Modern understanding of the cardiovascular system began with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733.[152][153] However, hypertension as a clinical entity came into its own with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896.[154] This allowed easy measurement of systolic pressure in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculated with a stethoscope while the sphygmomanometer cuff is deflated.[153] This permitted systolic and diastolic pressure to be measured.

^ Jump up to: a b Burt VL, Cutler JA, Higgins M, et al. (July 1995). "Trends in the prevalence, awareness, treatment, and control of hypertension in the adult US population. Data from the health examination surveys, 1960 to 1991". Hypertension. 26 (1): 60–69. doi:10.1161/01.HYP.26.1.60. PMID 7607734. Archived from the original on 2012-12-20. Retrieved 5 June 2009.

Approximately half of individuals with hypertension have OSA, and approximately half with OSA have hypertension. Ambulatory BP monitoring normally reveals a "dip" in BP of at least 10% during sleep. However, if a patient is a "nondipper," the chances that the patient has OSA is increased. Nondipping is thought to be caused by frequent apneic/hypopneic episodes that end with arousals associated with marked spikes in BP that last for several seconds. Apneic episodes are associated with striking increases in sympathetic nerve activity and enormous elevations of BP. Individuals with sleep apnea have increased cardiovascular mortality, in part likely related to the high incidence of hypertension. http://www.sandysidhumedia.com/wp-content/uploads/2013/12/SSM_Logo_White.png
Polycystic ovarian syndrome. Thought to be related to insulin resistance, this disorder involves the release of extra male hormones by the ovaries, which can lead to abnormal menstrual bleeding, excessive hair growth, acne, and fertility problems. It is also associated with an increased risk for obesity, hypertension, and — in the long-term — diabetes, heart disease, and cancer.
^ Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents, National Heart, Lung, and Blood Institute (Dec 2011). "Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report". Pediatrics. 128 Suppl 5: S213–56. doi:10.1542/peds.2009-2107C. PMC 4536582. PMID 22084329.
With secondary hypertension, if the condition causing the high blood pressure can be resolved (e.g., by removing an adrenal tumor or stopping a medication) or controlled (e.g., by controlling diabetes or thyroid disease), then blood pressure levels may fall to normal or near normal levels. When a cure is not possible and control of the underlying condition consists of minimizing further damage, as may occur with kidney disease, then hypertension will be controlled with a combination of medications and the person will be monitored closely to help maintain organ function and address acute problems as they arise.
Emergency department visits for hypertension with complications and secondary hypertension also rose, from 71.2 per 100,000 population in 2006 to 84.7 per 100,000 population in 2011, while again, admission rates fell, dropping from 77.79% in 2006 to 68.75% in 2011. The in-hospital mortality rate for admitted patients dropped as well, from 1.95% in 2006 to 1.25% in 2011. [37]
Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. [14, 15]

Although treatment of sleep apnea with continuous airway positive pressure (CPAP) would logically seem to improve CV outcomes and hypertension, studies evaluating this mode of therapy have been disappointing. A 2016 review of several studies indicated that CPAP either had no effect or a modest BP-lowering effect. [29] Findings from the SAVE study showed no effect of CPAP therapy on BP above usual care. [30] It is likely that patients with sleep apnea have other etiologies of hypertension, including obesity, hyperaldosteronism, increased sympathetic drive, and activation of the renin/angiotensin system that contribute to their hypertension. Although CPAP remains an effective therapy for other aspects of sleep apnea, it should not be expected to normalize BP in the majority of patients.
Naturally, since the metabolic syndrome is a disorder of energy distribution and storage, fat accumulation explains for a significant proportion of cardiovascular risk. However, obesity without metabolic syndrome does not confer a significant cardiovascular risk, whereas metabolic syndrome without obesity is associated with a significant risk of diabetes and cardiovascular disease. This association of metabolic syndrome with diabetes can be illustrated by generalized lipodystrophy (near complete absence of adipose tissue). The animals and humans with generalized lipodystrophy develop signs of metabolic syndrome in the absence of adipose tissue; and the metabolic syndrome progresses to type 2 diabetes. Adipose tissue transplantation in transgenic mice with lipodystrophy can cure the type 2 diabetes.
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).

Creatinine is a chemical waste molecule that is generated from muscle metabolism. Creatinine is produced from creatine, a molecule of major importance for energy production in muscles. Creatinine has been found to be a fairly reliable indicator of kidney function. As the kidneys become impaired the creatinine level in the blood will rise. Normal levels of creatinine in the blood vary from gender and age of the individual. https://s10721.pcdn.co/wp-content/uploads/2009/05/when-meditation-gets-hard.jpg
Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality.[6] It works by decreasing the liver's production of glucose.[87] Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, and agents that make the body more sensitive to insulin.[87] When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.[6] Doses of insulin are then increased to effect.[6][88]

Your doctor may recommend a 24-hour blood pressure monitoring test called ambulatory blood pressure monitoring to confirm if you have high blood pressure. The device used for this test measures your blood pressure at regular intervals over a 24-hour period and provides a more accurate picture of blood pressure changes over an average day and night. However, these devices aren't available in all medical centers, and they may not be reimbursed.


^ Jump up to: a b Campbell, NR; Lackland, DT; Lisheng, L; Niebylski, ML; Nilsson, PM; Zhang, XH (March 2015). "Using the Global Burden of Disease study to assist development of nation-specific fact sheets to promote prevention and control of hypertension and reduction in dietary salt: a resource from the World Hypertension League". Journal of clinical hypertension (Greenwich, Conn.). 17 (3): 165–67. doi:10.1111/jch.12479. PMID 25644474.
^ Xie, X; Atkins, E; Lv, J; Bennett, A; Neal, B; Ninomiya, T; Woodward, M; MacMahon, S; Turnbull, F; Hillis, GS; Chalmers, J; Mant, J; Salam, A; Rahimi, K; Perkovic, V; Rodgers, A (30 January 2016). "Effects of intensive blood pressure lowering on cardiovascular and renal outcomes: updated systematic review and meta-analysis". Lancet. 387 (10017): 435–43. doi:10.1016/S0140-6736(15)00805-3. PMID 26559744.
^ Jump up to: a b Go, AS; Bauman, M; King, SM; Fonarow, GC; Lawrence, W; Williams, KA; Sanchez, E (15 November 2013). "An Effective Approach to High Blood Pressure Control: A Science Advisory From the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention". Hypertension. 63 (4): 878–85. doi:10.1161/HYP.0000000000000003. PMID 24243703. Archived from the original on 20 November 2013. Retrieved 20 November 2013.

[Guideline] Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018 Jun. 71(6):e13-e115. [Medline]. [Full Text].

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