Antiarrhythmic Drugs & Cardiac Glycosides Flashcards
(36 cards)
0
Q
Procainamide
A
- Block Na+ channel
- Weaker K+ channel effects than Quinidine
- Metabolized into NAPA increases K+ blocking effects
- Used for:
1. Atrial & vent arrhythmias
2. Not usually used long term (due to lupus)
1
Q
Quinidine
A
- Blocks Na+ channels, decreasing excitability & conduction velocity in fast tissue (vent & atrium)
- Block of K+ channels prolonging refractory period which can inhibit re-entry arrhythmias
- Used for:
1. Aflutter
2. Afib
3. Supravent arrhythmias
4. Vtachy - not first line due to effects
2
Q
Lidocaine
A
- Slows conduction in depolarized fast tissue (ischemic)
- Blocks Na+ channel (open & inactivated Na+ channels more than closed)
- Used for:
1. Vtach & arrhythmias s/p MI - Must be IV or IM due to first pass metabolism
- Prophylactic use with MI lowers survival rate
3
Q
Flecainide
A
- Potent Na+ blocker reducing excitability in fast tissue
- Strong effects on his/purkinje fibers
- Used for:
1. Supravent arrhythmias (Afib) - Adverse reactions:
1. Proarrhythmic causing death in prolonged use
4
Q
Propranolol
A
- Blocks beta stimulation of Ca+2 channels
- Negative inotropic & chronotropic effects
- Block Na+ & K+ at high doses
- Used for:
1. Vent arrhythmias due to exercise or emotion
2. After MI to prevent recurrent
3. Supravent arrhythmias (Afib, Aflutter & supravent tachy)
4. CHF (Metoprolol) - No effect on fast tissue
5
Q
Amiodoraone
A
- K+ blocker = prolonged APs duration
- Na+ blocker in inactivated state
- Ca+2 blocker
- Long half life (13-103 days)
- Used for:
1. Supravent and vent tachycardia
2. Small beneficial effect on mortality for Tx of AMI
6
Q
Sotalol
A
- L isomer=non selective B blocker decreasing AV transmission (reduced Ca channels); negative inotropic & chronotropic effects
- D isomer=blocks K+ increasing APs
- Used for:
1. Aflutter & Afib
2. Vtach
7
Q
Dofetilide
A
- Selective blocker of delayed K+ channels (cardiac K channels) so APs prolonged
- Used for:
1. Only physicians that have special training
8
Q
Verapamil & Diltiazem
A
- Ca+2 channel antagonist on cardiac cells (decrease excitability & conduction velocity in SA/AV node)
- direct action on SA nodal cells slowing HR
- Used for:
1. First choice for supravent tachy due to AV nodal reentry
2. Reduce vent rate in Aflutter - 4 min half life
9
Q
Verapamil & Diltiazem side effects
A
- VFib & hypotension if Vtachy is misdiagnosed as supravent tachy
- lead to AV block in high doses
- negative inotropic effect (limit use in diseased hearts)
- constipation, peripheral edema & CNS effects
- bradycardia or AV block with B blockers or Digoxin
10
Q
Adenosine
A
- Adenosine receptor activation leads to opening K+ channels which hyperpolarizes AV nodal tissue
- shorter half life than verapamil (seconds)
- IV terminates supravent tachy
11
Q
Quinidine cardiac side effects
A
- Risk of arrhythmias increases with lengthening QRS & Q-T interval
- Syncope (torsade de pointes where APs travel different direction); can degenerate into VFib.
12
Q
Quinidine extra cardiac side effects
A
GI disturbances
Cinchonism (tinnitus, dizzy, HA)
Fever, angioedena, thrombocytopenia & hepatitis
13
Q
Class 1a
A
Quinidine
Procainamide
(Na+ & K+ blockers)
14
Q
Class 1b
A
Lidocaine
Block Na+ channels in depolarizer tissue
15
Q
Class 1c
A
Flecainide
Potent/selective Na+ channel blockers
16
Q
Class 2
A
Propranolol
Block beta receptor; blocks NE stimulation of Ca+2 channels
17
Q
Class 3
A
Amiodarone
Sotalol
Difetilide
(K+ blockers)
18
Q
Class 4
A
Verapamil
Diltiazem
(Ca+2 blocker)
19
Q
Procainamide cardio effects
A
- Torsades de pointe less common than Quinidine (increases with elevated NAPA)
- Hypotension
20
Q
Procainamide non cardiac side effects
A
- Drug induced lupus (reversible)
2. N/D, rash, hepatitis, fever & agranulocytosis
21
Q
Lidocaine side effects:
A
CNS: paresthesias, drowsy, tinnitus & blurred vision
22
Q
Adverse side effects of beta blockers
A
- SA & AV block = bad
- Sudden withdrawal may worsen angina & arrhythmias
- SOB
23
Q
Amiodoraone side effects
A
- Yellow/brown corneal microdeposits
- Cutaneous sensitivity or blue-gray skin
- GI
- Neuro = neuropathy, fatigue and motor issues
- Hypotension
- Life threatening pulmonary toxicity
- Hepatotoxicity
- Thyroid dysfunction
24
Amiodoraone drug interactions
- increase plasma anti arrhythmia drugs
| - with B or Ca blockers, worsen CHF (sinus arrest or AV block)
25
Sotalol side effects
1. Torsade de pointes
2. SA/AV block
3. Sudden withdrawal worsens angina & arrhythmias
4. SOB
26
Dofetilide side effects
1. Torsade de pointes
| 2. Few extra cardiac effects due to selectivity
27
Digoxin Overview
- From foxglove & lily of the valley
- Used for CHF
- Reduces hospitalization for CHF & does not improve mortality
28
Digoxin Use:
- Direct effects on cardiac muscle (CHF)
| - Indirect effects mediated by autonomic nervous system (arrhythmias)
29
Digoxin Effects:
- Positive inotropic effect by inhibiting Na+/K+ ATPase
| - Low doses = increase PNS & decrease ventricular rate during Aflutter & Afib.
30
Digoxin contraindicated in:
- WPW
| - Worsens Vtachy
31
Digoxin pharmacokinetics:
Do not use with Abx which can lead to sudden increase in Digoxin availability & toxicity ( since Abx kill off normal GI flora which degraded Digoxin)
32
Direct membrane effects of Digoxin
- inhibits Na/K ATPase ( increasing Intracellular Na)
- decreases Na/Ca exchanger (increase Intracellular Ca)
- increase myocyte contractility
- increase cardiac output
33
Digoxin toxicity
- serious and common
- 3x the therapeutic dose
- due to K depletion from diuretics combined with Digoxin ( low K enhances digoxin binding to ATPase)
34
Cardiac Toxicity in Digoxin:
1. Premature ventricular beat (Ca overload)
2. Vtachy & fib
3. AV junctional rhythm (block Na/K ATPase~membrane depolarization)
4. AV block (PNS too great)
35
Other Digoxin effects:
1. GI
2. Neuro/visual at high []
3. Gynecomastia
