Pictures from my backyard

At this time of year (late November), I like to post pictures from my yard—mainly to show off our nice weather to relatives in snowy parts of the country (they get to boast about the low cost of housing—we have similar sizes of house, but my siblings’ houses are ⅓ to ⅒ the price of mine, according to Zillow).

This flower is from a common houseleek (Sempervivum tectorum, which translates to “live-forever of the roofs”).

You may know the common houseleek better as hens-and-chicks. Here is a rosette, removed from the plant with the flower spike and planted separately. Supposedly the rosette dies after the flower spike is formed, though the side rosettes continue to grow.

Our rosemary is still doing ok, though it is getting choked out a bit by the Sweet 100s tomatoes.

The tomatoes are mostly done for the year, though there are a few still ripening.

The tomatoes are in turn getting choked out by the nasturtiums, which germinated after our October rain.

I have about 60 small pots of succulents that I’m growing from cuttings—I plan to give them away next fall to students at UCSC. The 27 that I gave away last September all were taken in about 80 minutes, so I’ll probably pot up another 40 cuttings before next summer, so that I’ll have 100 to give away in the fall.

I’ve found that I can get free (used) plastic pots from San Lorenzo Lumber, by their back gate.  The potting soil is also free, as I’m just potting the plants in sifted compost from around my compost heap.  That is really a bit too rich for succulents, but buying sand or vermiculite to reduce the organic content is too much trouble.

Holter monitor results

I got back the results from wearing the Holter monitor for 14 days today, and they were not what I expected.  I was expecting to see frequent PVCs, particularly when I was resting or sleeping. Instead the report had almost no PVCs but frequent PACs (premature atrial contractions) with runs of supraventricular tachycardia (runs of more than 3 PACs without normal beats in between).  “Isolated SVEs [supraventricular ectopy] were frequent (10.3%, 114645).” “2161 Supraventricular Tachycardia runs occurred, the run with the fastest interval lasting 6 beats with a max rate of 176 bpm, the longest lasting 26.7 secs with an avg rate of 133 bpm.”

Asymptomatic PACs (like asymptomatic PVCs) do not generally call for any treatment, but “many idiopathic PACs are relatively benign in the short term, although they can be associated with an increased risk of cardiac and all-cause mortality if they occur frequently.” [https://www.ncbi.nlm.nih.gov/books/NBK559204/] Most of the medical treatments seem to be focussed on lowering heart rate or blood pressure, neither of which seem appropriate for me (I have normal blood pressure and a low heart rate). The followup recommended for frequent PACs is an echo cardiogram, which I have now scheduled for mid-January (the soonest date that the clinic had available).

My sinus heart rate was about what I expected with “a min HR of 36 bpm, max HR of 160 bpm, and avg HR of 55 bpm”, though the 36 bpm minimum was a little lower than the 40bpm I expected—my sinus rate drops a little lower when I sleep than I expected. The recording of the 36bpm period does not look like my normal sinus rhythm—it looks like a series of ectopic beats with really tiny QRS complexes to me, but it did occur when I was asleep (in the middle of a period of very low heart rate). On another day, there was a recording of 37 bpm which showed normal QRS complexes, so my sinus rate does indeed drop that low.

The max of 160 bpm occurred when I was exercising fairly hard—pushing myself a bit on bicycling uphill to campus.  It is probably not my real maximum heart rate (I was not doing an all-out effort).  I looked up estimates of maximum heart rate and found three formulas: (220 – age), (207 – 0.7 age), and (211 – 0.64 age).  The first is very common, but clearly wrong for me, the second is adjusted for people over 40 years old and pretty accurately matches the observed maximum on the Holter monitor, and the third is adjusted for active people and may slightly overestimate my max heart rate.  If I ever need to take a stress ECG or stress echocardiogram, I’ll argue for them using the second formula rather than the first in estimating my max heart rate, so that the stress level is appropriately set.

One thing I wanted to know that is not reported in the short summary report from the Holter monitor is whether there was any correlation between the sinus rhythm and the ectopic beats—in particular, I wanted to know whether the ectopic beats occurred primarily when my sinus rhythm was very low.  If that is the case, then a pacemaker set to maintain a minimum sinus rhythm might be a possible treatment, should treatment ever be needed.  I downloaded the full report, which shows when the SVT runs occurred, and they seem to be primarily when I’m awake and active, which is the opposite of what I expected based on my observations of PVCs earlier in the year.

I wasn’t sure how one distinguishes a PAC from a PVC on a one-lead Holter monitor, so I watched a video (https://www.youtube.com/watch?v=7Vz8olVnGgU) from “Catalyst University”, which showed the difference between PVCs and PACs on a one-lead ECG. The crucial differences are whether the P-wave (from atrial depolarization) is observed and whether the resulting QRS complex is more or less normal or much longer duration that usual.  If the P-wave is observed and the QRS spike is normal duration and shape (though usually lower amplitude), then you have a premature atrial contraction.  If there is no P-wave and the QRS complex is much longer than usual, you have a PVC.  By these criteria, the observations I made earlier (see PVC again, for example) were clearly PVCs, and the examples of SVT runs shown in the report were indeed PACs. My most recent home ECG recordings have not shown me PVCs, but if I now have PACs instead, my inability to find PVCs may represent a change in what my heart is doing, rather than a failure in my rather crude code for detecting them.

I looked for genetic causes of PACs, but have not found much. Deletion of the STK11 gene is the only thing I’ve found so far, and there is no hint of that in my genome—I do have a SNP in an intron of a gene whose protein that interacts with it: STK11IP, as well as some SNPs in the intergenic region upstream of STK11.  None of these SNPs seem likely to be a major cause of problems.

Holter monitor

For the past 10 days, I’ve been wearing a Holter monitor made by Zio, in order to determine the real frequency of my premature ventricular complexes (PVCs).

I’ve checked the PVCs myself with my own home-made ECG starting about a year ago, but my ECG can only be used when I’m awake and generally sitting in one place, so it does not catch the full range of my heart activity. Because the amplifier board had to be connected to PteroDAQ running on a breadboard connected to a laptop, the ECG setup is not very portable, and I had to sit still to avoid disturbing the circuitry. I couldn’t even use the laptop to browse the web or read email while recording, since changing my contact with the laptop changed the bias voltage on my body, which the amplifier took a second or two to recover from.  So I only recorded about 5–10 minutes at a time.

Some of my recordings got a lot of PVCs, and some got almost none. I did notice that raising my heart rate through exercise seemed to abolish the PVCs. So I think that my PVCs are “slow-rate-dependent” PVCs—that is, that I only get the extra ventricular contractions when my sinoatrial node does not start frequent enough contractions.  Because my heart rate is most likely lowest when I’m sleeping, the ECGs that I did myself probably missed most of the PVCs.

I mentioned my curiosity about what my real PVC burden was at my annual checkup, so my doctor ordered a 14-day recording with a Holter monitor.

Holter monitors have gotten quite small. This Zio monitor has electrodes about 9cm apart and just sticks onto the chest.

Here is a closeup of the Zio Holter monitor.

The adhesive that holds the Zio on sticks well to dry skin (though it makes my skin itch a bit), but one day this week I got a bit sweaty cycling up to campus in my rain suit, and the monitor started to slide around. It seems to be firmly in place again after my skin dried, but I think it is slightly lower than its original placement.

I have to mail the Zio back to the manufacturer for them to unload the recorded data and send a report to the cardiology department.  I’m hoping that the cardiologist will provide me with the information I’m interested (things like what my minimum heart rate is when I’m sleeping, what the PVC burden is when I’m sleeping and overall, whether my PVCs are indeed slow-rate-dependent, whether there is a minimum heart rate for me above which very few PVCs are seen, … ).

Right now the PVCs are completely asymptomatic, which just means that I can’t tell when I have them without using an ECG. For asymptomatic PVCs, all the treatments are worse than the PVCs, so nothing needs to be done now, but if anything changes, I’ll want to know.  The treatments I’m aware of include ablation of the cells that trigger the premature complex, beta blockers to lower heart rate (not appropriate for slow-rate-dependent PVCs), and electrical pacemakers to start extra heartbeats at the sinoatrial node when the pacemaker cells fail to do so on their own.  I believe that my father had a pacemaker just for that purpose, and I suspect I may be getting one in a decade or so.

Halloween 2022

This year, we had a small turnout: only 22 kids, which is even less than last year’s small number.  We were not very ambitious in our decorations either.

I put the old packing-tape head sculpture on top of a pumpkin with 42 holes drilled in it (using 3 different sizes of Forstner bits).

The same 4-board strobe light that I used last year was inside the pumpkin lighting up the holes and the head, for a somewhat sci-fi look. I had the idea of putting the head on the pumpkin, but my wife was the one who suggested doing an abstract theme for the pumpkin itself. (The picture is a bit shaky, because I was too lazy to get out a tripod.)

My wife went with a more conventional carving.

She also had the carving conventionally lit with candles.

Our skeleton (Kyle) has been in the dining-room window since last year, but I put in the flashing lights again and gave him a cap.

I tied a rather random web this year and lit it with a UV LED strip. I apologize for using a non-web-spinning tarantula as the spider, but it was the only big spider toy I had.

My wife put all her Halloween effort this year into her costume as Puss in Boots. She works at an elementary school, so is almost required to wear a costume. They are not permitted to have weapons or gore as part of their costumes, so she substituted a feathered cat toy for the sword that Puss in Boots would usually have.

LED board schematic

I did a series of posts about the LED boards that I designed for lighting and strobes (starting with Summer project in 2014), but I just realized in going over the posts that I never posted the schematic nor explained how the board worked. I had to dig out the Eagle files on my old laptop to find the schematic, then redo it in Scheme-It to make it look reasonable.

Schematic for the LED board. This design is version 8, and is the one I actually had made.

The resistor R1 is a current-sensing resistor, measuring the current through the nFET Q2 and the LED. When the current is high enough, the voltage on the base of Q1 becomes large enough to turn on the NPN transistor Q1, lowering the gate voltage on Q2 and starting to turn the nFET off.  When the current is low, Q1 is off and the resistor R2 pulls the gate voltage for Q2 up, turning on the nFET more strongly. The Schottky diode D1 is just there to protect the LED from large reverse voltages if the board is hooked up backwards.

Power is dissipated in 4 places: the LED itself, Q2, R1, and D1. Based on the measurements in LED board I-vs-V curve,  the current is limited to about 118mA, so the voltage on the base is about 0.555 V when Q1 starts to turn on and R1 dissipates about 65mW. There is some current going through R2 and Q1 that doesn’t go through the LED (probably about 1–2mA), depending on the voltage applied to the whole board, but it is only about 1% of the total current, so I’ll ignore it—we may have another 30mW dissipated in R2.

I probably should measure the voltages across R1, on the base of Q1, on the gate of Q2, on the drain of Q2,  and across D1 to get detailed information about where the power is really being dissipated.  I think that the voltage across the LED should be about 6V when the board is fully on, and the voltage drop across the Schottky diode should be small (maybe 0.1V for 12mW).  For board voltages before the current limitation cuts in, almost all the power goes to the LED.  At higher voltages, the extra voltage drop and power dissipation is all in Q2, with around 700mW dissipated in Q2 when the board voltage is 6V higher than where the current limitation starts and 700mW delivered to the LED. That’s about as high as I’d be willing to go for continuous lighting, even with a heat-sink on the board.

I should be able to make the measurements fairly easily with the Analog Discovery 2, and I might do so later this week. One thing I’m curious about is whether the drop in current with higher board temperature is due to changes in the characteristics of the NPN transistor or the nFET.  The nFET is dissipating most of the power, so its junction temperature is probably changing much more, though the LED and the nFET together warm up the whole board, so the NPN transistor is getting warm also.