When Your Ticker Is Marching to the Beat of a Different Drummer

Doc Gumshoe looks at arrhythmia

By Michael Jorrin, "Doc Gumshoe", November 30, 2016

[ed note: Michael Jorrin is longtime medical writer who has been sharing his thoughts with our readers as “Doc Gumshoe” for several years (he’s not a doctor, I gave him the name). He generally covers medical and health news and sometimes health promotions and hype, but he rarely opines about investments or specific stocks. All of his past commentaries can be seen here]

Is it merely annoying, but essentially trivial? Or does it mean something that needs attention? That depends on what it’s doing, of course.

My motivation to devote a Doc Gumshoe piece to this complicated subject is that I know that it’s common to wonder what the heck that vital organ of ours is doing at any particular moment, and why. We expect our hearts to speed up when we’re exercising – in fact, a lot of exercise machines have built-in heart monitors, so that when we grip the handlebars it tells us our heart rates, and we’re supposed to raise our heart rates by a pretty big margin when we work out. We’re not surprised if we feel our hearts pounding after we race up a flight of stairs. But what if our hearts start beating fast and hard for no obvious reason? We’re concerned, and no wonder.

Most of the time, our hearts tick along without our paying much attention. We don’t have to will our hearts to beat; in fact, we cannot will our hearts to beat. Our hearts are governed by the autonomic nervous system, and the rhythm of our heart beat is controlled by small strips of specialized tissue within the heart called nodes, which emit the signals that trigger the contraction of cardiac tissue. You might think of the autonomic nervous system as your foot on the gas or brake pedals, which control the overall speed of your heart, while the nodes within the heart are the spark plugs that fire each heart beat.

Our two distinct autonomic nervous systems

However, the autonomic nervous system has two subdivisions which operate independently of one another. These are the sympathetic nervous system and the parasympathetic nervous system. The two systems transmit impulses through entirely different networks of nerves. The sympathetic nervous system employs chains of ganglia most of which originate in the vertebral column and run close to the sides of the vertebral column before branching off into the tissues that they innervate. The fibers of the parasympathetic nervous system, in contrast, mostly originate in the brain itself. The impulses of the parasympathetic nervous system do not pass through the vertebral column, as do those of the sympathetic nervous system. About three quarters of all the parasympathetic fibers are in the vagus nerve, which originates in the brain stem and goes all the way to the colon.

Why am I going into all that perhaps unnecessary detail? Because these two nervous systems have quite different effects on a great many of our physiologic functions, including – and especially! – the heart. Going right to the heart of the matter, so to speak: the sympathetic nervous system increases the overall activity of the heart, speeding up the rate and increasing the force of the heart’s contraction. The parasympathetic nervous system has the opposite effect. It slows down heart rate and decreases the force of the contraction. The sympathetic nervous system is like the gas pedal, and the parasympathetic nervous system is the brake.

The effects of those two nervous systems on bodily functions are, in many cases, opposites. The sympathetic nervous system acts on two kinds of receptors, dubbed alpha and beta. Activity at the alpha receptor tends to constrict coronary arteries as well as the pulmonary vasculature. The parasympathetic nervous system, on the other hand, tends to dilate both coronary and pulmonary arteries. The sympathetic nervous system also dilates the bronchi in our lungs, while the parasympathetic nervous system constricts the bronchi. The sympathetic nervous system tends to slow digestive activity, while the parasympathetic nervous system speeds it up.

What do those two kinds of actions imply for us? Under the effects of one of our two autonomic nervous systems, the heart beats faster and with more force, the lungs take in more air, and our digestion slows down. Under the other, the heart slows down, the lungs take in less air, and we dedicate our body’s energy to digesting our food. Sounds like the sympathetic nervous system is in charge when we’re up and about, doing our hunting and gathering and escaping the saber-toothed tiger. Then, when we’re back in the cave having eaten whatever we’ve managed to scrounge, and we stretch out on the nice comfortable cave floor and try to catch a snooze, the parasympathetic nervous system takes over and lets us relax.

Most of the time, the transition between the sympathetic and parasympathetic phases is relatively gradual, but it the effects can, in some cases, manifest with startling rapidity. The sympathetic nervous system has the capacity to double the heart rate within three to five seconds, and to double arterial pressure within about 15 seconds; this is termed the “fight or flight response.” In other words, we don’t have leisure to dawdle when faced by an immediate threat, real or imagined. And, similarly, within a few seconds the parasympathetic nervous system can lower arterial pressure enough to cause fainting. This is termed “vasovagal syncope.” Episodes of vasovagal syncope can be triggered by a fairly wide range of stimuli. For example, some people faint at the sight of blood, or when they taste something that they perceive is rotten or toxic, or when they are overheated, or simply when they have been standing too long.

These two divisions of the autonomic nervous system work by secreting molecules called neurotransmitters – a word concocted simply to describe substances that transmit nervous impulses. The molecule mostly employed by the sympathetic nervous system is norepinephrine, which used to be called adrenalin; thus, the sympathetic stimuli are termed adrenergic. The parasympathetic nervous system uses acetylcholine, so those stimuli are termed cholinergic.

What accounts for the way these two nervous systems alternate?

We observed, a couple of paragraphs back, that the sympathetic nervous system appears to be in charge when we‘re awake and active, and the parasympathetic nervous system more or less takes over to permit us to relax and maybe catch some sleep. These alternating phases of our lives are largely governed by our circadian rhythm, a 24-hour internal clock that all earthly creatures seem to have permanently hard-wired in their systems. (That, by the way, seems to include plants as well as animals.) In mammals, the clock is the suprachiasmatic nucleus (SCN), which is in the hypothalamus, just above the optic chiasm (from the Greek letter Χ, or chi), where the two optic nerves cross over. This clock very closely coincides with the 24-hour period of the earth’s rotation. It can be reset; over a few days a person traveling from Calais, Maine to Calais, France adjusts his or her internal clock so that it more or less lines up with local time. Artificial light delays the transition from sympathetic to parasympathetic nervous system to some degree. When subjects – humans as well as non-humans – are totally deprived of light, the natural circadian rhythm has nonetheless been measured at just a few minutes over 24 hours.

The circadian rhythm affects our physiologic function in several ways. For example, on average, our body temperature reaches a minimum about 5:00 AM, or about two hours before the usual wake-up time, then we start to warm up in preparation for the business of the day. Melatonin, a hormone that induces sleep, is absent from the system during the day, but starts to be secreted, on average, at around 9:00 PM, to get us ready for bed-time. Another hormone whose release is closely related to the circadian rhythm is cortisol, secreted by the pineal gland. It has a fairly wide range of physiologic functions, many of which are related to managing stress. We could say that it is another component of our fight-or-flight response. Cortisol is a day-time hormone; melatonin is a night-time hormone.

All of these have important effects on our heart. But there are quite a few other factors that affect our heart rhythms. Before we go any further down that path, let’s take a look at the cardiac cycle itself – the sequence of heart actions that take care of the job of pushing our blood through the circulatory system to where it needs to go.

What does the cardiac cycle consist of?

At those moments when we’re aware of our heart rhythms, such as when we’re lying in bed in certain positions, or when we have been exerting ourselves more than usual, what we hear and feel is usually a sort of double beat – luh-DUB – the first part quieter and the second part much more emphatic. The first part is the sound produced when the two atrial valves close. As perhaps you remember from biology, blood flows into the left and right atria before being moved along into the ventricles, which are the chambers that push them out into the circulation. The louder part of the double beat is the sound of the contraction of the ventricles.

The atrial valves prevent backflow from the left atrium and the right atrium into the respective veins that fill them. (Atrium is Latin for antechamber; the heart has four chambers – the two atria and the left and right ventricles.) These atrial valves are called the mitral valve and the tricuspid valve. A good part of the blood flow from the atria to the ventricles is passive, but the contraction of the atria, which rather gently push blood into the ventricles, completes the ventricular filling. Then, when the ventricles contract with much greater force, we hear and feel the second part of the heart-beat. (Actually, what we mostly hear when we listen to the heart-beat is the closing of the valves that prevent back-flow from the arteries into the ventricles.) The two parts of the beat are separated by a small fraction of a second. Those two actions, by the way, are not evident in the pulse, which only reflects the ventricular contraction.

So, what are all those parts of our hearts doing? Consider the round trip our blood takes in our bodies, starting from where blood from our veins enters the heart. I’m using that as a starting point in the description of the round trip because the amount of blood entering the heart from the veins is what determines the amount pumped out; more venous return stretches the heart muscle and induces stronger pumping action. This is known as the Frank-Starling mechanism.

Venous blood, as I’m certain you know, has given up its oxygen and is returning to the heart to be replenished. Venous blood from the lower body is forced upward, against gravity, by the pressure of blood entering the venous system, which, in turn, is pushed through the tissue by the pressure of arterial blood. The veins have small valves which permit the blood to flow in one direction, and prevent it from flowing backwards and pooling in our legs. Venous blood from all parts of the body merges into the vena cava and enters the right atrium. The right atrium then contracts and sends the blood into the right ventricle, which contracts much more strongly and pushes the blood into the pulmonary arteries.

From the pulmonary arteries, the blood enters the lungs, and eventually winds up in capillaries in the alveoli, which are minute air bags. Here, a process which is essential to life takes place: carbon dioxide (CO2) from the blood is exchanged for oxygen (O2) from the air. The diffusion process is somewhat random, but a driving force is that the CO2 pressure in the venous blood is higher than the O2 pressure, while in the air in the alveoli, the reverse is true, so the CO2 tends to diffuse across the membrane into the alveoli, and the O2 diffuses across the membrane into the blood. It also helps that our red blood cells (erythrocytes) are avid for O2, and don’t care much for CO2, so when O2 molecules are available they snap them up. All this in aid of keeping us alive and kicking!

Now, after spending a recuperative spell in the lungs, the blood is pushed back into the heart via the pulmonary veins, and into the left atrium. The left atrium contracts, pushing the blood into the left ventricle, which then contracts about a tenth of a second later, forcing the newly oxygenated blood into the aorta for distribution throughout the body.

What makes all this happen?

When we come right down to it, our hearts run on electricity. (So do many other body functions, as it happens, but let’s just stick with the ticker.) Fortunately, we don’t have to be connected to a wall socket or change our batteries periodically. We ourselves generate the electrical impulses that trigger those necessary heart actions.

The source of those electrical impulses are ions in our body fluids, the principal ones being sodium ions (Na+), potassium (K+), and calcium (Ca++). Ions, in case you don’t remember, are atoms whose outer shell of electrons is either absent, as in those aforementioned three ions, or those whose outer shell of electrons has been completed, as in chlorine (Cl-). When the outer shell is absent, the ions have a positive charge, because there are more protons in the nucleus than electrons in the shell; conversely, when the outer shell is filled, the ions have a negative charge, because the electrons outnumber the protons. (I hope the Gumshoe Denizens who remember their chemistry will forgive me for this elementary review, but when we come to a discussion of the drugs that are used to treat cardiac arrhythmias, it will probably be helpful to know something about the ion channels and pumps that these drugs address.)

For our hearts to function properly, the contraction and relaxation of the heart muscles has to be synchronized quite precisely. The heart needs to be relaxed in order to fill, and then there has to be a short delay, about a tenth of a second, between the contraction of the atrial muscle and the contraction of the ventricular muscle. It’s during that delay that the blood from the atria flow into the ventricles – the ventricles need to be relaxed at that point, so that blood can enter. After that delay, the ventricles contract and expel the blood into the aorta and the pulmonary arteries. The contraction of the atrial muscles takes about two tenths of a second, and of the ventricular muscle, about three tenths of a second.

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All of these contractions and relaxations are governed by the entrance of the aforementioned ions through ion channels and ion pumps. The changes in electric potential of the cardiac muscles are detected by means of an electrocardiogram (EKG). (Electrocardiograms are abbreviated that way because the procedure was developed by a Dutch physiologist, Willem Einthoven, in 1893, and he spelled it with a “k.”) EKGs record changes in electric potential at different points in the heart muscle, and give your examining physician a pretty good idea of what’s going on in your ticker. Here’s a representation of a normal EKG tracing:

EKG Tracing

Where the line begins, at the left of the picture, and ends at the right, the heart muscles are in a resting state. In this state, they have a small electric charge; this is referred to as a polarized state. The P wave in the tracing is evidence of a small electric discharge, or depolarization, which causes the contraction of the atria. There is a little dip towards point Q, initiating repolarization, caused by the rapid opening of the sodium channels, which permit a very rapid entry of sodium ions into the cardiac muscle cells. Repolarization – a sharp increase in the electric charge – peaks at point R in the electrocardiogram, and it is followed by an equally sharp depolarization, or discharge of electric potential. The discharge, represented by the steep decline from point R to point S, is what causes the contraction of the ventricles and the expulsion of blood into the arterial system.

The QRS complex on the EKG tracing represents systole – the term you know from systolic blood pressure. The more gradual increase in electric potential (repolarization) represented by the ST segment and the U wave takes place during diastole, when the heart muscle is relaxed. This phase of the cardiac cycle is when the cardiac muscle cells recover their positive electric charge, in preparation for the next discharge, which powers the contraction.

(When the ST segment on the EKG is elevated, that’s definitely a bad sign, characterizing one kind of heart attack, or myocardial infarction – an ST-elevation MI, or STEMI. The underlying cause of this change in the EKG tracing is a degree of ischemia – i.e., oxygen deprivation – in some of the cardiac muscle cells. What happens is that the oxygen shortage hampers the activity of the ion pump that brings sodium ions into the heart muscle cells and essentially recharges the batteries for the next contraction. Decreased repolarization leads to decreased pumping action, which leads to decreased oxygen perfusion and increased ischemia. In other words, a heart attack. That, however, is far from a cardiac arrhythmia. )

Here’s another representation of the cardiac cycle. This is not an EKG tracing, but a simplified representation of the changes in electric potential.

Electric Potential

Let’s start with the 4 on the left side of the diagram. This represents the resting state of the cardiac cycle. The 0 represents the rapid polarization of heart tissue, which corresponds with the sharp upward slope of the QRS complex on the EKG tracing. Each of these segments on the diagram is linked to a specific ion channel or ion pump, and deviations from normal functioning in those channels or pumps are associated with one or more particular classes of cardiac arrhythmias.

That rapid increase in polarization is due to the action of the fast sodium channels, which permits the rapid entry of sodium ions into myocardial tissue and a sharp rise in voltage, reaching a maximum at point 1. When I say “fast sodium channels,” I mean fast. Those channels stay open only a few ten-thousands of a second. After the electric potential reaches a peak at point 1, there is a plateau, designated 2 in our diagram. This is when the slow calcium-sodium channels open. These stay open for a few tenths of a second, during which there is a period of depolarization. During this plateau, the contraction of the heart muscle is greatly enhanced by the calcium ions. Finally, the potassium channels open (3), allowing potassium ions to diffuse from the cardiac fibers, returning the potential to the resting state, (4).

I hope this is not more unnecessary detail? But I want to give you an idea of the great number of disparate factors that can contribute to cardiac arrhythmia – or, rather, of all the factors that have to work in perfect synch to keep the heart ticking along in a healthy rhythm. To sum up briefly, there are those two separate divisions of the autonomic nervous system and the neurotransmitters that they deploy either to ramp up or calm down cardiac activity. But then there are a number of different little sparkplugs in the heart itself – the sinoatrial node, the atrioventricular node, and various bundles of fibers that conduct electrical impulses through the cardiac muscle. The speed at which those electrical impulses travel is a vital part of maintaining heart rhythm – the dilation and contraction of the atria and the ventricles has to be precisely coordinated. And then there are those ions, carrying electric charges. All these elements – neurotransmitters, the automaticity of the various cardiac fibers, the ions themselves – have to be in pretty good running order to keep the heart ticking along regularly.

Cardiac arrhythmias and what makes them happen

Let’s now consider the types of heart rhythm aberrations and their likely causes.

Tachycardia. When the heart rate exceeds 100 beats per minute (bpm) under normal conditions, this is called tachycardia. Most people can get their heart rate over that mark through vigorous exercise, but a heart rate over 100 bpm during normal activity or at rest is abnormal. Among the usual causes of tachycardia is fever. The heart rate increases about 10 bpm for every degree Fahrenheit over the normal 98.6⁰ mark; translated to the Celsius scale, that’s 18 bpm for every degree over the 37.6⁰ mark. The rate of increase tapers off after 105⁰ F (41⁰ C) because the cardiac tissues begin to weaken at that point. The underlying cause is that the increase in temperature speeds the rate at which the sinoatrial node emits the electrical impulses that control the sequence of heart contractions.

Heart rate also increases in response to events that shock they system, such as blood loss; the heart speeds up the pumping action to keep the body adequately supplied with oxygen. Any external threat that triggers the response of the sympathetic nervous system will increase the heart rate through the activity of the neurotransmitter norepinephrine; internal psychological stress may have the same effect. Conditions that weaken cardiac tissue, such as congestive heart failure, also result in tachycardia. This is essentially a homeostatic mechanism – if the heart is pumping a smaller volume of blood with each beat, then, in order to maintain adequate flow, it needs to pump more often.

Bradycardia. This term describes a heart rate less than 60 bpm. In athletes and individuals with exceptionally strong hearts that pump out greater volume of blood with each beat, requiring less frequent contractions to maintain optimum perfusion, a slow heart rate is normal. However, events or stimuli that trigger a response by the parasympathetic nervous system can result in release of acetylcholine by the vagus nerve, slowing the heart rate. For example, mild external pressure on the necks of some persons with carotid artery atherosclerosis can cause the heart to slow markedly, and even to stop beating totally for a good part of a minute.

Arrhythmias due to blocks in electric conduction. The impulse that starts off the cardiac cycle originates in that bit of fiber called the sinoatrial (SA) node. Blockage of this impulse takes place rarely, and when it does occur, there an impulse is usually emitted by the atriovenricular (AV) node, which delays but does not alter the QRS complex, that being the contraction of the ventricles – in other words, the heartbeat.

The AV node, on the other hand, is the site of several types of cardiac arrhythmias, which can be the result of factors including lack of oxygen, and also compression of the AV node by scar tissue, or inflammation. Any of these can delay or block conduction from the atria to the ventricles. These arrhythmias can result in a delay in the contraction of the ventricle (a first-degree block), but also in erratic heartbeat patterns. In a second degree block, the atria may contract twice for each ventricular contraction, and sometimes three times for each ventricular contraction. In a third degree block, the relationship between atrial and ventricular contraction disappears; the atria may contract as fast as 100 times per minute while the ventricles contract 40 times per minute, with no coordination between the contractions.

When a person is experiencing tachycardia, with a heart rate well above 100 bpm, sometimes it’s impossible for parts of the heart muscle to recover from a relaxed phase called the refractory period, such that those parts do not contract in synch with the heart as a whole.

Premature contractions. Electrical impulses can be generated from other places in the heart other than nodes that keep the whole organ marching to the same beat. These are called ectopic foci, and they can trigger premature contractions that throw off the efficient succession of atrial and ventricular filling and contraction. Usual causes of ectopic impulses are small areas of ischemia or calcification and toxic irritation, such as from drugs, caffeine, or nicotine. Premature contractions of the atria can occur in persons whose hearts are strong and healthy.

Atrial fibrillation. This is one of the more common arrhythmias, which can occur as a fairly consistent condition or only on occasion. It can affect persons with no underlying diseases or conditions, and may be caused by emotional stress, acute alcoholic intoxication, or following exercise or surgery. It can also affect patients with heart or lung disease, especially rheumatic heart disease, hypertensive heart disease, or mitral valve disease. What happens in atrial fib is that the atria do not fill and contract properly to move blood into the ventricles. Instead, different sections of the atria contract in no fixed order, resulting in a less efficient pumping sequence.

In most cases, atrial fib is a relatively benign condition, but there are some consequences of concern. Atrial fib can reduce overall cardiac output, causing fatigue. Also, when episodes of atrial fib are over, there can be a marked pause before the next contraction, which in some cases can result in syncope, or fainting. But by far the most common concern is that the inefficiency of the atrial contraction leaves blood pooling in the atria, possibly resulting in clot formation. What could happen, and what your doctor will try to prevent, is that a clot forms in one of the atria and then travels to a spot in your body where it can do real harm – the lungs, the brain, the coronary arteries. Thus, patients with atrial fib are usually given anti-clotting medications, such as aspirin or warfarin.

Because the atria are separated from the ventricles by a layer of fibrous tissue, atrial fib does not transmit to the ventricles to cause fibrillation.

Ventricular fibrillation. This is, by any measure, the single most serious cardiac arrhythmia, which, if not rapidly resolved, is fatal within a few minutes. Serious, sober writers of medical textbooks speak of electrical impulses in the heart going berserk within the cardiac muscle mass. In ventricular fib, some sections of the ventricular muscle are contracting while others are relaxing. The ventricles stop pumping blood, and within a few seconds a person loses consciousness because of lack of blood to the brain. Death follows in a few minutes, unless the fibrillation is reversed. Ventricular fib is probably the single most common cause of fatal cardiac arrest; about three-quarters of cardiac arrest incidents recorded while patients were wearing Holter monitors occurred during episodes of ventricular fibrillation.

Ventricular fib frequently follows ventricular paroxysmal tachycardia. This is a serious condition mostly seen in persons who have extensive ischemic damage in the ventricles. (Paroxysmal is the term used to specify that the episodes of tachycardia are sudden and occasional, and that it is not a chronic condition.)

One cause of ventricular fib is electric shock from a 60 cycle alternating current, which is our usual house current. Other than external electric shock, the most common cause of ventricular fib is ischemia of the heart muscle or of the specialized cardiac conducting system. The particular malfunction that occurs in ventricular fib is that the electric impulses that drive the QRS complex, or systole, do not quit after they have travelled through the cardiac muscle tissue. In the normal cardiac cycle, the cardiac tissue is in a refractory state after the contraction and cannot transmit another impulse. But the perpetuation of the impulse can take place for several reasons. If the heart is unusually dilated, the path the electric impulse takes is longer, permitting the muscle tissue to recover from the refractory state. In that case, the electric impulse keeps travelling, and causing repeated contractions in that part of the tissue that are not synchronized with the ventricle as a whole. Slower electric impulses and shorter refractory periods can have the same effect. A number of external factors can affect these mechanisms, including some drugs and elevated blood potassium levels.

The most effective intervention for ventricular fibrillation is external electric shock defibrillation. Electrodes externally applied to the two sides of the heart can deliver a shock that stops all internal electric conduction by throwing all the cardiac muscle tissue into the refractory phase, so that none of the internal electric impulses can travel through the tissue. The heart stops completely for a few seconds, and then the normal sinus rhythm can return. Defibrillators, such as those that are carried by emergency medical personnel, deliver a single shock of several thousand volts for about one thousands of a second. If defibrillation takes place very quickly after the onset of ventricular fibrillation, the heart will usually return to its normal rhythm. But if ventricular fib has been going on for much longer than one minute, the heart may be too weak from lack of oxygen to resume beating on its own, in which case cardiopulmonary resuscitation will be required.

Where do we go from here?

My main effort in this perhaps overlong post has been to try to give the curious among you an idea of the many factors that affect the way our hearts function. Yes, it is exceedingly complicated! From my perspective, the bottom line is that in many cases – perhaps even most – the discomfort and anxiety from occasional skipped beats or extra beats or episodes of fast beats does not add up to a life-threatening condition. However, there are conditions that are genuinely life-threatening, and it takes an expert to distinguish the arrhythmias that you can live with from the ones that could lead to something worse.

I have not mentioned many other types of arrhythmias, for instance, torsade de pointes, which is frequently the result of drug interactions. Nor have I even touched on the many, many drugs that are used to manage arrhythmias. The choice of antiarrhythmic drugs depends on very precise analysis of EKG patterns; these can suggest which of the ion channels and receptors the drug needs to address in order to be effective.

So it looks like I’ll be back with more on this topic! Thanks for your comments, and best to all! Michael Jorrin (aka Doc Gumshoe)