Obstructive sleep apnea (OSA) occurs when the throat-supporting muscles relax, which blocks or constricts the airway, ceasing sleep breathing. Obstructive sleep apnea and hypertension have been reported to coexist in individuals. Evidence suggests that OSA can be a potential secondary contributor to elevated blood pressure in patients with resistant hypertension. Alternatively, OSA patients are at high risk for developing resistant hypertension. Resistant hypertension is that state when the blood pressure persistently remains high even with concurrent use of maximal doses of three different classes of antihypertensive drugs (one of them should be a diuretic).
Who Is Susceptible to OSA With Hypertension?
About 50 percent of OSA patients have been reported with preexisting hypertension, and the vice-versa holds true for 30 percent of hypertensive cases. This independent association of OSA with hypertension is primarily seen in elderly women, prehypertensive individuals, primary care patients, spinal cord injury, and stroke patients. The study of the association in children is yet pending, but the relationship stands ground in this population as well.
What Are the Different Associations of OSA With Hypertension?
OSA and resistant hypertension.
OSA and nocturnal hypertension.
OSA and masked hypertension.
What Is the Cause of OSA Associated Hypertension?
In normal individuals, there is a diurnal variation of blood pressure, also known as the dipping phenomenon. This phenomenon defines that the blood pressure dips by 10 to 15 percent during sleep than the waking blood pressure. Autonomic nervous reflexes carry a big influence over circadian pressure variation. The dipping of pressure is also characterized by cardiovascular stability.
Sleep can be divided into two halves: rapid-eye movement (REM) sleep and non-rapid-eye movement (NREM) sleep. NREM is characterized by lower blood pressure, bradycardia (decreased heart rate), reduced cardiac output, systemic vascular resistance, and serum catecholamines. REM sleep, occurring during the second half of sleep, is characterized by surges in sympathetic neural output, tachycardia, and increased blood pressure. These REM changes are diagnostic notes for preexisting cardiovascular conditions. More than NREM sleep, REM holds the more significant pathologic role in OSA as REM is also associated with widespread muscle atonia, which makes the upper respiratory tract prone to collapse. Additionally, OSA is associated with REM due to disadvantageous pulmonary mechanisms and associated profound oxyhemoglobin desaturations.
What Is the Pathophysiology of OSA Associated Hypertension?
The exact relationship between OSA and hypertension is minutely studied to conclude the presence of multifactorial pathophysiology.
OSA induces hypoxia which causes systemic inflammation and oxidative stress, which results in increased endothelin-1 and a decrease in the nitric oxide content of endothelial cells, increased arterial peripheral resistance, and hypertension.
Periodic hypoxemia (periodic decrease in oxygen saturation), frequent arousals (regular waking up from sleep), and sleep deprivation activate the sympathetic neural pathways, which increase the cardiac output and induce peripheral vasoconstriction, which further elevates the blood pressure.
OSA patients, comparatively, have higher levels of renin production, which leads to elevated levels of plasma angiotensin-II and aldosterone. These, together, cause hypertension due to vasoconstriction and sodium-water retention.
What Is the Pathophysiology of OSA Associated Cardiovascular Diseases?
OSA has a profound defect on the cardiovascular system via various mechanisms.
Periodic hypercapnia (increase in partial pressure of carbon dioxide above 45 mm Hg) and hypoxemia (oxygen deficiency) cause sympathetic pathway activation and elevation of catecholamines (adrenal gland hormones) which increase the blood pressure and heart rate.
Secondarily, frequent arousal and sleep deprivation resulting from asphyxia can also activate the sympathetic nervous system. According to studies, hypoxemia increases oxidative stress, systemic inflammation, and endothelial dysfunction. Over time, these factors and hemodynamic changes largely contribute to the onset of atherosclerotic cardiovascular diseases, left ventricular hypertrophy, and heart failure.
Thirdly, the body generates negative intrathoracic pressure in response to the narrowing of the pharynx (during OSA episodes), which further increases mechanical stress over the ventricles and atria.
Over time, cardiac remodeling can occur as left ventricle hypertrophy and left atrial enlargement, which can ultimately lead to diastolic heart failure and atrial fibrillation. Additionally, impaired baroreflex sensitivity and regular activation of the renin-angiotensin-aldosterone axis (RAAS) collectively add up to cardiovascular disorders.
How to Manage OSA Associated with Hypertension?
Hypertension needs to be managed with a pharmacotherapeutic and lifestyle modification like management of comorbidities like obesity, smoking, alcohol abuse, etc. Hypertension can be managed with drugs from classes of ACE inhibitors, diuretics, calcium channel blockers, and beta blockers. These medications are prescribed by a cardiologist even through online consultations and prescriptions. Individuals already on these medications can also get a prescription refill online to ensure continuation of the treatment as advised by the cardiologist.
Managing OSA is completely another approach. Usually, OSA management is done via the usage of oral appliances and CPAP (continuous positive airway pressure) machines. Oral appliance therapy, reportedly, not just improves OSA but also aids in blood pressure reduction. Studies have shown that CPAP treatment also substantially reduces daytime and nighttime systolic blood pressure and nighttime diastolic blood pressure. CPAP has been more beneficial against nocturnal systolic pressure than diurnal pressure. Resistant hypertension, which is nonresponsive to many drugs, seems to respond to CPAP therapy.
CPAP treatment has been associated with the following:
Improvement of hypoxemia (declined oxygen saturation).
Decreased nocturnal sympathetic nervous activation.
Improvements in arterial oxygen saturation.
This aids in mitigating systemic inflammation and oxidative stress. Additionally, a reduced negative intrathoracic pressure (by the positive ventilation of the CPAP) results in advantageous hemodynamic results. Diuretic drugs have a better response against OSA-associated hypertension by improving parapharyngeal edema (swelling in the deep neck space). Usually, diuretics are added to the general antihypertensive modalities of OSA-hypertensive cases.
Since the incidence of hypertension, OSA and their association is on a rapid rise. So regular monitoring of pressure is absolutely necessary to keep a check and introduce management protocols accordingly. Control in the nascent stages is the need of the hour as persistent events (even isolated hypertension) can cause cardiovascular structural changes which are etiologic to heart diseases like heart failure and stroke. Further studies are required in the younger population to control OSA-associated hypertension in very early stages, hence, creating a good prognosis. It is the prerogative of the general physician to advise, prescribe, and formulate modalities to ideally manage hypertension, OSA, and, ultimately, cardiovascular diseases.