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Blood pressure rises while sleeping
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Blood pressure rises while sleeping

I am 46 yrs. old. I have high blood pressure. My doctor has changed my bp medicine twice & next week I am to see a cardiologist. My blood pressure rises while I am asleep & at times wakes me up because I have fast palpitations in my heart. I get up & check my bp & it ranges from 165 - 190 to 110 - 128. So basically the minimum is 165/110. During the day it ranges from 140/96 - 160/108. Basically I have hard time getting back to sleep because my heart is racing. I also have asthma. I have tried finding on the computer why my bp rises while sleeping & really can't find answers. It usually say's bp lowers while sleeping & mine rises while sleeping. I wake up a few times a night. I am calm when I  go to bed at nights. I don't have anxiety. It just scares me how high my bp gets while I am sleeping. Any advice. Should I be concerned or is it okay for me to go the cardiologist a week from tomorrow. I worry I may have a heart attack or some kind of heart failure while asleep. I would say 80% of the time my blood pressue rises while I am asleep.
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I am having same problem.  Have been on 20mg lisinoprol for many years but doctor has just upped it to 40mg daily.  I decided insted of taking it all at once, I am taking 20mg in a.m. and 20 mg about l2 hours later and it seems to keep my pressure down while sleeping  I was getting up at night and taking the bp and it was l60/90, now with taking the two doses separately my sleeping bp has gone down to l30/80.  I hate taking these meds and am looking into other alternatives.  I am looking into an herb called Ashwaghanda and also an hibiscus tea.  I am sorry I cannot report anything to you on this as I have not yet tried them...they are coming in the mail. From what I have read the problem might also be caused by adrenal gland dysfunction, or problem with blood flow through kidneys.  You might want to research this before your visit to the doctor as I feel the more information you have on a medical visit the more will be considered.  Good luck
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I just saw a television show about a man who was going through a similar situation as yours.  His blood pressure and heart rate would go up significantly when he was sleeping; it was so bad, his wife would have to take him to the hospital.  The doctors didn't know why it was happening.  It turned out he had obstructive sleep apnea...he would actually stop breathing for several seconds while he was sleeping and this would cause the dramatic rise in his bp and heart rate.  His problem was found when he spent the night in a sleep clinic.  They gave him a c-pap machine and he hasn't had the problem since.  Perhaps you should look into this.  If you're married, ask your spouse to watch you when you sleep to see if you stop breathing intermittently.  Do you snore?  That is a sign of sleep apnea.  I wish you the best.
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QUOTE: I have tried finding on the computer why my bp rises while sleeping & really can't find answers.

Does the following information add to what you have have learned from the internet?

Mayo Clinic:Having an abnormal blood pressure pattern, such as high blood pressure in the morning, can mean that you have a health problem. Potential problems include:

■Poorly controlled high blood pressure
■Sleep apnea
■Tumors of the adrenal gland
■Kidney disease


Obstructive sleep apnea: one hypoxic (decrease of oxygen level in the blood/decreased oxygen to heart cells) night increases daytime blood pressure.  Also, asthma decreases oxygen level in the blood and can contribute to higher than normal bp.


Severe intermittent hypoxia, such as that experienced during episodes of obstructive sleep apnoea, results in a maintained elevation in blood pressure and a sympathetic hyperactivity, French researchers report in the European Respiratory Journal.

Obstructive sleep apnea syndrome (OSAS) is associated with nocturnal chronic intermittent hypoxia that leads to excess cardiovascular morbidity. Some of the proposed contributing mechanisms are an increased vascular sympathetic tone, resulting in an elevated systemic resistance and hypertension, an impaired arterial vasodilatory capacity, and chronic inflammation leading to endothelial dysfunction and atherosclerosis.

In order to better understand the pathophysiological events triggered by intermittent nocturnal hypoxia, Dr Tamisier and colleagues of the Laboratoire d'Exploration Fonctionnelle Respiratoire at the University Hospital in Grenoble examined whether the effect of intermittent nocturnal hypoxia on arterial blood pressure is sustained throughout the waking hours and whether it extends beyond the acute episodes.

The authors tested if, in young and healthy subjects, after 2 weeks of hypoxic attacks with 30 desaturations per hour, arterial blood pressure would remain elevated and if this would relate to increased sympathetic activity to muscle vasculature, decreased flow-mediated dilatation and increased circulating biomarkers of inflammation. They performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of exposure to intermittent hypoxia. They also assessed haemodynamic parameters, muscle sympathetic nerve activity, the baroreflex control of sympathetic response and inflammatory markers in the blood before, during and after exposure.

After a single night of intermittent hypoxia, mean blood pressure during the day increased by 3 mmHg and further increased after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean sympathetic nerve activity to the muscles increased across exposure time and the baroreflex control of sympathetic outflow declined. There were no evident changes in either vascular reactivity or systemic inflammatory markers.

Although intermittent hypoxia was applied during sleep, increased blood pressure occurred during the daytime and not the night-time, the authors report. The rise in blood pressure was sustained throughout the daytime, beyond the acute phase of severe intermittent hypoxia, but returned to baseline after 5 days of recovery.

These data are the first to show that increased sympathetic activation induced by intermittent hypoxia probably contributes to blood pressure elevation and may derive from a decreased baroreflex function. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.

However, one cannot extrapolate from these findings in young, healthy individuals to the typical (overweight and middle-aged) obstructive sleep apnoea patients. In this very young and lean cohort, intermittent hypoxia did not lead to any increase of nocturnal catecholamine excretion. Moreover, the employed model of hypoxia itself is not comparable to OSAS: a patient with OSAS experiences asphyxia during sleep, i.e. he suffers from both hypoxia and hypercapnia, whereas the experimental model reduces oxygen as well as carbon dioxide. This may lead to an underestimation of the effect of hypoxia, since increased carbon dioxide enhances the cardiovascular responses to hypoxia in both healthy individuals and sleep apnoea patients, the authors caution.

Reference:
14  nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans.

Tamisier R et al. Eur Respir J. 2011; 37: /119 N 128.

Thanks for sharing and if you have any other questions or comments you are welcome to respond.  Take care and I wish you well going forward.

Ken

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