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

Antiarrhythmic Drugs (part 1) Flashcards

(60 cards)

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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
QT interval:
duration of ventricular action potential
26
What does a normal cardiac rhythm = SINUS RHYTHM look like:
note - action potential differences!! SLOW rise & NO plateau spontaneous discharge RAPID DEpolarization with plateau
27
What are action potential differences due to?
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
Most Antiarrhythmic Drugs Act on...
Ion Channels (act directly/indirectly on them)
29
What are the Class 1 antiarrhythmic drugs? What do they act on?
- Procainamide - Lidocaine - Flecanide primarily block Na+ channels
30
What are the Class 2 antiarrhythmic drugs? What do they act on?
- Propranolol - Metoprolol - Esmolol primarily block B-adrenergic receptors (INDIRECTLY influence electrical activity of heart)
31
What are the Class 3 antiarrhythmic drugs? What do they act on?
- Amiodarone - Sotalol primarily block K+ channels
32
What are the Class 4 antiarrhythmic drugs? What do they act on?
- Verapamil primarily block Ca2+ channels
33
What are the Class 5 antiarrhythmic drugs? What do they act on?
- Magnesium - Adenosine - Digoxin other mechanisms
34
What happens when Na+ channels open?
explosive Na+ INFLUX driven by both chemical & electrical forces!!
35
What happens when K+ channels open WHEN MEMBRANE IS DEPOLARIZED?
explosive K+ EFFLUX driven by both chemicals & electrical forces!!
36
Describe Non-pacemaker cells
FAST atria, ventricles, pukinje fibres phases 0-4
37
Describe Pacemaker cells
SLOW SA node; AV node phases 0, 3, & 4
38
What are the phases of non-pacemaker cells?
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
What is hERG?
imp. family of K+ channel in heart ex: 1st gen of anti-histamines
40
Non-pacemaker (fast) cells Phase 4
– 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
Non-pacemaker (fast) cells Phase 0
- 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
Non-pacemaker (fast) cells Phase 1
- slight repolarization chloride channels open briefly and chloride enters cell
43
What is a main difference b/t pacemaker & non-pacemaker cells?
have extended plateau phase (pacemaker cells don't)
44
Non-pacemaker (fast) cells Phase 2
- plateau - opening of voltage gated L-type Ca CHANNELS - Ca enters cell -- causes further release of Ca from sarcoplasmic reticulum - Ca dependent CONTRACTION
45
Non-pacemaker (fast) cells Phase 3
- 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
Why is Na+ channel inactivation important:
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
When inactivated Na+ channels are closed and thus...
unavailable
48
repolarization allows Na+ channels to recover from ______ and return to the “resting” state
inactivation
49
Describe the Absolute & Relative Refractory Period
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
Reduced Na+ channel availability during the Absolute/Relative Refractory Period...
limits how quickly this tissue can be stimulated
51
Availability of _____ Na+ channels is key for allowing rapid phase 0 depolarization
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
Availability of resting Na+ channels is key for allowing rapid phase 0 depolarization CONSEQUENTLY...
decreased Na+ channel availability will: - decreases the rate of depolarization - decreases the strength and speed of the impulse
53
Na+ channel availability is decreased by
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
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?
Class I (block Na+ influx) & Class III (block K+ efflux) drugs
55
What does the Pacemaker (slow) look like?
0 - Ca2+ influx 3 - K+ efflux 4 - K+ efflux
56
What are the 3 main differences that Pacemaker (slow) cells have?
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
Sinoatrial (SA) Node / Atrioventricular (AV) Node
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
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?
Non-pacemaker (fast) - Class 1 - Na+ influx - Class III - K+ efflux Pacemaker (slow) - Class II - block Na+ influx (If) - Class IV - Ca2+ influx
59
Sum up Pacemaker (slow)
SA node & AV node RMP (mV): -40 to -65 Phase 0: Calcium Phase 2: no Automaticity: yes (property of cells that spon. depolarize)
60
Non-pacemaker (fast)
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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