Discussion Cont’d

Treating Atrial Fibrillation:

The treatment of atrial fibrillation must take into account the clinical situation, the chronicity of the fibrillation, the patients level of anti-coagulation and other stroke risk factors, the patients symptoms, the ventricular rate, and most importantly, the hemodynamic status of the patient. There are several treatment strategies depending on the above factors and also partly on patient preference. If the patient is hemodynamically stable, and the atrial fibrillation is new in onset, an attempt is made to convert the patient out of the rhythm, with either anti-arrhythmics or electrical cardioversion. If the rhythm is persistent or chronic, a strategy of ventricular rate control and anti-coagulation to prevent complications is generally used. If the patient is unstable, emergent cardioversion is warranted. Surgical catheter ablation therapy or AV node ablation with ventricular pacing are other options for patients with persistent atrial fibrillation and more bothersome symptoms.

Up to 2/3 of patients with new onset atrial fibrillation will spontaneously revert to sinus rhythm in 24 hours, so temporary rate control is appropriate. However, if it persists longer than a week, spontaneous conversion is unlikely and other measures should be attempted to either terminate the rhythm or control the rate.

            For new onset atrial fibrillation, especially if it is thought to be of recent onset, termination of the rhythm is generally attempted with elective cardioversion during short-acting anesthesia using a 200 joule biphasic synchronized shock. It may also be attempted in patients with bothersome symptoms despite adequate rate control. Elective cardioversion must follow at least 4 weeks of anti-coagulant therapy with warfarin to prevent embolization of a thrombus with the cardioversion. The recurrence rate after elective cardioversion is significantly high, so anti-coagulation therapy is generally maintained until sinus rhythm can be proven for at least 6 months straight. Pharmacological therapy to convert the rhythm is less reliable than cardioversion. It can be instituted to maintain sinus rhythm after it has been achieved either by spontaneous conversion or cardioversion or it can be started in anticipation of cardioversion. The agents most commonly used are sotolol, amiodarone, procainamide, ibutilide or dofetilide. In the absence of structural heart disease or hypertensive heart disease, the use of class IC anti-arrhythmics flecainide or propafenone is well tolerated. Many of the anti-arrhythmic agents are associated with an increased risk of arrhythmias and many other adverse effects and these risks must be weighed against the benefit to the patient of maintaining sinus rhythm.

In the setting of chronic atrial fibrillation that has recurred despite the attempts described above, a strategy of ventricular rate control and anti-coagulation is used. Rate control is generally achieved with beta-blockers, non-dihydropyridine calcium channel blockers, and/or digoxin. In older, less active patients, control can generally be achieved with one agent, but in younger more active people, a combination may be necessary. Hypertensive patients should receive either a beta-blocker or calcium channel blocker and coronary disease patients and patients with heart failure should receive a beta-blocker. Heart rates over 80 beats per minute are an indication that rate control is inadequate. Anti-coagulation with warfarin to a target INR of 2-3 is necessary to prevent embolic events and stroke. An exception to the need for anti-coagulation is the patient with “lone atrial fibrillation” (no known heart disease, hypertension, atherosclerotic coronary disease, or diabetes) who is under 65 years old. These patients should however be treated with aspirin.

The AFFIRM and RACE trials compared outcome with respect to survival and thromboembolic events in patients with atrial fibrillation and risk factors for stroke in the above to treatment approaches. They favored the rate control strategy over the rhythm control strategy. There was no higher risk of death or stroke in the rate control group. There was only a mildly increased risk of hemorrhagic events in the rate control and anti-coagulation group. However, the decision of which strategy should be used is still controversial and many times is the patient’s preference.

Atrial Fibrillation very commonly co-exists with congestive heart failure, either as an exacerbating factor or as a cause. Some recent studies have suggested that atrial fibrillation is an independent predictor of mortality in patients with CHF with an ejection fraction of less than 35%. As such, a recent study has examined the relationship between atrial fibrillation and the incidence of death due to congestive heart failure. This study by Talajic et al, examined the relationship between the presence of sinus rhythm and outcomes in patients with a history of CHF and atrial fibrillation. In the study, patients were randomized into either a rate control or rhythm control group and their symptoms and EKG’s were monitored to determine the effects of both treatment strategies and sinus rhythm on the course of CHF. It was found that atrial fibrillation is not predictive of cardiovascular mortality, total mortality, or worsening heart failure. There was not a significant difference in mortality or worsening heart failure found between patients that had a high versus low prevalence of sinus rhythm. The most probable explanation for the findings of this study is that atrial fibrillation is a marker of more advanced heart failure but that it is not etiologically linked to a poorer outcome.

In the acute setting urgent cardioversion is usually indicated for patients with shock or severe hypotension, pulmonary edema, or ongoing myocardial infarction or ischemia. There is a potential risk of a thromboembolic event with this treatment if atrial fibrillation has been present for over 48 hours, but the need for immediate rate control outweighs the risk. Just like stable patients, an initial shock of 100-200 joules of synchronized, biphasic cardioversion is applied and if rhythm is not restored, an additional shock at 360 joules is indicated. If this still fails, cardioversion may be successful after loading with IV ibutlide over 10 minutes. If the onset of atrial fibrillation is acute and the conditions that precipitated it are expected to spontaneously resolve over a period of a few days (post-surgery, pericarditis, alcohol) a strategy of rate control is appropriate. Again, beta-blockers are generally first line. However, if hypertension is present or beta-blockers are contraindicated, calcium channel blockers are used. If rate control is still inadequate, digoxin may be used; however, rate control is generally slow, may affect the bronchial tree, and may be inadequate. Amiodarone may also be used if rate control is still inadequate or if cardioversion is planned in the near future.

If cardioversion and drugs are not successful in controlling the symptoms of atrial fibrillation or left ventricular function is worsening due to persistent tachycardia despite rate control treatment, radiofrequency AV nodal ablation may be performed with permanent ventricular pacing to ensure rate control. Another option is catheter ablative therapy of foci around the pulmonary veins that initiate atrial fibrillation. Elimination of atrial fibrillation generally occurs in 50-80% of individuals after catheter ablation. Catheter ablation even holds promise in patients with persistent atrial fibrillation, even those with severe atrial dilation. It does carry risks of pulmonary vein stenosis, atrioesophageal fistula, embolic events, or perforation and tamponade. These risks must be weighed against the benefit to the patient. Surgical ablation is typically only performed at the time of other necessary cardiac surgery.

Future options for the control of atrial fibrillation include, surgical elimination or isolation of the left atrial appendage where most thrombi form or by endovascular insertion of a left atrial appendage-occluding device. These strategies are currently undergoing investigation and may eliminate the need for anti-coagulation.



Fauci, Anthony S., and Tinsley Randolph Harrison. Harrison’s Principles of Internal             Medicine. New York [etc.: McGraw-Hill, Medical Division, 2008. Print.

Talajic, Mario, Paul Khairy, Sylvie Levesque, and Stuart J. Connolly. “Maintenance of             Sinus Rhythm and Survival in Patients with Heart Failure and Atrial             Fibrillation.” Journal of the American College of Cardiology 55.17 (2010):            1796-802. 27 Apr. 2010. Web. 23 Jan. 2011. <www.sciencedirect.com>.

Ferry, David R., and David R. Ferry. ECG in 10 Days. New York: McGraw-Hill,             Medical Pub. Division, 2007. Print.



            Atrial fibrillation is the most common chronic (sustained) arrhythmia. Its incidence increases with age such that >5% of the population over 70 years of age will experience atrial fibrillation in some form. The definition of atrial fibrillation is a rapid atrial rate with an irregular rhythm and an irregular ventricular rhythm, with a rate that may be either tachycardic, bradycardic, or regular. In untreated individuals, the ventricular rate is more likely to be rapid, but is entirely dependent on the conduction properties of the AV junction. The ventricular rate typically varies between 120-160 beats per minute, but may be over 200 beats per minute in certain individuals. In other individuals with high vagal tone or intrinsic AV nodal conduction problems the ventricular rate may be less than 100. The EKG in atrial fibrillation demonstrates erratic, disorganized atrial activity between discrete QRS complexes occurring in an irregular rhythm. The atrial activity varies from a very fine baseline to course baseline. Atrial fibrillation generally occurs paroxysmally in elderly individuals before becoming the established, chronic rhythm. It is extremely uncommon in children, occurring mainly in children with a structural heart disease. The mechanism of initiation and perpetuation of atrial fibrillation requires both a large atrial area and irritable foci that demonstrate abnormal automaticity and take over control from the SA node by virtue of a faster rate. Atrial fibrillation is a re-entry arrhythmia. The requirements for a re-entry arrhythmia include, at least 2 conduction pathways, and a variable block in one of the pathways, which is usually caused by a premature atrial contraction (PAC) that makes the pathway refractory. Once that pathway is no longer refractory, the impulse may travel back up the previously refractory conduction pathway the wrong way creating a re-entry loop. The irritable foci that cause the PACs are generally found around the insertion of the pulmonary veins into the atria.

Atrial fibrillation can be caused by really any condition that causes the atria to enlarge, including rheumatic and other forms of valvular heart disease, dilated cardiomyopathy, atrial septal defect, hypertension, or coronary artery disease. It can be the initial presenting episode in thyrotoxicosis. Pericarditis, chest trauma, thoracic surgery, pulmonary disease, beta-adrenergic agonists, and alcohol can all cause an acute attack of atrial fibrillation in individuals with normal hearts (atria are not enlarged). It can also be triggered by other supraventricular arrhythmias such as AV nodal re-entry tachycardia. Perhaps the most important complication of atrial fibrillation is the propensity for clot formation secondary to blood stasis in the atria and subsequent embolization, causing stroke. If the ventricular rate is too fast, it can cause hypotension, myocardial ischemia, or tachycardia-induced myocardial dysfunction.

Many patients with atrial fibrillation are asymptomatic and have no hemodynamic consequences. Mainly, patients complain of fatigue and younger, more active people may complain of bothersome palpitations or the sense that their pulse is irregular. Other patients can experience severe palpitations and anginal symptoms resulting from hypotension. In patients with hypertension, hypertrophic cardiomyopathy or obstructive aortic valve disease that cause diastolic dysfunction, the symptoms may be even more pronounced. However, exercise intolerance and easy fatigability are the hallmark symptoms. Occasionally, the only symptoms of atrial fibrillation are dizziness and syncope associated with the pause that occurs before normal rhythm reappears.


Shall I share a case study…

History and Physical

NAME: Jane DOE                     DOB: 06/26/1934                         SEX: Female

RACE: Caucasian                         PA: Math, James PA-C             DATE: 01/24/2011


CHIEF COMPLAINT: Shortness of breath and palpitations

HISTORY OF PRESENT ILLNESS: This is a 76-year-old female who is presenting to clinic for a 4-month follow-up visit for paroxysmal atrial fibrillation. She reports mild shortness of breath, fatigue and bothersome palpitations that have decreased since she has been on amiodarone. She also reports 2-pillow orthopnea and mild pedal edema. She does report a 1-month history of diarrhea, for which her primary physician prescribed Flagyl, which as it turns out, she is allergic to. She developed hives and had to be taken off the medication. The diarrhea and hives have resolved at this time. She denies any chest pain, dizziness or loss of consciousness, cyanosis, hemoptysis or edema.


PAST MEDICAL HISTORY: Paroxysmal atrial fibrillation, hypertension, COPD, hypothyroidism, chronic low back pain, GERD, and hypercholesterolemia.


ALLERGIES: Flagyl- hives.

MEDICATIONS: Amiodarone 400 mg PO QDAY, Levoxyl 25 mcg PO QDAY, Bystolic 10 mg PO BID, Zocor 10 mg PO QDAY, Aciphex 20 mg PO BID, Spiriva 18 mcg INH QDAY, Albuterol 2 puffs Q4-6 hours PRN and Naproxen 250 mg PO BID.

SURGERIES/HOSPITALIZATIONS: One past hospitalization for CHF exacerbation 2/2 onset of atrial fibrillation.

SOCIAL HISTORY: Denies tobacco use, alcohol use and drug use. Patient lives at home with her husband.

FAMILY MEDICAL HISTORY: Mother- type II diabetes and HTN. Father- Roofer in Scranton, died of an MI at 68 y/o.


  • General: increased fatigue, no weight loss or gain, no fever, chills or sweats.
  • SKIN: no rashes, easy bruising, bleeding or cyanosis.
  • HEENT: denies any URI symptoms, eye pain or pressure, visual changes, hearing difficulty, dizziness or vertigo and headaches.
  • Cardiovascular: denies chest pain, cyanosis, dizziness or LOC. + edema of feet. + increased fatigue, + palpitations + orthopnea
  • Respiratory: + shortness of breath, denies wheezing, cough, hemoptysis. No history of tobacco use.
  • GI: denies abdominal pain, nausea, and vomiting. Recent diarrhea.
  • Neuro: denies memory problems, LOC, weakness, tremors, lightheadedness/dizziness, difficulty walking, changes in hearing, and headache. Denies paresthesias.



  • Vital Signs: P 72 R 16 BP 130/60 Weight: 184 lbs
  • General: alert and oriented x3. Slightly overweight female in no acute distress.
  • HEENT: Head-normocephalic, atraumatic; Eyes- PERRLA, EOM-intact, conjunctiva clear, no scleral icterus. Ears- intact, no discharge; Nose- patent, no discharge.
  • Skin: warm and dry, no cyanosis, pallor, bruising or rashes.
  • NECK: trachea midline, no adenopathy, full ROM, no JVD.
  • CHEST: stable, equal rise and fall, no retractions, no instability or crepitus. Non-TTP.
  • LUNGS: mild rales bilaterally, no wheeze or rhonchi. no pericardial friction rub, normal respiratory effort.
  • CVS: regular rate, regular rhythm, no murmurs, rubs, or gallops. 2+ radial pulses bilaterally, 2+ femoral, posterior tibial and dorsalis pedis pulses bilaterally. + edema in bilateral lower extremities.
  • Abdomen: soft, non-distended, non-tender, bowel sounds present and normoactive in all 4 quadrants, no organomegally, masses, or guarding. No abdominal jugular reflex.
  • Extremities: no obvious deformities. Normal capillary refill. Normal movement and sensation. + edema in bilateral lower extremity.
  • Neuro: Cranial nerves II-XII grossly intact. Mental status: alert and oriented x 3.


  • Chemistry (CMP)
    • K: 4.5, Na: 141, Cl: 101, HCO3: 24, BUN: 12, Cr: 0.6, Glucose: 130, Ca: 8.5, Phos: 3.9, Mg: 1.5.
  • Hematology
    • WBC: 9.2, Hgb: 14.0, Hct: 36, Plt: 260
  • LFT’s
    • TBili: 0.4. AST: 25 ALT: 23 ALP: 110 LDH: 120 Lipase: 87 Amylase: 118
  • PFT’s
    • DLCO- 70% predicted. FVC-78% predicted. FEV1/FVC- 0.65
  • CPK-89 Troponin- 001
  • PT- 2 INR-1.2 PTT-22
  • BNP- 67
  • Stress ECHO- EF of 55% pre-exercise increasing to 65% post-exercise. Mild mitral regurgitation and tricuspid regurgitation. Right Ventricular systolic pressure = 45 (mild pulmonary hypertension).
  • CXR- No cardiomegally. Normal pulmonary vasculature, no evidence of interstitial edema. No pleural effusion or infiltrates.
  • EKG- normal sinus rhythm with a rate of 77 beats per minute. No QT prolongation. No ST or T wave changes. Evidence of LVH with LBBB.



1.) Paroxysmal atrial fibrillation

2.) Pulmonary Fibrosis- 2/2 amiodarone

2.) CHF

3.) COPD exacerbation



1.) Paroxysmal atrial fibrillation- Currently in normal sinus rhythm. Continue amiodarone if PFT’s and LFT’s are within normal range, if not, consider switching to Multaq 400 mg BID.

2.) Pulmonary Fibrosis- DLCO mildly decreased, but not indicative of pulmonary fibrosis. Continue to monitor PFT’s.

3.) COPD- order repeat pulmonary function tests to monitor lung function on amiodarone, which can cause pulmonary fibrosis and shortness of breath and to determine the severity of her COPD. Continue Spiriva and Albuterol as needed.

4.) CHF- no evidence of cardiomegally, BNP not elevated and no indications of heart failure on stress echo, continue to monitor CXR, BNP, and Stress Echo yearly. Continue Bystolic to prevent re-modeling, consider addition of a diuretic in the future if edema and SOB persist.

5.) Hypertension- controlled on Bystolic, continue current dose.

6.) Hypercholesterolemia- controlled on Zocor, continue current dosage.

7.) Hypothyroidism- controlled on Levoxyl, continue current dosage.

8.) Chronic Low Back pain- controlled on Naproxen, continue current dosage.

9.) GERD- controlled on Aciphex, continue current dosage.



Learning is In-tents

“Learning is in tents”

Seriously, did you think I was going to be serious this entire blog? Well.. if ya did.. sorry. While I still be learning some things, and teaching others I am still the kinda guy who likes to have a good time. Why? because learning is intense! Speaking of “tents” I am just getting ready for a party at my house, which leads me to the pun of my post… in tents.

I am currently researching an affordable tent rental company in Scranton. I have called around and asked around. It is important that you gather as much information as possible before you purchase your tent since it may make or break your party. Make sure the tent rental place is reliable and insured. Compare prices, even drive to the dealer and look at what they have. Don’t assume that you know exactly what you are getting into before you do the research. Some tent rental companies can be really shady, some just downright will scam you. Others are more reputable and offer special prices for event planning, photo booth and even silverware rental. It is important that you go with a local company who knows the area. This will ensure you that you will get the best bang for your buck. Different types of tents are available based on your budget so it is important to plan ahead and know that you can and cannot afford. Do not be afraid to ask questions about your rental prices and quality.

Whether you are in a big city or small town, your special day matters and it is important to get all of your ducks in a row beforehand. Doing the research, getting various quotes and actually laying eyes on the rentals will do you good. I will guarantee that if you follow these simple steps, you will not make a bad purchase.

Talk with you soon

You can find more info Here

The Village Idiot.