Shocked

by David Casarett

  One of the prize exhibits here is—improbably—a large fiberglass heart. At about two stories tall, it’s scaled to fit inside a 220-foot man. That’s large enough to walk through, which many people seem to be doing with the giddy enthusiasm one might expect while about to do something otherwise considered impossible.

  Even from across the room, the enormous red-and-purple blob is immediately and unmistakably recognizable as the muscle that keeps us alive. A heart has four chambers that pass blood from the right side of the heart to the left. Blood flows in through one small chamber, the right atrium, which pushes it into a larger, more muscular chamber, the right ventricle. From there the blood goes through vessels in the lungs and then through the left atrium, left ventricle, and out into the aorta. In this fiberglass model, the larger ventricles are clearly visible near the top, as is the massive vein (the vena cava) that wraps around its right side like a pillow. Helpfully color-coded, the structure offers viewers a cheat sheet to figure out what’s what. The blue-painted vessels coming back from the body contain blood that is deoxygenated and full of carbon dioxide, and the red-painted vessels denote blood that has been stripped of carbon dioxide in the lungs, and then filled with oxygen. And the centerpiece of this display is the bright red aorta, carrying oxygenated blood out to the brain and all of the other gigantic organs of that 220-foot-tall man.

  Alas, today I don’t have this magnificent view all to myself. I’m accompanied, it seems, by every second-grader currently enrolled in the Philadelphia school system. The resulting din is overwhelming. On the bright side, the packed masses provide a vivid sense of what it’s like to be a red blood cell making your way slowly—painfully slowly—through a heart. Imagine a river of red blood cells each approximately three feet tall, all wearing knapsacks and carrying clipboards, and screaming at the top of their lungs. Which is exactly what these red blood cell reenactors around me are doing.

  Tuning them out, at least temporarily, it’s possible to get a unique glimpse of what the inside of this fancy machine looks like. And it’s at this point I realize with some relief that this refresher course won’t take too long. Because however important the heart may be, its mechanics are designed at a second-grade level.

  If your heart were a car, it would be that old 1978 MG convertible that your father kept, rusting, in the back of the garage. Like that old machine, the heart has only a few moving parts. And their actions are motivated by a simple logic, and ruled by even simpler laws of physics.

  Just as those old MGs were tinkerers’ cars, the heart is a tinkerer’s organ. Its collection of muscle and nerves and blood vessels is as susceptible to modification and improvement as the engine of a 1978 MG is. And not just susceptible—it’s almost as if the heart is asking to be patched up, tweaked, and improved. You can almost imagine a cardiac surgeon looking down at an open chest in the same way that a weekend mechanic might peer down into an MG’s open hood, thinking pretty much the same thing: “Hey, I bet if I upgraded that wiring, and cleaned out that hose, this baby would run a lot smoother.” And indeed, that seems to be the philosophy of two centuries of doctors and scientists who have been trying to patch and fix and improve the heart, as we’ll see.

  The heart is mostly just a muscle. Inside the giant fiberglass heart, it’s a couple of feet thick in places, and its thick cords give the walls a rough texture a little like corduroy. It’s solid and comforting. Sort of like being wrapped in a four-ton steak.

  As muscles go, the heart is more essential for life than, say, the quadriceps muscle running down the front of your leg that lets you kick a soccer ball. And it’s a little more complex, too, as we’ll see. But not much.

  The heart contracts one time per second, and that’s really all it has to do. Like an MG’s engine, it just does what it’s told to do by a neural center called the sinoatrial (SA) node, which serves as the heart’s natural pacemaker. The SA node tells the heart to beat, and it beats. Simple.

  The fact that the heart comes from the dealership nicely equipped with this SA node means that it keeps beating without our having to think about it. The beat, as they say, goes on. To appreciate the value of this standard feature, imagine just for a moment what life would be like if we had to concentrate on making our hearts beat in the same way that we need to concentrate on, say, kicking a soccer ball. Now imagine having to do that once every second. Life would be very different. Life would also be very, very short.

  The SA node is safely buried between the right and left atria, where blood enters the heart from the body and lungs, respectively. So it’s out of sight of the hordes of backpack-toting red blood cells around me. Left to its own devices, and kept out of the reach of meddling second-graders, the SA node produces an electrical impulse about once a second at a comfortable idle. But it can modify its rate, much as a car engine’s revolutions can be slowed down or sped up. That impulse travels out to the atria and down through the center of the heart, between the left and right sides. There it reaches the atrioventricular (AV) node, whose not-very-creative name is inspired by its position between the atria and the ventricles. The AV node then regulates each impulse, speeding it up or slowing it down as needed, and sending it on to the heart’s ventricles. The impulses go through progressively smaller bundles of nerve fibers known as, in descending order: the bundle of His, the right and left bundle branches, and the Purkinje fibers that carry the signal to muscles.

  It takes about 0.19 second for an impulse to travel from the SA node to a muscle fiber. Then the whole process starts over again. The result is a precise choreography that ensures that the atria and ventricles contract in sequence, pushing blood from atrium to ventricle and from the right side of the heart to the left. This choreography is essential. The heart needs carefully calibrated delays so that each part of the heart fires in sequence, in the same way that the cylinders of a car’s engine do. For instance, the right atrium needs to contract while the right ventricle is relaxed, because if they contracted at the same time, the larger, stronger ventricle would overpower the atrium, pushing blood backward.

  This would cause your cardiac output to drop to zero. Very quickly, you would become unhappy, you would turn blue, and you would pass out. Then you’d be dead. So coordination is a very good thing.

  Normally, all this coordination is invisible. But you can see what it looks like if you happen to be looking at an EKG monitor. You can also get a pretty good look if, like me, you happen to be in a two-story fiberglass heart surrounded by pulsing displays.

  The heartbeat on an EKG monitor has four main components. First, there’s a little bump known as the p wave that indicates the initiation of the heartbeat in the SA node. As this happens, the left and right atria contract, pushing blood into the ventricles. Then there is a long, flat segment—a straight line—during which the signal moves from the SA node through the AV node and down to the ventricles. The length of that segment depends on how much of a delay the AV node is imposing, and whether there are any problems along the signal’s path. This is a common place for the signal to get hung up, resulting in varying degrees of a condition called heart block, which is just about as bad as it sounds.

  If all goes well, though, next you’ll see a series of squiggles as the heart muscle membrane develops a negative charge, and then a positive charge. This is the QRS complex that corresponds to the contraction of both ventricles. Finally, there is the t wave at the very end, when the muscle cells in the ventricle restore their equilibrium and get ready for the next heartbeat. (In the time it’s taken you to read this, your heart has gone through fifteen or twenty of these cycles.)

  As that electrical impulse moves through the heart, it causes the muscle to contract and relax in sequence. First the atria contract, pushing blood into the ventricles. Then the ventricles contract, pushing blood into the lungs (from the right ventricle) and out into the body (from the left ventricle). Timing is everything. Each chamber has to contract and relax at ex
actly the right time, so blood flow is coordinated.

  If this sounds like a simple system, it is, but only up to a point. The interesting thing about it—and where the analogy to the wiring system in a 1978 MG breaks down—is that the heart doesn’t rely only on neural fibers to carry a signal throughout the heart. Unlike the muscles in your leg, for instance, the muscles in your heart form what is called a functional syncytium. In other words, there is a loose aggregation of cells that are all connected to one another, allowing electrical impulses to flow in every direction. This is possible because the muscle cells of the heart don’t rely on nerves. Instead, they propagate electrical impulses by way of gap junctions that let signals jump between muscle fibers.

  To see why this is important, you have to forget the model of electrical wiring in a car. That wiring goes from point to point, with fuses and switches that can be described in a schematic of lines and boxes. But the heart muscle doesn’t really have a schematic. Instead, think of a computer-to-computer Internet network that uses Wi-Fi. Rather than plugging into an access port, a computer in the network grabs a signal from other computers nearby and passes that signal along to others. So as long as someone has a connection, everyone is connected. In the same way, as long as a little chunk of heart muscle is getting a signal, it can propagate that signal to its neighbors. Whereas a signal traveling down a nerve stops if that nerve is severed, if a section of heart muscle is injured, the signal just takes a detour around the affected area.

  This system is elegant, and avoids the need for complex wiring to reach every muscle fiber. It also makes the heart more resistant to damage. If some part of the heart muscle is damaged (by a heart attack, for instance), signals can still find their way around. In this respect it’s resilient in the same way that a distributed computer-to-computer Internet network in an airport lounge still functions when one person leaves to catch a flight.

  There are disadvantages of this arrangement, though. For example, because all heart muscle can conduct electrical activity, a disruption can set up strange patterns in which impulses circle and loop back. This causes heart muscle to contract out of sequence and can lead to sometimes fatal arrhythmias. Indeed, this is the typical cause of arrhythmias after a heart attack. That might happen during the heart attack itself, or in the recovery phase. Still, as a redundant system, in which each backup plan has another backup plan, the heart is really quite well designed.

  Next on our tour, there are valves that keep blood flowing in the right direction. Clearly the designers of this 220-foot-tall man’s heart had some fun with these, because they’re molded with amazing attention to detail. Now my fellow red blood cells and I are passing through the tricuspid valve, which leads from the right atrium to the right ventricle. From the right atrium, we can see three “leaflets,” each about the size of a café table. In the body, they are made of connective tissue that flip forward to let blood through, and then snap back to form a seal that prevents blood from moving backward. If these fiberglass leaflets were moving right now, they’d swat us like giant tennis rackets. But they’re not moving now, fortunately, and we push our way through, yelling and screaming.

  Now we’re in the right ventricle, where the most important part of the valve is located. I take a moment to pause and turn around, incurring the wrath of a dozen eager red blood cells behind me. For a moment, I am an unwanted obstacle. I am an adult-size clot.

  Soon, though, a red blood cell turns around to see what I’m looking at. From this angle, we can see that each leaflet is tethered to the wall of the heart by perhaps a dozen cords of muscle. Each is as big around as your waist where they leave the wall, tapering to the diameter of your wrist by the time they attach to the valve.

  “What are they?” the other red blood cell asks no one in particular.

  I explain, over the din, that they’re called chordae tendineae. Literally: heart strings.

  “Cordy what?”

  I tell him that chordae tendineae are strips of connective tissue attached to muscle that keep the valve leaflets from collapsing backward into the right atrium. The mitral valve between the left atrium and left ventricle is similarly equipped. (The valves that guard the exit of the right and left ventricles don’t have chordae, and rely instead on rigid cartilage for structure.) Without them, the leaflets would just wave back and forth. Blood would move from the atria to the ventricles, and then back, effectively reducing your blood flow to zero. And then, I add, you’d die.

  The red blood cell nods. He gazes around vacantly. Then he lets out a yell, dodges around me, and rejoins the bloodstream.

  The beauty of this system is that these valves are mostly passive. With the right timing of contractions, they open in response to increased pressure on one side, and then they slam shut when they’re supposed to. That is, they function a little like the exhaust valves of a car’s engine, allowing only one-way flow. They’re ingenious devices, and researchers have spent decades trying to create facsimiles that work as well (and last as long).

  My part of the red-blood-cell parade has now passed through the pulmonic valve and has summited the top of the heart. If we were in a real 220-foot-tall man, we’d be floating out into his 30-foot lungs. There we’d pick up oxygen and release carbon dioxide, moving on through the left atrium, left ventricle, and out into the body. That’s one of the trickiest parts of the heart’s function, and where accidents often happen. For instance, blood can clot in the smaller vessels, and fluid can leak out into the lungs if the left side of the heart isn’t keeping pace with the right.

  Perhaps sensing the potential danger ahead, it’s at this point that the whooping scrum of little second-grade red blood cells around me becomes densest. And loudest. Then the clot dissolves and we’re flowing into the left side of the heart.

  As we do, we get an up-close glimpse of the aorta—the largest artery in the body that emerges from the heart and branches repeatedly until blood flows into tiny capillaries. Curious to see how authentic this model is, I look closely at the root of the aorta where it leaves the heart. Sure enough, there are a few small vessels—coronary arteries—branching off and wrapping back around the heart. All muscle needs oxygen to survive, and the heart is no exception. So laced across the outside of the heart is a network of increasingly fine blood vessels that feed oxygen to the heart muscle.

  Of all of the pieces of this mechanical puzzle, these little arteries are the ones that are most likely to cause trouble. The valves we just passed through are amazingly durable, as is the neural wiring that surrounds us. But these blood vessels are thin and fragile. They’re also not very redundant, meaning they feed a very clearly defined territory. If you develop a clot or a bit of cholesterol plaque in one, it’s unlikely that the heart muscle downstream has a plan B. With no other source of blood and oxygen, the heart becomes vulnerable and dies, as do you.

  Nevertheless, even these blood vessels are susceptible to tinkering. When they’re clogged with blood clots, for instance, they can be cleared with so-called thrombolytic drugs that dissolve blood clots that have blocked off an artery. Balloons inserted on a wire through an artery and then inflated can open a narrowed passage. (Although no respectable cardiologist would explain these interventions this way, you can think of these thrombolytic drugs and balloons as a little like using Drano and a Roto-Rooter, respectively, to open a clogged pipe.) And when all else fails, heart surgery and bypass grafts can route blood around the closed-off sections of blood vessels.

  It’s so simple, in fact, that it’s tempting to try a little tinkering yourself. I mean, how hard could open-heart surgery be? It’s just muscle, right?

  THE HISTORY OF CHICKEN RESUSCITATION

  To say that the mechanics of the heart are simple is true enough. However, that statement ignores the rather important role that the heart plays in keeping us alive.

  I’m reminded of this as I watch the man on the operating table in front of me. He’s u
nder deep anesthesia, and his chest is wide-open, his rib cage held in place by stainless-steel retractors. But the scariest part of this scene is his heart.

  When the heart beats normally in the chest, it’s a reassuring metronome, ticking away no matter what physiologic chaos is unfolding around it. But this heart isn’t beating. Instead, it’s fibrillating—quivering with a frail, fine tremor.

  Oddly, no one around the operating table seems the least bit concerned about this heart’s lack of activity. They’re so nonchalant, in fact, that I’m tempted to point out that this particular heart isn’t doing what it’s supposed to be doing.

  But I don’t say anything. I think this is all part of a plan. At least, I hope it is.

  The person on the operating table in front of me is a sixty-three-year-old man named Allan. I’m watching his open-heart surgery to get an up-close look at a real heart. About three hours ago, Allan started having crushing chest pain that started in the center of his chest and radiated down his left arm. His wife called 911 and he was rushed to the nearest hospital. An EKG and lab tests found that he was having a massive heart attack. A clot-dissolving drug didn’t work, so he was whisked to the cardiac catheterization lab, where dye introduced into his aorta flowed out into the systemic circulation but bypassed his coronary arteries almost entirely. It was as if they weren’t there at all.

  He had a blockage in his left main coronary artery—the same blockage that killed Joe, the man I introduced you to in chapter 1. From the catheterization lab Allan went straight to the operating room. Now, less than three hours after his chest pain began, his chest is open, he’s on cardiac bypass, and he has less than a 50 percent chance of waking up and seeing his wife and grandchildren again.