Heart Throbs

Transcription

You’ve seen this before in a TV show or a movie. A patient is on the table in the emergency room, bleeding from a stab wound or having ODed on drugs, when suddenly, an alarm goes off and the beep beep beep on the heart monitor flatlines. It’s cardiac arrest, and you can tell just by that sound that it’s terrible. Doctors swarm around, barking orders, and McDreamy or Dr. Grey -- or whoever the latest foxy doctor is on the TV show that you’re addicted to -- grabs the paddles, pushes them down on the patient’s chest, and is all CLEAR! Then the patient’s chest jumps up, and everyone stares at the monitor waiting for those steady beeps to reappear. That is a pretty classic scene. When it comes to medical crises you see in popular culture, it’s probably only rivaled by the pool-side CPR scene, or someone shaking an unconscious body, pounding on their chest and saying “Don’t you die on me!” Which hopefully you know is no way to keep someone alive. These are classic script tropes, but they contribute to some misconceptions about how defibrillators, CPR, and the electricity of the heart work. Because the truth is, CPR can help prolong heart function during cardiac arrest, but it usually can’t save a life without help from a defibrillator. And when McDreamy -- may he rest in peace -- finally bursts out those paddles, that high-voltage shock isn’t turning the heart back on -- it’s actually stopping it. Confused? Well, I’m here to get your head to understand your heart. We’ll get back to hot TV doctors in a coupla minutes, I promise. But in order to understand what’s actually going on during cardiac arrest, we have to understand some basics about your heart cells. We’ve learned a lot about skeletal muscle tissue -- how it’s striated, and contracts using the actin-myosin sliding filament dance you’ve heard so much about. Your cardiac muscle is also striated, and uses sliding filaments to contract, but the similarities end there. For one, their cells look pretty different. Skeletal muscle tissue has long, multinucleate cells, while cardiac cells are squat, branched out, and interconnected, each one with one or two central nuclei. The cells are separated by a loose matrix of connective tissue called the endomysium, which is chock full of capillaries, to serve up a constant supply of oxygen. Cardiac cells are also loaded with energy-generating mitochondria. In fact, mitochondria take up as much as 25 to 35 percent of each cell, making it resistant to fatigue, which is partly why your heart can beat nearly 3 billion times in a lifetime. Not surprisingly, the differences between skeletal and cardiac muscle tissues are key to understanding their functions. Skeletal muscle fibers are both structurally and functionally separate from each other, meaning that some cells can work while others don’t -- that’s why you can grasp a delicate flower with the same hand that you can use crush a soda can. Cardiac cells, on the other hand, are both physically and electrically connected, all of the time. It takes precise coordination to create the high and low pressures required to pump your blood after all, and cardiac cells need to be linked in order to have that perfect timing. And there’s one more thing you need to know about your heart’s cells: Some of them can generate their own electricity. How in the name of Raymond de Vieussens can that be? Well, rewind your brain to when we explored the electrical marvel that is the action potential, and how it triggers both neurons and muscle cells. That process started by depolarizing the cell -- that is, pushing the cell’s membrane potential from negative toward positive, past a threshold that triggered voltage-gated ion channels to open. Most cells in your body only depolarize after being triggered by an external stimulus, or by a neighboring cell, in a long chain reaction of action potentials that’s set off by the nervous system. But that is not the case for a special group of cells found only in your heart -- ones that can trigger their own depolarization. These are your pacemaker cells. Pacemaker cells are what keep your heart beating at the correct rhythm, and ensure that each cardiac muscle cell contracts in coordination with the others, because you don’t want your brain to have to send a series of action potentials every time you need your heart to beat. Your brain has got other stuff to do. So pacemaker cells are, in a way, your heart’s very own brain, generating the initial spark that sends a current through your heart’s internal wiring system, known as the intrinsic cardiac conduction system. This system transmits electricity along a precisely-timed pathway that ends with atrial and ventricular contractions -- also known as heart beats. And it begins with pacemaker cells generating their own action potentials. In most cells, the action potential starts with the resting potential, which the cell maintains by pumping sodium ions out and potassium ions in, Right? Then, when some stimulus causes the sodium channels open up, the sodium ions flood back in, which raises the membrane potential until it reaches its threshold. Pacemaker cells operate the same way, except for that initial stimulus. They don’t need it. Their membranes are dotted with leaky sodium and potassium channels that don’t require any external triggers. Instead, as their channels let sodium ions trickle in, they cause the membrane potential to slowly and inevitably drift toward its threshold. Since the leaking happens at a steady rate, the cells fire off action potentials like clockwork. And the leakier the membrane gets, the faster it keeps triggering action potentials. The pacemaker cells at the start of the conduction system have the leakiest membranes, and therefore the fastest inherent rhythms, so they control the rate of the entire heart. And those fast, leaky cells are found in the sinoatrial node, or the SA node, up in the right atria. They essentially turn the whole SA node into your natural pacemaker. After those pacemaker cells make themselves fire, they spread their electrical impulses to cardiac muscle cells throughout the atria. The impulses leap across synapse-like connections between the cells called gap junctions, and continue down the conduction system until they reach the atrioventricular node, or AV node, located just above the tricuspid valve. Now, when the signal hits the AV node, it actually gets delayed for like, a tenth of a second -- so the atria can finish contracting before the ventricles contract. Without that delay, all the chambers would squeeze at once, and the blood would just splash around and not go anywhere. So instead, the atria contract and blood drops down into the ventricles, and then a moment later, the signal moves on and triggers the ventricles to squeeze, making the blood flow out of the heart. And there are two tricks to a good ventricular contraction. One, the ventricles are so large that the signal has to be distributed evenly to ensure a coordinated contraction. And two, the ventricles need to squeeze like their squeezing a tube of toothpaste -- from the bottom up -- to accelerate the blood through the big arteries at the top of the heart. So from the AV node, the signal travels straight down to the inferior end of the heart and gets distributed to both sides. The path the electrical impulse takes to the bottom of the heart is called the atrioventricular bundle, also known by the more rad name, the bundle of His, where it branches out to the left and right ventricles. Finally, the signal disperses out into Purkinje fibers, which trigger depolarization in all surrounding cells, causing the ventricles to contract from the bottom up like toothpaste tubes, at which point the whole cycle starts all over again. And everything I just described to you -- from when the SA node fires to when the last of the ventricular cells contract -- takes about 220 milliseconds. So that is how your heart beats. But I know what you want -- you want to get back to talking about TV shows and McDreamy and his paddles. It’s totally understandable. OK, so picture all your individual heart cells as a bunch of musicians in an orchestra. They all sound really great together, but then the conductor suddenly needs to go to the bathroom. And it sounds OK at first, but then the tuba gets a little weird, and the triangle is half a beat off, and soon everyone is playing a different note at a different time, jamming to their own personal rhythm. In the heart, we call this out-of-sync behavior fibrillation, and it can be caused by all sorts of problems, especially ones that affect the pacemaker cells in the SA node. In an orchestra, this just sounds really terrible. In a heart, there’s no coordinated contraction, no lub-dub, no blood moving through the body. Which means you will soon be dead. But then the conductor comes back from the bathroom break, taps her wand, and everybody stops. It’s silent for a second before the wand comes up, and then they all start playing again, this time in unison. If your heart in fibrillation is an out-of-sync orchestra, then a defibrillator is that conductor. It stops the chaotic noise by overriding all the individuals, and hits a sort of reset button so everyone can start again on the same page. The paddles send so much electricity through the heart that they trigger action potentials in all of the cells at once. Then, the cells repolarize, and start leaking again, and then the most leaky cells, in the pacemaker SA node, reach their threshold and fire first, re-setting the rhythm that keeps everyone in harmony so your heart functions properly. And that is how hot doctors and their paddles actually stop hearts to save lives. Now the thing about CPR -- or cardiopulmonary resuscitation -- is that it can’t correct fibrillation. What those chest compressions can do is force a fibrillating heart to keep circulating oxygenated blood until help arrives. But if a person is in cardiac arrest, just breathing into their mouth and compressing their chest won’t deliver the electricity needed to give the pacemaking cells a chance to reset. I think I just figured out why they call those TV doctors heart throbs. That’s a terrible joke. Anyway, today you learned how your heart’s pacemaker cells use leaky membranes to generate their own action potentials, and how the resulting electricity travels through the cardiac conduction pathway from SA Node to Purkinje fibers, allowing your heart to contract. And if you weren't too busy daydreaming about TV doctors, you also learned how defibrillators work to reset the rhythm of your heart. Thank you to our Headmaster of Learning, Thomas Frank, and to all of our Patreon patrons who help make Crash Course possible through their monthly contributions -- not just to themselves but to everyone in the world for free. If you like Crash Course and want to help us keep making these videos, you can visit patreon.com/crashcourse. Crash Course is filmed in the Doctor Cheryl C. Kinney Crash Course Studio. The episode was written by Kathleen Yale, edited by Blake de Pastino, and our consultant is Dr. Brandon Jackson. It was directed by Nicholas Jenkins; the script supervisor and editor is Nicole Sweeney; our sound designer is Michael Aranda, and the Graphics team is Thought Cafe.