additional thoughts...

Yesterday's meeting was so packed with information, that I missed recording a couple things, that if not for the occasional reader, I need to record for myself.

The biggest omission was info on albuterol (sulfate). This is the substance in the most common form of inhaler, prescribed for shortness of breath, ie, wheeziness. I have had one for a couple years. Jan has one too, suggesting its further commonness. Each inhaler contains 200 doses. The fact that I still have 50 huffs left testifies to the fact that I don't use it all the time. In fact I use it very little. Such was not the case during the pneumonia where I would sometimes take a hit to open the lungs up enough for O2 in order to get to sleep. One can take a couple hits every 4-6 hrs several times per day.

Albuterol apparently is a CNS stimulant. One of its effects is to speed up heart rate. Since speeded up heart rate may be a pre-cursor to SVT, in my case it is surely contraindicated, The cardio doc suggests that the next time I need to work on shortness of breath, I get an inhaler which is steroidal. This dovetails very nicely with what the pulmonologist in PHX did. My last bout of wheezing in AZ, he gave me a cortisone shot, and some prednisone pills to be taken in a decreasing order (eg, 4,3,2,1 per day). (He added a very short course of antibiotic as well.) That did the trick for me. Not incidentally, my sister-in-law has been treated the very same way.

I have already reported that my heart rate is much more sensitive now without the attenolol doing its thing. And I am much more sensitive to caffeine. It follows that I will also be much more sensitive to albuterol.

Therefore: no albuterol for me!

Watching and waiting...

At long last, I've heard back from my cardiologist. A week late is much better than never. Last week when I took the Holter monitor in, the tech who read it reported to me that he didn't see anything crazy, which I took to mean not too many critical values. Longest pause between heart beats was 2.16 sec. The cardiologist said we can live with that. I did have one period of low rate at 4 am one morning where the HR was at 37. Take 60 sec (1 min), divide by 2 sec and you get 30 beats per minute. A beat every other second means a 2 sec pause. So this is where the pausing was seen. He was not too concerned about that either.(He recalled an emergency room case where the patient had two periods of absence of HR, one of 10 sec and one of 20 sec and was asymptomatic of it!) What this means is that discontinuing the attenolol was the right thing to do. Its absence has led to the absence of longer pausing in my heart beats.

The bps that I have been worried about--elevated as much as 150/95--actually just crack the threshold now of hypertension. Definitions of hypertension have tended to wander about as much as what is on the food pyramid. I am to keep recording these and discuss with my primary guy. We may or may not go back on the lisonopril at that time. (My earlier dose was a half of a 20 mg tablet, daily.) I think the cardio guy thinks that my body may still be adjusting to the new reality of no beta blocker, so more time free of heart meds will be good to see whether I am symptomatic in any other way. Again today, when the nurse took my bp in the office, it was like 110/71. I could live a long time with that! So there is some disconnect between what is seen when I am up and about, and what is seen after I have been sleeping. This data, too, needs to figure into lisonopril usage. (HR during this measurement was 115.)

I am getting a little pre-syncope, which is probably orthostatic but I can usually control it by moving my head down, or breathing rapidly for a moment. It is not happening when I am active. These are not daily, more like weekly. I am to track those events.

The other half is what is happening in the upper chambers. There there were instances of SVT--which stands for supra-ventricular tachycardia--but the longest one was for just more than a minute. And, moreover, these were not all that speedy, for example, less than 130 bpm. And it wasn't clear that there were a great many of these. He said I can also live with this. Again, I am not sure when or if I feel these instances, so I appear to be asymptomatic. If I do feel them, I am to take my pulse (like I can do that reliably). Even get a bp measure at that time. And if they continue seek help.

So no ablation at this time. No pacemaker at this time. I'm happy. I'll just have to see whether I can progress to feeling less fatigued by doing some walking and see whether I can improve the condition my condition is in that way.

Attenolol, wherefore art thou..?

I have been 5 days without attenolol (50 mg), a beta blocker, which I have taken since I was roughly 50, that is, 27+ years. It was prescribed to counter a couple experiences that I had at that age, which resulted in fibrillation. Both experiences involved pushing my body too hard. The first was a work out outcome--I both ran and lifted weights in the same session. A carotid massage by the physician on call at Budge Clinic at the time (Ed Redd), brought the HR down into normal territory.  The second, a year or two later, was an extended trumpet solo in a big band that put me back into fibrillation. This was during a performance of the second tune from the end of the concert (Take the A Train by Duke Ellington). I had a feeling (high) that all was not right, but finished the concert and then Jan and I drove leisurely to the hospital and hung around in the parking lot deciding whether I should go in. 45 min after the onset of the event, we went in and my HR was 245 bpm. The nurse doing the measurement mused that after that long in fibrillation, I should be dead. On that occasion the heart did not come down in the right rhythm. So I was hospitalized until such time as it did and then went to SLC for electrophysiology of the heart. The outcome there was not significant for any ablation, but they found out that attenolol would nicely limit my heart rate. Too late, I found out that I could have maintained my trumpet playing during this period, under the medication, but instead I took almost 2 decades off. Bummer!

Which brings us to today, the fifth attenolol free day. But first, a digression. When we were invited to Mexico by good friends a number of years ago, I decided I would like to try snorkeling. I never really did this in earlier days, but during my 40s, I was swimming 3 miles per week, in 1-mile workouts. (This probably saved my fibrillating heart!). I did this workout faithfully for 12 years from age 39 to age 51. In anticipation of the Mexico event, I got back in the pool. Granted, a large number of years had passed since I was a regular swimmer, but in a lap and a half, I was totally out-of-breath. So out-of-breath in fact that I had to grab onto the lane rope. It was like a huge stop was placed on my heart. This was the most noticeable time when I think the attenolol was at work. It stopped the planned snorkeling in its nascent tracks. (It is also possible, in retrospect, that I was already down to the 44% lung capacity caused by my recently-discovered, lamed-assed left diaphragm muscle.)

Oh yes, the anecdotal effects of being attenolol free.

1. Two cups of tea in the morning with breakfast has been a part of my morning for many years. Real tea. No camomille. This past five days, this amount of tea has made me so high and jittery, it is unbelievable. So I cut back to one cup. More tolerable, but still high. In fact, when I began typing this post, I was quite high. A minute or so ago, I felt myself finally coming down some, and immediately experienced some pre-syncope--almost fainting--light headedness.   I still feel somewhat high.

2. Increased variability in heart functions. My heart rate after just walking from one room to the other now is in the 90s. Prior to this during a workout on the exercycle, it would take me 10 min to get my HR to 100 and to keep it there. In fact the first day without the attenolol it seemed to me that my HR was almost always at >90 bpm whenever I measured it (a lot!). By the second day I was beginning to see some returns to resting rates = for me, low 60s. Perhaps there was an anxiety component, I don't know. 

The hour before rising this morning after nearly 10 hours of sleep, I dozed in bed in that relaxation state of well being in which respiration is slow and deep. I was in it for quite a while, it seemed. When I got to the breakfast table, I immediately took a bp reading. Nasty surprise: it was 155/95! I have never had such a high reading that I can recall. But we all know that bp is amazingly variable, so after breakfast and all the normal activity that goes with it, I repeated the test. BP now at 110/66 = fantastic! So normal variability? I don't know. I am guessing that the attenolol would have prevented the high reading. 

So, in part, what the docs want to see appears to be happening. My heart is beating faster. Still don't know whether this will result in less ventricular pausing as well. 

The sleep cycle difficulties appear to be on the wane. I have a new CPAP machine and perhaps that has something to do with it. But also, I am remarkably free of nasal congestion right now. Not taking any Nasonex. Perhaps it is a low season for allergens. In any case, without a nap yesterday, I was dead in the water by 7:30 last night and turned the light off at 7:45 with the Utah Jazz behind by 9. I awakened at 5:40 for 9:55 hrs of sleep. I think I arose just once during the night. This makes a cumulative third or fourth night of successful sleep. Yet right now I am still tired. Also, no melatonin helper on the front end.

Still to come: I am back on the Holter monitor for 24 hrs commencing Friday am. So in the absence of readouts Saturday won't know more about current heart function until early next week.

Until then..

living in personally interesting times

The psychology involved with conscious breathing is interesting. For the most part we don't think about the process. It is automatic. But when one lacks O2 (or perceives that), it is both automatic--one tries to suck in air and conscious as in "Oh my God, I can't breathe." One then may do several things consciously: breathe forcefully several times and wait for the feeling of insufficiency to subside; monitor one's state alertly, for instance, no longer sleeping, or relaxing.

The one-two punch that I have experienced this past couple years has consisted of: 1. apnea, where one unconsciously stops breathing for more than 10 sec at a time (the break in the snoring), and 2. the additional insufficiency of O2 produced by restricted lungs (at 44% of normal) and pneumonia where the lungs are further compromised in re their processing of O2.

Here is how these two conditions appear to be compromising my ability to get to sleep, and once there to stay asleep, or to get back to sleep. Under normal circumstances, when I approach sleep, I slow (or automatically my body slows) my respiration rate. An outcome of this slowing is a relaxation response, felt as coming down, or indeed, going to sleep. Ordinarily this proceeds and one goes blissfully to sleep. However, a correlate of having sleep apnea, is that the slowing of respiration leads to an apnea. This, too, may pass unconsciously and any insufficiency is dealt with by the CPAP machine which is pumping air into the nostrils. (The theory is that this increased pressure of air keeps the soft palate from collapsing, which is the cause of the apnea. No air pressure, as in slow respiration, increases the likelihood of an apnea, since there is no air flow to keep the soft palate open.) And, for the 7 years that I have had the machine it has worked beautifully. I have slept like a baby and have been alert all day. Post chemo, and then post pneumonia, this has all changed.

Pavlov, in the earliest days of modern psychology, showed that any neutral stimulus could, if paired in time with a stimulus significant to the organism, acquire a similar significance as the natural one. (Does the  name Pavlov ring a bell?) In his experiments where his dogs were hungry, food was the significant stimulus, and bells, tones and what not were the neutral stimuli. In a few "associations" of the neutral and biological stimulus the neutral stimulus would produce some of the same response seen to the biological one. Much later it would be shown that if the biological stimulus was a very, very powerful one, for example, the animal was sickened--as happens with food poisoning--this process did not require a precise pairing of the neutral stimulus and the biological one in time, nor did it require a number of pairings--the conditioning happened in a single trial. This is the case known to many of you as taste aversion. You get sick some time after eating a food and you avert to the taste of the food thereafter. The very thought of the food may make you queasy.

So now that first apnea, leads to a quick alerting, increased respiration rate, and indeed, some panic. This set of events has occurred more than I like to think about since I started with the pneumonia but was particularly acute whilst in PHX this winter. It has led to truly fucked up sleeping times. Jerking awake at 2 a.m. and then staying awake until after breakfast when one may (or just as likely may not) successfully get to sleep. Definite, not to be denied, urges to sleep during the day (a feature of narcolepsy). Being foiled in the subsequent attempt, until the sleep deprivation reaches such a level sleep occurs no matter. Even then, the sleep cycle that ensues may be shortened to three instead of 4 hours. Inadvertent self-treatment with alcohol helps with the first cycle, but repeated use shortens the first sleep cycle.  Mike Stones' suggestion of melatonin at bedtime has also helped. In fact, I have used it successfully the last 2-3 nights and spent the full night in bed, rather than sleeping sitting up or leaving the bedroom to do computer puzzles and read the op-eds of the day.

Yesterday, a particularly acute failure to sleep mid-afternoon led me to plead with Mike for some other alternative and he said he would prescribe some tramazepan (xanax). That fell through the cracks of the system and I ended up again with the melatonin which was satisfactory. Indeed the failure to deliver on services may be good, as I don't want to be taking anything stronger.

Now we know that these sleep symptoms are also related to what is happening with my heart. The relaxation response associated with the apnea is probably also associated with the slowing of ventricular movement in the bottom chambers of the heart. Discontinuing the Tenormin (attenolol), we'll see, may decrease that slowing. Will it decrease anything else? Will it increase anything else? After 27+ years what will happen? The docs are banking on the fact that I have had little light headedness or fainting (none) during the day, so I should be able to tolerate the offset of the attenolol. We'll see.

reality ain't what it used to be

Cardiology wanted their monitor back this morning and I was surprised when I was asked to sit so they could get the preliminary results from the 48-hr ECG. They were looking for significant events and they immediately found them. In general, they found a number of instances where my heart stops beating for a couple seconds, but one reading was as high as 5 sec. These were ostensibly during sleep, but could also have been when I was trying to get back to sleep (eg., 2:30 am). This was enough to have a cardiologist read the printouts, which do a mighty fine summary of their own. There were multiple instances of SVT anomalies, to wit: speeded up areas (in the heart above the ventricles) and a number of instances where the heart slowed down in the ventricles. This condition is called tachycardia/brachycardia and is difficult to treat because one wants to slow down one area of the heart while speeding up another. And most medications are too general for that. For example, the attenolol, a beta blocker, that I have taken for 28 years has the effect of slowing the heart, so that while that is good for the supra-ventricular regions, it's contrary to the speeding up needed in the ventricles. Can you say Pacemaker? But wait.

First we are going to see whether simply dc'ing the attenolol allows the ventricles to speed up some, without the SVT going beserk, This would be the best outcome, and we will explore that first. So, no more attenolol. It will take 4-5 days to clear the system and I will go back on the Holter monitor to see what the undrugged heart looks like. I am to watch for palpitations, flutters and the like. Normal activity; no working out (doh!). Trumpet okay, nothing above a high C the doc said and smiled.

It appears as though the ventricular slowing is happening primarily at night, so I am at low risk of passing out during the day. Therefore we take this first step and if successful outcomes, then no pacemaker. If not, and the SVT area speeds up and has its own anomalies, then it may be an ablation study where they check for the electrical path causing the SVT anomaly and burn it out. Good outcome, still no pacemaker,  Otherwise, pacemaker.

Ya learn something new everyday...