Complete HB, bradycardia, and hypertension

NorthER,RN · Mar 23, 2005

Hi Zacarias. I'm no pro any more with cardiac - used to work CCU...

The high blood pressure may be firstly a response to hypovolemia - due to his illness he may not have been consuming sufficient fluids - a common problem with older patients, and I bet that he's on some Lasix or HCTZ. He may not have sufficient fluid for the pump, the receptors in his kidneys, brain and arteries may have caused a narrowing of the arteries to provide sufficient pressure for perfusion. Secondly with the 3rd degree heart block, there is a mismatch of the atria and ventricles, out put is very limited, and once again, poor perfusion which the body will try to respond to with an increase in blood pressure.

I look forward to the next person's response..... :rolleyes:

zacarias, ASN, RN · Mar 23, 2005

The high blood pressure may be firstly a response to hypovolemia - due to his illness he may not have been consuming sufficient fluids - a common problem with older patients, and I bet that he's on some Lasix or HCTZ. He may not have sufficient fluid for the pump, the receptors in his kidneys, brain and arteries may have caused a narrowing of the arteries to provide sufficient pressure for perfusion. Secondly with the 3rd degree heart block, there is a mismatch of the atria and ventricles, out put is very limited, and once again, poor perfusion which the body will try to respond to with an increase in blood pressure.
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North ER,

Thanks for the reply. He may have been hypovolemic although he's in pretty good health. NO meds at home for any illnesses. I like your theory though, just like we get tachy with low BP, he may have become hypertensive in response to the brady. I, however, believe he had been hypertensive for weeks prior to the HB.

athomas91 · Mar 23, 2005

i will go out on a limb here - but hypovolemia never causes hypertension in any way shape or form. his hypertension could have multiple causes - does he have a pheochromocytoma?? how's the thyroid? what meds did they have him on for the heart block as a adjunct for the pacer?? it could be circulating catecholamines due to the trauma of heartblock, hospitalization, and pacer insertion (pending surgery)...

all in all - 3rd degree heartblock nor hypovolemia cause hypertension - the body is only able to compensate so much - if one vasoconstricted THAT much in response to hypovolemia or heartblock - they would be losing digits and ears due to the effects on the smallest capillary systems.

his hypertension may be essential

NorthER,RN · Mar 23, 2005

Thanks Athomas and Zacarias: - I went back to the books for this Critical Care Nursing 2nd edition, chapter 26:

"Blood pressure is determined by cardiac output (blood flow) and the resistance to flow or total peripheral resistance. Simply put, arterial pressure equals cardiac output times total peripheral resistance. Total peripheral resistance is the sum of resistance in all vascular beds. Direct determinants of arterial pressure include cardiac output, aortic impedence and vascular resistance". "Indirect determinants that maintain control of arterial pressure are the autonomic nervous system, hormonal regulation, the renin-angiotensin pressor system, and the volume of extracellular fluid." When the blood pressure is inadequate to maintain sufficient blood flow through the kidneys, as may have initially happened, the juxtaglomerular cells of the kidney secrete renin which through the angiotensin presor system acts as a powerful vascoconstrictor.

The autonomic nervous system's mechanisms for control of arterial pressure include the baroceptor reflex, the chemoreceptor reflex and the central nervous system ischemic mechanism.... When arterial pressure is too low, the baroreceptor reflex system creates the opposite effect, resulting in a rise in blood pressure."

Once there is a critical degree of hypertension there are 2 pathways.

1. Local effects such as prostaglandins, free radicals, etc. lead to endothelial damage which leads to platelet deposition which causes an increase in mitogenic and migration factors which increases myointimal proliferation which leads to a further rise in blood pressure and vascular damage.

2. systemic effects such as renin-angiotensin pathways, catechol and vasopressin leads to pressure natriuresis which leads to hypovolemia and a further increase in vasopressors and a further rise in blood pressure and vascular damage.

So this is where my concern re: decreasing output relating to his heart block, decreased volume status came from.

But, having gone through pages of brilliant, concentrated stuff.... Was the guy taking cold medicine? Lots of those meds are a no no for hypertensive people. That, plus the essential hypertension may have been a problem. Was he obese? Was he a smoker, what were his lipids like, what was his previous cardiac status... so while I was off checking out the zebras, there was a horse. Thanks for the opportunity to read and think.

CritterLover, BSN, RN · Mar 23, 2005

blood pressure will often increase to compensate for low heart rate, in order to maintain adequate cardiac output.

this can sometimes be seen in people on high doses of beta blockers. more that once, i have pushed labatelol and watched the blood pressure go up, to compensate for the lowered heart rate (much easier to see this occur when you have an art line). the last time this happened to one of my patients was in the cath lab.....and the cardiologist had me push some atropine in order to raise the heart rate and allow the blood pressure come down :rolleyes: .....a little backwards, if you ask me, but it did actually work.

i have also seen it in some of the patients i saw in home health on clonidine. their bps would be running a little high, so the docs would increase the clonidine.....at the next visit the blood pressure would be even higher, and the heart rate lower.

Speculating · Mar 23, 2005

That's what I thinking his body is simply compensating for the extremely low HR. Secondly, from the original post it sounds as if this pt went to a tele/pcu floor. I not sure I would accept a third degree heart block on a pcu floor unless it was a dnr. I'm not sure I would accept anything short of a critical care bed for a pt in third degree. There's just to good of a chance that a third degree will convert to an arrest being on a pcu floor at night you've probable got about 6 pts. which wouldn't allow you adequate time to watch the HB pt

athomas91 · Mar 23, 2005

clonidine is an alpha 2 adrenergic agonist - it lowers blood pressure not heart rate. if heart rate is lowered it is a side effect (a rare one) but the blood pressure should not go up in response to this.

blood pressure has NOTHING to do with cardiac output

here is why - CO=HRXSV cardiac output = heart rate X stroke volume........ so if the heart rate drops the only way to compensate CO is to increase stroke volume... the only way to do that is to increase fluid volume (blood volume) the body does this via ADH (released from the juxtaglomerular cells in the macula densa in the wall of the distal tubule of the kidney) - ADH is released in response to decreased Renal blood flow, sympathetic nervous stimulation and decreased glomerular filtration rate. The body also responds via the renin-angiotensin-aldosterone system - which vasocontricts as well as aldosterone decreasing the reabsorbtion of H20 in the distal tubule. the RAA system however has a negative feedback mechanism - meaning that it turns itself off...renin is converted to angiotensin I which is converted to angiotensin II in the lung which is further hydrolyzed the angiotensin III which is responsible for inactivating the renin system.

as you can see - the body attempts to raise BP by vasoconstriction and increasing plasma volume but this increase only offsets the decrease due to the dramatic drop of CO due to a HR of 35. this man's hypertension was not caused by these things because of his heart rate. there was something else going on.

nursbee04 · Mar 23, 2005

(I may not be remembering this right.)

COxSVR=BP

If the CO goes down, then the SVR goes up to compensate. If the SVR goes down, then the CO increases to compensate.

Am I way off base? So could the SVR compensate enough for a SBP in the 200's? Or maybe there was something else going on?

hollyster · Mar 23, 2005

(I may not be remembering this right.)
COxSVR=BP
If the CO goes down, then the SVR goes up to compensate. If the SVR goes down, then the CO increases to compensate.
Am I way off base? So could the SVR compensate enough for a SBP in the 200's? Or maybe there was something else going on?

You are right. SVR is responsible for the hypertension. BP does not go up when a pt goes into heartblock or is hypovolemic. Pt's vascular system is clamped down in response to low CO.

Stress is also a factor. Knowing that this little box is the only thing keeping you alive would be terrifying. I do not understand why they would make him wait. Was he on anti-coagulants?

The pt may not of infarcted. Heart is an electrical system sometimes the pathway wears out with age. I have seen quite a few pts who showed no signs of MI (negative troponin,cpk and cath) but were in 3rd degree.

This happened to my 78 year old father. He c/o fatigue after his morning bike ride. When rescue arrived he was in third degree heart block. They did a full work up(including cath) and everything was negative. They put a permanent in him and he is fine. He rides a bike five miles a day.

zacarias, ASN, RN · Mar 24, 2005

What great responses everyone!

I tend to agree with Hollyster and athomas in that there's no way this man could have compensated to that high of a BP. I tend to think that his essential hypertension precipitated the block. A BP of 230-260/60 could indeed cause ischemia leading the HB.

One of you said stress could have been a factor because of him knowing he had HB. Well, which came first. He was at home not feeling well for a couple weeks. How long was he actually in HB? We don't know...I can't imagine too long, his ventricular rate was dang low. Who knows. Don't worry folks, they ordered thyroid and coag studies. :)

As for his placement, he was very stable (as stable as you can be with a temp. tranvenous pacer). He showed no signs of overload, pump failure, or and active MI that would absolutely necessitate him being in the ICU. It's kind of like the other thread where some people think all 'R/O MI' should be on a CCU. I don't agree but I see where they're coming from.

Thanks again all for your comments.

tenale123 · Nov 23, 2011

very interesting subject. I,ve actually looked after 2 pts now with same scenario. The first pt, the cardiologist did not want to treat BP cos he said that PPM will sort it. is there anyone who can have access to this research

http://www.ncbi.nlm.nih.gov/pubmed/7457024 would be interesting to know in detail the findings