Facilitator Version
Module #23 Atrial Fibrillation
Created by Dr. Percy Pentecost
10/1/2013
Objectives:
1. Recognize atrial fibrillation by clues found on EKG, physical exam and by history
2. List risk factors and symptoms of atrial fibrillation
3. Describe the management of acute atrial fibrillation
4. Describe the management of chronic atrial fibrillation
References:
Concepts and Cautions in Electrocardiography (Nelson 2007)
Harrisons Principles of Internal Medicine, 15th Edition
MKSAP 16
Uptodate.com
Case
A 67 year old male with DM, HTN, hyperlipidemia and obesity presents to the faculty
clinic at UNMH for routine follow up of his chronic medical issues. At triage, he reports a
feeling of anxiety and a “fast heartbeat.” As it is very busy in clinic, your medicine team is
called to evaluate/admit the patient. An EKG has been ordered.
On physical examination, vital signs are significant for a heart rate of 127 and a blood
pressure of 103/ 61. In general, the patient is an obese male in no acute distress, who looks
his stated age. HEENT exam is within normal limits. Neck is large and JVP cannot easily
be assessed. Cardiac exam reveals an irregularly irregular heart beat that is obviously
tachycardic. Lungs are clear to auscultation bilaterally though diminished at the bases. GI
exam shows an obese abdomen but is otherwise benign. MS exam shows trace LE edema.
Neurologic exam is non-focal grossly.
Labs will be ordered after an appropriate encounter has not been created in the computer
EKG has been obtained and is shown below:
What is the diagnosis and what data support the diagnosis (studies, exam, history)?
The EKG shows an absence of P waves, and QRS complexes are irregularly irregular. Likewise,
physical exam shows an irregularly, irregular heart beat that is tachycardic. The patient’s history
suggests risk factors: male gender; HTN; possible OSA; possible CAD/MI history (patient has
DM).
What other conditions are associated with atrial fibrillation? Other symptoms?
Heart failure, hyperthyroidism, WPW, cardiac surgery, MI, myocarditis, pericarditis, pulmonary
disease, mitral valvular disease. Symptoms can include none (asymptomatic), chest discomfort,
palpitations, dyspnea, dizziness, fatigue and syncope.
How common is atrial fibrillation and which patients are most likely to get it?
The prevalence of atrial fibrillation in the United States is approximately 2.2 million cases. Men
are more likely to have atrial fibrillation than women. Older age is also a risk factor: the
prevalence of 80 year olds with atrial fibrillation approaches 10%.
Your team is successful in admitting the patient and he is transferred to a monitored bed.
By the time you see him on the floor his heart rate is 155 and his blood pressure is 93/51.
He is able to converse and complains of palpitations and lightheadedness with
ambulation—which resolves when he is in bed (though he still feels fatigued). On exam he
appears mildly short of breath but has good color. The rest of his exam is unchanged.
What is the initial decision tree for atrial fibrillation and what are the treatment options
for each branch? What are the costs and benefits of the treatment options?
The initial decision/assessment to make is: stable or unstable? This decision is clinical and is
based on a number of parameters (e.g. AMS? Evidence of poor perfusion?). Cardioversion is
the treatment for unstable atrial fibrillation. Direct current is often used but chemical
cardioversion is also used (e.g. with amiodarone). Medical management with IV rate control
agents can be used for stable atrial fibrillation. Agents typically include beta blockers such as
esmolol or metoprolol, and, calcium channel blockers such as diltiazem or verapamil. Digoxin is
also used but usually as an adjunct for one of these other medications. In a situation where the
patient is doing well, oral medications can be utilized. If the need for cardioversion is not
emergent then medications that could convert the patient to NSR should be avoided as
conversion could dislodge a LA thrombus and cause a CVA or other embolic event.
Your patient’s rate is decreased with IV Diltiazem. His labs come back and the following
are noted:
CBC: WBC=7.8, H/H=18/55, Plt=392,000. Chem 10: Na=132, K=3.1, Cl=108, HCO3=20,
BUN=24, Cr=01.4, Glu=183, Ca=8.4, Mag=1.8, Phos=2.3
What conditions do you note that are potentially contributing to your patient’s atrial
fibrillation and how might treatment help his condition? What other labs should you order
and what would you be looking for?
Patient may be dehydrated based on his BUN/Cr and perhaps his sodium. Low potassium could
be a contributing factor. Elevated H/H could be from dehydration but it could also suggest
obstructive sleep apnea. IV fluids could reduce the stimulus for tachycardia. Oxygen therapy
and potassium replacement may make the myocardium less “irritable.”
LFTs could show underlying liver disease or, perhaps, suggest alcohol consumption. TSH could
show hyperthyroidism. BNP could suggest CHF. Troponin could suggest MI (but may be
resultant of a demand supply issue because of tachycardia). D dimer could suggest PE (in the
right situation).
After IV fluids, potassium replacement and titration of the diltiazem drip, your patient
feels better. His HR is in the high 90s. His BP is 119/81. He asks the nurse to page a a
team member because he has a number of questions, the first being: “Can you get me back
in a good rhythm?” What can you tell your patient in answer to his question?
Atrial fibrillation often converts spontaneously. But if it does not, there are 2 strategies for
effecting non-acute cardioversion: 1) The patient starts warfarin and achieves a therapeutic INR,
and 4 weeks later elective cardioversion is undertaken. 2) The patient starts on therapeutic
anticoagulation immediately (e.g. Lovenox) and undergoes a TEE. If no intra-cardiac thrombus
is seen, cardioversion can follow. In either case, the patient should be anti-coagulated for 4
weeks after cardioversion as there is an increased risk of thrombus and CVA until the
myocardium “wakes up” and contracts effectively. Cardioversion can be either chemical (e.g.
Amiodarone or Flecanide) or via direct current. The latter usually is undertaken with sedation.
Unfortunately, cardioversion often fails within days and patients again are in Afib.
Your patient is worried about cardioversion failure. And he really does not want to be on
Warfarin. But he does not like the idea of a CVA. What can you tell him about his CVA
risk?
CHADS2 score allows for risk stratification and suggests appropriate anticoagulation strategy:
1 point is given for CHF, HTN, Age greater than 75 years, and Diabetes. 2 points are given for
prior CVA or TIA. A score of 0 imparts a 1.9 % annual stroke risk and recommended treatment
is ASA or no treatment. A score of 1 imparts a 2.8% annual stroke risk and recommended
treatment is ASA or Warfarin. A score of 3 to 6 carries an annual stroke risk of from 5.9% to
18.2% and Warfarin is the treatment of choice.
Your patient reluctantly agrees to start Warfarin and a rate control medication. What can
you tell him about rate control medications’ side effects? What can you tell him about his
goal INR, maintaining this level, and, about following up with a practitioner for Warfarin
maintenance?
Beta blockers’ side effects include cardiovascular troubles such as AV block, but also
depression, fatigue, pulmonary spasm, erectile dysfunction, and masking of hypoglycemia.
Diltiazem side effects include cardiac difficulties such as AV block, but also, dizziness, gout and
edema. Digoxin has a narrow therapeutic window and toxicities include arrhythmias, AMS, and
visual disturbances.
Goal INR is usually 2-3. With a prosthetic valve it is 2.5—3.5. Diet needs consistency. Other
medications interfere with Warfarin metabolism (can increase or decrease). Follow up is usually
more in the beginning and less when INRs become consistent. Lab draws can be by
venipuncture or finger stick.
If time: Your patient has concern about his upcoming trip to Europe. He does not know
how he will follow his INR for the 2 months he will be there. What suggestions can you
make?
Newer oral anticoagulants such as Dabigatran are now available. These do not require
monitoring. Their long term efficacy is not well studied. ASA and Plavix combination offers
more protection from CVA than ASA alone but bleeding risk is higher. Lovenox or
Fondaparinux shots might also be an option but may not be covered by insurance.
MKSAP 16 Questions
CV Question 10-nonpharmacological strategies for atrial fibrillation. – Answer C
CV Question 30-heart failure and atrial fibrillation. – Answer A
CV Question 37-paroxysmal atrial fibrillation. – Answer E
CV Question 52-pharmocoprophylaxis in atrial fibrillation. – Answer A
CV Question 55-repaired tetralogy of Fallot and atrial fibrillation. – Answer B
CV Question 68-mitral regurgitation and atrial fibrillation. – Answer A
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to Dr.
Wendy Gerstein, Department of Medicine, VAMC (111) or give to Dr. Patrick Rendon at UNM
Hospital.
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment below:
_____________________________________________________________________________________
_____________________________________________________________________________________
_____________________________________________________________________________________
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4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient curriculum in
general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
Medical student