Zoobiquity

  But a whole other category of cardiac woe comes from inborn or acquired damage to the electrical system. Its health can be discerned from an electrocardiogram (EKG)—the jagged, steep slopes that shoot up and down across graph paper or scroll along a computer monitor. You’ve seen these representations of the heart’s steady current countless times on medical dramas and in pharmaceutical ads. And you’ve heard audio translations of that electricity, too. When wired to an alarm signal, the clockwork electrical current creates that stable beep … beep … beep that indicates all is well. Nothing calms a nervous on-call doctor better than news that her patient’s heart is beating in that pattern. We call it normal sinus rhythm.

  Tragically, however, this steadfast, pulsing electrical system fatally short-circuits in seven hundred human hearts every day in the United States‡ and in many thousands more worldwide. The dependable throb suddenly races out of control or becomes floppy and unpredictable. When you listen with a stethoscope, the lub-dubs take on an anxious, irregular, and muffled quality. When the beat speeds up—a condition we call ventricular tachycardia, or VT—it’s unmistakable on the EKG. The assembly-line predictable peaks and valleys of normal sinus rhythm loosen into rolling, closely spaced “hills.” The lopsided, irregular rhythm, on the other hand, is called ventricular fibrillation (VF). It’s equally easy to recognize. The jagged visual static lurches across the monitor or graph paper with a sickening randomness.

  To those in the know, the sounds and sights of VT and VF instantly convey one thing: the urgent need for someone to place shock paddles on the sufferer’s naked chest; call “All clear!”; and send a few hundred joules coursing toward the malfunctioning heart. If this specialized electrical therapy doesn’t arrive immediately, the EKG landscape will devolve from the hilly and craggy warning shapes to the infamous horizontal configuration we refer to—with dreaded respect—as a flatline. The shift in rhythm from “life-sustaining” to “malignant” causes the heart’s pumping to decrease or stop. With more precision than poetry, doctors call this electrical cardiac catastrophe sudden cardiac death (SCD or sudden death for short).§

  Cardiac death can come rather predictably after years of plaque buildup in the brittle arteries of an overweight smoker. Or it can strike with a shock as happens when a high school athlete drops dead from a congenital defect he didn’t know he had. The “final common pathway” is the same. It’s an electrical malfunction, the shift from a life-sustaining, normal rhythm to the death-heralding arrhythmia of VF or VT.

  But certain victims of sudden cardiac death have no previously identified heart problems. In these otherwise healthy patients, a massive emotional jolt alone converts the cardiac rhythm from safe and steady to malignant and deadly. Startled, terrified, horrified, or aggrieved, these patients spew stress hormones, including adrenaline, from their highly activated central nervous systems. These catecholamines gush into the bloodstream. Like a chemical cavalry they appear on the scene, ready to boost strength and stamina to aid an escape. But instead of rescuing the patient, this neuroendocrine burst may rupture plaque deposits, lodge a blocking clot in an artery, and cause a fatal heart attack. It might trigger an extra beat at just the wrong moment and send the heart into VT. And in huge amounts and all at once, the chemicals themselves can be enough to poison muscles, including some of the two billion heart muscle cells in a human ventricle. In these patients, the weapon is essentially the reactive nervous system itself, fully loaded with dangerous catecholamines, waiting for terror to pull the trigger.

  That’s what happens with takotsubo. Whether activated by lost love or war, geological heaving or a ball game, the catecholamine torrent damages heart muscles, creates the octopus pot–shaped bulges, and sometimes causing dangerous arrhythmias.

  But takotsubo is only a small part of the story, as I figured out when I started comparing notes with veterinarians.

  • • •

  Dan Mulcahy is the kind of guy you’d want along if you ever found yourself stranded in a Category 5 blizzard with the gas gauge on your Arctic Cat F1000 Sno Pro on empty. Part MacGyver, part Davy Crockett, with a full mustache, wire-rimmed glasses, and a basso profundo rumble, Mulcahy occupies that rare and desirable zone on the Venn diagram where superhero and supernerd overlap. At forty-one, after two decades as a microbiologist studying fish diseases, he switched careers and became a wildlife veterinarian. When I met him, he was working in Alaska, tracking and treating walruses, tundra swans, caribou, and other endangered northern creatures. His job requirements ran from the delicate surgery of installing satellite transmitters in spectacled eider ducks to the bravura choreography involved in collaring a half-ton polar bear as part of a worldwide team monitoring and trying to preserve these animals’ disappearing hunting grounds.

  When we met, we quickly discovered that we shared a professional and personal fascination—with the ways death lurks in the interplay of the heart and the mind. We bonded, as only two doctors can, by trading ghoulish yet exciting tales of fear-based sudden death we’d seen and treated.

  Mulcahy’s interest had a poignant and frustrating root: every once in a while, an animal—especially, for some reason, certain birds—would silently die in his hands after being chased, captured, and handled. Sometimes they seemed to get through the medical procedure just fine, only to weaken and die the minute they were reintroduced to a new habitat. Mulcahy knew it wasn’t anything he was doing wrong. In fact, his supervision made these important surveys carried out by field biologists much safer for the animals.‖

  Veterinary textbooks describe a heartbreaking yet eerily predictable reality: animals consistently die from the stress of chase and handling. Veterinarians call it capture myopathy. The term describes a syndrome of illness and death seen in animals who are terrified, captured, or running for their lives from predators, hunters, or well-intentioned but underinformed wildlife biologists. Sometimes the affected animals expire on the spot, crumpling to the ground like a maiden in a gothic novel. Sometimes they endure for a few hours after the stressful incident before expiring. Other times they linger for days or weeks, listless and depressed, unable to walk or even stand, refusing food and water, until they die. In any case, postcapture death rates are disturbingly consistent.a It’s usually about 1 to 10 percent of a population, sometimes as high as 50 percent, depending on the species.

  Capture myopathy was first noticed by human hunters a hundred or so years ago. It was initially thought to be an exclusive syndrome of big prey, like zebra, buffaloes, moose, and deer. These animals often died mysteriously after a hearty chase, even when the hunters’ weapons had left no mark on their bodies.

  But then ornithologists started noticing capture myopathy’s fingerprint on the muscles of birds from tiny parakeets to lanky whooping cranes to brawny, ostrichlike rhea. Marine biologists described cases in dolphins and whales. Fishermen trawling for wild Norway lobsters off the coast of Scotland saw it pinch their bottom line. The meat of chased lobsters was discolored and had an unappealing, watery texture. It looked spoiled—in a way, it was deader than dead. It rotted faster. At the market, it was rejected on sight.b

  Soon wildlife veterinarians realized that pursuit—chasing without rest—was killing animals from every corner of the food web. In South Africa, where animals frequently need to be moved around to accommodate national park boundaries and human encroachment, capture myopathy is a serious health threat and a major cause of death. Special care is taken when capturing sensitive giraffe, which aren’t as a rule accustomed to running long distances and are also known for their anxiety. Deer, elk, and reindeer in North America have capture myopathy mortality rates from relocation and hunting as high as 20 percent. The Bureau of Land Management’s yearly helicopter roundups of wild mustangs in Nevada result in the deaths of a certain number of horses every year from capture myopathy.

  Fueling an animal’s escape from threat is a powerful neurochemical response: a catecholamine dump. Pushed beyond a safe limit, though, catecholamines
can overwhelm the skeletal and cardiac muscles and cause them to break down. When significant chunks of skeletal muscle are degraded, massive amounts of their proteins are released into the bloodstream. These proteins can overpower and eventually shut down the kidneys. The medical name for this muscle damage is rhabdomyolysis. “Rhabdo”—as it’s widely known in clinical shorthand—can be fatal, but if it is caught early, it can be effectively treated with hydration and supportive care. In people, it’s most often seen in extreme cases of trauma and immobility: an earthquake victim pinned under steel beams and rubble, for example, or a motorcyclist thrown from his bike with multiple skeletal fractures and overwhelming soft-tissue injuries. Veterinarians and physicians alike know that a telltale sign of rhabdo is rust-colored urine—tinged that shade by the overflow of toxic muscle enzymes that the kidneys couldn’t filter out.

  Military physicians from the U.S. Navy and Marine Corps noted as early as the 1960s that during the intense repetitive calisthenics of basic training, recruits sometimes developed the exhaustion, muscle breakdown, and cola-colored urine seen with rhabdomyolysis. Extreme athletes like cyclists, runners, weight lifters, and even high school football players occasionally report similar symptoms after grueling workouts. Animal athletes are also vulnerable to rhabdo, racehorses in particular. Extreme athletes—whether animal or human—push themselves to perform, often through pain, which sometimes results in rhabdo. “Mind over myocardium” can trigger quiet but deadly effects in both humans and animals.

  But sometimes wildlife veterinarians finger capture myopathy as the killer even in cases in which there has been no prolonged chase, no skeletal muscle breakdown, no rhabdomyolysis.

  A form of capture myopathy can appear when an animal is simply handled, noosed, netted, corralled, crated, penned, or transported. “Running for your life” is terrifying, but at least you have a fighting chance. Being caught, on the other hand, is the step right before the worst-case scenario: “game over.”

  As Dan Mulcahy put it, for an animal, “the only time they’re caught is when something’s going to eat them.” Restraint usually means one thing: another animal wants you not to move. Capture and restraint, from an evolutionary perspective, spell a single state of affairs: imminent predation or death. Understandably, brains have evolved an all-systems-go response, a massive, last-ditch catecholamine tsunami.

  Examples of animals dying when they’ve been captured or restrained abound. In species as varied as Irish hares, white-tailed deer, cotton-top tamarins, and antelopes, this combination can equal death. Experts on pikas, the rabbitlike “tundra bunnies” of South America, have learned the hard way that holding a captured pika firmly around its middle can scare it to death. A safer approach is to allow it to stand, unrestrained, in your open hands. And the risk exists not just for flighty prey animals. Top carnivores like brown bears, lynxes, wolverines, and gray wolves have died after being trapped.

  Loud noises and heat can intensify the hazard of entrapment. Bighorn sheep in California’s Mojave Desert that were rounded up for a relocation program fared especially poorly when a thundering helicopter hovered nearby. Pet rabbits have been known to expire in the presence of blaring rock music and even loud arguments between their owners. Fireworks blasts have reportedly startled and killed pets and livestock from parrots to sheep.

  In Copenhagen in the mid-1990s, the Royal Danish Orchestra was performing Wagner’s Tannhäuser in a public park. Abutting the park was the Copenhagen Zoo. As the chorus keened and the soloists belted out their highest pitches, a six-year-old okapi anxiously circled her enclosure and tried to escape. After struggling for several stressful minutes, she keeled over and died. The vets diagnosed capture myopathy.

  Loud, frightening noises—not only those passing through a soprano’s warbling epiglottis—have recently been shown to be risk factors for adverse cardiac effects in a variety of populations. One study published in the journal Occupational and Environmental Medicine found that people laboring in workplaces so persistently noisy they had to shout to have a normal conversation had twice the risk of serious cardiac events as people whose workplaces were quieter. And in some inherited cardiac conditions, startling loud noises can trigger a disturbance in the heart rhythm that leads to death.c

  Interestingly, there’s a breed of dog that seems to have evolved a defense against noise’s jolting effects. Dalmatians born with long QT syndrome, and therefore susceptible to noise-induced sudden death, fortuitously sometimes also carry a genetic mutation that causes deafness. The auditory disability becomes a cardiac blessing in disguise as their muffled experience of sound may protect their vulnerable hearts from fatal cardiac arrhythmias.

  Startling sounds and the feeling of confinement signal danger to animals and humans. Like the okapi trapped at the opera, noise and the perception of entrapment can be enough to ignite a fatal brain-heart reaction. Animal and human sensory systems provide information about the outside world that their brains convert to evasive action. But it’s not just noise or restraint that can create terror.

  In some cases, the mere thought of restraint can induce comparable physiology. Like the anxious and scared humans watching the events of 9/11 on TV, other animals, too, can experience an intense brain-heart reaction simply by seeing a threat.

  Four captive zebras at a zoo in Vancouver once died from what was diagnosed as capture myopathy. They hadn’t been chased. The stressor was the simple presence of two intimidating Cape buffalo that had been placed in the zebras’ enclosure, an enclosure whose fences and moat would prevent their escape.

  A sudden and unexpected appearance of predatory threat can also endanger animals. Some bird-watchers described observing a flock of cinnamon-bellied shorebirds called red knots calmly wading along the water of an Australian beach. Suddenly, a raptor swooped down and grabbed one of the unsuspecting waders with its lethal talons. As the raptor flew off, the observers noticed something interesting. Although untouched by the predator, several nearby birds suddenly became unsteady and weak. Some fell over when they tried to walk.

  Ornithologists call this kind of stress-induced muscle disease “cramp.” The adrenaline spew would have affected the birds’ heart muscles, too. The red knots, like the zebras, succumbed after merely witnessing a terrifying sight.

  Circumstances that are not directly life-threatening can induce potent physiologic responses in humans, too. If, while traveling at ten thousand feet, your airplane hits an air pocket and plunges, your adrenal glands and brain release catecholamines. Your heart rate accelerates and your blood pressure rises. You may feel as though you’re going to die. And, worse, as with a restrained animal facing predation, your inability to escape heightens your body’s physiologic response.

  Your brain processes the threat, but your body generates the response. That sickening, activated state you feel is fear. And fear, say veterinarians, is a key factor in capture myopathy. Some say it’s the single most important factor. This leads us to an internal but dangerous contributing element to capture myopathy: the captured animal’s activated emotional state.

  We’ve seen that animal brains, human and nonhuman, respond and in some cases overrespond to entrapment. It’s possible that our imaginative human minds take it a step further, triggering heart responses to traps that are not actually physical: an abusive relationship, crushing debt, an impending prison sentence.

  Consider disgraced Enron chief Kenneth Lay’s cardiac arrest weeks before being sentenced for an embezzlement conviction. Douglas P. Zipes, an expert in sudden cardiac death (SCD) and the editor in chief of the journal Heart Rhythm, told a Florida journalist, “We know that stress about which you can do nothing—the death of a spouse, the loss of a job, or facing life imprisonment—can be associated with sudden cardiac death. I can’t crawl into [Lay’s] head, but there is no question that the head talks to the heart and can have an impact on heart function.”

  Overwhelming fear responses to entrapment and threat may not be all that different whe
ther you’re a zebra facing a glowering Cape buffalo or a white-collar criminal facing life in prison. Indeed, studies have demonstrated that abusive, unfair bosses; negative, conflict-ready spouses; and suffocating debt substantially up the risk of heart-related death.

  Given the power of fear and restraint to cause harm in humans and animals, it’s surprising there’s not a diagnostic term for these types of deaths. Because capture myopathy in animals and fear-induced cardiac effects in humans are related but complex, it might be helpful to find a way to identify cases in which fear and restraint were at fault. More than a decade ago the Harvard neurologist Martin A. Samuels called for “a unifying hypothesis … to explain all the forms of sudden death based on the anatomic connection between the nervous system and the heart and lungs.”

  The takotsubo moment that started my zoobiquitous journey began with placing the features of stress-induced heart failure in humans side by side with capture myopathy in animals and seeing the many similarities. When doctors notice a pattern of symptoms or physical findings, we create syndromes, which we then name. Veterinarians and physicians might consider adopting a new, common term to describe the role of fear in capture myopathy in animals and sudden cardiac death in humans. I propose the acronym FRADE: fear/restraint–associated death events. FRADE is broad enough to describe emotionally triggered fatalities in both animals and humans but narrow enough to filter out nonemotional causes. It would centralize the clinical anecdotes emerging from both human ERs and wild animal field sites. It could link, say, a takotsubo death in a terrified elderly woman to a capture myopathy death in a trapped okapi. In medicine, as in other fields, commonalities go unnoticed until they’re named. Eventually, the neuroanatomical and neuroendocrine systems underlying fear- and restraint-related deaths will be fully characterized and better understood. But until then, using a common term to classify this particular kind of death will help veterinarians and physicians compare these sudden fatal events in ways that may lead to prevention strategies.