21 - Atrial Fibrillation Flashcards

1
Q

What are the different classifications of atrial fibrillation?

A
  • Paroxysmal AF
  • Persistent AF
  • Long standing persistent AF
  • Lone AF
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2
Q

What is paroxysmal AF?

A
  • episodes may last 1-7 days
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3
Q

What is persistent AF?

A

not self-limited; lasts for longer than 7 days

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4
Q

What is long standing persistent AF?

A

lasts over a year

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5
Q

What is lone AF?

A

Used less often; young, low risk, CHADS2=0 (qv)

Don’t know why they have it and they’re young

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6
Q

What pathophysiological elements will you see in atrial fibrillation patients?

A
  • Atrial enlargement (wall stretch)
  • Ischemia
  • Toxins
  • Metabolic disease
  • Hemodynamic impairment
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7
Q

Describe the atrial wall enlargement

A
  • Can be due to mitral valve disease or rheumatic heart disease
  • Wall stretch – start to break apart the conduction fibers in the atria due to increased pressure
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8
Q

Describe toxins that can cause atrial fibrillation

A

ALCOHOL = classic example

  • Holiday heart symptoms because they went on a “bender” over the holidays and it is causing heart symptoms
  • Direct cardiac toxin
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9
Q

What type of metabolic disease can send a patient into AF?

A
  • Hyperthyroid
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10
Q

What type of hemotynamic impairment results from AF?

A
  • Loss of atrial addition to the systolic volume

- Tachyarrhythmia

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11
Q

Describe the cardiomyopathy seen in AF

A
  • Dilated cardiomyopathy
  • Will see dilation in the left atrium and left ventricle
  • The size of LA and LV will be increased in size
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12
Q

What types of things will you ask in the history for an AF workup?

A
  • hypertension
  • rheumatic heart disease
  • valvular heart disease
  • myocardial ischemia/ infarction (CAD)
  • alcoholism
  • palpitations
  • symptoms of heart failure (SOB, PND, etc.)
  • thyroid disease
  • stroke
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13
Q

What types of things will you look for in the physical exam?

A
  • “irregularly irregular” pulse
  • variable intensity S1 (softer with long cycles)
  • heart murmur (e.g. MR/MS)
  • pulmonary rales/rhonchi
  • hepatic edema (enlarged liver)
  • peripheral edema
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14
Q

Why will S1 vary in intensity? Why will the mitral valve closure sound different?

A

Why will S1 vary? Why will mitral valve closure sound different?

  • Varying levels of blood
  • Varying stroke volume
  • Some have more time to fill, some have less
  • Mitral regurgitation – the base of the valve (circle) widens but the valves themselves do not get larger, so they pull apart
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15
Q

What will you do for lab tests?

A

Chest x-ray

  • may suggest heart failure:
  • pulmonary congestion
  • cardiac enlargement

Lab tests

  • may relate to myocardial ischemia (e.g. troponin)
  • may relate to toxic/metabolic disease (e.g. thyroid fnx)
  • no findings in “lone” Afib

Echocardiography

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16
Q

What are you looking for in echocardiography?

A

This is CRUCIAL

Looking for…

  • Valvular disease
  • Chamber enlargement
  • Intracardiac thrombi
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17
Q

What is the main consequence of AF?

A

Thromboembolism

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18
Q

What are other consequences of AF?

A
  • Thrombi can be present in Left Atrium
  • Nonvalvular AF most common (~50%)
  • Stroke (low risk in lone AF)
  • Diminished cardiac output
  • Ischemic events
  • Exercise capacity diminished (HR does not respond to demand)
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19
Q

Why does the heart not respond to increased demand in cases of AF?

A

Loss of vagal and adrenergic chronotropic influences

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20
Q

What are causes of AF that are not due to pathology in the heart valves?

A
  • Age >65
  • Hypertension
  • Rheumatic heart disease(also valvular)
  • Prior stroke or transient ischemic attack
  • Diabetes mellitus
  • Congestive heart failure
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21
Q

What are the treatment goals in atrial fibrillation?

A

Rhythm and rate control

You can either try to control the rhythm (get them back in to normal sinus rhythm) or you can try to get control over the rate

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22
Q

Describe the goal of rhythm control

A

Rhythm control: restore/maintain sinus rhythm, may

  • improve symptoms
  • improve hemodynamics
  • reduce stroke risk
  • avoid anticoagulation
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23
Q

Describe the goal of rate control

A

maintain acceptable ventricular rate in chronic AFib

24
Q

Describe the treatment of AF in terms of what is better - rate or rhythm control?

A
  • No survival advantage with either strategy
  • Rhythm control patients hospitalized more for adverse drug problems
  • Stroke risk similar between groups

According to AFFIRM study

25
Q

What did a different test say about mortality rates?

A

Rhythm control may be lightly more effective than rate control, but it is not a significant difference, can be due to chance

26
Q

In which patients would you try to first control the rhythm?

A

Rhythm control: restore/maintain NSR

- Most common to try on your patient who wants great quality of life and minimal risk – younger patients

27
Q

In which patients would you try to first control the rate?

A

Rate control: maintain acceptable ventricular rate in chronic AF

  • Most common overall
  • Most common in elderly procedure
28
Q

What is the main goal in all patients?

A

Avoid embolic events!!!

29
Q

Describe the process of rhythm control (younger, healthy)

A
  • DC conversion to NSR usually preferred (v. drug tx) - shock the patient into normal sinus rhythm

Urgent DC cardioversion needed if:

  • current myocardial ischemia
  • evidence of hypoperfusion
  • severe heart failure symptoms
  • pre-excitation present

Infrequent episodes that don’t convert spontaneously

30
Q

What do you do if shocking the patient into NSR doesn’t work?

A

Pharmacologic treatment

  • Not as successful
  • Not primary choice
31
Q

What drugs can be used to get gain rhythm control for up to 1 week?

A
dofetilide (Class III) 
flecainide (Class IIC)
ibutilide (Class III)
propafenone (Class IIC)
amiodarone (Class III) – most common
32
Q

What drugs can be used to gain rhythm control for longer than 1 week?

A

dofetilide, amiodarone, ibutilide

33
Q

Describe the goal of rate control

A
  • only ~30-35% remain in NSR after conversion
  • goal HR ~80 - ~110 (“lenient” rate control)*
  • control of rapid rate may improve hemodynamics
  • long-term, may avoid cardiomyopathy mediated by high HR
34
Q

What are today’s standards for rhythm vs rate control?

A

rate control is currently preferred unless:

  • symptoms persist despite good HR
  • unable to control HR
35
Q

What are common agents for ACUTE rate control?

A
Beta blockers (metoprolol)
Ca++ channel blockers (verapamil, diltiazem)
36
Q

When would you admit an AF patient from the ER?

A

Hospitalize:

  • to initiate heparin or other anticoag
  • if ablation being considered
  • to treat associated medical problem
  • elderly
  • acute coronary syndromes
37
Q

When would you send home from ER?

A

Send home from ER:

  • no clear indication to admit (above)
  • successful cardioversion
  • no evidence of significant comorbidities
  • “lone” AF
38
Q

What other drugs would you prescribe in AF?

A

ANTITHROMBOLYTICS***

  • In both rate and rhythm control
  • If you’re cardioverting over a period of more than 48 hours, need to give antithrombolytics for at least three weeks before, during and at least four weeks after

KNOW THIS ***

39
Q

When would you not give antithrombolytics?

A
  • under 60yr

- “lone AF”

40
Q

What are some antithrombolytic drugs that are used?

A

These are actually anticoagulants… I think what he is trying to say is that these are the agents we would use in order to PREVENT THROMOEMBOLISM!!! (main goal)

  • Heparin
  • Warfarin
  • Aspirin
41
Q

What are the benefits of warfarin?

A
  • Reduce stroke risk by 60%
  • Higher risk of hemorrhage
  • Need to keep INR between 2.0-3.0
42
Q

What are the benefits of aspirin?

A
  • Reduces stroke risk by 45%
  • Easy to use
  • Indicated if warfarin cannot be used
43
Q

What is the protocol when a patient cannot tolerate warfarin?

A

Aspirin alone or aspirin with clopidogrel

44
Q

Does the addition of clopidogrel to an aspirin regimen alter the stroke incidence?

A

Yes

Aspirin alone: 3.4%/year
With clopidogrel: 2.4%/year

45
Q

Does the addition of clopidogrelto an aspirin regiment alter the incidence of major bleeding?

A

Yes

Aspirin alone: 1.3%/year
With clopidogrel: 2.0%/year

46
Q

What are NOACs?

A

Non-vitamin K antagonis
Oral
Anti-
Coagulants

They are a newer treatment option for atrial fibrillation and other conditions requiring blood thinners

47
Q

What are some examples of NOACs?

A
  • Dabigatran
  • Rivaroxaban
  • Abaxiban
48
Q

What are the pros and cons of NOACs?

A
  • No diet restrictions
  • Rapid onset and offset
  • Costly ($400/month) which is 100x more expensive than warfarin
  • No testing available to monitor
  • No reversal agent
  • Limited data is available for comorbidities (restricted use in kidney disease)
49
Q

What is DC cardioversion?

A

Shocking the patient to get them to snap out of the atrial fibrillation

50
Q

When would you elect for DC cardioversion as the treatment of choice?

A

It is required emergently in cases of hemodynamic collapse

51
Q

What are the pros and cons of DC cardioversion?

A
  • Effective in more than 90% but does not provide a permanent solution - 30-50% revert back into AF
  • May be better than pharmacological treatment
  • Requires pre-cardioversion anticoagulation to decrease the risk of thromboembolism (heparin or warfarin)
52
Q

What are some other treatment options for AF?

A
  • Ablation of AV node plus VVI-R pacer
  • Dual chamber (DDD-R) pacemaker (which is more effective in stroke prevention)
  • Maze procedure
  • Atrial defibrillator
53
Q

Main point: what is AF?

A

AF is a defect of cardiac rhythm control which is governed by random static electricity

54
Q

Main point: what are the consequences of AF?

A
  • Clot formation in the atria

- 30% decrease in stroke volume

55
Q

Main point: what are the symptoms of AF due to?

A

Symptoms are from decreased cardiac output and embolic vascular catastrophes

56
Q

Main point: what are the treatments for AF focused on?

A

Treatment focuses on rate and rhythm control and prevention of clot formation