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Pharmacology (Fall) > Antiarrhythmic Drugs (part 1) > Flashcards

Antiarrhythmic Drugs (part 1) Flashcards

1
Q

Arrhythmias frequent problem which occurs in:

A

25% of patients with heart failure

50% of anesthetized patients

80% of patients with myocardial infarction

anti-arrhythmic drugs also produce arrhythmia

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2
Q

What are the 3 requirements for normal cardiac excitation?

A
  1. PACEMAKER (impulse generator; normally the sinoatrial (SA) node)
  2. CONDUCTION FIBRES (atrioventricular (AV) node; bundle of His; Purkinje Fibers)
  3. healthy MYOCARDIUM (atria, ventricles)
    ie capable of robust excitation-contraction coupling
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3
Q

Describe the pathway of a normal cardiac excitation?

A
  1. SA node
  2. To both Atrium’s (contraction)
  3. AV node
  4. Purkinje Fibers (for rapid excitation - so that it is a timely manner)
  5. Ventricle (contracts) - allows blood to be expelled into rest of body
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4
Q

What are the 2 reasons why AV node is imp.?

A
  1. Normally only electrical activity b/t atrium & ventricle
  2. Opposes a delay in conduction - allows atrium to contract & ventricles to fill
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5
Q

Normal cardiac rhythm =

A

SINUS RHYTHM

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6
Q

Arrhythmia =

A

any rhythm that is not a normal sinus rhythm with normal atrioventricular (AV) conduction

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7
Q

What 3 things are apart of the Cardiac Conduction System?

A
  1. SA node
  2. AV node
  3. Conduction fibres
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8
Q

What is the MAIN PACEMAKER & initiator of heartbeat?

A

SA node

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9
Q

What spontaneously discharges 60 to 100 beats per minute (bpm)?

A

SA node

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10
Q

What rate can be changed by nerves innervating the heart?

A

both the SA node & AV node

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11
Q

What is the only normal ELECTRICAL CONNECTION BETWEEN ATRIA AND VENTRICLES?

A

AV node

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12
Q

What DELAYS CONDUCTION of action potential by 0.1 sec. Important to allow atria to contract and ventricles to fill before

A

AV node

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13
Q

What spontaneously discharges at 40 to 60 bpm (normally overridden)?

A

AV node

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14
Q

What function is to excite the ventricular mass as near simultaneously as possible?

A

Conduction fibres

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15
Q

What spontaneously discharge at 20 to 40 beats bpm (overridden)?

A

Purkinje fibres (Conduction fibres)

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16
Q

What has specialization due to unique ELECTRICAL PROPERTIES of myocytes in each area?

A

Conduction fibres

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17
Q

What is the Internal & External Electrodes of the Cardiac Action Potentials?

A

Internal Electrodes

  1. SA node pacemaker impulse
  2. Conduction to atria
  3. AV node
  4. Bundle of His - Purkinje fibres
  5. Contraction

External Electrodes (ECG)

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18
Q

What falls under the waves?

A
  • P wave
  • QRS complex
  • T wave
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19
Q

What falls under the intervals?

A
  • PR interval
  • QRS interval
  • QT interval
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20
Q

P wave:

A

atrial DEpolarization

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21
Q

QRS complex:

A

ventricular DEpolarization

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22
Q

T wave:

A

ventricular REpolarization

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23
Q

PR interval:

A

conduction time atria to ventricles

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24
Q

QRS interval:

A

time for all ventricular cells to be activated

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25
Q

QT interval:

A

duration of ventricular action potential

26
Q

What does a normal cardiac rhythm = SINUS RHYTHM look like:

A

note - action potential differences!!

SLOW rise & NO plateau

spontaneous discharge

RAPID DEpolarization with plateau

27
Q

What are action potential differences due to?

A

action potential differences due to different ion channels expressed in myocytes
PACEMAKING vs NON-PACEMAKING cells
(the drugs target either pacemaking or non-pacemaking cells)

28
Q

Most Antiarrhythmic Drugs Act on…

A

Ion Channels (act directly/indirectly on them)

29
Q

What are the Class 1 antiarrhythmic drugs? What do they act on?

A
  • Procainamide
  • Lidocaine
  • Flecanide

primarily block Na+ channels

30
Q

What are the Class 2 antiarrhythmic drugs? What do they act on?

A
  • Propranolol
  • Metoprolol
  • Esmolol

primarily block B-adrenergic receptors (INDIRECTLY influence electrical activity of heart)

31
Q

What are the Class 3 antiarrhythmic drugs? What do they act on?

A
  • Amiodarone
  • Sotalol

primarily block K+ channels

32
Q

What are the Class 4 antiarrhythmic drugs? What do they act on?

A
  • Verapamil

primarily block Ca2+ channels

33
Q

What are the Class 5 antiarrhythmic drugs? What do they act on?

A
  • Magnesium
  • Adenosine
  • Digoxin

other mechanisms

34
Q

What happens when Na+ channels open?

A

explosive Na+ INFLUX driven by both chemical & electrical forces!!

35
Q

What happens when K+ channels open WHEN MEMBRANE IS DEPOLARIZED?

A

explosive K+ EFFLUX driven by both chemicals & electrical forces!!

36
Q

Describe Non-pacemaker cells

A

FAST

atria, ventricles, pukinje fibres

phases 0-4

37
Q

Describe Pacemaker cells

A

SLOW

SA node; AV node

phases 0, 3, & 4

38
Q

What are the phases of non-pacemaker cells?

A

each event is mediated by diff. ion channels

Phase 0 - Na+ INward

Phase 2 - Ca2+ INward

Phase 3 - K+ OUTward

Phase 4 - Pacemaker current

39
Q

What is hERG?

A

imp. family of K+ channel in heart
ex: 1st gen of anti-histamines

40
Q

Non-pacemaker (fast) cells

Phase 4

A

– diastolic (resting) potential
- NO TIME-DEPENDENT CURRENTS DURING PHASE 4
- as a result, resting potential is substantially more negative (-80 mV) than SA/AV nodes

41
Q

Non-pacemaker (fast) cells

Phase 0

A
  • depolarization
  • lots of voltage gated Na CHANNELS,
    – low threshold potential - easily opened
  • threshold reached - “active” voltage gated Na channels open
    – rapid depolarization
  • Na channels quickly become “INACTIVE” - ends depolarization
42
Q

Non-pacemaker (fast) cells

Phase 1

A
  • slight repolarization
    chloride channels open briefly and chloride enters cell
43
Q

What is a main difference b/t pacemaker & non-pacemaker cells?

A

have extended plateau phase (pacemaker cells don’t)

44
Q

Non-pacemaker (fast) cells

Phase 2

A
  • plateau
    • opening of voltage gated L-type Ca CHANNELS
    • Ca enters cell
      – causes further release of Ca from sarcoplasmic reticulum
    • Ca dependent CONTRACTION
45
Q

Non-pacemaker (fast) cells

Phase 3

A
  • repolarization
    • K CHANNELS activate (open)
    • movement of K out of the cell repolarizes the membrane
      – returns to resting membrane potential
    • Ca is removed from the cytoplasm and tissue relaxes
    • REPOLARIZATION ALLOWS Na+ CHANNELS TO RECOVER FROM INACTIVATION
46
Q

Why is Na+ channel inactivation important:

A

Physiological: limits Na+ channel availability, which is establishes how quickly tissue can be stimulated

Pharmacology: Class I and III primarily act by reducing Na+ channel availability by increasing their inactivation

47
Q

When inactivated Na+ channels are closed and thus…

A

unavailable

48
Q

repolarization allows Na+ channels to recover from ______ and return to the “resting” state

A

inactivation

49
Q

Describe the Absolute & Relative Refractory Period

A

during phase 3 – Na+ channels recover from “INACTIVE” to “RESTING” state

if the MAJORITY of Na+ channels remain in the “INACTIVE” state
- myocyte can not be depolarize – this is the ABSOLUTE REFRACTORY PERIOD (ARP)

if only a PORTION of the Na+ channels are in the “INACTIVE” state
- myocyte may depolarize, but will do so less rapidly – this is the RELATIVE REFRACTORY PERIOD (RRP)

50
Q

Reduced Na+ channel availability during the Absolute/Relative Refractory Period…

A

limits how quickly this tissue can be stimulated

51
Q

Availability of _____ Na+ channels is key for allowing rapid phase 0 depolarization

A

resting

a rapid phase 0 depolarization results in a strong and rapid transmission of this impulse to surrounding fibers (propagation) = strong/effective contraction of atria and ventricles

52
Q

Availability of resting Na+ channels is key for allowing rapid phase 0 depolarization

CONSEQUENTLY…

A

decreased Na+ channel availability will:
- decreases the rate of depolarization
- decreases the strength and speed of the impulse

53
Q

Na+ channel availability is decreased by

A

pathological conditions: e.g. hypokalemia, ischemia will cause slow depolarization of the resting membrane potential

drug treatment: e.g. Class 1 and III antiarrhythmic drugs

favours ectopic foci/re-entry mechanisms

54
Q

How would altering the Na, Ca and/or K channels in the “fast” cells (atria, purkinje fibers, ventricles) alter the appearance of the action potential?

A

Class I (block Na+ influx) & Class III (block K+ efflux) drugs

55
Q

What does the Pacemaker (slow) look like?

A

0 - Ca2+ influx

3 - K+ efflux

4 - K+ efflux

56
Q

What are the 3 main differences that Pacemaker (slow) cells have?

A
  1. Pace heart (spon. depol) - automaticity
  2. No phase 1 - therefore no role of Cl- in these cells
  3. Don’t have plateau phase
57
Q

Sinoatrial (SA) Node / Atrioventricular (AV) Node

A

Phase 4
SPONTANEOUS DEPOLARZATION (and thus capable of pacemaker activity/automaticity)
pacemaker current - = increased Na+ influx
increased Ca influx
decreased K efflux
intrinsic firing rate: SA > AV > Bundle of His > Purkinje fibers
note Bundle of His and purkinje fibres are “fast” cells, but with very slow Phase 4 depolarization

Phase 0
threshold reached - voltage gated L-type Ca CHANNELS open
rapid depolarization
then L-type calcium channels close

Phase 1 or Phase 2 is absent in SA/AV node

Phase 3
voltage gated K CHANNELS open and membrane repolarizes

58
Q

How would altering the Na?, Ca and/or K channels in the “slow” cells (SA node, AV node) alter the appearance of the action potential?

A

Non-pacemaker (fast)
- Class 1 - Na+ influx
- Class III - K+ efflux

Pacemaker (slow)
- Class II - block Na+ influx (If)
- Class IV - Ca2+ influx

59
Q

Sum up Pacemaker (slow)

A

SA node & AV node

RMP (mV): -40 to -65
Phase 0: Calcium
Phase 2: no
Automaticity: yes (property of cells that spon. depolarize)

60
Q

Non-pacemaker (fast)

A

Atrial & Ventricular muscle

RMP (mV): -80 to -95
Phase 0: Sodium (inactivation/refractory period)
Phase 2: yes
Automaticity: no

Pharmacology (Fall) (28 decks)

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