Sleep Apnea Syndrome as a Cause of Secondary Hypertension

Sleep Apnea Syndrome as a Cause of Secondary Hypertension

   Jul 30 , 2018

   Michael White

A case report.

Poreba R, Derkacz A, Andrzejak R.

Pracownia Hemodynamiki, Klinika Kardiologii, Akademia Medyczna, ul. M. Sklodowskiej-Curie 66, 50-369 Wroclaw, tel./faks: +48 71 784 09 38, e-mail:

A case of a 51-year old man, suffering from drug-resistant hypertension, complaining of hypersomnia and fatigue during the day, is presented. In the course of diagnostic procedures the diagnosis of sleep apnea syndrome was established. Continuous positive airway pressure (CPAP) therapy was successfully started. Examination carried out 3 months later revealed good response to pharmacological treatment with normal levels of blood pressure.

PMID: 16362859 [PubMed - in process]

From Mike: Apnea causes or worsens HBP. Optimal Breathing improves BOTH. Begin here

Blood Pressure Evolution After Acute Ischemic Stroke in Patients With and Without Sleep Apnea

Selic C, Siccoli MM, Hermann DM, Bassetti CL.

Neurology Department, University Hospital of Zurich, Zurich, Switzerland.

BACKGROUND AND PURPOSE: Sleep apnea (SA) is an independent risk factor for arterial hypertension and is present in 50% to 70% of patients with ischemic stroke. The effects of SA on blood pressure (BP) and stroke outcome in the acute stroke phase are essentially unknown. 

METHODS: We studied 41 consecutive patients admitted within 96 hours after stroke onset. Stroke severity on admission (National Institutes of Health Stroke Scale [NIHSS]) and stroke outcome at discharge (modified Rankin Disability Scale [mRS]) were assessed. Nocturnal breathing was assessed with an ambulatory device the first night after admission. SA was defined by an apnea-hypopnea-index (AHI) > or =10/hour, and moderate-severe SA (MSSA) was defined by an AHI >30/hour. BP monitoring was performed during the first 36 hours after admission. A nondipping status (NDS) was defined by a ratio >0.9 of mean systolic BP during nights 1 to 2/mean systolic BP during day 2. 

RESULTS: SA was found in 28 (68%) and MSSA in 11 (27%) of 41 patients. A correlation was found between AHI and both NIHSS (r=0.331; P=0.035) and mRS (r=0.341; P=0.031). Patients with MSSA had higher systolic and diastolic BP values during night 1 (P=0.003), day 2 (P=0.004), and night 2 (P=0.03). NDS was found in 26 (63%) patients. Nondippers had a similar AHI but higher NIHSS (P=0.004) and mRS (P=0.005) than dippers. AHI and NDS were confirmed to be independent predictors for both stroke severity and stroke outcome in a multiple stepwise linear regression model. 

CONCLUSIONS: SA severity is associated with high 24-hour BP values but only weakly with stroke severity and outcome. Conversely, NDS is linked with a more severe stroke and a poorer evolution but not with SA severity. These data suggest different, although overlapping, pathophysiological and clinical implications of circadian and nocturnal BP values in acute stroke.
PMID: 16282549 [PubMed - indexed for MEDLINE] Email induced sleep apnea

From Mike: Optimal breathing development lowers blood pressure and reduces or eliminates waking up not breathing.   Begin here  Diaphragm strength and sleep.
It's a little known fact that your diaphragm muscles can be a HUGE help in reducing sleep apnea. How? 
The diaphragm muscles are responsible for breathing – weak muscles mean your breathing isn't as strong as it should be.
But there is hope!
There are a few key breathing exercises that are meant to strengthen the diaphragm and increase oxygen intake. 
If you're like most people, you know that one of the biggest dangers of untreated sleep apnea is a reduction in the body's intake of oxygen.
Without the right amount of oxygen, we experience fatigue and depression, and low oxygen levels can also lead to serious health conditions such as heart failure. 
By following the breathing exercises included in our Sleep program you'll be well on your way to a stronger diaphragm - and much better oxygen intake.