Published in the October 2007 issue of Today’s Hospitalist
To evoke the challenge of managing atrial fibrillation, electrophysiologist Darryl Elmouchi, MD, likes to use an unusual metaphor: the Whac-a-Mole game that kids love to play at arcades and summer carnivals.
“With atrial fibrillation, you keep hitting it, but it pops up again,” he said. “You keep chasing it, but you never get rid of it.”
Given atrial fibrillation’s recurring nature, Dr. Elmouchi urged physicians to keep their treatment goals realistic when trying to prevent recurrences and reduce the severity of patient symptoms. And while atrial fibrillation is rarely life-threatening, he noted that a major part of managing this arrhythmia is safeguarding patients against potentially deadly thromboembolic complications.
At the Spring 2007 Hospitalist CME Series meeting held this year in Cambridge, Mass., Dr. Elmouchi walked hospitalists through protection strategies and outlined management techniques for both acute and chronic atrial fibrillation.
AF’s clinical manifestations
Although plenty of younger patients present with atrial fibrillation, the condition is directly related to age. Dr. Elmouchi, a cardiac electrophysiologist with West Michigan Heart PC in Grand Rapids, Mich., said that 2 million patients have the arrhythmia, and that 15 million patients are projected to have atrial fibrillation in the U.S. by 2015.
While many factors predispose patients to atrial fibrillation, Dr. Elmouchi flagged one in particular: thyroid disease. “Hyperthyroidism is definitely associated with atrial fibrillation, and it is one of very few reversible causes,” he pointed out. For patients with atrial fibrillation, checking thyroid function can help identify “that one out of every 150 patients where you catch hyperthyroidism,” he said. By treating it, “the atrial fibrillation may not recur.”
The clinical manifestations of atrial fibrillation vary, he said. Many cases are rate-related and stem from the loss of AV synchrony or atrial asystole.
Most patients with rate-related atrial fibrillation “go fast,” said Dr. Elmouchi, although occasionally patients go “very, very slow, usually because of polypharmacy in people on digoxin and various other medications.”
Physicians will also see patients with very slow atrial fibrillation in whom the post-conversion pauses can be “very scary” and last as long as 10 seconds. “Post-conversion pauses do reflect that the sinus node is a little weak,” he explained, “but they are a natural phenomenon that you don’t have to worry about unless patients are symptomatic.”
Managing acute AF
When patients present with atrial fibrillation and are unstable, the obvious course is cardioversion. More typically, however, you’ll see stable patients in the emergency department with atrial fibrillation, a heart beat of 160 per minute and a systolic blood pressure of 85 or 90.
“Someone in the emergency room will give them 20 mg of IV diltiazem because that’s the bolus dose listed in Epocrates and Pocket Pharmacopeia,” he said. “You get called because their blood pressure is now 60 and they look terrible.”
When giving IV calcium-channel blockers or beta-blockers, Dr. Elmouchi said, think in terms of very small boluses. Give 2.5 mg of diltiazem, then wait a few minutes and give another bolus.
“It may take 30 minutes to give patients the full 20 mg,” he explained, “but their blood pressure may rise if you give the bolus gradually.”
If you have a stable patient with atrial fibrillation and rapid heart rate, the best choice for acute rate control is oral or IV non-dihydropyridine calcium-channel blockers or beta-blockers. For patients who do not have an accessory pathway (as in Wolff-Parkinson-White syndrome), American Heart Association guidelines released last year call for prescribing esmolol, metoprolol, propranolol, diltiazem or verapamil. (The guidelines recommend amiodarone for patients with an accessory pathway.)
One drug to avoid in acute treatment is digoxin. “It takes a very long time to work,” Dr. Elmouchi said, “and it has very little effect on people with high sympathetic tone, which is most of the people you’ll see.”
The exception is patients without an accessory pathway who have heart failure. “A big slug of diltiazem or IV metoprolol might decrease their systolic output,” he pointed out. “Digoxin does not work very well, but it is relatively safe.” Another alternative for heart failure patients is amiodarone.
Beware of thromboemboli
While heart rate is the first big consideration, an equally important issue is the potential for thromboembolic problems. That’s particularly true for patients who have one or more of six risk factors in the CHADS2 scoring system. (See “Risk factors for thromboembolic complications with AF,” left.)
“Blood is pooling in the atrium that quivers,” Dr. Elmouchi explained. “Blood that pools can clot.” Patients are particularly vulnerable to clots forming in the left atrial appendage, a small vestigial part of the atrium.
Even if an echocardiogram shows no clots, you can’t feel confident that the patient does not have an intracardiac thrombus, he said. “You need a transesophageal echocardiogram [TEE], which is currently the gold standard,” although cardiac CT is getting “better and better.”
Using the CHADS2 scoring system, weigh patients’ thrombus risk against their risk of bleeding. Patients with no risk factors run an annual thromboembolic complication rate from persistent atrial fibrillation of less than 2%. The complication rate of those with all six risk factors, on the other hand, tops 18% per year.
“The guidelines say that first-line is full-strength aspirin, not baby aspirin,” Dr. Elmouchi said. And for patients who have two or more risk factors, consider discharging them on warfarin.
While the risk of a serious bleeding complication with warfarin runs about 2%, “someone with a 15% or higher risk of stroke per year can live with that small risk from Coumadin.”
Cardiovert or not?
The issue of thromboembolic complications plays into the decision of when to cardiovert a stable patient. “If you cardiovert them,” Dr. Elmouchi said, “they may end up throwing a clot. Cardiovert them only when it is appropriate.” But knowing when it’s safe to cardiovert patients can be difficult unless you now exactly when their atrial fibrillation began.
“Even if patients say they started feeling palpitations six hours ago, you do not know when the fibrillation started,” said Dr. Elmouchi. And because between one-third and one-half of atrial fibrillation patients are asymptomatic, patients may be able to offer no help at all in giving you a timeline. “Even patients who present with symptomatic atrial fibrillation often have asymptomatic episodes,” he added.
Before shocking stable patients, Dr. Elmouchi said that physicians should consider several options. The first is anticoagulation.
“Let patients get three weekly therapeutic INRs that are greater than or equal to 2,” he said. Then cardiovert the patient, either with medications or electrical cardioversion.
Option No. 2 is to send patients for cardioversion if they have had atrial fibrillation for less than 48 hours.
And option No. 3 is the one to choose for symptomatic patients whom you’re having a tough time getting under control.
“Give them a low-molecular-weight heparin or unfractionated heparin along with warfarin, and get a TEE,” Dr. Elmouchi said. If you still see no clot, you can cardiovert the patient, but keep in mind that you’ll need to prescribe some form of anticoagulation for at least four weeks. “People are actually at a higher risk for a thromboembolic complication in the two-to-four week period after a cardioversion,” he explained.
Medical therapies and refractory AF
In addition to electricity, Dr. Elmouchi said, several drugs work well to cardiovert patients. For younger patients with structurally normal hearts, guidelines recommend a class I-C antiarrhythmic such as flecainide or rhythmol or a class III antiarrhythmic.
“More than 50% of these patients will cardiovert just with meds,” he pointed out, “and you will not need to shock them, which will make them your friend.”
He mentioned that amiodarone is not widely used, nor is IV ibutilide, although the latter remains a favorite of electrophysiologists. “If a patient is well-monitored, this is an excellent drug with very good efficacy.”
Keep in mind, however, that IV ibutilide shouldn’t be used in anyone whose ejection fraction is less than 20%. In addition, the drug shouldn’t be given to patients with a prolonged QT interval. That’s because ibutilide significantly prolongs the QT interval for a short period of time, putting patients at risk of torsades.
Then there are patients with refractory atrial fibrillation, whose heart rates are very difficult to control, for whom you cannot get their resting heart rate below 100 beats per minute or who fail cardioversion.
For these patients, he said, you have two options. The first is an atrial fibrillation ablation procedure that is rarely done in an acute setting.
The second is a pacemaker with AV node ablation, which “is the only way we have currently of invasively controlling ventricular response to atrial fibrillation,” he noted. “These are great procedures, but in select individuals.”
Dispelling rate vs. rhythm control myths
Finally, Dr. Elmouchi addressed findings from the AFFIRM and the RACE trials, both published in the Dec. 5, 2002, New England Journal of Medicine, on the advantages of rate vs. rhythm control strategies for atrial fibrillation.
In the AFFIRM trial, which was the larger of the two, patients in the rhythm-control arm were anticoagulated at their physician’s discretion, while those in the rate-control arm were receiving life-long anticoagulation.
“There was no significant difference in quality of life or total mortality,” Dr. Elmouchi said. “So what did everyone say? ‘There is no reason to get people out of fibrillation because if we slow them down, they will do fine.’ ”
The problem with that conclusion, he pointed out, is that patients in the study were asymptomatic, which isn’t the case for many atrial fibrillation patients.
“In totally asymptomatic patients, rate control is reasonable,” he pointed out. For patients with symptoms, however, even when you achieve rate control, they will still feel fatigue, palpitations and symptoms of heart failure.
The other important take-home message from the AFFIRM trial, he added, is that the rhythm-control arm in which patients were taken off of anticoagulation had a higher incidence of cardiovascular events.
“Regardless of whether patients are converted to sinus rhythm,” he concluded, “anticoagulation is very important.”
Phyllis Maguire is Executive Editor of Today’s Hospitalist.
To illustrate how variable ventricular tachycardia (VT) can present, Darryl Elmouchi, MD, a cardiac electrophysiologist with West Michigan Heart PC in Grand Rapids, Mich., recalled two patients he’d seen recently with VT.
One had been exercising on a stationary bicycle when his heart began to “feel funny,” and he came in with VT and a heart rate of 280 beats per minute. The other patient, an 80-year old, had VT at 140 beats per minute.
“The speed of the VT is not that important,” Dr. Elmouchi told attendees at a Spring 2007 Hospitalist CME Series meeting. “If someone is clinically compromised and hemodynamically unstable, shock first and ask questions later.”
The newest guidelines call for shocking unstable VT patients with 360 joules, the maximum setting. “The old 200, 300 just doesn’t fly anymore,” he said. “The sooner you defibrillate someone, the better, so you might as well start with the most energy and then use pharmacotherapy adjunctively.”
For stable patients, on the other hand, “you can try to do this with medications.” IV amiodarone is the most frequently used, although IV lidocaine is another option.
Keep in mind, Dr. Elmouchi cautioned, that IV amiodarone “can lead to hypotension, particularly in the initial bolus.” Guidelines indicate using a 300 mg bolus, but “if you have someone who is a little more stable,” he pointed out, give 150 mg over 10 minutes, “and usually the hypotension will not be severe.”
Among patients with ventricular tachycardia, 90% have structural heart disease, either from prior CV surgery, a prior MI, dilated cardiomyopathy or structural heart disease.
But 10% of patients with ventricular tachycardia have completely normal hearts. “You can echo them, get cardiac CTs or MRIs,” he explained, “and their hearts and coronaries are completely normal.”
That small subset of patients, who are said to have idiopathic VT, have an excellent prognosis. For patients with idiopathic VT and a structurally normal heart, IV calcium-channel blockers, beta-blockers or even adenosine may be
able to convert VT back to sinus rhythm.
For patients in VT who have an existing implantable cardioverter-defibrillator, however, Dr. Elmouchi suggested calling your local electrophysiologist or the pacemaker company. “They can actually overdrive pace or pace the VT
faster, and sometimes that will terminate it.”