For those articles where there’s such overwhelming study findings that I feel comfortable presenting information as fact, I won’t put a “byline” picture at the top of the article.

You’ll see there’s a byline picture on this article. And with that byline I’m hoping you’ll let me express some frustration with the medical community. Palpitations, PVCs, PACs and other various arrhythmia are suffered by a huge portion of the population. Huge. And there are thousands upon thousands of pages on the web of women suffering through arrhythmia that seems to coincide with their cycles, and nobody’s able to provide them with a straight answer for why it happens.

The medical community just collectively pats women on the head, says “everything will be ok,” then sends them on their way. And nobody’s ever made to understand WHY this is happening. I even read an article by the female director of women’s cardiovascular health at University of Pennsylvania. ^[1] I mean, you can’t even dream up a better resource, right? She provided responses no better than you’d find at Yahoo! Answers.

Why is there no science on this topic? Why no studies? The results of those studies and presenting the science in lay terms would probably add hundreds of thousands of productive hours back into the lives of women across the world, instead of having them take time away from career or family, either at a doctor’s office or just withdrawing from the world for fear of dying of cardiac arrest.

That seems worth the effort and expense of a single study and comprehensive, scientific breakdown.

But we don’t have that. So I’ve gone over, under and through the web to find and piece together as much information about female menstrual cycles and causes for arrhythmia. The results of that research I present here. I hope it can give you some degree of peace.

Before I get too deep into how a woman’s menstrual cycle might affect heart rhythm, I think it’d be worthwhile to have a refresher on how it is, exactly, that a heart is able to beat. Just like every other muscle cell in your body (arms, legs), each cell in your heart holds a tiny little electrochemical charge (think of your car battery and the sloshy fluids inside it - same sort of thing). When that cell is ready to discharge, it becomes permeable by other electrolytes (like sodium ions (Na+)). When those electrolytes rush into the newly permeable cells, it starts an electrochemical chain reaction, moving from cell to cell to cell, resulting in the coordinated contraction of the muscles in your heart, squeezing to pump blood to the rest of your body.

That’s how your heart works. And I feel more than a little ridiculous, being a man, about to explain how the menstrual cycle works. But here I am, doing it anyway. At least a part of it.

As the female body performs it’s monthly task of preparing for pregnancy, making conditions optimal for creating a baby, then purging all evidence of that preparation (only to do it all over again the next month), hormones are coursing through a woman’s veins. During the first phase (of two) in the cycle, the follicular phase, the level of estrogen in the body is increased up until the point that it peaks, at ovulation. Post-ovulation, the amount of estrogen in the body decreases. Part of the reason that occurs is because the estrogen did it’s job: it initiated ovulation. The other part of the reason estrogen levels decrease is because (as is hypothesized by some in the medical profession), progesterone levels in the body increase just prior to ovulation, peaking in about the middle of the luteal phase (second phase) of the menstrual cycle. The theory is this: progesterone aids the body in metabolizing excess estrogen or as an antagonist to it’s production ^[2], so as progesterone levels increase, estrogen levels decrease. (I should note that the graphic here, courtesy of Wikipedia, seems to counterindicate that relationship between progesterone and estrogen levels. But for this discussion about heart rhythm, it isn’t relevant, so I won’t do anything beyond mentioning that I question the validity of the hypothesis about metabolizing estrogen with progesterone.)

And every month, this hormonal battle is waged within a woman’s body.

So. How does this relate to heart rhythm and palpitations? It wasn’t until I found a power point presentation on the American Heart Association’s website discussing the use of progesterone as a possible treatment for Long QT Syndrome (LQTS) that I was able to find other data points and start putting a few pieces together.^[3]

According to Cardiovascular Research, a magazine of the European Society of Cardiology, women have a slightly longer QT interval than men when corrected for heart rate (QTc), which is to say that women also have a slightly higher heart rate than men.^[4]

The article stated that for women at risk of suffering an episode of torsades de pointes (a type of extremely dangerous ventricular tachycardia), those episodes almost never happened during the luteal phase of the menstrual cycle, suggesting a tie between progesterone and the rate of repolarization of ventricular heart cells. As a refresher, if ventricle cells are slow to repolarize (regain their electrical charge), they may not be ready to initiate muscle contraction when needed, meaning blood pushed into them from the atria doesn’t get pushed from the ventricles into the body in a timely fashion. Also, it can result in ventricle cells being asked to depolarize (begin the process of contraction) right at the moment they are repolarizing - this is what can initiate torsades de pointes, which can turn into ventricular fibrillation, which is deadly without medical intervention.

But I don’t mention all that to scare you. Torsades is extremely rare, and is more common in heart attack survivors than the general population (because of the electrical problems associated with the tissue death that accompanies a heart attack), and also tends to be hereditary. I only mention it to show that the effect of progesterone on the cardiac system of the female body has been investigated.

In other studies there was indication that progesterone enhanced action potential adaptation during rapid heart rates.^[3][5] In English? A woman’s tiny batteries in each heart muscle cell recharged faster in the presence of progesterone. Again, the study was relative to the problems associated with Long QT Syndrome, something that in all likelihood most all readers of this article do NOT have.

But the relevant part in my mind is that repolarization happened more quickly, making each of those heart cells ready to discharge and initiate a contraction earlier. If some of those cells are already predisposed to discharging early due to having a lower electrochemical threshold (the permeability I mentioned earlier), then those cells are just sitting there, all charged up, ready to set off a PVC, and they have an itchy trigger finger.

The result? A woman potentially getting more PVCs and palpitations during certain parts of her monthly cycle, every cycle. And for women who are taking birth control pills, this is likely to be exaggerated due to the increase in hormone levels from ingesting the pills.

Because there can literally be a hundred different reasons why a person experiences skips and flutters, the monthly increase in progesterone might not always be enough to cause skipped heartbeats. Maybe that month the person is under less stress and there’s been a lower quantity of catecholemines (a stress hormone) flowing through the body. Or other electrolytes are in better balance. Or she’s gotten enough sleep. Really, the reasons are too numerous to list.

But the doctors were right. Getting skips and bumps in your heart rhythm during the same part of your cycle is not an indication of anything sinister. In fact, it’s a sign that your reproductive system is working the way it’s supposed to, that progesterone is being produced, and that it’s making your heart a little jumpy. That’s all.

References

Whenever news of a professional athlete dying from heart-related causes hits the breakfast tables and living rooms of people living with various benign or more serious heart conditions, it gives them pause.  And sometimes worry.

If someone that young can die from cardiac arrest, why can’t you?

He was in fantastic physical health and he still died.  You’re in terrible shape.  Who’s to say you won’t drop tomorrow from cardiac arrest, if someone so healthy could?

First, let’s look at a common sense analysis.  NFL offensive and defensive lineman are huge.  Gaines Adams was a defensive end, and while men playing that position are much larger than any normal human, they aren’t usually the largest men on the field.   That distinction is held by the men playing on the interior of the defensive line and all of the offensive line, with most players in those positions weighing in excess of 300 pounds, some as much as 400 pounds - all packed onto frames in the 6′2″ - 6′6″ range.

Any everyday person with a body that large is putting their heart under tremendous stress.   Pushing blood through the miles of fat-clogged veins under higher than normal pressures makes the heart, a muscle like any other, grow in size.  Unfortunately, hearts almost never grow outward, or if they do, it’s a very small percentage of the total growth.  Usually the muscle mass gained in an enlarged heart is gained inside the chambers of the heart, taking up the space and reducing the volume of blood that can be pumped with each contraction of the heart.

This starts a downward spiral where the heart must work even harder to pump sufficient blood volume throughout the body which makes the heart gain even more muscle mass.  And in the bodies of NFL lineman, the stress is that much greater, as they are capable of and do perform physical feats that many amateur athletes 100 pounds lighter can’t perform.  The vicious cycle of enlargement of the heart, if not caught, stopped and reversed, results in what happened this morning.

But let’s even set aside the common sense and anecdotes.  Let’s look at some facts about the life expectancies of NFL players and lineman in particular.

A 1994 study of 7,000 former players by the National Institute of Occupational Safety and Health found linemen had a 52 percent greater risk of dying from heart disease than the general population. While U.S. life expectancy is well over 70 years years, this ‘94 study suggests the average for NFL players is 55.  And worst of all, 52 for linemen.

The stories and statistics abound.

From ESPN: Heavy NFL players twice as likely to die before 50

From the St. Petersburg Times: A huge problem - Strength isn’t enough: NFL linemen have to be so big, their health may be at risk

From MSNBC: Retired NFL players focus of health push - Stars of the past feeling effects of tackle-filled careers

From Time: The NFL’s Huge Linemen: Healthier Than You Think?

While the death of any young person in the prime of their lives is tragic, in this particular case, unless you’re 6′5″ and weigh 290 pounds, there’s no reason the sadness over the loss of a player on your favorite team needs to become anxiety that you’ll suffer the same fate.  The genetics of these NFL linemen coupled with the terrible health habits they learned throughout high school, college and the pros, all in the name of being massive and able to throw their weight around, are the reasons for their early demise - NOT a benign rhythm gone bad.

I’ve experienced PVCs for at least the last decade. During that time I’ve spent months having 5-10,000 PVC per day, every single day. I’ve also spent months where I’ve lost count of the number of days between feeling even a single PVC. I can only estimate that my heart has kicked out millions of PVCs since I first experienced them. I mention all this to explain that when it comes to premature heart contractions, I’ve built up a substantial body of work. I know what they feel like, where I feel them and how strong they are.

But in December 2008 I began having what felt like small explosions in my chest. They felt like they originated in the same place as my PVCs - my heart. Only it felt like someone had placed a firecracker inside of my chest and lit it.

And as quickly as one would appear, it would disappear, and leave me wondering what the hell had just happened, and if I should be calling a doctor.

As many of you do, I Googled. And I Googled. I was fortunate in that I was able to capture one of these “explosions” during an event monitoring, which helped to put my mind at ease but also presented me with more questions that needed answers.

Because I’m not a doctor and I don’t have access to text and other professionals in the field, I had to reach my own conclusion: I was having esophageal spasms.

If you look at the ecg tracing above from my event monitoring in early 2009, you’ll see several negative spikes in the highlighted green area.  You’ll also notice that the large positive spikes, the QRS complexes of my heartbeat, are unchanged during this time.  No difference in heart rate, no change QRS adjustments because of an early beat.

Clearly this ECG is showing an electrochemical discharge, but not one inside the chambers of my heart, because heart rate was completely unaffected.

Through the process of elimination and a careful review of my symptoms, it appears that esophageal spasms are the most likely cause of these explosion sensations in my chest, which is great news because while they can stop me in my tracks, they aren’t dangerous.

So if you’re feeling something similar, you may be experiencing the same thing as I was, which is anything but the end of the world and the end of you.

I did find one reference study worth noting, but it involved people already suffering from some form of angina and/or coronary artery disease.  So bear that in mind when you read about the study.

-Jeff

You’ve called your doctor and he’s run any number of tests, from as little as a stethoscope to your chest to as much as an ECG, Holter monitor, event monitor or echocardiogram.

And then he prescribes an SSRI for you, which sounds fine at the time because what do you know about acronyms and what medications treat which conditions. But you like to know what you’re being told to take and how it might affect you, so you Google SSRI.

Hmm. Serotonin reuptake inhibitor? That’s a drug for the brain, right? And it’s an antidepressant. The doctor thinks I’m depressed and that’s what’s causing my arrhythmia?

Now you feel worse than you did before you saw the doctor. Not only is he not addressing the cardiac issues, he’s trying to pigeon-hole you as a simple worry-wart and mollify you by filling you full of “happy” pills.

Before you go into a tailspin, Googling all the terrible things that might (but in all likelihood will never) happen to you by leaving your primary symptom untreated, please read on.

It’s true that SSRIs like Zoloft and Prozac are antidepressants. They’re also used as anti-anxiety medication, too, and for those of us who suffer from benign heart rhythm abnormalities, they can be a godsend.

What Do SSRIs Do? Do They Work?

Without getting overly technical, an SSRI is designed to help stimulate synaptic cells in the brain by keeping the neurotransmitter serotonin at the surface of a synaptic receiving cell for a longer period of time. The result of this stimulation, as you might expect from a drug called an antidepressant, is to make a person less depressed, or put another way, more happy. Less anxious.

And if stress is a concomitant factor in your arrhythmia, this may be exactly the thing you need to wrangle control of your health and well being back from the brink.

Stress can be a cagey animal. It hits some people long before an upcoming, worrisome event. It hits others during the event. Still others it affects after the event. For some the stress grows little by little, every single day. Just like an animal you feed each day, it grows a bit here and there, but it happens so slowly that you never realize how big it’s become until it’s snarling in your face, demanding all of your attention. And throwing your formerly metronomic heart into fits and quivers.

SSRIs can help you fight this stress animal by keeping your worry and anxiety at manageable levels and maybe even allow your mind to return to a time when your life was simpler. When the weight of the world wasn’t on your shoulders, worrying about your job, mortgage, kids, parents, neighbors, coworkers, spouse and all the rest.

Because SSRIs affect brain chemistry slowly, it takes awhile for them to take full affect. Pharmacists will tell you it’ll take 2-3 weeks and even after that initial “break-in” period you may continue to improve over the following months. And once the stress is wiped away, often times so are the palpitations, skips and spurts.

So don’t dismiss your doctor as an uncaring and self-absorbed just yet. Give your SSRI a few weeks before you decide. It may be just the thing you need to treat your arrhythmia.

Being able to feel a person’s pulse means that blood is actually being pumped; when you place your fingers on the inside of your wrist, you’re feeling the rush of blood being pushed through the artery by your heart’s contraction.

So in the case of pulseless electrical activity, depolarization and repolarization of heart tissue is occuring but blood isn’t being pumped.

How does this happen? Most often it occurs when there has been a significant loss of fluid volume in the body, to the point that such small amounts of blood are being pumped with each contraction as to not be able to detect the pulsing of the blood through arteries and veins. Called hypovolemia, the loss of fluid volume could be from blood loss due to an injury, or surgery, severe dehydration or the use of diuretics (causing excessive urination).

Other causes for PEA include:

Hypoxia
Hydrogen ion (acidosis)
Hypokalemia/hyperkalemia
Hypoglycemia
Hypothermia
Toxins
Tamponade, cardiac
Tension Pneumothorax
Thrombosis (coronary or pulmonary)
Trauma

If a person remains in a state of asystole for 15 minutes or more, they are most likely brain dead, and in a study of 1,635 asystolic patients, only 10% survived long enough to be admitted to the hospital and only 2% survived long enough to be discharged from the hospital.^[1] Asystole is more often used as a confirmation of death than as an arrhythmia to be treated.

References

Heart Failure doesn’t mean the heart stops.  It just means the heart isn’t able to keep up with the demands your body is placing on it.  This inability to keep up can be caused by several things:

• High blood pressure: if your heart has had to work against the added pressure in your arteries and veins for years, your heart can become weakened and unable to pump blood throughout your body as it used to.
• Narrowed arteries: if your arteries have narrowed due to plaque buildup or some other reason, they may nto be capable of carrying the full volume of blood your body’s organs need.  Your heart has to pump more often, which over time makes it weaker.
• Previous heart attack:  if you had a previous heart attack there may be dead muscle tissue in your heart, making it less efficient than it was prior to the heart attack.
• Heart defects: hearts that are malformed at birth can cause congestive heart failure.
• Infections of the heart and heart valves.
• Cardiomyopathy:  disease of the heart muscle itself.

The reason this condition is called “congestive” is because it’s much like an arterial roadway at rush hour.  Because the heart isn’t pushing out as much blood as wants to come in, blood gets backed up, like a congested highway.  One of the symptoms of congestive heart failure is swelling in the lower extremities – that’s blood getting backed up in arterial and venous highways.  Swelling can happen in other places, too.

Another common symptom is shortness of breath (sob), especially during physical activity.  Your body is burning through it’s store of oxygen to do the work you’re asking it to do (such as running on a treadmill), but your heart can’t replace those stores fast enough, putting you in a state of oxygen deficit.  This makes you tired, you fatigue easily and you struggle to fill your lungs with as much air as can fit.

The good news is there are many ways to treat CHF.  Treatment usually includes modifying what you do at home, such as changing your food intake and losing weight if you’re overweight.  There are also medications that can make your heart’s job easier, by dilating (making bigger, expanding) blood vessels, reducing the pressure required to pump blood through your body.  They can also improve the pumping function of your heart muscle.

In a worst-case scenario, if congestive heart failure gets so bad that medications and lifestyle changes don’t help, a heart transplant can be considered.

AED - automated external defibrillator

A-fib - atrial fibrillation

ARVD - arrhythmogenic right ventricular dysplasia

AV node - atrioventricular node

AVNRT - atrioventricular nodal reentrant tachycardia

AVRT - atrioventricular reentrant tachycardia or atrioventricular reciprocating tachycardia

BID - “bis in die” (Latin), which means twice per day

CABG - coronary artery bypass graft surgery

CAD – coronary artery disease

CHF – congestive heart failure

COPD – chronic obstructive pulmonary disease

CT – computed tomography

ECG – electrocardiogram (used interchangeably with EKG)

EF – ejection fraction

EKG – electrocardiogram (used interchangeably with ECG)

EP - electrophysiologist - a specialty of cardiology

EP Study - a study of the electrical systems of the heart, performed by an electrophysiologist

FP – family practice or family practitioner

GP – general practice or general practitioner

HCM – hypertrophic cardiomyopathy

ICD – implantable cardioverter defibrillator

IST – inappropriate sinus tachycardia

LBBB – left bundle branch block

LQTS – long QT syndrome

LVOT – left ventricular outflow tract

MI – myocardial infarction (heart attack)

MRI – magnetic resonance imaging

MVP – mitral valve prolapse

NSR – normal sinus rhythm

NSVT – non-sustained ventricular tachycardia

PAC – premature atrial contraction

PAT – paroxysmal atrial tachycardia

PCP – primary care physician

PEA - pulseless electrical activity

PJC – premature junctional contraction

PNC – premature nodal contraction

POTS – postural orthostatic tachycardia syndrome

PSVT – paroxysmal supraventricular tachycardia

PVC – premature ventricular contraction

QD - “quaque die” (Latin), once a day

QID - “quater in die” (Latin), four times a day

RFA – radiofrequency ablation

RBBB – right bundle branch block

RVOT – right ventricular outflow tract

SA node – sinoatrial node

SCA – sudden cardiac arrest

SCD – sudden cardiac death

SOB – shortness of breath

SSRI – selective serotonin reuptake inhibitors

SVT – supraventricular tachycardia

TEE – transesophageal echocardiogram

TID - “ter in die” (Latin), three times a day

V-fib – ventricular fibrillation

V-tach – ventricular tachycardia

WPW - Wolff-Parkinson-White syndrome

Explaining it more technically, the sinoatrial node (SA node) in your heart (located at the top of your right atrium) is a special cluster of heart cells called “pacemaker cells.”  These cells have electrochemical properties that allow them build a store of electrical charge and then release that electrical charge, all in regular intervals.  When this wave of electricity reaches the other cells in your heart they discharge as well, passing the electrical charge on to the next cells, generating a coordinated contraction.  What’s special about the SA node cells is that they don’t need a signal from a cell further up the line to tell them to discharge, and their threshold for releasing their electrical charge (called depolarization) is lower than that of other heart cells, making it that much easier for them to lead the other cells into contractions.

Put another way, if a sports stadium were a heart, those over-exuberant guys in section 14B would be the sinoatrial node, starting “The Wave” and getting all the other cells in the stadium to stand up and wave their arms at just the right time.

Nobody told them to do it.  They just did it spontaneously.  Automatically.  And everyone else just followed along.  Maybe it was the 320 drinks that section consumed during the first half that lowered their threshold for depolarization, enhancing their automaticity (for doing the wave).

Arrhythmia problems arise when the automaticity of the SA node fails to be regular, causing arrhythmia.  Automaticity can be affected by electrolyte levels, certain medications, forms of heart disease or changes in autonomic nervous system tone.

When your blood pressure is being taken, your diastolic pressure (the second number) is the measure of the pressure in your arteries just before the next ventricular contraction, when the pressure is at it’s lowest.