Arrhythmias Flashcards

(47 cards)

1
Q

What sxs might be associated with a-fib?

A

-palpitations, SOB, dyspnea, dizziness, fatigue

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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
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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

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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
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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
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6
Q

What CCB are used for a-fib rate control?

A

-non-dihydropyridines: diltiazem and verapamil

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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

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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

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9
Q

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

A
  • atenolol

- metoprolol

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10
Q

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

A
  • BP for HoTN
  • bradycardia
  • exacerbation of CHF
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11
Q

Adverse Effects of BBs in A-fib Rate Control

A

-CNS: fatigue, lethargy, depression, sexual dysfunction

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12
Q

MOA of Digoxin in A-fib Rate Control

A

-increases vagal tone to slow conduction at AV node

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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

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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
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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

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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

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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
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18
Q

MOA of Procainamide/Quinindine/Disopyramide

A
  • inhibit fast sodium channels
  • decreases conduction velocity
  • increases refractory time
  • decreases automaticity
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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
What are some problems associated with ibutilide/dofetilide use?
-can cause QT prolongation, proarrhythmias, torsades de pointes
26
What is important to remember about dofetilide dosing?
-adjust for renal function (lower doses for poorer CrCl)
27
What is sotalol indicated for?
- BB with additional anti-arrhythmic properties | - indicated for maintaining NSR once converted
28
What must happen with paroxysmal supraventricular tachycardia in order to convert to NSR?
-must break the re-entry pathway in the AV node
29
How is PSVT treated and what is the DOC?
- initially, carotid sinus massage - use drugs to slow AV nodal conduction - adenosine is DOC, but verapamil, diltiazem and BBs also work
30
MOA of Adenosine
-briefly interrupts conduction at AV node to break re-entry
31
What must be monitored with adenosine use?
-peripheral vasodilation: HoTN, flushing, SOB, chest tightness, apprehension
32
When is adenosine contraindicated?
-in heart transplant patients
33
What is primary prevention of ventricular arrhythmias?
-at elevated risk of ventricular arrhythmias, but have never experienced an episode
34
What is secondary prevention of ventricular arrhythmias?
-have survived or experienced v-tach w/o a precipitating cause or experience syncope thought to be caused by tachyarryhthmias
35
How is stable v-tach (non-cardiac arrest) treated?
-with amiodarone
36
How is unstable v-tach (non-cardiac arrest) treated?
-with cardioversion
37
Besides amiodarone, what other drugs can be used for v-tach (non-cardiac arrest)?
- lidocaine | - procainamide
38
How is torsades de pointes with a prolonged QT interval corrected?
- correct electrolytes | - give magnesium
39
What are the various ventricular arrhythmias?
- v-fib - v-tach - asystole - pulseless electrical activity (PEA)
40
During v-fib/v-tach, asystole or PEA, what drugs can improve perfusion?
-epinephrine or vasopressin
41
During v-fib/v-tach, what drugs can "fix" the rhythm?
- amiodarone - lidocaine - procainamide
42
During asystole or PEA, what drugs can "fix" the rhythm?
-atropine possibly
43
MOA of Epinephrine
- improves perfusion to heart and brain during CPR | - peripheral vasoconstriction = increased cardiac conduction and improved cardiac contractility
44
MOA of Vasopressin
- improves perfusion to heart and brain during CPR - alternative to epi - increase coronary perfusion pressure, vital organ blood flow, cerebral blood flow
45
Indications for Mag Sulfate
- torsades de pointes - suspected hypomagnesemic state - refractory ventricular arrhythmias - digoxin toxicity
46
MOA of Atropine
-anticholinergic effects --> increased SA node firing and AV node conduction
47
How much epi is given to a patient in cardiac arrest?
1 mg IV q3-5 minutes