Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fall 2014 - Pharm Cardio > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What sxs might be associated with a-fib?

A

-palpitations, SOB, dyspnea, dizziness, fatigue

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

What are the 3 goals in management of a-fib?

A
  1. control rate
  2. prevent thromboembolism
  3. correct to normal sinus rhythm, maintain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the goal of pharm therapy to control the ventricular rate in a-fib?

A
  • slow the conduction velocity

- increase refractory period at AV node

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

What drugs can be used to control ventricular rate in a-fib?

A
  • beta blockers
  • non-dihydropyridine calcium channel blockers
  • digoxin and amiodarone are alternative choices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MOA of Non-Dihydropyridines in A-fib Rate Control

A
  • work at AV node to decrease conduction velocity and increase refractory period
  • slows down the ventricular rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What CCB are used for a-fib rate control?

A

-non-dihydropyridines: diltiazem and verapamil

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

What must be monitored when using CCB for a-fib rate control?

A
  • BP because diltiazem and verapamil are vasodilators

- signs of CHF due to negative inotropic effect

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

MOA of Beta Blockers in A-fib Rate Control

A
  • block beta adrenergic receptors in heart

- decreased conduction at AV node and increased refractory period

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

What oral BBs are commonly used in a-fib rate control?

A
  • atenolol

- metoprolol

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

What must be monitored when using BB for a-fib rate control?

A
  • BP for HoTN
  • bradycardia
  • exacerbation of CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adverse Effects of BBs in A-fib Rate Control

A

-CNS: fatigue, lethargy, depression, sexual dysfunction

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

MOA of Digoxin in A-fib Rate Control

A

-increases vagal tone to slow conduction at AV node

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

It is advantageous to use digoxin in 2 circumstances for a-fib control. What are they?

A
  • pt HoTN: other agents reduce BP, dig has no effect on BP

- advantage in CHF exacerbation: other agents may decrease heart’s contractility

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

What must be monitored when using digoxin in a-fib rate control?

A
  • HR, BP, electrolytes (for hypokalemia/magnesemia)
  • rhythm for any new arrhythmias
  • signs of toxicity: hallucinations, N/V, AV block
  • serum level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of Amiodarone in A-Fib Rate Control

A
  • beta blocker and CCB to slow down heart rate

- also has anti-arrhythmic actions to convert a-fib

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

When is anticoagulation needed when converting a-fib to NSR?

A

-if a-fib 48 hours or unknown, anticoag is needed: 3 weeks of warfarin before cardioversion

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

What are some of the agents that can be used to convert a-fib to NSR?

A
  • procainamide, quinindine
  • propafenon, flecanide
  • amiodarone
  • ibutilide, dofetilide, sotalol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MOA of Procainamide/Quinindine/Disopyramide

A
  • inhibit fast sodium channels
  • decreases conduction velocity
  • increases refractory time
  • decreases automaticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In what patients do propafenone and flecanide need to be avoided?

A

-pt with with structural heart dz like CAD or CHF

20
Q

MOA of Amiodarone

A
  • provides rate control

- may convert to NSR and maintain NSR once converted

21
Q

What are some downsides of amiodarone use?

A
  • potentially serious long term risk of pulmonary fibrosis
  • hypo or hyperthyroidism
  • hepatic dysfunction
  • skin discoloration
  • ocular toxicities
22
Q

What must be monitored short term with amiodarone?

A
  • bradycardia
  • heart block
  • HoTN
  • drug interactions w/ warfarin, digoxin, statins
  • GI disturbances
23
Q

What must be monitored long term with amiodarone?

A
  • PFT and CXR at baseline then annual CXR
  • LFTs at baseline and q6 months
  • thyroid function test at baseline and 2-3x/yr thereafter
24
Q

How is ibutilide used?

A

-one time IV dose to convert to NSR

25
Q

What are some problems associated with ibutilide/dofetilide use?

A

-can cause QT prolongation, proarrhythmias, torsades de pointes

26
Q

What is important to remember about dofetilide dosing?

A

-adjust for renal function (lower doses for poorer CrCl)

27
Q

What is sotalol indicated for?

A
  • BB with additional anti-arrhythmic properties

- indicated for maintaining NSR once converted

28
Q

What must happen with paroxysmal supraventricular tachycardia in order to convert to NSR?

A

-must break the re-entry pathway in the AV node

29
Q

How is PSVT treated and what is the DOC?

A
  • initially, carotid sinus massage
  • use drugs to slow AV nodal conduction
  • adenosine is DOC, but verapamil, diltiazem and BBs also work
30
Q

MOA of Adenosine

A

-briefly interrupts conduction at AV node to break re-entry

31
Q

What must be monitored with adenosine use?

A

-peripheral vasodilation: HoTN, flushing, SOB, chest tightness, apprehension

32
Q

When is adenosine contraindicated?

A

-in heart transplant patients

33
Q

What is primary prevention of ventricular arrhythmias?

A

-at elevated risk of ventricular arrhythmias, but have never experienced an episode

34
Q

What is secondary prevention of ventricular arrhythmias?

A

-have survived or experienced v-tach w/o a precipitating cause or experience syncope thought to be caused by tachyarryhthmias

35
Q

How is stable v-tach (non-cardiac arrest) treated?

A

-with amiodarone

36
Q

How is unstable v-tach (non-cardiac arrest) treated?

A

-with cardioversion

37
Q

Besides amiodarone, what other drugs can be used for v-tach (non-cardiac arrest)?

A
  • lidocaine

- procainamide

38
Q

How is torsades de pointes with a prolonged QT interval corrected?

A
  • correct electrolytes

- give magnesium

39
Q

What are the various ventricular arrhythmias?

A
  • v-fib
  • v-tach
  • asystole
  • pulseless electrical activity (PEA)
40
Q

During v-fib/v-tach, asystole or PEA, what drugs can improve perfusion?

A

-epinephrine or vasopressin

41
Q

During v-fib/v-tach, what drugs can “fix” the rhythm?

A
  • amiodarone
  • lidocaine
  • procainamide
42
Q

During asystole or PEA, what drugs can “fix” the rhythm?

A

-atropine possibly

43
Q

MOA of Epinephrine

A
  • improves perfusion to heart and brain during CPR

- peripheral vasoconstriction = increased cardiac conduction and improved cardiac contractility

44
Q

MOA of Vasopressin

A
  • improves perfusion to heart and brain during CPR
  • alternative to epi
  • increase coronary perfusion pressure, vital organ blood flow, cerebral blood flow
45
Q

Indications for Mag Sulfate

A
  • torsades de pointes
  • suspected hypomagnesemic state
  • refractory ventricular arrhythmias
  • digoxin toxicity
46
Q

MOA of Atropine

A

-anticholinergic effects –> increased SA node firing and AV node conduction

47
Q

How much epi is given to a patient in cardiac arrest?

A

1 mg IV q3-5 minutes

Fall 2014 - Pharm Cardio (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions