Cardiac physiology

I wonder if physiology professors everywhere hack on about the same things: action potentials in muscle cells, both cardiac and skeletal, and the contents of the cell. So many things I’m more curious about, like the human genome and DNA, transcription, meiosis and mitosis, brain chemistry, kidney function, etc etc. But somehow it seems to me that the longest lessons always wind up being on action potentials, with their sodium and potassium channels, depolarization, and concentration and ion gradients. Maybe it’s just UofO and ESO. Maybe these are just the ones I understood the first time (thanks Grant and Greg!).

So let me explain it to you, to test my knowledge!

The heart has two types of muscle cells: autorhythmic and contractile. Autorhythmic cells control the electric signal that initiates the beat of your heart. Contractile cells cause the actual beat you feel, pumping blood through the body, and coordinate the timing. Both of these work in a never-ending cycle of depolarization and repolarization.

Hokay, so… in autorhythmic cells, like any cell, sodium is constantly being pumped out and potassium is constantly being pumped in by ion pumps that live in the membrane. They do this to build up a concentration of sodium outside and potassium inside, which creates stored energy (because they want to mix evenly, not be divided up and shoved together) that can be used to move other molecules, contract muscle fibers, or do other “cell work”. These cells also have leaky sodium channels, allowing constant slow diffusion back into the cell. This influx is essentially defeating the purpose of the pumps, causing the membrane potential, or voltage difference, to gradually decrease, rising from its resting rate of -60mV. Once it reaches -40mV, calcium channels suddenly open, which flood the cell with + charges. This depolarization very quickly takes the internal cell membrane to around +10mV. At this voltage potassium pumps are signaled to open, letting some + charge leave the cell, reducing the charge inside.  All the while sodium and potassium pumps are working to build concentrations of these molecules, sodium outside, potassium inside, and concentration gradually returns to -60 and we start again. Each time this cycle reaches the threshold level, it sends a stimulus to the contractile cell. This cycle is your pacemaker, setting your heart rate at around 100 beats per minute, and is automatic.

The contractile cells have the same sodium and potassium pumps working to build the concentration gradient on either side of the membrane. These cells are connected to the autorhythmic cells (and each other) by gap junctions, like the door between two halves of a duplex. These cells work towards -90mV. When their neighbor cells depolarize and flood with calcium, some travels through the open “doorway,” and when enough gets through  they, in turn, depolarize, suddenly opening sodium channels. They ride this wave up to +30mV, when sodium channels close. At this time slow calcium channels open and it enters. Remember that sodium is still being pumped out all the while. This allows the voltage to remain near 0 for a prolonged period, called the plateau phase, as calcium and sodium exchange balance each other. Calcium diffuses through the cell, and also into the next contractile cell, propagating this cycle. The plateau period allows time for this diffusion down the line, so that the cells can contract together in coordination. Once around 20% of the cells have enough calcium for contraction, the ventricles contract, pushing blood out of the heart. After a set duration, potassium channels open, which allows potassium to leave the cell, and voltage drops, returning the cell to an excitable state. During the plateau phase repeated stimulus  cannot speed up contractions, effectively limiting the heart rate. This is call the refractory period.Make sense? :)

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