Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

RC Test 1 > B4.017 Prework 3 Treatment of Cardiac Arrhythmias > Flashcards

B4.017 Prework 3 Treatment of Cardiac Arrhythmias Flashcards

(65 cards)

Start Studying
1
Q

2 main classes of drugs used to treat arrhythmias

A

rate control agents

rhythm control agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

rate control agent classes

A

b-blockers (metoprolol, atenolol)
Ca2+ channel blockers (verapamil, diltiazem)
digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

rhythm control agents

A

Na+ channel blockers (Procainamide, quinidine, disopyramide, flecainide, propafenone)
K+ channel blockers (amiodarone, ibutilide, sotalol, dofetilide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class I overview

A

Na+ channel blockers
decrease HR by:
-elevating threshold for excitation
-decreasing slope of phase 4 depol in SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Class II overview

A

B blockers

-decrease HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Class III overview

A

K+ channel blockers

-prolong AP duration and refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Class IV overview

A

Ca2+ channel blockers

-decrease conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Class IA overview

A

moderate Na+ channel block
dissociate with intermediate kinetics
prolong AP duration
also inhibit K+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Class IB overview

A

mild Na+ channel block
fast dissociation
shorten AP duration
shortened repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Class IC overview

A

strong Na+ channel block
slow dissociation
minimal effects on AP duration
no change in repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

members of Class IA

A

procainamide
quinidine
dispyramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

members of Class IB

A

lidocaine

mexiletine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

members of class IC

A

flecainide
propafenone
moricizine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

procainamide cardiac effects

A

increases effective refractory period of the atria and ventricles
can directly depress SA and AV nodes
prolongs AP duration by nonspecific blocking K+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

procainamide extracardiac effects

A

has ganglion blocking activity

reduced peripheral vascular resistance can lead to hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

procainamide toxicity

A

cardiotoxic: excessive AP prolongation, QT prolongation, induction of torsades de pointes, arrhythmia and syncope
long term: reversible lupus like syndrome (rash, arthralgia, arthritis, pericarditis)
other: nausea/diarrhea, rash, fever, hepatitis, agranulocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

procainamide therapeutic use

A

effective against most atrial and ventricular arrhythmias
short half life (3-4 hrs): oral dosing every 6 hours
less useful for long term (shoft half life and adverse effects)
2nd or 3rd choice for sustained ventricular arrhythmias associated w MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

quinidine cardiac effects

A

slows upstroke of action potential
slows conduction
QT prolongation due to K+ channel blocking
modest antimuscarinic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

quinidine extracardiac effects

A

blocks a-adrenergic receptors to cause vasodilation

-hypotension and reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

quinidine toxicity

A 
increase plasma digoxin
precipitate digoxin toxicity
thrombocytopenia
syncope (due to torsades de pointes)
adverse GI effects (30-50%), cinchonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

quinidine therapeutic use

A

rarely used

better tolerated drugs available

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

disopyramide cardiac effects

A

similar to quinidine and procainamide but more antimuscarinic effects (tend to accelerate HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

disopyramide toxicity

A

adverse effects caused by its pronounced atropine like activity

  • urinary retention
  • dry mouth, blurred vision, constipation
  • worsening of preexisting glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

disopyramide therapeutic use

A

not used often bc of antimuscarinic effect
not first line bc negative inotropic action may induce CHF
ventricular arrhythmias only**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
similarities between class IA antiarrhythmics
all block Na+, K+ channels, and can induce torsade de pointes
26
lidocaine administration
must be given IV | high first pass hepatic metabolism (only 3% in plasma)
27
lidocaine therapeutic use
ventricular arrhythmias associated with MI or digoxin toxicity relatively ineffective in normally polarized tissues as in atrial flutter or fibrillation cardiac events
28
lidocaine toxicity
low incidence of toxicity and high degree of effectiveness
29
mexiletine administration
lidocaine analog, resistant to first pass hepatic effect so effective orally
30
mexiletine uses
electrophysiologic and antiarrythmic actions like lidocaine useful for ventricular arrhythmias relief of chronic pain, esp diabetic neuropathy and nerve injury (off label)
31
mexiletine adverse effects
predominantly neurologic | tremor, blurred vision, lethargy, nausea
32
similarities of all Class IC drugs
all oral | increase mortality from cardiac arrest or arrhythmic rudden death in pts with recent MI
33
flecainide mechanism
blocks Na+ and K+ channels, no QT prolongation | no antimuscarinic effects
34
flecainide therapeutic use
supraventricular arrhythmias | very effective in suppressing premature ventricular contractions
35
propafenone mechism
blocks Na+ channels | structurally similar to propranolol, thus weakly B blocking activity
36
propafenone adverse effects
metallic taste | may exacerbate arrhythmias and cause constipation
37
propafenone therapeutic use
supraventricular arrhythmias very effective in suppressing premature ventricular contractions (same as flecainide)
38
moricizine mechanism
potent Na+ channel blocker that does not prolong action potential
39
moricizine therapeutic uses
was used for ventricular arrhythmias | withdrawn from US market
40
propranolol (nonselective) and atenolol (b1) therapeutic uses
rate control supraventricular and ventricular arrhythmias caused by SYM stim prevent v-fib
41
esmolol (b1) therapeutic use
acute tachycardias occurring during surgery
42
beneficial effects of b blockers
diminished SYM activation of heart and blood vessels | decreased cardiac workload
43
harmful effects of b blockers
negative inotropy | may induce or worsen HF in patients w acute MI
44
amiodarone therapeutic use
oral or IV maintain normal sinus rhythm in patients with a-fib prevent recurrent ventricular tachycardia
45
amiodarone cardiac effects
prolongs AP duration (and QT interval) by blocking K+ channels decreases rate of firing in pacemaker cells by blocking Na+ channels blocks a and b adrenergic receptors and Ca2+ channels and this inhibits AV node conduction to produce bradycardia
46
amiodarone extracardiac effects
peripheral vasodilation, esp after IV admin
47
amiodarone toxicity
aymptomatic bradycardia and AV block in pts with AV/SA node disease resp difficulties leading to fatal pulm fibrosis (1%) abnormal liver function and hepatitis skin deposits (grayish blue skin) after a few weeks in essentially all pts: corneal microdeposits, reduced visual activity, optic neuritis, can progress to blindness blocks thyroid function T4 to T3, can result in hyper or hypothyroidism
48
amiodarone pharmacokinetics
long half life rapid 3-10 days (50% of drug) slow for several weeks> toxicity long after its discontinues
49
amiodarone metabolism
CYP3A4 | drug drug interactions
50
dronedarone mechanism
structural analog of amiodarone without iodine | blocks several K+ and Na+ channels
51
dronedarone adverse effects
no thyroid or pulm toxicity liver toxicity black box warning of increased death, stroke, a d heart failure in pts with decompensated heart failure and permanent a-fib
52
sotalol mechanism
nonselective b adrenergic blocker that also prolongs AP duration and has antiarrhythmic properties may cause prolonged repol resulting in torsade de pointes (6% at highest dose)
53
sotalol therapeutic use
life threatening ventricular arrhythmias maintaining sinus in a-fib treatment of supraventricular and ventricular arrhythmias in pediatrics
54
dofetilide (oral) and ibutilide (IV) mechanism
block rapid component of the delayed rectifier K+ current to slow cardiac repolarization
55
dofetilide (oral) and ibutilide (IV) therapeutic use
restore normal sinus rhythm in a-fib or flutter
56
dofetilide (oral) and ibutilide (IV) adverse effects
prolonged QT and torsade de pointes in 10% of pts
57
verapamil and diltiazem mechanism
``` orally active block L type Ca channels in myocardium and vascular smooth muscle depress SA/AV nodes directly to: -decrease contractility -reduce SA not automaticity -slow AV node conduction ```
58
verapamil and diltiazem therapeutic use
supraventricular arrhythmias | rate control in a-fib
59
adenosine mechanism
opens inward rectifier K+ channels> hyperpolarization inhibits L-type Ca channels > inhibits Ca entry and conduction CV in AV node inhibits pacemaker current > decreases HR mainly affects AV > SA
60
adenosine therapeutic uses
IV injection converts paroxysmal supraventricular tachycardia to sinus highly efficient (90-95%) very short half life
61
adenosine adverse effects
``` flushing SOB chest burning headache hypotension nausea paresthesia ```
62
digoxin mechanism
potent and selective inhibitor of NA+/K+ ATPase > increased Ca2+ > positive inotrope stimulated vagus nerve and thus decreases HR
63
digoxin therapeutic use
can be used in a-fib to decrease rate narrow window other antiarrhythmic drugs enhance toxicity many antibiotics increase digoxin absorption drugs that produce hypokalemia will enhance toxicity (K+ is a competitor)
64
digoxin toxicity
GI: nausea, vomiting, diarrhea, ab discomfort cardiac: almost all arrhythmias
65
magnesium therapeutic use
mag chloride or sulfate (parenteral) mechanism unknown prevent torsade de pointes used against digoxin induced arrhythmias

RC Test 1 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions