Lecture 4 - Antiarrhythmics Flashcards
1
Q
In what type of patients is arrhythmia a frequent problem?
A
- 25% of patients with digitalis (heart failure)
- 50% of anesthetized patients
- 80% of patients with MI
2
Q
T or F: anti-arrhythmic drugs can produce arrhythmia
A
true
3
Q
What is the normal pacemaker?
A
SA node
4
Q
What are the conduction fibres??
A
AV node, bundle of His, Purkinje fibres
5
Q
What is included in the term “healthy myocardium”?
A
atria and ventricles
6
Q
Super briefly describe how atria and ventricles contract using SA and AV nodes
A
- SA node causes atria to contract
- AV node allows for a pause for ventricles to fill
- Then ventricles contract
7
Q
Normal cardiac rhythm = ?
A
sinus rhythm
8
Q
Define arrhythmia
A
any rhythm that is not a normal sinus rhythm with normal AV conduction
9
Q
What is the main pacemaker and initiator of heart beat?
A
SA node
10
Q
SA node = ____bpm
A
60-100
11
Q
AV node spontaneously discharges at ____ bpm (normally overridden)
A
40-60
12
Q
What is the function of conduction fibres?
A
to excite the ventricular mass as near simultaneously as possible
13
Q
Purkinje fibres spontaneously discharge at ___bpm (overridden)
A
20-40
14
Q
P wave
A
atrial depolarization
15
Q
QRS complex
A
ventricular depolarization
16
Q
T wave
A
ventricular repolarization
17
Q
PR interval
A
conduction time atria to ventricles
18
Q
QRS interval
A
time for all ventricular cells to be activated
19
Q
QT interval
A
duration of ventricular action potential
20
Q
Most anti arrhythmic drugs act on ___ _____
A
ion channels
21
Q
Class 1 Antiarrhythmic drugs block __ channels
A
Na
22
Q
Class 2 Antiarrhythmic drugs block _______
A
B-receptors
**class 2 antiarrhythmics are B-blockers lol
23
Q
Class 3 Antiarrhythmic drugs block __ channels
A
K
24
Q
Class 4 Antiarrhythmic drugs block ___ channels
A
Ca
25
Class __ Antiarrhythmic drugs have other mechanisms
5
26
List some Class 1 Antiarrhythmic drugs
procainamide, lidocaine, flecanide
27
List some Class 2 Antiarrhythmic drugs
propranolol, metoprolol, esmolol (B blocker)
28
List some Class 3 Antiarrhythmic drugs
amiodarone, sotalol
29
List some Class 4 Antiarrhythmic drugs
Verapamil
30
List some Class 5 Antiarrhythmic drugs
magnesium, adenosine, digoxin
31
Class 2 and 4 antiarrhythmic drugs act on _____ cells
pacemaking
32
Class 1, 3, and 5 antiarrhythmic drugs act on _____ cells
non-pacemaking
33
Na is higher _____
extracellular
34
K is higher ______
intracellular
35
Cl is higher ______
extracellular
36
Ca is higher _____
extracellular
37
The only ion higher intracellular is __
K+
38
What causes depolarization?
positive charge in cell (Na+ and Ca2+ entering)
39
What causes repolarization?
negative charge in cell (K+ leaving)
40
What are the pacemaker cells?
SA node
| AV node
41
What are the non-pacemaker cells?
atria
ventricles
purkinje fibres
42
Describe the electrophysiology of non-pacemaker cells:
| Phase 0
Phase 0 - Depolarization:
- voltage gated Na channels open
- rapid depolarization
- Na channels
43
Describe the electrophysiology of non-pacemaker cells:
| Phase 1
Phase 1 - Slight Repolarization:
* Distinctive to non-pacemaker cells
- Cl channels open briefly and chloride enters cell
44
Describe the electrophysiology of non-pacemaker cells:
| Phase 2
Phase 2 - Plateau:
* Distinctive to non-pacemaker cells
- Opening of Ca channels
- Ca enters cell
- Causes further release of Ca from SR
- Ca dependent contraction
45
Describe the electrophysiology of non-pacemaker cells:
| Phase 3
Phase 3 - Repolarization:
- K channels 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
46
Describe the electrophysiology of non-pacemaker cells:
| Phase 4
Phase 4 - Diastolic (resting) potential:
- no time-dependent currents during phase 4
- as a result, resting potential, is substantially more negative (-80mV) than SA/AV nodes
47
Describe the electrophysiology of non-pacemaker cells:
| Absolute/Relative Refractory Period
Phase 3:
- Na channels recover from inactive to resting state
- Repolarization switches sodium channels from inactive to resting
- If the Na channels are in the inactive state the myocyte cannot be depolarized = absolute refractory period
- If only a portion of the Na channels are in the inactive state the myocyte may depolarize but a less rapid depolarization = relative refractory period
48
What does Depolarization of the resting membrane potential in non-pacemaker (fast) cells cause?
- decreases the number of sodium channels available
- decreases the rate of depolarization
- decreases the strength and speed of the impulse
*slow depolarization of the resting membrane potential caused by hyperkalemia, schema, drugs blocking sodium channels will decrease the upstroke of eliminate it all together
49
So, need completely ____ membrane and "resting" sodium channels
repolarized
50
Describe the sodium channel gates in resting conformation
- m gate closed
| - h gate open
51
Describe the sodium channel gates in activated conformation
- m gate open
| - h gate open
52
Describe the sodium channel gates in inactivated conformation
- m gate closed
- h gate closed
*absolute refractory period
53
How do Class 1 Antiarrhythmics alter the appearance of the action potential in non-pacemaking (fast) cells?
Class 1 are the Na channel blockers
- so they would prevent the rising phase of depolarization (phase 0)
- only affects non-pacemaking cells
54
How do Class 3 Antiarrhythmics alter the appearance of the action potential in non-pacemaking (fast) cells?
Class 3 are K channel blockers
| -so they would prevent K+ efflux and delay repolarization
55
Describe the electrophysiology of pacemaker cells:
| Phase 0
- threshold reached - Ca channels open
- rapid depolarization
- then Ca channels close
56
Describe the electrophysiology of pacemaker cells:
| Phase 3
-voltage gated K channels open and membrane repolarizes
57
Describe the electrophysiology of pacemaker cells:
| Phase 4
- spontaneous depolarization
- pacemaker current - I f (funny current) = increased Na+ influx
- increased Ca influx
- decreased K efflux
- intrinsic firing rate: SA > AV > bundle of his > purkinje fibres
* *note: bundle of his and purkinje fibres are "fast" cells but have very slow Phase 4 depolarization
58
How do Class 4 Antiarrhythmics alter the appearance of the action potential in pacemaking (slow) cells?
Class 4 block Ca channels
| -so this would prevent Ca influx and slow the depolarization phase
59
How do Class 2 Antiarrhythmics alter the appearance of the action potential in pacemaking (slow) cells?
Class 2 are Beta blockers
- prevent increased Na+ influx (If)
- prevent increased Ca2+ influx (ICa)
**don't really understand this right now...look into it
60
Non-pacemaker (fast) cells:
| RMP = ?
-80 to -95 mV
61
Non-pacemaker (fast) cells:
| Phase 0 current = ?
sodium
62
Non-pacemaker (fast) cells:
| Phase 0 kinetics = ?
fast
63
Non-pacemaker (fast) cells:
| Conduction velocity = ?
0.5 - 5 m/sec
64
Non-pacemaker (fast) cells:
| Automaticity = ?
yes ??
65
Pacemaker (slow) cells:
| RMP = ?
-40 to -65 mV
66
Pacemaker (slow) cells:
| Phase 0 current = ?
calcium
67
Pacemaker (slow) cells:
| Phase 0 kinetics = ?
slow
68
Pacemaker (slow) cells:
| Conduction velocity = ?
0.01 to 0.1 m/sec
69
Pacemaker (slow) cells:
| Automaticity = ?
yes
