The Heart, Part 2 – Heart Throbs: Crash Course A&P #26

The Heart, Part 2 – Heart Throbs: Crash Course A&P #26


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.

15 Replies to “The Heart, Part 2 – Heart Throbs: Crash Course A&P #26”

  1. whenever i learn about anatomy i'm like what the FLIP how are our bodies that WILD. It's insane how much happens just for us to like…survive another 30 seconds. Crazy stuff.

  2. Hank saving my life with midterms. Learning a whole chapter in 9.5 minutes when my professor spends 3+ hours explaining it LOL

  3. "Confused? Well I'm here to help your head understand your heart."
    Speak, wise one. We listen in desperation. Your words can teach more in ten minutes then the last 3 weeks (9+ hrs of just lecture, not counting lab) of class.

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