At the beginning of today’s class I took some questions about the quiz that the students had just redone as homework, and some about the class-D power amplifier lab that they had worked on yesterday and will work on more tomorrow. I don’t think that most of the groups got far enough in the lab yesterday—they barely finished the pre-amp and had not yet wired up the comparators—I’m a little worried about how long the lab might take tomorrow. Other than taking orders for T-shirts, I spent most of the rest of the time on cardiac action potentials.
This year I decided to try to give a lecture on action potentials myself, rather than having a guest lecturer, as I did last year. In part I wanted to try to strengthen my own knowledge (which comes mainly from Wikipedia’s cardiac action potential article), and in part I wanted to cover muscle action potentials, rather than neural ones, so I needed to bring calcium ions into the picture.
Fortunately for me, one of the students in the class had had a neuroscience course (all the students have had more biology than me), so could remember words I had forgotten (like sarcoplasmic reticulum for the organelle that stores Ca++ ions in cardiac cells).
I was able to give rough electronic analogs for some of the components (like a capacitor for the membrane and an FET for the voltage-gated ion channels), but I did not include some of the things that the bio professor had included last year (like references to the Nernst equation).
I tried to explain how the EKG signal we record corresponds to the dipole that results from the movement of the waveform across the heart, but I think I did a poor job of it. I got confused about whether the Sinoatrial node was in the upper right or upper left atrium (it is the upper right), and did not remember the polarity of Lead I (which is left arm – right arm). The P and R depolarizations are upright (positive voltage) in Leads I and II, because the depolarizations travel from upper right to lower left of the heart.
I think I’m still a little confused why the dipole points the way it does. As best I can figure out, the leading edge of the depolarization wave lowers the voltage outside the cell quickly, giving a + potential in front of the wave and a – potential during it. The trailing edge of the depolarization wave is much slower and so does not produce a strong dipole? I’m not quite sure how this dipole interacts with the volume conduction of the body to produce the waveforms we observe on the EKG electrodes, though.
I did get out a sketch of the PQRST waveform and a brief interpretation of it.
There are some cool animations at http://thevirtualheart.org/CAPindex.html that I did not get a chance to use. Perhaps I can make use of them on Friday. I should also point students to the filter information in the Wikipedia ECG page, because they will need to set up their 1-lead EKGs in “monitor mode”.