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RRCCPA Clinical Medicine I > A-fib (Exam 4) > Flashcards

A-fib (Exam 4) Flashcards

1
Q

Most common clinically significant arrhythmia?

A

A-fib (about 2% of the population)

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2
Q

What is the epidemiology of a-fib

A
  • Prevalence increases with age
  • Men > Women
  • More prevalent in north america
  • White > Black
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3
Q

Most common predisposing diseases for A-fib?

A
  • HTN
  • CAD
  • CHF
  • Valvular disease
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4
Q

Basic pathophys of A-Fib

A

Many reentrant circuts in the atria -> not all beats make it through -> irregularly irregular ventricular rythm

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5
Q

Some triggers for A-Fib

A
  • Spontaneous ectopy in atrialized musculature of pulmonary veins often triggers AF
  • Surgery (esp. CT surgery)
  • Infection
  • Acute MI
  • Acute alcohol consumption (holiday heart)
  • Thyrotoxicosis
  • Acute pericarditis
  • PE or acute lung condition
  • Heart Failure
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6
Q

Classifications of A-fib

A
  • Paroxysmal
    • Self-terminates within 7 days
      • Most within <24-48 Hrs
  • Persistent
    • Lasts > 7 days
  • Longstanding Persistent
    • Continuous AF >/= 12 months
  • Permanent
    • Efforts to restore or maintain NSR have either failed or been abandoned

Important to note there is no “Chronic AF” classification

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7
Q

What is Paroxysmal AF?

A

Self terminates within 7 days most within < 24-48 Hrs

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8
Q

What is persistent AF

A

Lasts > 7 days

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9
Q

What is longstanding persistent AF?

A

Continuous AF >/= 12 months

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10
Q

What is permanent AF

A

When efforts to restore or maintain NSR have either failed or been abandoned

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11
Q

What are the most common symptoms of AF?

A
  • May be asymptomatic
  • Palpitations
  • Fatigue, dyspnea, dizziness, diaphoresis
  • Symptoms of heart failure or other underlying disease
  • S/S of hemodynamic compromise
    • CP, pulmonary edema, syncope
  • Irregularly irregular pulse palpated/auscultated
  • CVA/TIA (often Pts will be asymptomatic until they have a CVA/TIA)
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12
Q

Key features of a EKG showing A-fib

A
  • Absence of P waves
  • Irregularly irregular QRS intervals
  • Irregular or fluctuating baseline
  • Rate often uncontrolled
    • Usually 110-150 BPM
    • Termed AF with RVR one rate > 100
  • Usually narrow complex
  • Many see fine or coarse fibrillatory waves
    • Can trick you into thinking P waves are there
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13
Q

Ways to test for A-fib

A
  • Ambulatory monitoring
    • Holter monitor, implantable loop monitor
      • Good for finding a-fib if it is intermittent
  • TSH
  • CBC
  • BMP, Mg
  • Others based on likely triggers/underlying factors
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14
Q
  • You have an unstable patient with A-fib, what is the first line treatment?
    • Examples of unstable Pateint
      • Active ischemia
      • Evidence of organ hypoperfusion
        • Severe manifestations of heart failure
A

Cardiovert them!!!

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15
Q

Why do we want to control the heart rate in patients with A-fib?

A
  • Avoid hemodynamic instability and symptoms
  • Avoid tachycardia-mediated cardiomyopathy
    • Rate tends to increase the longer someone has A-fib
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16
Q

What are the two HR goals for a Pt with AF?

A
  • Strict: <80
  • Lenient: <110

RACE II trial compared strict vs lenient HR goals in pateints with permanent AF and found that Lenient HR control was noninferior to strict rate control

Rate control is generally preferred over rhythm control

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17
Q

Generally Rate control for Pts with Af is preferred over rhythm control, this is especially true in Pts > 80 years old. Why?

A

Pts over 80 are usually more sensitive to antiarrhythmics having worse S/E, and their AF is often permanent so rhythm control would do nothing for them.

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18
Q

If emergent or urgent rate control is needed what are the two classes of drugs used?

A
  • IV beta blockers: Slow sinus rate, decrease AV nodal conduction
    • Esmolol
      • Very rapid acting (duration 10-20 minutes)
    • Metoprolol
    • Propranolol
  • IV Calcium channel blockers
    • Diltiazem (Cardizem) preffered
      • Can usually control the rate within several minutes with bolus -> drip
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19
Q

Name the IV beta blockers for emergent/urgent rate control

A
  • Esmolol
  • Metoprolol
  • Propranolol
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20
Q

What is the preferred IV calcium channel blocker for emergent/urgent rate control?

A

Diltazem (Cardizem)

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21
Q

Chronic use of Beta Blockers can be used for long term rate control in patients with AF, what do they do?

A
  • Decrease resting HR and blunt HR response to exercise
  • M&M benefit to Pts with HFrEF
  • Most Beta blockers are equally effective
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22
Q

Name some of the Beta Blockers used for long term rate control in Pts with AF and their side effects

A
  • Atenolol
  • Metoprolol
  • Nadolol
  • Bisoprolol
  • Carvedilol

S/E: Wrosening CHF, bradycardia, hypotension, bronchospasm, reduced exercise tolerance, AV block

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23
Q

Calcium channel blockers can also be used for long term rate control in AF. What are the two most commonly used ones?

A
  • Diltiazem (Cardizem)
    • 30 mg QID
    • Sustained release pill available
  • Verapamil (Calan)
    • 40 mg TID-QID
    • Sustained release pill avalible
  • Cautions when using CCBs: Pts with CHF (can exacerbate CHF and worsen edema associated with it), combination with beta blockers, significant hypotension, verapamil increases serum digoxin, heart block.
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24
Q

Digoxin can also be used to control rate in Pts with Af. What are the two circumstances when it would be used?

A
  • Patients with HFrEF and AF
    • Improves contractility and reduces ventricular rate
  • Patients whose rate isn’t adequately controlled with BB and/or CCB
    • Digoxin can be added on as a medication as well as BB and/or CCB
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25
Q

What are some disadvantages to using Digoxin?

A
  • Not as effective as BB/CCB
  • May be associated with higher mortality
  • Narrow therapeutic window and levels can be increased by many medications
  • Renally cleared but cannot be removed by dialysis
  • Can cause: Caridac arrhythmias, visual distrubances (blurred or yellow vision), n/v, anorexia
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26
Q

What methonds may be used to attempt to restore sinus rhythm in Pts with AF

A
  • Antiarrhythmic drugs
  • Radiofrequency catheter ablation
  • Surgical procedures
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27
Q

What is the goal of rhythm control for Pts with AF?

A

Reduce symptoms

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28
Q

Pts with A-fib who have their rhythm controled and maintained in sinus rhythm still need to be on anticoagulants, why?

A
  • Maintaining sinus rhythm does NOT reduce the frequency of thromboembolism
    • AFIRM and RACE trials found that embolic events happened at equal frequency regardless of whether a Pt was rate or rhythm controlled
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29
Q

When is the best time to attempt rhythm control for Pts with AF?

A

Early in the course of AF

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30
Q

When initiation of rhythm control is done the Pt often needs to be hospitalized for a day or two, why?

A

So they can be put on tele monitoring. 10-15% of Pts can go into a concerning rhythm (risk for this is highest during the first 24 hours of rhythm control initiation)

31
Q

What is the main antiarrhythmic med used for rhythm control in AF?

A
  • Amiodarone
    • Best chance of maintaining NSR
32
Q

Of the antiarrhythmic meds used to control rhythm in AF, Amiodarone has the highest risk of long-term complications, what are they?

A
  • Cough
  • Thyroid dysfunction
  • Bradycardia/AV block
  • Transaminitis
  • Corneal microdepositis
  • Photosensitivity
  • Blue discoloration to skin
  • n/v
  • CNS manifestations
33
Q

What other antiarrhythmic meds can be given besides Amiodarone and why are they given?

A
  • Sotalol
    • Given to those with structural heart disease
  • Flecainide
    • Good for those without structural heart disease
  • Dofetilide
    • Given to those with structural heart disease
  • Propafenone
    • Good for those without structural heart disease
34
Q

What is the pill in pocket approach?

A
  • To terminate out-of-hospital paroxysmal AF
    • Pts can take an antiarrythmic med if they feel early symptoms of conversion to a-fib to try and abort the process
35
Q

What antiarrhythmic meds are used in the Pill out of Pocket approach?

A
  • Flecainide
  • Propafenone
36
Q

In the pill in pocket approach the Pt takes a dose of diltiazem or a beta blocker 30 minutes before taking the antiarrhythmic med. Why?

A
  • To prevent RVR if conversion to atrial flutter occurs
  • Some providers also have patients take NOAC (novel oral anticoagulants) at this time as well
37
Q

Indications for cardioversion

A
  • Hemodynamic instability
  • First episode of AF, esp. if symptomatic
  • Before initiating long-term rhythm control (mades or catheter ablation)
  • Symptomatic persistent AF
38
Q

What are reasons not to cardiovert?

A
  • Asymptomatic/minimally symptomatic
  • Low likelihood of success
    • Continuous AF > 1 year
    • Marked enlargment of LA
    • Recently failed cardioversion + antiarrhythmic meds
    • Underlying precipitant has not been corrected
39
Q

Anticoagulation meds must be given prior to cardioversion, why and what is the process?

A
  • Conversion to sinus rhythm is associated with a transient increase in the risk of thromboembolism
    • Those in AF > 48 hours are at especially high risk
    • Most often occurs in first 10 days after cardioversion
  • Need to treat Pt with anticoagulant for 1 month before and after cardioversion
  • If there is concern about delay:
    • TEE and short duration anticoagulation
      • Inpatient: Lovenox or UFH (unfractionated heparin) and simultaneous warfarin OR 48Hrs of NOAC
      • Outpatient: Start warfarin 5 days before TEE.
        • Minimal INR: 2.0 OR NOAC
40
Q

Before cardioversion Pts need to be treated with an anticoagulant for how long? For how long after cardioversion must they be treated with an anticoagulant?

A

1 month before cardioversion and one month after.

41
Q

There are two types of cardiac ECHO used for Pts with AF. What are they?

A
  • TTE
    • Gives info about
      • LA size
      • Vavular function
      • LVEF/function
  • TEE
    • Better than TTE for detecting LA and LAA thrombi
42
Q

Catheter ablation is used to control cardiac rhythm in Pts with AF, describe it.

A
  • Done by electrophysiology
  • Catheter maneuvered to LA
  • Abnormal electrical pathways are mapped to find a target area
    • Radiofrequency ablation or cryotherapyy delivered to destroy that area
  • Complications
    • Cardiac tamponade
    • Pulmonary vein stenosis
    • Phrenis nerve paralysis
    • Stroke
    • Atrioesophageal fistula
43
Q

Surgical ablation is used to control refactory AF, describe it.

A
  • Usually done in Pts who will be undergoing cardiac surgery for another reason
  • MAZE procedure:
    • Lines of ablation/scars are created in an attempt to create a “maze” of functional myocardium that allows for atrial depolarization and avoids microreentry
    • LAA (Left Atrial Appendage) may be removed
  • Effective at eliminating or reducing the frequnecy of AF in a high percentage of Pts.
44
Q

Why do Pts with Af need to be on anticoagulation meds?

A
  • Pts with AF are at a 4-6x increased risk of having a thromboelitic event
    • Anticoagulation decreases ischemic events by about 2/3
  • Decreases the severity if Pt has a CVA/TIA
    • Better long term outcome.
45
Q

What does CHADS2 stand for?

A
  • CHF
  • HTN
  • Age >/= 75
  • Diabetes
  • Stroke/TIA/TE
    • 2 points
46
Q

What does CHA2DS2-VASc stand for?

A
  • CHF
  • HTN
  • Age >/= 75
    • 2 points
  • Diabetes
  • Stroke/TIA/TE
    • 2 points
  • Vascular disease (MI, PAD, Aortic plaque, ect.)
  • Age 65-74
  • Female sex category
47
Q

Your Pt has a CHADS2 or CHA2DS2-VASc score of zero what do you do?

A
  • This is the low risk category
  • Recomendations depend on the organization
    • ACC suggests no antiplatelet or anticoagulant therapy
    • ACCP suggest no antiplatelet or anticoagulant therapy OR can use ASA 75-325 mg daily or ASA + plavix
48
Q

Your Pt has a CHADS2 or CHA2DS2-VASc score of 1, what do you do?

A
  • Intermediate risk
  • Who the hell knows, tons of different recomendations depending on the organization
  • WE WON’T BE TESED ON A SCORE OF 1
  • Just in case, just know that some recommend giving anticoags or ASA other recommend doing nothing and just watching.
49
Q

According to ACTIVE-A and ACTIVE-W studies what is the hierarchy of thrombolitic preventative meds for AF patients?

A
  • Warfrin is better than ASA + Plavix
  • ASA + Plavis is better than ASA alone
  • ASA alone is better than nothing

The studies also found that ASA + Plavix significantly increased the risk of major bleeding.

50
Q

Honestly not sure if we need to know the various studies cited in the Powerpoint. But if so what was the only study that showed the benefit of ASA alone in preventing stroke in Pts with AF?

A

SPAF-1

51
Q

Your Pt has a CHADS2 or CHA2DS2-VASc of 2, what do?

A
  • High risk for thrombolitic event
  • Oral anticoagulation recommended
    • For Pts with Paroxysmal a-fib
    • Pateints with rhythm control methods
52
Q

Even though they have been found to have a poor predictive value by the ACC what are some of the bleeding risk calculators?

A
  • HAS-BLED
  • RIETE
  • HEMORR2HAGES
  • ATRIA
53
Q

What factors significantly increase bleeding risk?

A
  • Thrombocytopenia
  • Coagulation disorder associated with bleeding
  • Active bleeding or recent surgery with concern for active bleeding
  • Prior severe bleeding while on oral anticoagulant
  • Suspected aortic dissection
  • Malignant HTN
  • Combined use of anticoagulant and antiplatelet agents
54
Q

Warfrin is one anticoagulant med used to prevent thrombolitic events in Pts with AF. What is is?

A
  • Vitamin K antagonist
    • Vit K is reversal agent
  • Reduces stroke by 64% when compared to placebo
  • Monitored by the INR
    • ​Goal range is 2.0-3.0
55
Q

How do you start a Pt with AF on Wardarin?

A
  • Start with 5mg QD for 2 days, then check INR and adjust accordingly
    • For frail or elderly Pts, may start with 2.5 mg
  • Generally, bridging with heparin is not recommended
  • Full anticoagulant effect doesn’t occur for 2-3 days
56
Q

Dabigatran (PRADAXA) is a NOAC (Novel oral anticoagulant) med for AF what are its benefits?

A
  • Superior to warfarin in stroke prevention
  • Less fatal bleeding and ICH
    • More GI bleeding
  • Reversed with Praxbind (idarucizumab)
57
Q

What is the dosing for Dabigatran (PRADAXA)?

A
  • 150 mg PO BID
  • If CrCl (Creatinine Clearance) 15-30
    • 75 mg BID
  • Not recommended for CrCL < 15
58
Q

Contraindications for giving Dabigatran (PRADAXA)

A
  • Active pathological bleeding
  • Sypersensitivity
  • Mechanical valve
59
Q

Rivaroxaban (Xarelto) is another NOAC med for AF what are its benefits?

A
  • Noninferior to warfarin for stroke prevention
  • Less fatal bleeding and ACH
    • Higher rate of GI bleeding
  • Reversed with Andexxa
60
Q

Dosing for Rivaroxaban (Xarelto)

A
  • 20 mg PO QD
  • For CrCl 15-50
    • 15 mg QD
61
Q

Contraindications for Rivaroxaban (Xarelto)

A
  • Active pathological bleeding
  • Hypersensitivity to Rivaroxaban (Xarelto)
62
Q

Apixiban (ELIQUIS) is another NOAC med for AF what are its benefits?

A
  • Superior to warfarin for stroke prevention
  • Less fatal bleeding and ICH
    • Less GI bleeding
  • Reversed with Andexxa
63
Q

Dosing for Apixiban (ELIQUIS)

This one is important she told us to know it!!!

A
  • 5 mg PO BID
  • In patients with at least two of the following: Age >/= 80, weight = 60 kg, or serum Cr >/= 1.5 mg/dL
    • 2.5 mg BID
64
Q

Contraindications for Apixiban (ELIQUIS)

A
  • Active pathological bleeding
  • Hypersensitivity to Apixiban (ELIQUIS)
65
Q

Edoxaban (SAVAYSA) is another NOAC med for AF what are its benefits?

A
  • Noninferior to warfarin for stroke prevention
  • Less fatal bleeding and ICH
    • More GI bleeding
  • Reversed with Andexxa (off-label)
66
Q

Dosing for Edoxaban (SAVAYSA)

A
  • 60 mg QD for CrCl 50-95
  • 30 mg QD for CrCl 15-50
  • DO NOT USE if CrCl >95
67
Q

Contraindications for Edoxaban (SAVAYSA)

A
  • Active pathological bleeding
68
Q

Of the NOACs which is the only one that does not increase the risk of GI bleeding?

A

Apixiban (ELIQUIS)

69
Q

Benefits of Warfarin vs NOACs?

A
  • CHEAP!!!
  • Best for severe or ESRD (End stage renal disease) and valvular AF
  • Reversal aganet exists
70
Q

Downfalls of Warfarin vs NOACs

A
  • Many food and drug interactions
  • Narrow therapeutic window
  • Frequent blood monitoring needed
71
Q

Benefits of NOACs vs Warfarin?

A
  • Fewer interactions
  • LEss ICH and fatal bleeding
  • No blood monitoring needed
  • Rapid onset/offset
72
Q

Downfalls of NOACs vs Warfarin

A
  • Historically had a lack fo reversal agents (they have them now though)
  • Expensive
  • Generally have a higher rate of GI bleeding
73
Q

What is the prognosis for Atrial Fibrillation?

A
  • Lower life expectancy
    • 1.5-1.9 fold higher risk of death
  • Antiarrhythmic drugs and anticoagulants may contribute to increased mortality
  • AF development predicts HF, and is associated with a worse NYHA (New York Heart Association) class
  • If in the setting of MI, 40% increase in mortality with AF development.

RRCCPA Clinical Medicine I (49 decks)

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