretch, acidosis)

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18
Q

If some sodium channels reset too early what kind of disturbance in impulse formation can occur?

A

Afterdepolarizations which are abnormal depolarization occurring during phase 2, 3, or 4.

19
Q

When does EAD occur?
What causes this?

A

Depolarization in phase 2 or 3
Caused by sodium or calcium channels, increases in the QT interval

20
Q

When does DAD occur?
What causes this?

A

Depolarization occurs before a normal action potential (phase 4)
Caused by elevated intercellular Calcium, digitalis toxicity

21
Q

What are examples of Disturbances in Impulse Conduction

A

1st, 2nd, 3rd degree block
Reentry Block (Circus Movement)

22
Q

What is Reentry/Circus Movement

A

Block allowing one way “circus” conduction, where the conduction is slow enough where it can re-excite tissue that have been excited once.

23
Q

What are the requirements for a Reentry Block to occur?

A
  1. There must be an obstacle (usually scar tissue)
  2. Block must be unidirectional
  3. Conduction time must be long enough to reenter same areas AFTER refractory period
24
Q

How are Type II and Type III blocks treated?

A

Transcutaneous Pacing/ Pacemaker

25
Q

How are Reentry Blocks treated?

A

Slow down circular current to sync with the next action potential.
Drugs: Block sodium or calcium to lengthen or shorten effective refractory period (ERP)

26
Q

What are the four classes of Anti-arrhythmic Agents?

A

Class I - Sodium channel blockers
Class II - Sympatholytic
Class III - Prolong action potential duration (K+)
Class IV - Block cardiac calcium channel currents.

27
Q

What are the three subclasses of Class I Sodium Channel Blockers?

A

Class IA (Quinidine, Procainimide, Disopyramide)
Prolong APD, Increase ERP, Intermediate Dissociation

Class IB (Lidocaine, Mexiltine)
Shorten APD, Decrease ERP, rapid Dissociation
Quick reset of sodium channels

Class IC (Flecainide, Propafenone)
Minimal effect on APD, no effect ERP, Slow Dissociation

28
Q

Satolol
What’s the Class?
Whats the Activity?
What are the Effects?
Other Activity?

A

Class: II
Activity: Beta Blocker
Effect: Slows Rate
Other Activity: Slows APD

29
Q

Amiodarone
What’s the Class?
Whats the Activity?
What are the Effects?
Other Activity?

A

Class: III (but it can be all of them)
Activity: K+ Channel blocker
Effect: Prolongs APD
Other Activity: CCB, Sodium Channel Blocker, Adrenergic Inhibitor

30
Q

Verapamil
What’s the Class?
Whats the Activity?
What are the Effects?
Other Activity?

A

Class: IV
Activity: blocks both activated and inactivated Ca2+ Channels
Effect: Slows SA node, prolongs AV node.

Hypotensive action

31
Q

What is the half time of Amiodarone?

A

13-100 days!

32
Q

What is an alternative to Amiodarone?

What can it be used for?

A

Dronedarone
Less Toxic
Shorter Half-Life 24 hours
Not as effective as amio

Dronedarone is used more in A-fib.

33
Q

What is the drug of choice for V-tach?

A

Amiodarone because it lengthens the AP well in tachycardia, longer the AP, the longer it takes for the Na+ channels to reset.

It also can block Ca2+ channels, inhibit beta receptors, inhibit normal automaticity

34
Q

What are the side effects and toxicity of amiodarone?

A

Dilation in peripheral vasculature
Toxicity: can produce bradycardia, precipitate HF, Fatal pulmonary fibrosis, iodine staining.

35
Q

What is used to treat SVT?
How does it work?

A

Adenosine to treat SVT (6mg bolus)
Enhance conductance of K+
Inhibition of cAMP induced calcium influx
Half life: 10 seconds

36
Q

What can be given to treat digitalis induced arrhythmias?

A

Magnesium

37
Q

Bradycardia
Initial Treatment
Symptomatic Treatment
Chronic Treatment

A

Bradycardia
Initial Treatment: Underlying cause, d/c drugs
Symptomatic Treatment: 1st Atropine/ 2nd: Epi/Dopamine
Chronic Treatment: Pacemaker

38
Q

Heart Block
Initial Treatment
Symptomatic Treatment
Chronic Treatment

A

Heart Block
Initial Treatment: 1st degree (not treated)
Symptomatic Treatment: Atropine, transcutaneous pace
Chronic Treatment: Pacemaker

39
Q

SVT
Initial Treatment
Symptomatic Treatment
Chronic Treatment

A

SVT
Initial Treatment: Assess Cause
Symptomatic Treatment: Adenosine
Chronic Treatment: CCB, Beta Blockers

40
Q

Sinus Tach
Initial Treatment
Symptomatic Treatment
Chronic Treatment

A

Sinus Tach
Initial Treatment: Assess Cause
Symptomatic Treatment: Adenosine, CCB, Cardiovert
Chronic Treatment: Catheter ablation

41
Q

V-tach (wide complex)
Symptomatic Treatment
Chronic Treatment

A

V-tach (wide complex)
Symptomatic Treatment: Amio
Chronic Treatment: Amio, Satolol

42
Q

A-fib
Symptomatic Treatment
Chronic Treatment

A

A-fib
Symptomatic Treatment: Diltiazem, Verapamil
Chronic Treatment: Beta Blockers, Amiodarone

43
Q

V-fib
Symptomatic Treatment
Chronic Treatment

A

V-fib
Symptomatic Treatment: CPR, Defibrillation
Chronic Treatment: Amio, Lidocaine

Pharmacology Test 3 (6 decks)

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