A month or so ago one of our readers commented on the need for more information on atrial fibrillation, and, since I’m always happy to comply with requests to blather on about anything in this blog, I’ll gladly accommodate.

To understand atrial fibrillation (AF) you must first understand how normal electric activity in the works.  Once every second an area of cells known as the sinus node produces a spontaneous electrical impulse—a minute shock—that spreads throughout the muscle of the top chambers of the (the right and left atria).  The atria are responsible for pushing blood down into the ventricles, the muscular bottom chambers of the that pump blood out to the body and the lungs.  The electrical stimulus first causes contraction of the atria and then a split second later (one-fifth of a second to be more precise) makes its way down into the ventricles to cause contraction there.  The result is that the atria contract first followed by the ventricles.  Lub-dub.

Let me use an example to better illustrate the electrical rhythm of a beat.  Think of a big band orchestra (a la Tommy Dorsey or Count Basie) with a conductor leading the music, the musicians playing the music, and a room full of dancers.  Think of the sinus node as the conductor—constantly tapping out a rhythm, telling the to go slower or faster as needed.  The musicians represent the atrial muscle and follow the conductor impeccably.  Now pretend that the dancers, who in this scenario represent the ventricular muscle, move with the beat of the music.  Under normal circumstances the three parts—conductor, musicians, dancers—perform in perfect synchrony.

Now let’s pretend that a clarinetist decides to spin off into an allegretto while the rest of the orchestra is in the middle of an andante.  He plays fast and furious, and so loud that the neighboring instruments get confused and start their own solos.  This behavior makes its way through the orchestra until all musicians are playing their own tunes, to their own beat.  Nothing that the conductor can do will matter since he has lost control of the musicians.  The dancers, in turn, hear the cacophony and dance faster and faster, trying their best to keep up with the flood of rhythms they perceive.

This is what happens with AF.  The top atrial chambers descend into a chaotic dervish and the ventricles do their best to follow, but tend to beat so fast and irregularly that the person starts to have symptoms of palpitations, shortness of breath, and lightheadedness. 

To add to this, since the atria are no longer contracting in a coordinated fashion, the blood that normally courses smoothly through the atria with each squeeze begins to coagulate along the corrugated walls of the chambers.  In the left atrium this represents a particular problem since any clot that forms there and breaks free will migrate through the left ventricle and out the , coming to rest only when it lodges in a small artery in the brain (causing a stroke) or elsewhere in the body.

Therapy for AF really needs to focus on two areas:

1. Decreasing risk of stroke
2. Slowing the rate

To decrease the risk of clot to the brain we generally employ the age-old drugs warfarin and aspirin.

Slowing the rate is a little more complicated.  We generally adopt one of two strategies:

1. Promote normal rhythm.  The most common way to do this is to add a medication that pushes the toward normal rhythm and decreases the likelihood of AF.  For this we frequently use propafenone (Rythmol), amiodarone (Pacerone), sotalol (Betapace), flecainide (Tambocor), and a few others.  Adding one of these drugs is like hiring the club’s bouncer to stand over the shoulder of the wayward clarinetist and whack him every time he falls out of tempo.

A second way to keep the patient out of atrial fibrillation is to do an invasive procedure called pulmonary vein isolation (also referred to as AF ablation).  In many patients we know where the AF starts (at the inlet of the 4 pulmonary veins) before it expands to involve the whole upper half of the .  If we encircle the pulmonary veins with a scar line we can insulate the rest of the from the abnormal electrical activity of this small area.  It’s like taking the troublesome clarinet player and moving him to another room where he can’t bother anyone.

This procedure is done either through the veins (by an electrophysiologist) or through a small hole in the chest wall (by a surgeon).  Our group offers both approaches.

2.   Allow AF to continue but control rate.  We do this mostly with medications like beta-blockers, calcium blockers, and digoxin.  This therapy is akin to allowing the band to play as chaotically as they want but limiting how fast the dancers move. 

Most older patients and those with valve problems have s that are so stubbornly stuck in AF that we can’t get them back into normal rhythm despite our best efforts.  Allowing the AF to continue and simply controlling the rate doesn’t seem as glamorous an approach as rhythm control, but in reality patients can live long and healthy lives with ongoing AF as long the ventricular rate is in a comfortable range ( rate between 50 and 80 at rest and up to 120 or 130 with activity) and the patient is on some type of anti-clotting medication (aspirin or warfarin).  A couple of large research studies suggest that this approach may actually be safer in many people.

Atrial fibrillation is a very complicated issue that we often take for granted because we see it so frequently.  With the right medications AF should be no more than a nuisance issue for the patients who suffer from it and they should be able to continue with full physical activity—even if that includes dancing and clarinet playing.

I was recently reading an article published in the British Journal of Medicine in 1987 on the history of coronary care units.  As you may know, the coronary (or cardiac) care unit (CCU) is the specialized ward of the hospital where patients with cardiac problems are closely monitored and intensively treated.  They are staffed by experienced nurses and monitored around the clock by technicians trained in recognizing rhythm problems.  The concept of the CCU is now so commonplace that it’s hard to imagine a time when it was considered revolutionary.

The CCU was developed in the 1960s in response to a rise in the perceived incidence of coronary artery disease and attacks.  Prior to World War II most of our civilian health casualties were victims of infectious diseases such as tuberculosis and pneumonia.  The recognized problems were principally those involving congenital abnormalities and acquired valvular problems (acute rheumatic fever).  In the entire year of 1959 only six articles in the British Heart Journal centered on coronary artery disease.  People were simply too busy dying from other things to bother themselves with attacks.

The advent of antibiotics, good nutrition, and workplace safety led the way for people to live long enough to develop coronary atherosclerosis.  Unfortunately there wasn’t much anyone could really do about it.  The mainstay therapy for a attack in the 1960s was to simply let the disease runs it’s course and offer bypass surgery only if the patient survived long enough to develop chronic chest pain.  Consider this quote cited in the BJM article by the early CCU advocate Gunnar Biörck:

“There are few diseases in the sphere of internal medicine where the average mortality during four to six weeks hospitalization is over 30%, and if the patients with shock are particularly considered, the figure is more than twice as large.”

Imagine that—30% death rate among attack patients (over 60% if the patient presents with shock)!  It was out of the recognition of this abysmal survival statistic that the concept of the CCU was born. 

As time progressed the medical community began to recognize the importance of aggressive therapies to restore blood flow to the blocked artery.  In the early 1970s the median time from the onset of symptoms to the initiation of therapy (at the time it was mainly nitroglycerin, oxygen and morphine) was greater than 8 hours.  These days the standard of care dictates that we reestablish blood flow within the first 90 minutes of the patient entering the emergency department.  It’s not unusual to have a patient resting in a CCU bed—having already undergone successful placement of a coronary stent—within an hour after presenting with chest pain.

Bear this historical progression in mind as I relate a conversation I recently had with a young man who came to our hospital with a attack.  When I met him in the emergency department he was sweaty and pale, wide-eyed with fear.  His EKG showed abnormalities reflective of a significant attack.  Because he came in during the day we were able to whisk him into the catheterization lab with very little delay and open his occluded artery.

The following morning, as I exhorted him to give up his cigarette habit, he interrupted me to share his thoughts on the need for change in his health habits:

“I don’t need to quit smoking.  This attack thing was a piece of cake. I figure if this happens again I’ll just come in here and you guys will take care of it just like you did yesterday.  By the way, when can I go home?”

I have to admit I couldn’t fault his logic even if his level of understanding was sorely deficient.  Dr. Biörck in the quote above spoke of a “four to six weeks hospitalization” as the norm for patients with attacks.  In the 1950s and 60s the average cardiac patient would lounge around the hospital for weeks with strict instructions to engage in no more exertion than was required to summon the pinafore-clad nurse for his daily constitutional.  The hard-driving business executive laid low by a coronary event would spend months away from the office as he recuperated amid doting family members.  Manual laborers would find themselves permanently disabled and incapable of resuming their usual employment.

Now, as suggested by my impulsive patient, it’s a totally different world.  These days, thanks to advances in coronary reperfusion (angioplasty, stents, bypass surgery), medications (beta-blockers, statins, aspirin), and aggressive early detection and treatment standards, we’ve chopped Dr. Biörck’s 4 to 6 weeks down to a mere 48 hours. 

Of course, this is all a very good thing and we should be nothing short of ecstatic that a attack is no longer the death sentence that it was 50 years ago.  I just wish sometimes that a few of my patients would get a little more spooked over the whole ordeal, that they would recognize this experience as a brief introduction to their own mortality and sincerely commit to the changes they need to make.

A number of years ago, as I was sitting in a college class, I reached down to pick up my backpack off the floor when I felt the sudden onset of intense pain in my left chest.  I sat there, unable to take a breath or even move without excruciating discomfort stabbing through my thorax.  When class ended I rushed over to the student health center and made it clear to the nurse that I was expiring from a attack, or something equally bad.  After some tests they concluded I wasn’t dying and let me go.  My question for them was the same that my patients ask me all the time: So, if it’s not my , what exactly is it?

I obviously recovered, but the episode made me aware of a general rule of thumb I invoke to people who are dissatisfied with the lack of diagnosis for their health ills.

Rule #1: The body will periodically exhibit strange, sometimes miserable, symptoms that eventually go away on their own and never lead to any long-term health problems.

That warm feeling that starts in the left shoulder and creeps up to the right ear, accompanied by tingling in the toes.  The pain in the neck that radiates into the arm whenever you breathe deeply or cough.  The sudden onset of inexplicable sweating followed by palpitations and the profound need to yawn.  A pain below the right breast that worsens when you bend over or laugh.

Frequently these symptoms lead people to seek an answer from me and other doctors.  Since some involve chest symptoms the patients are often put through a battery of tests to assess the health of the .  If they come through the emergency department they will receive an even more vigorous—and expensive—evaluation since their symptoms are perceived as being more acute and possibly life-threatening.  They get an EKG, echocardiogram, stress test, chest CT, lab work—all done in the outside chance that these strange symptoms may represent real disease.

In most cases all the testing comes up normal.  At that point the patient is dismissed from the doctor’s office or ER and told that their is okay.  “That’s great,” says the patient, “but you never told me what’s wrong.”

Rule #2: There are few things as frustrating as experiencing frightening symptoms for which no one can provide a satisfactory diagnosis.

I know the symptoms are real, therefore the problem must be real. What if they missed something?  What if I have a rare but deadly disease that a smarter doctor would have picked up on?  Where’s House MD when I need him?

Another experience from my youth: While I was on my surgical rotation in medical school, I developed an intense pain behind my left knee that gradually worsened to the point that I could no longer walk.  As background, you must know that the surgery training environment is no place for students to complain about ephemeral needs of the frail mortal coil—the expressed desire for sleep, bathroom breaks and food is seen as an explicit declaration of weak surrender.  As I hobbled from room to room on rounds my supervising interns and residents belittled and mocked my complaints as figments of my imagination.  Are you bleeding?  Do you have any exposed bone fragments?  No? Then you’d better get back to work.  One chief resident took enough pity on me to perform a cursory exam on my leg, but promptly declared me healthy.  This went on for several days until I was able to talk a friendly ultrasound technician into scanning my knee.  There, as plain as day, sat lodged in my vein a giant angry thrombus (I had severely injured that leg the previous year in a motorcycle accident).  At that point, armed with evidence of real disease, I was suddenly transformed from a weak medical student meriting nothing more than ridicule to a patient with a real pain deserving real sympathy. 

Within a few days the clot resolved and my aching vanished.  Of course I never forgot the frustration of not knowing.  In fact, the “not knowing” was in many ways even worse than the pain.  At least in this instance I had the satisfaction of ultimately learning the cause of my misery.

When I evaluate patients with odd (we call them “atypical”) symptoms and find no evidence of abnormality, I’m happy to be able to deliver the good news that their s are healthy. Indeed, most patients are relieved to find out that the unusual symptoms they are experiencing are not ominous harbingers of cardiac failure even if I can’t provide a diagnosis for what they have.  Others feel let down that my thorough evaluation has not led to what they want most, which leads me to my final rule:

Rule #3: In modern medicine we’re better at telling you what it isn’t than we are at telling you what it is.

And sometimes you just have to live with this.  Sure, we all know of someone whose diagnosis of some awful problem was delayed because their doctor didn’t look hard enough, but this is the exception rather than the rule.  In most cases our medical system is really quite good at evaluating symptoms and unearthing any potentially damaging diseases if they exist. But bear in mind that the body is full of glitches and quirks that lead to plenty of symptoms but no adverse consequences and may not merit the extensive time, expense and risk of elaborate medical evaluation.

Sometimes just knowing what’s not there has to be enough.