Question: I have mild-moderate HTN and have been on Bystolic 5mg/day for a little over a month with no problems. It seems to have stabilized me pretty well - better than the meds I took prior. In the last couple days, however, I have noticed readings were a little higher than they were the previous weeks, especially in the morning after waking and I was also feeling a bit more agitated but nothing to be alarmed about, as my BP would always level off for the rest of the day.

Just tonight, for no apparent reason, I started experiencing an adrenalin surge/anxiety/tachycardia. I took my BP and it measured 162/96. Pulse 96. 7h earlier it was 132/74. I also noticed my blood glucose was higher than usual @ 133. I usually am very relaxed at this time and start to fall asleep.

The only other time I had a similar hypertensive crisis similar to this was when I was trying to come off clonidine (stopped 04-08-14) which was the med I was on prior to Bystolic and experienced acute rebound hypertension. But those attacks only occurred in the early a.m. and involved tremor (this time, no tremor). My last dose of Bystolic was my usual 24h ago. It sure feels like rebound hypertension, but Bystolic is long acting, is taken once daily, and should not cause rebound this soon. The only other meds I take are for hypothyroid (Armour and T3/Cytomel) and for thrombosis (Xarelto).

I took my usual 5mg Bystolic dose tonight, but the BP decreased only moderately (152/93). I then took 0.5mg Xanax which seems to have helped (139/91).

I should also mention that I have a history of elevated serum and urine calcium, and passed a kidney stone 2 years back. I don't know if any of this is related to my elevated serum and urine calcium levels or to my diagnosis of primary hyperparathyroidism, but these surges are completely abnormal for me - other than being related to BP meds. I simply never had anxiety attacks/BP spikes like this before taking any BP meds!

On a side note, I showed within normal ranges on my urine catecholamines and metanephrine tests, so I don't think it's pheochromocytoma (although I was already taking Bystolic). Plus, if I did have pheo, wouldn't I have reacted sooner to the Bystolic since I read that certain beta blockers can worsen symptoms if you have pheo?
Bottom line: This occurrence makes zero sense to me, as Bystolic is suppose to block the adrenergic response like this, not make it worse, but the symptoms are almost identical to the rebound HTN I experienced with weaning off clonidine. Hopefully, someone can make sense out of this.
Less than 2h following the Xanax dose, I awoke from sleep and BP was back up to 160/98. This is crazy! I am going to ER.

I have already run most of those tests and all were normal. I also did a CCTA that showed a 0 calcium score - no plaque. BP was stable from starting Bystolic up through yesterday except after awakening, but then stabilized for rest of day up until after midnight. The BP spike I am experiencing is not my usual level. It is much higher than my pre-medicated level. I forgot to mention I was taking lisinopril concurrently with the Bystolic but stopped 2 weeks ago because of the dry cough. Even so, why would my BP level spike? The worst it should do is be slightly higher. It's like the Bystolic is no longer working and is causing a similar rebound.

Thanks for the quick response again.

As you have pointed out, I figured that stopping the lisinopril 2 weeks ago might be a factor, but the question that still remains is why would a spike ABOVE pre-medicated levels occur in the first place when I still was on Bystolic, especially when it seemed to be more effective than lisinopril? It baffles me me why a beta blocker couldn't keep it in check on its own. Perhaps because Bystolic is a selective beta blocker?

So, are you suggesting to stop Bystolic and then go with an ARB or use in combination? My docs have always suggested to employ a dual therapy. By the way, I did pop 10mg lisinopril 3h ago and my level is now 128/82, pulse 69. Don't know if it's due to the resuming lisinopril. I wouldn't think its onset of action is that quick?

I am fully aware that taking too much thyroid hormone of any kind whether it's synthetic T4 or T3 or even Armour can cause hyperthyroid symptoms which can cause exactly what I experienced (tachycardia, elevated BP, etc.), however, my thyroid levels were all within range (was tested 1 mo. ago), but are you saying it could still be a factor? Please elaborate.
A little BP meds history: The first BP med I started was HCTZ in the beggining of this year. I was on it for a month. It did nothing to lower BP, so I stopped it. The next one I tried was clonidine (2 mos.) which was a horrible mistake that caused varying BP levels, dry mouth, and sluggishness, and when I tried to wean off, gave the first symptoms of anxiety and acute rebound hypertension I ever experienced trying to come off it. Then Bystolic (1+ mo.), saved me from further spikes and rebounding from clonidine (I was also on lisinopril), until today. Prior to this, I had never touched a BP med nor ever had any "attacks" like this. Knowing that clonidine is a alpha blocker and Bystolic is s beta blocker makes me believe these reactions are related to the pharmacology of these drugs.

Thank you again for the timely response.

So, Bystolic is rarely used as a monotherapy? Also, it is my understanding that Bystolic also blocks the adrenergic response, thus I would think there might be a rebound effect similar to clonidine - or no? How else would I get a flood of adrenalin similar to clonidine rebound? Just am trying to understand the pharmacology here. It just would satisfy my curiosity to know the mechanism by which Bystolic induced an "overshoot" of catecholamines.

Regarding using an ARB, I do have a bottle of Losartan 50mg. The only question I have is that, unlike lisinopril, it shows as interacting with Bystolic via "pharmacodynamic synergism. Significant interaction possible, monitor closely." Which to me means it could lower BP too much? Thoughts?

Lastly, am I correct to assume that you feel Armour is a less predictable therapy because the amounts of the active hormones (T3, T4) can vary in a natural product than, say, synthetic T3 (Cytomel) and T4 (Levo), and therefore must be monitored?