We still don't know how it begins, but suddenly, it moves.
At some point, around the 22nd day of an embryo's life, there will be a flicker, and then another, and another. A cylinder of tissue, which had never moved before, suddenly oscillates. Random bursts of activity occur throughout, each jolt sparked by a puff of ions. They trigger a wave across the surface that gives it the appearance of a pond rippling in the rain. As the embryo grows, the activity will organize and the cylinder will balloon out and fold up into something that looks less like a tube and more like a heart.Though the events leading up to that initial spark are still a mystery, we know that these ripples will mature into strong, organized, dependable strokes—the first of 2 billion that will sustain you over a lifetime.
You now have a heartbeat.
The rhythmic thud of this vital organ is so fundamental that its march has become our most universal measurement. It is our benchmark for time (in a heartbeat), significance (the beating heart of it all), emotion (be still my beating heart), and even being (for as long as my heart beats). It is the stuff of poems, of vows, of anguished cries. It defines our love, our core, and—quite literally—our life. It is the alpha and omega of a human, the beginning and end of love, life, and goodness. A heartbeat: could there be a more meaningful unit?
And yet, while this cadence is our most palpably dependable reality, each one of those beats grants us only a few more ounces of blood, a few more seconds of consciousness, and a few more moments of life. We are dependent upon a process that must occur repeatedly and perfectly our entire lives, with each contraction hailing the successful integration of a myriad of complex processes. You might hope, then, that this mechanism on which life itself depends would be somewhat robust. But while there is some resilience built into the system, it shares with every other intricate machine a fragility endowed by so many moving parts. If the timing, degree, or substance fails even once, life altogether may stop.
Despite its omnipresence, this mechanism is so extensively complex and elusively mysterious that generations of scientists have not been able to answer its most basic questions: How does it start? Why doesn’t it stop? And will it, in the words of Celine Dion, “go on and on”?
Automaticity is the beginning of the answer. Automaticity is the capacity of a cell to spark an electrical impulse all on its own, and in the case of the heart to do so every second for an entire lifetime. Like many other tissues, the heart utilizes electrical signals as a means to communicate between cells and to ignite the molecular mechanisms that cause contraction.
While electricity inside the body looks less like a bolt of lightning and more like a puff of ions, the same principle that applies to batteries and power lines applies to a cell: Separating positively and negatively charged substances creates voltage. In cells, this means shuffling ions like potassium, calcium, sodium, and chloride across the membrane that insulates the interior of the cell from the outside world. And it means keeping the concentrations of these charged molecules different enough to generate a polarity. A sudden movement of those ions means a change in the voltage, which will incite a contraction in the cell. Most cells require a zap from a neighbor, a chemical change in their environment, or some other stimulus to change the voltage. But not automatic cells. Automatic cells can spark all on their own.
Cardiomyocytes—the brawny workhorse cells responsible for the heart’s squeeze—are all born with automaticity. Inside that early cylinder of tissue (inelegantly named your “heart tube”), every young heart cell has the ability to jolt itself and its neighbors into action. It’s an ability that no other muscle cell in the body can boast. But as the embryo grows, most cardiomyocytes lose their automaticity. Instead of all of them sparking at will, a single site near the top of the tube claims dominance over the generation of impulses.
This small clump of cells is formally known as the Sinoatrial Node, but is nicknamed for the vital and unique role that it performs for the rest of your life: it is the pacemaker. In a normal heart, these are the only cells that initiate a beat. The sparks they generate zip down the heart's conduction system to stimulate an organized contraction of your 3 billion cardiomyocytes. They set the pace that coaches your cardiomyocytes to work as a team. And because of that, your heart beats. Your blood moves.
We still don’t fully understand the mechanism behind automaticity. The most popular explanation, the “calcium clock” theory, speculates that pacemaker cells have channels that let positive calcium ions slowly and constantly leak out, preventing them from ever fully coming to rest. While the other cardiomyocytes linger at a negative electric potential until a spark from a neighbor initiates a change in their voltage (and with it, a contraction), the calcium clock theory says that maybe the pacemakers never get to just hunker down in the negative. Instead, like the dripping of a faucet or the cresting of waves, the cells constantly oscillate through a cycle of slowly accumulating a positive charge, reaching a tipping point that activates a sudden voltage change, then crashing back to where they started and beginning anew.
But the process is vulnerable. If the pacemaker cells become sick from any number of agents—a virus, a heart attack, blunt trauma, or even a change in the electrolyte concentrations—that steady tick becomes less reliable, and may even stop. Sometimes this means a complete cardiac arrest as the billions of cardiomyocytes lose their conductor and cannot organize on their own. Sometimes it means a cell elsewhere in the heart will remember the automatic ability it possessed during development and step forward to take over the pacing role. Though this stand-in pacemaker will often provide a less effective or inadequate heartbeat, it can give the body enough time to ride out the disturbance and give doctors enough time to address the disease. This resilience is imperfect, but sometimes it is enough.
While we don't know how that first beat starts, we do know that from the initial ripple of a heart tube your entire survival is contingent upon it never stopping.
“What is your life?” James wrote, “For you are a mist that appears for a little time and then vanishes.” Our entire existence hinges upon that next beat, and we are inextricably dependent on a process that could be terminally disrupted by the glitch of a cell, change in blood chemistry, decrease in oxygen delivery, or even a sharp blow to the chest. “Instead,” James says, “you ought to say, If the Lord wills, we will live.”
We are given only one beat at a time. We are a mist, a little puff of ions.
Lindsay Stokes is an emergency physician living in Albany, New York. She wrote about heart rest (diastole) for The Behemoth’s issue 23.
