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Cardiovascular 2 > Drugs for Arrhythmias - Konorev > Flashcards

Drugs for Arrhythmias - Konorev Flashcards

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1
Q

Sodium channel gates in a voltage-gated Na channel

A

M gates = open during activation (depolarization)

H gates = close during inactivation (repolarization)

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2
Q

The resting membrane potential is largely regulated by ____ channels

A

Potassium

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3
Q

In the resting (polarized) state, ____ potassium channels are open.

Is there a current through them?

A

Inwardly-rectifying

NO current - electric gradient in equilibrium with concentration gradient

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4
Q

During phase 3 of the action potential (repolarization), ____ potassium channels open up.

Function?

A

Voltage-gated

Limit the frequency and duration of action potentials and refractory period

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5
Q

Which cardiac tissues use a FAST action potential?

A

Myocytes and purkinje fibers

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6
Q

Which cardiac tissues use a SLOW action potential?

A

SA and AV nodes

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7
Q

Flow of which ion (channel) is responsible for phase 2 (plateau) of the fast action potential?

A

Slow voltage-dependent calcium (inward flow)

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8
Q

Flow of which ion is responsible for phase 0 (rise) of the fast action potential?

A

Sodium

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9
Q

Phase 0 channels

A

Voltage-gated fast Na+

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10
Q

Phase 1 ion flow (brief repol.)

A

Voltage-gated K+ OPEN

Fast Na+ CLOSE

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11
Q

Phase 3 ion flow (start of rapid repol.)

A

Ca+ channels close

K+ begins to exit more rapidly

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12
Q

Restoration of resting membrane potential (refractory period)

A

Na/K ATPase and Na/Ca exchanger

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13
Q

Phase 4 channels of pacemaker potential

A

Funny Na+ current (open during hyperpolarization)

Slow Ca+ T-type channels (just before depolarization)

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14
Q

Phase 0 channels of pacemaker potential

A

L-type (long-acting) Ca+ channels

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15
Q

Phase 3 of pacemaker potential

A

K+ efflux, closing of Ca+ channels

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16
Q

3 factors that influence the rate of the pacemaker

A
  • Rate of spontaneous depolarization in phase 4
  • Threshold potential (more negative = easier to depol.)
  • Resting potential (less negative = easier to depol.)
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17
Q

Function of sympathetics on pacemaker rate (pathway of events) - KNOW THIS

A

Beta-1 –> increased AC –> increased cAMP –> increased funny channel flow rate and decreased calcium channel threshold –> increased pacemaker speed

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18
Q

Function of parasympathetics on pacemaker rate (pathway of events) - KNOW THIS

A

M2 –> decreased AC and increased K+ opening –> slower funny currents, higher threshold (via less cAMP/PKA for Ca++ channels), and lower resting potential

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19
Q

What is an early afterdepolarization? Cause?

A

Another rapid depolarization during phase 2 or 3 of the previous action potential – caused by impaired K+ channels and prolonged repolarization period

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20
Q

Torsades de pointes - will see ______

A

Long QT syndrome (prolonged repolarization)

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21
Q

Do not give a Torsades de Pointes (long QT) inducing drug IF ______

Which ones are long-QT inducing?

A

QT is > 450 ms

  • Class 1A or Class C antiarrhythmics
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22
Q

What is a delayed afterdepolarization? Cause?

A

Another partial depolarization during phase 4 (hyperpol.) DUE TO INCREASED CYTOSOLIC Ca++

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23
Q

3 causes of increased cytosolic Ca++

A

Digoxin toxicity, catecholamine excess, myocardial ischemia/reperfusion

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24
Q

A patient is on Digoxin, but starts experiencing heart beat issues. Explain.

Study These Flashcards
A

Digoxin –> spontaneous Ca++ release from SR after an action potential –> 3Na/Ca exchanger –> net depolarization of membrane –> premature ventricular beats (bigeminy)

25
Class 1 antiarrhythmic drugs - function
Sodium channel blockers
26
Class 1A drugs - names
- Quinidine - Procainamide - Disopyramide
27
Class 1B drugs - names
- Lidocaine | - Mexiletine
28
Class 1C drugs - names
- Flecainide | - Propafenone
29
Class 2 antiarrhythmic drugs - function Names?
Beta blockers - Esmolol - Propranolol
30
Class 3 antiarrhythmic drugs - function Names?
K+ channels blockers - Amiodarone - Dronedarone - Sotalol - Dofetilide
31
Class 4 antiarrhythmic drugs - function Names?
Cardioactive CCBs - Verapamil - Diltiazem
32
Miscellaneous antiarrhythmic agents
- Adenosine | - Magnesium
33
State-dependent blocks
Drugs block ion channel during certain stage in the cycle (active, inactive, resting)
34
Functions of class 1A antiarrhythmics
- Slow impulse conduction and reduce rate of pacemaker cells - Binds ACTIVE sodium channels - Blocks potassium channels - Prolong action potential, QRS duration, and QT interval
35
Procainamide - Uses? (6) - Function? - Adverse effects?
- WPW, PAC, PVC, A fib, V tach, A flutter - Depress SA and AV nodes (sodium channel blocker) - QT prolong (TdP), lupus-like syndrome, hypersensitivity reactions
36
Quinidine - Functions? (3) - Uses? - Adverse effects?
- Slows velocity of conduction system, decreased automaticity of ectopic foci, and prolongs refractory period in heart - MAT, PAC, PVC, A. fib, V. tach. - QT prolongation (TdP), many neural symptoms, thrombocytopenic purpura
37
Disopyramide - Uses? (3) - Adverse effects?
- A fib, V tach, PAC | - QT prolongation (TdP), excess sympathetics effects
38
Functions of class 1b antiarrhythmics Benefit of these?
- Binds INACTIVE sodium channels, mostly in depolarized (damaged) tissue - Shorten action potential - Do NOT block K+ channels --> no prolonging QT or AP
39
Lidocaine - Uses? (4) - Functions? - Adverse effects?
- WPW, V tach, PVC, V fib - Silences ectopic foci, increases conduction in His-Purkinje system - Hypotension via inhibited contractility, neurologic deficits
40
Mexiletine - Uses? (2) - Functions? - Adverse effects?
- Life-threatening ventricular arrhythmias (VT), PVC - Silences ectopic foci and slows AV node, prolongs refractory period for junctional and ventricular pathways - Hepatotoxicity, seizures
41
Functions of class 1c antiarrhythmics
Binds ACTIVE sodium channels and some potassium channels
42
ECG effect of class 1c drugs
- LONG QRS
43
Flecainide | - Clinical use?
- Chronic therapy for long-term V. tach, supraventricular arrhythmias
44
Propafenone - adverse effects
- Metallic taste - Constipation - Exacerbation of ventricular arrhythmias or HF
45
Propafenone - MoA (2)
- Increase refractory period and decrease conduction velocity through heart - Weak BETA-BLOCKING ability
46
Functions of beta blockers (class 2 drugs) (2)
- Slow action potential (slow down SA and AV nodes) | - Prevent delayed afterdepolarizations (decrease Ca++ overload)
47
Uses of Propranolol and Esmolol with arrhythmias
- Stress-associated sinus tach. - AV nodal re-entrant tachycardia - A fib, A flutter - WPW syndrome
48
Function of class 3 drugs
- Block potassium channels -- prolong AP and QT
49
Amiodarone - Use? - Adverse effects?
- Ventricular arrhythmias | - AV block, bradycardia, pulmonary fibrosis, hepatitis, blue-gray skin discoloration, optic neuritis, thyroid problems
50
Dronedarone - Functions? - Use? - Adverse effects? - CONTRAINDICATION?
- Blocks K+ channels, Na+ current, L-type Ca++ current - A. fib/flutter - Worsening heart failure, GI stuff - INCREASED MORTALITY w/ decompensated HF
51
Sotalol - Functions? - Uses? - Adverse effects?
- Beta-blocker AND AP prolonger - Vent. arrhythmias, maintianing sinus rhythm w/ A. fib. - Cardiac depression, TdP INDUCTION
52
Dofetilide - Function? - CAUTION? - Use? - Adverse effect?
- Blocks rapid part of rectifier K+ current (lower HRs) - NARROW THERAPEUTIC WINDOW - Converts AF to sinus rhythm - QT prolongation, risk of ventricular arrhytmias
53
Function of class 4 drugs
- Blocks all L-type calcium channels - Decreased slope of phase 0 depolarization - Prolong SA and AV node APs and refractory periods
54
Uses of Cardiogenic CCBs
- Prevent paroxysmal SVT | - Control rate in AF and A. flutter
55
Adverse effects of cardiogenic CCBs
- AV block, weaken contractility, hypotension, CONSTIPATION (VERAPAMIL)
56
Function of Adenosine
- Activate K+ current, inhibit Ca++ and funny currents --> hyperpolarization of SA and AV nodes
57
Use of Adenosine Adverse effects?
- Convert paroxysmal SVT to sinus rhythm | - SoB, bronchoconstriction, chest burning
58
Uses of magnesium
- Digitalis arrhythmia | - TdP

Cardiovascular 2 (20 decks)

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