Sleep Apnea Syndrome as a Cause of Secondary Hypertension
Sleep Apnea is a serious sleep disorder in which breathing repeatedly stops and starts during sleep. The several risk factors include age and obesity. It's more common in men. The symptoms include snoring loudly, feeling restless during sleep and feeling drained and tired even after a full night’s sleep.
Main Types of Sleep Apnea are:
Obstructive sleep apnea, the more common form that occurs when throat muscles relax
Central sleep apnea, which occurs when your brain doesn't send proper signals to the muscles that control breathing
Complex sleep apnea syndrome, also known as treatment-emergent central sleep apnea, which occurs when someone has both obstructive sleep apnea and central sleep apnea
Your Diaphragm’s Role in Reducing Sleep Apnea
It's a little known fact that your diaphragm muscles can be a HUGE help in reducing sleep apnea.
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.
Scientific Studies to support Connection between Sleep Apnea and Secondary Hypertension
Poreba, R., Derkacz, A., & Andrzejak, R. (2005). Zespół bezdechu sennego jako przyczyna wtórnego nadciśnienia tetniczego. Opis przypadku [Sleep apnea syndrome as a cause of secondary hypertension. A case report]. Kardiologia polska, 63(5), 549–552.
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 a good response to pharmacological treatment with normal levels of blood pressure.
PMID: 16362859 [PubMed - in process]
Sleep Apnea causes or worsens High Blood Pressure. Optimal Breathing improves BOTH.
Blood Pressure Evolution After Acute Ischemic Stroke in Patients With and Without Sleep Apnea
Selic, C., Siccoli, M. M., Hermann, D. M., & Bassetti, C. L. (2005). Blood pressure evolution after acute ischemic stroke in patients with and without sleep apnea. Stroke, 36(12), 2614–2618. https://doi.org/10.1161/01.STR.0000189689.65734.a3
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 non-dipping 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]
Optimal breathing development lowers blood pressure and reduces or eliminates waking up, gasping for breath. Begin here for improved diaphragm strength and enhanced quality of sleep.
References: Mayo Clinic