Hypertension (HTN) or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated.

High blood pressure is said to be present if it is persistently at or above 140/90 mmHg.

Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorized as "primary hypertension" which means high blood pressure with no obvious underlying medical cause.[2] The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart or endocrine system.

Hypertension is a major risk factor for stroke, myocardial infarction (heart attacks), heart failure, aneurysms of the arteries (e.g. aortic aneurysm), peripheral arterial disease and is a cause of chronic kidney disease. Even moderate elevation of arterial blood pressure is associated with a shortened life expectancy. Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment is often necessary in people for whom lifestyle changes prove ineffective or insufficient

Signs and symptomsHypertension is rarely accompanied by any symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. A proportion of people with high blood pressure reports headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes.[3] These symptoms however are more likely to be related to associated anxiety than the high blood pressure itself.[4]

On physical examination, hypertension may be suspected on the basis of the presence of hypertensive retinopathy detected by examination of the optic fundus found in the back of the eye using ophthalmoscopy.[5] Classically, the severity of the hypertensive retinopathy changes is graded from grade I–IV, although the milder types may be difficult to distinguish from each other.[5] Ophthalmoscopy findings may also give some indication as to how long a person has been hypertensive.[3]

[edit] Secondary hypertension

Main article: Secondary hypertension

Some additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause such as kidney diseases or endocrine diseases. For example, truncal obesity, glucose intolerance, moon facies, a "buffalo hump" and purple striae suggest Cushing's syndrome.[6] Thyroid disease and acromegaly can also cause hypertension and have characteristic symptoms and signs.[6] An abdominal bruit may be an indicator of renal artery stenosis (a narrowing of the arteries supplying the kidneys), while decreased blood pressure in the lower extremities and/or delayed or absent femoral arterial pulses may indicate aortic coarctation (a narrowing of the aorta shortly after it leaves the heart). Labile or paroxysmal hypertension

accompanied by headache, palpitations, pallor, and perspiration should prompt suspicions of pheochromocytoma.[6]

[edit] Hypertensive crises

Main article: Hypertensive emergency

Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110 — sometime termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressures above these levels are known to confer a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases)[7] and dizziness than the general population.[3] Other symptoms accompanying a hypertensive crisis may include visual deterioration or breathlessness due to heart failure or a general feeling of malaise due to renal failure.[6] Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.[8]

A "hypertensive emergency", previously "malignant hypertension", is diagnosed when there is evidence of direct damage to one or more organs as a result of the severely elevated blood pressure. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilloedema and/or fundal hemorrhages and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the expectoration of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system.[8] Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur.[8] In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage.[8] In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks.[6] Use of oral medications to lower the BP gradually over 24 to 48 h is advocated in hypertensive urgencies.[8]

[edit] In pregnancy

Hypertension occurs in approximately 8-10% of pregnancies.[6] Most women with hypertension in pregnancy have pre-existing primary hypertension, but high blood pressure in pregnancy may be the first sign of pre-eclampsia, a serious condition of the second half of pregnancy and puerperium.[6] Pre-eclampsia is characterised by increased blood pressure and the presence of protein in the urine.[6] It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths globally.[6] Pre-eclampsia also doubles the risk of perinatal mortality.[6] Usually there are no symptoms in pre-eclampsia and it is detected by routine screening. When symptoms of pre-eclampsia occur the most common are headache, visual disturbance (often "flashing lights"), vomiting, epigastric pain, and edema. Pre-eclampsia can occasionally progress

to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, cerebral edema, seizures or convulsions, renal failure, pulmonary edema, and disseminated intravascular coagulation (a blood clotting disorder).[6][9]

[edit] In infants and children

Failure to thrive, seizures, irritability, lack of energy, and difficulty breathing [10] can be associated with hypertension in neonates and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis.[11][10]

[edit] Cause

[edit] Primary hypertension

Main article: Essential hypertension

Primary (essential) hypertension is the most common form of hypertension, accounting for 90–95% of all cases of hypertension.[2] In almost all contemporary societies, blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable.[12] Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified[13] as well as some rare genetic variants with large effects on blood pressure[14] but the genetic basis of hypertension is still poorly understood. Several environmental factors influence blood pressure. Lifestyle factors that lower blood pressure include reduced dietary salt intake,[15] increased consumption of fruits and low fat products (Dietary Approaches to Stop Hypertension (DASH diet)), exercise,[16] weight loss [17] and reduced alcohol intake.[18] Stress appears to play a minor role[4] with specific relaxation techniques not supported by the evidence.[19] The possible role of other factors such as caffeine consumption,[20] and vitamin D deficiency[21] are less clear cut. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension.[22] Recent studies have also implicated events in early life (for example low birth weight, maternal smoking and lack of breast feeding) as risk factors for adult essential hypertension,[23] although the mechanisms linking these exposures to adult hypertension remain obscure.[23]

[edit] Secondary hypertension

Main article: Secondary hypertension

Secondary hypertension results from an identifiable cause. Renal disease is the most common secondary cause of hypertension.[6] Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, hyperparathyroidism and pheochromocytoma.[6][24] Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta,

excessive liquorice consumption and certain prescription medicines, herbal remedies and illegal drugs

PathophysiologyMain article: Pathophysiology of hypertension

A diagram explaining factors affecting arterial pressure

In most people with established essential (primary) hypertension, increased resistance to blood flow (total peripheral resistance) accounting for the high pressure while cardiac output remains normal.[26] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[27] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[27] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[28] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[29] although a reduction in the number or density of capillaries may also contribute.[30] Hypertension is also associated with decreased peripheral venous compliance[31] which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction. Whether increased active vasoconstriction plays a role in established essential hypertension is unclear.[32]

Pulse pressure (the difference between systolic and diastolic blood pressure) is frequently increased in older people with hypertension. This can mean that systolic pressure is abnormally high, but diastolic pressure may be normal or low — a condition termed isolated systolic hypertension.[33] The high pulse pressure in elderly people with hypertension or isolated systolic hypertension is explained by increased arterial stiffness, which typically accompanies aging and may be exacerbated by high blood pressure.[34]

Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in renal salt and water handling (particularly abnormalities in the intrarenal renin-angiotensin system)[35] and/or abnormalities of the sympathetic nervous system.[36] These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction and vascular inflammation may also contribute to increased peripheral resistance and vascular damage in hypertension.[37][38]

[edit] Diagnosis

Typical tests performed in hypertensionSystem TestsRenal Microscopic urinalysis, proteinuria, serum BUN (blood urea nitrogen) and/or creatinine

Endocrine Serum sodium, potassium, calcium, TSH (thyroid-stimulating hormone).Metabolic Fasting blood glucose, total cholesterol, HDL and LDL cholesterol, triglycerides

Other Hematocrit, electrocardiogram, and chest radiographSources: Harrison's principles of internal medicine[39] others[40][41][42][43][44]

Hypertension is diagnosed on the basis of a persistently high blood pressure. Traditionally,[45] this requires three separate sphygmomanometer measurements at one monthly intervals.[46] Initial assessment of the hypertensive people should include a complete history and physical examination. With the availability of 24-hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocols. In the United Kingdom, current best practice is to follow up a single raised clinic reading with ambulatory measurement, or less ideally with home blood pressure monitoring over the course of 7 days.[45] Pseudohypertension in the elderly or noncompressibility artery syndrome may also require consideration. This condition is believed to be due to calcification of the arteries resulting an abnormally high blood pressure readings with a blood pressure cuff while intra arterial measurements of blood pressure are normal.[47]

Once the diagnosis of hypertension has been made, physicians will attempt to identify the underlying cause based on risk factors and other symptoms, if present. Secondary hypertension is more common in preadolescent children, with most cases caused by renal disease. Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension.[48] Laboratory tests can also be performed to identify possible causes of secondary hypertension, and to determine whether hypertension has caused damage to the heart, eyes, and kidneys. Additional tests for diabetes and high cholesterol levels are usually performed because these conditions are additional risk factors for the development of heart disease and may require treatment.[2]

Serum creatinine is measured to assess for the presence of kidney disease, which can be either the cause or the result of hypertension. Serum creatinine alone may overestimate glomerular filtration rate and recent guidelines advocate the use of predictive equations such as the Modification of Diet in Renal Disease (MDRD) formula to estimate glomerular filtration rate (eGFR).[1] eGFR can also provides a baseline measurement of kidney function that can be used to monitor for side effects of certain antihypertensive drugs on kidney function. Additionally, testing of urine samples for protein is used as a secondary indicator of kidney disease. Electrocardiogram (EKG/ECG) testing is done to check for evidence that the heart is under strain from high blood pressure. It may also show whether there is thickening of the heart muscle (left ventricular hypertrophy) or whether the heart has experienced a prior minor disturbance such as a silent heart attack. A chest X-ray or an echocardiogram may also be performed to look for signs of heart enlargement or damage to the heart.[6]

[edit] Adults

Classification (JNC7)[1] Systolic pressure Diastolic pressuremmHg kPa mmHg kPa

Normal 90–119 12–15.9 60–79 8.0–10.5Prehypertension 120–139 16.0–18.5 80–89 10.7–11.9

Stage 1 hypertension 140–159 18.7–21.2 90–99 12.0–13.2Stage 2 hypertension ≥160 ≥21.3 ≥100 ≥13.3

Isolated systolichypertension ≥140 ≥18.7 <90 <12.0

In people aged 18 years or older hypertension is defined as a systolic and/or a diastolic blood pressure measurement consistently higher than an accepted normal value (currently 139 mmHg systolic, 89 mmHg diastolic: see table —Classification (JNC7)). Lower thresholds are used (135 mmHg systolic or 85 mmHg diastolic) if measurements are derived from 24-hour ambulatory or home monitoring.[45] Recent international hypertension guidelines have also created categories below the hypertensive range to indicate a continuum of risk with higher blood pressures in the normal range. JNC7 (2003)[1] uses the term prehypertension for blood pressure in the range 120-139 mmHg systolic and/or 80-89 mmHg diastolic, while ESH-ESC Guidelines (2007)[49] and BHS IV (2004)[50] use optimal, normal and high normal categories to subdivide pressures below 140 mmHg systolic and 90 mmHg diastolic. Hypertension is also sub-classified: JNC7 distinguishes hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly.[1] The ESH-ESC Guidelines (2007)[49] and BHS IV (2004),[50] additionally define a third stage (stage III hypertension) for people with systolic blood pressure exceeding 179 mmHg or a diastolic pressure over 109 mmHg. Hypertension is classified as "resistant" if medications do not reduce blood pressure to normal levels.[1]

GENETICS

Evidence for genetic influence on blood pressure comes from various sources.[7] There is greater similarity in blood pressure within families than between families, which indicates a form of inheritance.[8] And it was proved that this finding wasn't due to shared environmental factors.[9] Single gene mutations is proved to cause Mendelian forms of high and low blood pressure.[10] almost 10 genes have been identified to cause this forms of hypertension.[10][11] These mutations affect blood pressure by altering renal salt handling.[12] Recently and with the aid of newly developed genetic analysis techniques researchers found statistically significant linkage of blood pressure to several chromosomal regions, including regions linked to familial combined hyperlipidemia.[13][14][15][16][17] These findings suggest that there are many genetic loci, each with small effects on blood pressure in the general population. Overall, however, identifiable single-gene causes of hypertension are uncommon, consistent with a multifactorial cause of essential hypertension.[2][7][18][19]

The best studied monogenic cause of hypertension is the Liddle syndrome, a rare but clinically important disorder in which constitutive activation of the epithelial sodium channel predisposes

to severe, treatment-resistant hypertension.[20] Epithelial sodium channel activation resulting in inappropriate sodium retention at the renal collecting duct level. Patients with the Liddle syndrome typically present with volume-dependent, low renin, and low aldosterone, and hypertension. Screenings of general hypertensive populations indicate that the Liddle syndrome is rare and does not contribute substantially to the development of hypertension in the general population.[21]

[edit] Autonomic nervous systemAlso the autonomic nervous system, plays a central role in maintaining the cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. Done by altering peripheral vasculature, and kidneys, causing increased cardiac output, increased vascular resistance, and fluid retention. Disorder of the system, as in case of sympathetic nervous system overactivity, increases blood pressure and contributes to the development and maintenance of hypertension.[22]

[23][24][25] In addition, autonomic imbalance (i.e. increased sympathetic tone accompanied by reduced parasympathetic tone) has been associated with many metabolic and hemodynamic abnormalities that result in increased cardiovascular morbidity and mortality.[24][26]

The mechanisms of increased sympathetic nervous system activity in hypertension are complex and involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized.[8][27][28] Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II.[29][30][31] Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin.[32][33] Some studies shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls.[34] And that hypertensive patients do not show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and its believed that this abnormal response is genetically inherited.[35]

Exposure to stress increases sympathetic outflow, and repeated stress-induced vasoconstriction may result in vascular hypertrophy, leading to progressive increases in peripheral resistance and blood pressure.[2] This could partly explain the greater incidence of hypertension in lower socioeconomic groups, since they must endure greater levels of stress associated with daily living. Persons with a family history of hypertension manifest augmented vasoconstrictor and sympathetic responses to laboratory stressors, such as cold pressor testing and mental stress, that may predispose them to hypertension. This is particularly true of young African Americans. Exaggerated stress responses may contribute to the increased incidence of hypertension in this group.[36]

[edit] Renin-angiotensin-aldosterone system

Another system maintaining the extracellular fluid volume, peripheral resistance and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular volume, and arterial vasoconstriction, Thus it contributing to regulation of the blood pressure, it performs this function through breaking down (hydrolyzes) angiotensinogen secreted from the liver into the peptide angiotensin I, Angiotensin I is further cleaved by an enzyme that is located primarily but not exclusively in the pulmonary circulation bound to endothelium, that enzyme is angiotensin converting enzyme (ACE) producing angiotensin II, the most vasoactive peptide.[37][38] Angiotensin II is a potent constrictor of all blood vessels. It acts on the musculature of arteries and thereby raises the peripheral resistance, and so elevates blood pressure. Angiotensin II also acts on the adrenal glands too and releases Aldosterone, which stimulates the epithelial cells of the kidneys to increase re-absorption of salt and water leading to raised blood volume and raised blood pressure. So elevation of renin level in the blood, which is normally in adult human is 1.98-24.6 ng/L in the upright position.[39] will lead to hypertension.[2][40]

Recent studies claim that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS) in adipose tissue,[41][42] and also linked renin-angiotensin system with insulin resistance, and claims that anyone can cause the other.[43] Local production of angiotensin II in various tissues, including the blood vessels, heart, adrenals, and brain, is controlled by ACE and other enzymes, including the serine proteinase chymase. The activity of local renin–angiotensin systems and alternative pathways of angiotensin II formation may make an important contribution to remodeling of resistance vessels and the development of target organ damage (i.e. left ventricular hypertrophy, congestive heart failure, atherosclerosis, stroke, end-stage renal disease, myocardial infarction, and arterial aneurysm) in hypertensive persons.[40]

[edit] Endothelial dysfunctionThe endothelium of blood vessels produces an extensive range of substances that influence blood flow and, in turn, is affected by changes in the blood and the pressure of blood flow. For example, local nitric oxide and endothelin, which are secreted by the endothelium, are the major regulators of vascular tone and blood pressure. In patients with essential hypertension, the balance between the vasodilators and the vasoconstrictors is upset, which leads to changes in the endothelium and sets up a “vicious cycle” that contributes to the maintenance of high blood pressure. In patients with hypertension, endothelial activation and damage also lead to changes in vascular tone, vascular reactivity, and coagulation and fibrinolytic pathways. Alterations in endothelial function are a reliable indicator of target organ damage and atherosclerotic disease, as well as prognosis.[44]

Multiple evidences suggest that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension.[45][46][47] Normally nitric oxide is an important regulator and mediator of numerous processes in the nervous, immune and cardiovascular systems, including smooth muscle relaxation thus resulting in vasodilation of the artery and increasing blood flow, suppressor of migration and proliferation of vascular smooth-muscle cells.[2] It has been suggested that angiotensin II enhances formation of the oxidant superoxide at concentrations that affect blood pressure minimally.[48]

Endothelin is a potent vasoactive peptide produced by endothelial cells that has both vasoconstrictor and vasodilator properties. Circulating endothelin levels are increased in some hypertensive patients,[49][49][50] particularly African Americans and persons with hypertension.

[edit] Children

Hypertension in neonates is rare, occurring in around 0.2 to 3% of neonates, and blood pressure is not measured routinely in the healthy newborn.[11] Hypertension is more common in high risk newborns. A variety of factors, such as gestational age, postconceptional age and birth weightneeds to be taken into account when deciding if a blood pressure is normal in a neonate.[11]

Hypertension occurs quite commonly in children and adolescents (2-9% depending on age, sex and ethnicity)[51] and is associated with long term risks of ill-health.[52] It is now recommended that children over the age of 3 have their blood pressure checked whenever they attend for routine medical care or checks, but high blood pressure must be confirmed on repeated visits before characterizing a child as having hypertension.[52] Blood pressure rises with age in childhood and, in children, hypertension is defined as an average systolic or diastolic blood pressure on three or more occasions equal or higher than the 95th percentile appropriate for the sex, age and height of the child. Prehypertension in children is defined as average systolic or diastolic blood pressure that is greater than or equal to the 90th percentile, but less than the 95th percentile.[52] In adolescents, it has been proposed that hypertension and pre-hypertension are diagnosed and classified using the same criteria as in adults.[52]

PreventionMuch of the disease burden of high blood pressure is experienced by people who are not labelled as hypertensive.[53] Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive drug therapy. Lifestyle changes are recommended to lower blood pressure, before starting drug therapy. The 2004 British Hypertension Society guidelines[53] proposed the following lifestyle changes consistent with those outlined by the US National High BP Education Program in 2002[54] for the primary prevention of hypertension:

maintain normal body weight for adults (e.g. body mass index 20–25 kg/m2) reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of

sodium per day) engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most

days of the week) limit alcohol consumption to no more than 3 units/day in men and no more than 2

units/day in women consume a diet rich in fruit and vegetables (e.g. at least five portions per day);

Effective lifestyle modification may lower blood pressure as much an individual antihypertensive drug. Combinations of two or more lifestyle modifications can achieve even better results.

[edit] Management

[edit] Lifestyle modifications

The first line of treatment for hypertension is identical to the recommended preventative lifestyle changes[55] and includes: dietary changes[56] physical exercise, and weight loss. These have all been shown to significantly reduce blood pressure in people with hypertension.[57] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication. Different programs aimed to reduce psychological stress such as biofeedback, relaxation or meditation are advertised to reduce hypertension. However, in general claims of efficacy are not supported by scientific studies, which have been in general of low quality.[58][59][60]

Dietary change such as a low sodium diet is beneficial. A long term (more than 4 weeks) low sodium diet in Caucasians is effective in reducing blood pressure, both in people with hypertension and in people with normal blood pressure.[61] Also, the DASH diet, a diet rich in nuts, whole grains, fish, poultry, fruits and vegetables promoted in the USA by the National Heart, Lung, and Blood Institute lowers blood pressure. A major feature of the plan is limiting intake of sodium, although the diet is also rich in potassium, magnesium, calcium, as well as protein.[62]

[edit] Medications

Several classes of medications, collectively referred to as antihypertensive drugs, are currently available for treating hypertension. Prescription should take into account the person's cardiovascular risk (including risk of myocardial infarction and stroke) as well as blood pressure readings, in order to gain a more accurate picture of the person's cardiovascular profile.[63] Evidence in those with mild hypertension (SBP less than 160 mmHg and /or DBP less than 100 mmHg) and no other health problems does not support a reduction in the risk of death or rate of health complications from medication treatment.[64]

If drug treatment is initiated the Joint National Committee on High Blood Pressure (JNC-7)[1] recommends that the physician not only monitor for response to treatment but should also assess for any adverse reactions resulting from the medication. Reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.[65] The aim of treatment should be to reduce blood pressure to <140/90 mmHg for most individuals, and lower for those with diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).[63][66] If the blood pressure goal is not met, a change in treatment should be made as therapeutic inertia is a clear impediment to blood pressure control.[67]

Guidelines on the choice of agents and how to best to step up treatment for various subgroups have changed over time and differ between countries. The best first line agent is disputed.[68] The Cochrane collaboration, World Health Organization and the United States guidelines supports low dose thiazide-based diuretic as first line treatment.[68][69] The UK guidelines emphasise calcium channel blockers (CCB) in preference for people over the age of 55 years or if of African or Caribbean family origin, with angiotensin converting enzyme inhibitors (ACE-I) used first line for younger people.[70] In Japan starting with any one of six classes of medications including: CCB, ACEI/ARB, thiazide diuretics, beta-blockers, and alpha-blockers is deemed reasonable while in Canada all of these but alpha-blockers are recommended as options.[68]

[edit] Drug combinations

The majority of people require more than one drug to control their hypertension. JNC7[1] and ESH-ESC guidelines[49] advocate starting treatment with two drugs when blood pressure is >20 mmHg above systolic or >10 mmHg above diastolic targets. Preferred combinations are renin–angiotensin system inhibitors and calcium channel blockers, or renin–angiotensin system inhibitors and diuretics.[71] Acceptable combinations include calcium channel blockers and diuretics, beta-blockers and diuretics, dihydropyridine calcium channel blockers and beta-blockers, or dihydropyridine calcium channel blockers with either verapamil or diltiazem. Unacceptable combinations are non-dihydropyridine calcium blockers (such as verapamil or diltiazem) and beta-blockers, dual renin–angiotensin system blockade (e.g. angiotensin converting enzyme inhibitor + angiotensin receptor blocker), renin–angiotensin system blockers and beta-blockers, beta-blockers and centrally acting agents.[71] Combinations of an ACE-inhibitor or angiotensin II–receptor antagonist, a diuretic and an NSAID (including selective COX-2 inhibitors and non-prescribed drugs such as ibuprofen) should be avoided whenever possible due to a high documented risk of acute renal failure. The combination is known colloquially as a "triple whammy" in the Australian health industry.[55] Tablets containing fixed combinations of two classes of drugs are available and while convenient for the people, may be best reserved for those who have been established on the individual components.[72]

[edit] In the elderly

Treating moderate to severe hypertension decreases death rates and cardiovascular morbidity and mortality in people aged 60 and older.[73] There are limited studies of people over 80 years old but a recent review concluded that antihypertensive treatment reduced cardiovascular deaths and disease, but did not significantly reduce total death rates.[73] The recommended BP goal is advised as <140/90 mm Hg with thiazide diuretics being the first line medication in America,[74] and in the revised UK guidelines calcium-channel blockers are advocated as first line with targets of clinic readings <150/90, or <145/85 on ambulatory or home blood pressure monitoring.[70]

[edit] Resistant hypertension

Resistant hypertension is defined as hypertension that remains above goal blood pressure in spite of concurrent use of three antihypertensive agents belonging to different antihypertensive drug

classes. Guidelines for treating resistant hypertension have been published in the UK[75] and US.[76]

[edit] Epidemiology

Disability-adjusted life year for hypertensive heart disease per 100,000 inhabitants in 2004.[77]   no data  <110  110-220  220-330  330-440  440-550  550-660

  660-770  770-880  880-990  990-1100  1100-1600  >1600

As of 2000, nearly one billion people or ~26% of the adult population of the world had hypertension.[78] It was common in both developed (333 million) and undeveloped (639 million) countries.[78] However rates vary markedly in different regions with rates as low as 3.4% (men) and 6.8% (women) in rural India and as high as 68.9% (men) and 72.5% (women) in Poland.[79]

In 1995 it was estimated that 43 million people in the United States had hypertension or were taking antihypertensive medication, almost 24% of the adult United States population.[80] The prevalence of hypertension in the United States is increasing and reached 29% in 2004.[81][82] As of 2006 hypertension affects 76 million US adults (34% of the population) and African American adults have among the highest rates of hypertension in the world at 44%.[83] It is more common in blacks and native Americans and less in whites and Mexican Americans, rates increase with age, and is greater in the southeastern United States. Hypertension is more prevalent in men (though menopause tends to decrease this difference) and in those of low socioeconomic status.[2]

[edit] In children

The prevalence of high blood pressure in the young is increasing.[84] Most childhood hypertension, particularly in preadolescents, is secondary to an underlying disorder. Aside from obesity, kidney disease is the most common (60–70%) cause of hypertension in children. Adolescents usually have primary or essential hypertension, which accounts for 85–95% of cases.[85]

Prognosis

Main article: Complications of hypertension

Diagram illustrating the main complications of persistent high blood pressure.

Hypertension is the most important preventable risk factor for premature death worldwide.[86] It increases the risk of ischemic heart disease [87] strokes,[6] peripheral vascular disease,[88] and other cardiovascular diseases, including heart failure, aortic aneurysms, diffuse atherosclerosis, and pulmonary embolism.[6]Hypertension is also a risk factor for cognitive impairment and dementia, and chronic kidney disease.[6] Other complications include hypertensive retinopathy and hypertensive nephropathy.[1]

Many guidelines exist for the management of hypertension. Two of the most widely used recommendations are those from the American Diabetes Association (ADA) and the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7).

ADA 2011 standard of medical care

The ADA 2011 standard of medical care states that in individuals with diabetes and mild hypertension, it may be reasonable to begin treatment with a trial of nonpharmacologic therapy (diet, exercise, and other lifestyle modifications.) Mild hypertension as defined by the ADA guideline (systolic blood pressure 130-139 mm Hg or diastolic BP 80-89 mm Hg) may be classified as prehypertension by other organizations.[38]

The ADA 2011 standards of medical care in diabetes also indicate that a majority of patients with diabetes mellitus have hypertension. In patients with type 1 diabetes, nephropathy is often the cause of hypertension, whereas in type 2 diabetes, hypertension is one of a group of related cardiometabolic factors.[38, 39] Hypertension remains one of the most common causes of congestive heart failure (CHF). Antihypertensive therapy has been demonstrated to significantly reduce the risk of death from stroke and coronary artery disease.

Other studies have demonstrated that a reduction in BP may result in improved renal function. Therefore, earlier detection of hypertensive nephrosclerosis (using means to detect

microalbuminuria) and aggressive therapeutic interventions (particularly with ACE inhibitor drugs) may prevent progression to end-stage renal disease.[4]

JNC 7

Key messages of the JNC 7 are as follows[1] :

The goals of antihypertensive therapy is the reduction of cardiovascular and renal morbidity and mortality, with the focus on controlling the systolic BP, as most patients will achieve diastolic BP control when the systolic BP is achieved

Prehypertension (systolic 120-139 mm Hg, diastolic 80-89 mm Hg) requires health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and cardiovascular disease

In uncomplicated hypertension, a thiazide diuretic, either alone or combined with drugs from other classes, should be used for the pharmacologic treatment of most cases

In specific high-risk conditions, there are compelling indications for the use of other antihypertensive drug classes (eg, angiotensin-converting enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], beta blockers, calcium channel blockers)

Two or more antihypertensive medications will be required to achieve goal BP (< 140/90 mm Hg or < 130/80 mm Hg) for patients with diabetes and chronic kidney disease

For patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using 2 agents, one of which usually will be a thiazide diuretic, should be considered

Regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan

Note that the JNC 8 is expected to be released in 2012.

Lifestyle modifications

Lifestyle modifications are essential for the prevention of high BP, and these are generally the initial steps in managing hypertension. As the cardiovascular disease risk factors are assessed in individuals with hypertension, pay attention to the lifestyles that favorably affect BP level and reduce overall cardiovascular disease risk. A relatively small reduction in BP may affect the incidence of cardiovascular disease on a population basis. A decrease in BP of 2 mm Hg reduces the risk of stroke by 15% and the risk of coronary artery disease by 6% in a given population. In addition, a prospective study showed a reduction of 5 mm Hg in the nocturnal mean blood pressure and a possibly significant (17%) reduction in future adverse cardiovascular events if at least one antihypertensive medication is taken at bedtime.

Surgical intervention

Aortorenal bypass using a saphenous vein graft or a hypogastric artery is a revascularization technique for renovascular hypertension that has become much less common since the advent of renal artery angioplasty with stenting. Surgical resection is the treatment of choice for pheochromocytoma and for patients with a unilateral solitary aldosterone-producing adenoma,

because hypertension is cured by tumor resection. In patients with fibromuscular renal disease, angioplasty has a 60-80% success rate for improvement or cure of hypertension.

Consultations

Consultations with a nutritionist and exercise specialist are often helpful in changing lifestyle and initiating weight loss. Consultations with an appropriate consultant are indicated for management of secondary hypertension attributable to a specific cause.

Nonpharmacologic Therapy

Lifestyle modifications

JNC 7 and AHA-ASA lifestyle modification recommendations

The Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommendations to lower blood pressure (BP) and decrease cardiovascular disease risk include the following, with greater results achieved when 2 or more lifestyle modifications are combined[1] :

Weight loss helps to prevent hypertension (range of approximate systolic BP reduction [SBP], 5-20 mm Hg per 10 kg); recommendations include the DASH (Dietary Approaches to Stop Hypertension) diet (range of approximate SBP reduction, 8-14 mm Hg), which is rich in fruits and vegetables and encourages the use of fat-free or low-fat milk and milk products

Limit alcohol intake to no more than 1 oz (30 mL) of ethanol per day for men (ie, 24 oz [720 mL] of beer, 10 oz [300 mL] of wine, 2 oz [60 mL] of 100-proof whiskey) or 0.5 oz (15 mL) of ethanol per day for women and people of lighter weight (range of approximate SBP reduction, 2-4 mm Hg)

Reduce sodium intake to no more than 100 mmol/d (2.4 g sodium or 6 g sodium chloride) (range of approximate SBP reduction, 2-8 mm Hg)

Maintain adequate intake of dietary potassium (approximately 90 mmol/d) Maintain adequate intake of dietary calcium and magnesium for general health Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall

cardiovascular health Engage in aerobic exercise at least 30 minutes daily for most days (range of approximate

SBP reduction, 4-9 mm Hg)

The 2010 American Heart Association-American Stroke Association (AHA-ASA) guidelines for the primary prevention of stroke makes the following recommendations:

Hypertension: the AHA-ASA guidelines recommend regular blood pressure screening, lifestyle modification, and drug therapy; lower risk of stroke and cardiovascular events are seen when systolic blood pressure levels are lower than 140 mm Hg and diastolic blood pressure levels are less than 90 mm Hg

In patients who have hypertension with diabetes or renal disease, the BP goal is lower than 130/80 mm Hg

Diet and nutrition: a diet that is low in sodium and high in potassium is recommended to reduce BP; diets that promote the consumption of fruits, vegetables, and low-fat dairy products, such as the DASH-style diet, help lower BP and may lower the risk of stroke

Physical inactivity: increasing physical activity is associated with a reduction in the risk of stroke; the goal is to engage in 30 minutes or more of moderate intensity activity on a daily basis

Obesity and body fat distribution: weight reduction in overweight and obese persons is recommended to reduce BP and the risk of stroke

In a study that attempted to formulate a predictive model for the risk of prehypertension and hypertension, as well as an estimate of expected benefits from population-based lifestyle modification, investigators reported that the majority of risk factors have a larger role in prehypertension and stage 1 hypertension than in stage 2 hypertension. The investigators derived multistep composite risk scores by assessing significant risk factors in the progression from prehypertension to hypertension, as well as the regression of prehypertension to normal; they indicated that as the number of risk factors included in intervention programs increases, the size of the expected mean risk score decreases. In men, the 5-year predicted cumulative risk for stage 2 hypertension decreased from 23.6% (in the absence of an intervention program) to 14% (with 6-component intervention); the results were similar in women.

Dietary changes

A number of studies have documented an association between sodium chloride intake and BP. The effect of sodium chloride is particularly important in individuals who are middle-aged to elderly with a family history of hypertension. A moderate reduction in sodium chloride intake can lead to a small reduction in blood pressure. The American Heart Association recommends that the average daily consumption of sodium chloride not exceed 6 g; this may lower blood pressure by 2-8 mm Hg. Higher sodium intake is associated with higher levels of serum uric acid (SUA) and urine albumin excretion (UAE). In individuals with higher SUA and UAE, higher sodium intake is an independent risk factor for hypertension.[40]

One randomized controlled trial published found that moderate dietary sodium reduction (approximately 2500 mg Na+ per day or 6 g NaCl per day) added to angiotensin-converting enzyme inhibition was more effective than dual blockade (angiotensin-converting enzyme inhibitor and angiotensin receptor blocker) in reducing both proteinuria and blood pressure in nondiabetic patients with modest chronic kidney disease. Furthermore, a low sodium diet added to dual therapy yielded additional reductions in both blood pressure and proteinuria, emphasizing the beneficial effect of dietary salt reduction in the management of hypertensive patients with renal insufficiency.

The DASH eating plan encompasses a diet rich in fruits, vegetables, and low-fat dairy products and may lower blood pressure by 8-14 mm Hg. The 2011 ADA standard of care supports the DASH diet, with the caution that high-quality studies of diet and exercise to lower blood pressure have not been performed on individuals with diabetes.[38]

Dietary potassium, calcium, and magnesium consumption have an inverse association with blood pressure. Lower intake of these elements potentiates the effect of sodium on blood pressure. Oral potassium supplementation may lower both systolic and diastolic pressure. Calcium and magnesium supplementation have elicited small reductions in blood pressure.

In population studies, low levels of alcohol consumption have shown a favorable effect on blood pressure, with reductions of 2-4 mm Hg. However, the consumption of 3 or more drinks per day is associated with elevation of BP. Daily alcohol intake should be restricted to less than 1 oz of ethanol in men and 0.5 oz in women. The 2011 ADA standard supports limiting alcohol consumption in patients with diabetes and hypertension.[38]

Although many studies implicate a high fructose diet as a contributing factor to the metabolic syndrome and hypertension, a 2012 review of Cochrane database disputed this relationship.[41]

Weight loss and exercise

Up to 60% of all individuals with hypertension are more than 20% overweight. The centripetal fat distribution is associated with insulin resistance and hypertension. Even modest weight loss (5%) can lead to reduction in BP and improved insulin sensitivity. Weight reduction may lower blood pressure by 5-20 mm Hg per 10 kg of weight loss in a patient whose weight is more than 10% of ideal body weight.

Regular aerobic physical activity can facilitate weight loss, decrease BP, and reduce the overall risk of cardiovascular disease. Blood pressure may be lowered by 4-9 mm Hg with moderately intense physical activity.[1] These activities include brisk walking for 30 minutes a day, 5 days per week. More intense workouts of 20-30 minutes, 3-4 times a week, may also lower BP and have additional health benefits.[1]

In a study by Faselis et al, the authors showed that in a population of middle-aged and older male veterans, degree of fitness (based on peak metabolic equivalents, METs) was a strong and independent predictor of the rate of progression from prehypertension to hypertension. The adjusted risk for developing hypertension was 72% higher for the least-fit individuals (≤6.5 METs) compared to the high-fit individuals (>10 METs). The protective effects of fitness were evident when exercise capacity exceeded 8.5 METs.[42]

Blumenthal et al found that in overweight or obese patients with high BP, adding exercise and weight loss to the DASH diet resulted in even larger reductions in BP and cardiovascular biomarkers of risk.[43] The trial showed that after 4 months, clinic-measured BP was reduced by 16.1/9.9 mm Hg in patients in the DASH-plus-weight management group; by 11.2/7.5 mm Hg in the DASH-alone group; and by 3.4/3.8 mm Hg in a control group eating a usual diet. Compared with DASH alone, DASH plus weight management also resulted in greater improvement in pulse wave velocity, baroreflex sensitivity, and left ventricular mass.[43]

Moderate to high cardiorespiratory fitness has been shown to decrease the risk of hypertension in individuals with a parental history of hypertension.[44]

The 2011 ADA diabetes standards support increasing physical activity. The recommendations emphasize that exercise is an important part of diabetes management in addition to reducing cardiovascular risk factors, contributing to weight loss, and improving overall well-being.[38]

Moreover, patients with diabetes and severe hypertension (SBP ≥140 mm Hg or DBP ≥90 mm Hg) at diagnosis or afterward should receive drug therapy along with lifestyle modifications

Management of Diabetes and HypertensionHypertension is not only disproportionately high in diabetic individuals, but it also increases the risk of diabetes 2.5 times within 5 years in hypertensive patients.[1] In addition, hypertension and diabetes are both risk factors for cardiovascular disease, stroke, progression of renal disease, and diabetic retinopathy.[1]

The JNC 7 and the 2011 American Diabetes Association (ADA) standard of medical care recommend blood pressure control in diabetic individuals be controlled to 130/180 mm Hg or lower, primarily to prevent or lower the risk of progression from diabetic nephropathy to end-stage renal disease.[1, 38]

In general, patients with diabetes type 1 or type 2 and hypertension have shown clinical improvement with diuretics, ACE inhibitors, beta-blockers, ARBs, and calcium antagonists.[1]

Most studies, however, have shown superiority of ACE inhibitors or ARBs over calcium antagonists in diabetic patients. A notable exception is the ACCOMPLISH trial, which showed that, in patients at high risk for cardiovascular events, the combination of benazepril (an ACE inhibitor) and amlodipine (a CCB), was superior to the combination of benazepril plus hydrochlorothiazide (a thiazide diuretic).[45] About 60% of the patient cohort had diabetes.).

Two or more antihypertensive drugs at maximal doses should be used to achieve optimal BP targets in patients with diabetes and hypertension.[38] Either an ACE inhibitor or an ARB is usually required in patients with diabetes and hypertension. If the patient cannot tolerate one class of drugs, the other should be tried. If needed to achieve BP goals, a thiazide diuretic is indicated for those patients with an estimated GFR of 30 mL/min/1.73 m2 or greater, and a loop diuretic is indicated for those with an estimated GFR of less than 30 mL/min/1.73 m2. Regardless of which antihypertensive drugs are used, kidney function and serum potassium levels should be monitored.[38]

In a subgroup analysis from the TRINITY study ( TRI  ple therapy with olmesartan medoxomil, amlodipine, and hydrochlorothiazide in hyperte N  sive patien T  s stud Y), Chrysant et al reported that in patients with hypertension and diabetes, triple-combination drug therapy resulted in greater BP reductions and BP-goal achievement (< 130/80 mm Hg) than dual-combination drug therapy. The triple-combination regimen consisted of olmesartan medoxomil, 40 mg; amlodipine besilate, 10 mg; and hydrochlorothiazide, 25 mg.

Ruggenenti et al found that in patients with type 2 diabetes who have hypertension, combined manidipine and delapril therapy helped improve health in patients with cardiovascular disease, retinopathy, and neuropathy, as well as stabilized insulin sensitivity.[46] However, neither of these agents are available in the US.

Management of Hypertensive EmergenciesHypertensive emergencies are characterized by severe elevations in BP (>180/120 mm Hg) associated with acute end-organ damage.[1] Examples include hypertensive encephalopathy, intracerebral hemorrhage, acute myocardial infarction, acute left ventricular failure with pulmonary edema, aortic dissection, unstable angina pectoris, eclampsia,[1] or posterior reversible encephalopathy syndrome (PRES) (a condition characterized by headache, altered mental status, visual disturbances, and seizures).[30] Patients with hypertensive emergencies should be monitored and managed in an intensive care unit.[13, 47]

The primary goal of the physician is to determine which patients with acute hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous parenteral antihypertensive therapy. That is, the fundamental principle in determining the necessary emergent care of the hypertensive patient is the presence or absence of end-organ dysfunction.

Initial treatment goals are to reduce the mean arterial BP by no more than 25% within minutes to 1 hour. If the patient is stable, reduce the BP to 160/100-110 mm Hg within the next 2-6 hours.[1]

Several parenteral and oral therapies can be used to treat hypertensive emergencies, such as nitroprusside sodium, hydralazine, nicardipine, fenoldopam, nitroglycerin, or enalaprilat. Other agents that may be used include labetalol, esmolol, and phentolamine.[1] Avoid using short-acting nifedipine in the initial treatment of this condition because of the risk of rapid, unpredictable hypotension and the possibility of precipitating ischemic events.[1] Once the patient’s condition is stabilized, the patient’s BP may be gradually reduced over the next 24-48 hours.

Exceptions to the above recommendation include the following[1] :

Patients with an ischemic stroke (currently, no clear evidence exists for immediate antihypertensive treatment)

Patients with aortic dissection (their systolic BP should be lowered to <100 mm Hg, if tolerated)

Patients in whom BP is lowered to allow thrombolytic therapy (eg, stroke patients)

Approximately 3-45% of adult patients presenting to an emergency department have at least one increased BP during their stay in the ED, but only a small percentage of patients will require emergency treatment. However, medical therapy and close follow-up are necessary in patients who present to the ED with acutely elevated BPs (systolic BP >200 mm Hg or diastolic BP >120 mm Hg) that remain significantly elevated until discharge.[48]

For further information, see the Medscape Reference article Hypertensive Emergencies in Emergency Medicine.

Management of Hypertension in PregnancyIn patients who are pregnant, the goal of antihypertensive treatment is to minimize the risk of maternal cardiovascular or cerebrovascular events. Hypertensive disorders—categorized as

chronic hypertension, preeclampsia, chronic hypertension with superimposed preeclampsia, gestational hypertension, and transient hypertension (see Table 3, below)— may contribute to maternal, fetal, or neonatal morbidity and mortality, particularly in the first trimester.[1]

Table 3. Hypertensive Disorders in Pregnancy (Open Table in a new window)

Classification CharacteristicsChronic hypertension Prepregnancy or before 20 weeks’ gestation; SBP =140 mm Hg or

DBP 90 mm Hg that persists >12 weeks postpartumPreeclampsia After 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg

with proteinuria (>300 mg/24 h)

Can progress to eclampsia

More common in nulliparous women, multiple gestation, women with hypertension =4 years, family history of preeclampsia, previous hypertension in pregnancy, and renal disease

Chronic hypertension with superimposed preeclampsia

New-onset proteinuria after 20 weeks in hypertensive woman

In a woman with hypertension and proteinuria before 20 weeks’ gestation

Sudden 2- to 3-fold increase in proteinuria

Sudden increase in BP

Thrombocytopenia

Elevated AST or ALT levels

Gestational hypertension Temporary diagnosis

Hypertension without proteinuria after 20 weeks’ gestation

May be a preproteinuric phase of preeclampsia or a recurrence of chronic hypertension that abated in mid-pregnancy

May lead to preeclampsia

Severe cases may cause higher rates of premature delivery and growth retardation relative to mild preeclampsia

Transient hypertension Diagnosis made retrospectively

BP returns to normal by 12 weeks’ postpartum

May recur in subsequent pregnancies

Predictive of future primary hypertension

ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; DBP = diastolic BP; SBP = systolic BP. 

Adapted from:  Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52.[1]

In normal pregnancy, women’s mean arterial pressure (MAP) drops 10-15 mm Hg over the first half of pregnancy. Most women with mild chronic hypertension (ie, systolic BP 140-160 mm Hg, diastolic BP 90-100 mm Hg) have a similar decrease in BP and may not require any medication during this period. Conversely, diastolic BP greater than 110 mm Hg has been associated with an increased risk of placental abruption and intrauterine growth restriction, and systolic BP greater than 160 mm Hg increases the risk of maternal intracerebral hemorrhage.

Lifestyle modifications are generally sufficient for the management of pregnant women with stage 1 hypertension who are at low risk for cardiovascular complications during pregnancy.{{Re1} Restrictions to lifestyle modifications may include aerobic exercise (theoretical increased preeclampsia risk from inadequate placental blood flow) and weight reduction, even in obese pregnant women. Reduction of sodium intake and avoidance of tobacco and alcohol use are similar to those for individuals with primary hypertension.[1]

Although the primary risk of chronic hypertension in pregnancy is development of superimposed preeclampsia, no evidence suggests that pharmacologic treatment of mild hypertension reduces the incidence of preeclampsia in this population.

Antihypertensive therapy should be started in pregnant women if the systolic BP is greater than 160 mm Hg or the diastolic BP is greater than 100-105 mm Hg. The goal of pharmacologic treatment should be a diastolic BP of less than 100-105 mm Hg and a systolic BP of less than 160 mm Hg.

Women who have preexisting end-organ damage from chronic hypertension or who have previously required multidrug therapy for BP control should have a lower threshold for starting antihypertensive medication (ie, >139/89 mm Hg) and a lower target BP (<140/90 mm Hg). The JNC 7 recommendations are to continue antihypertensive medication as needed to control BP and to reinstate antihypertensive therapy when the SBP is 150-160 mm Hg or the DBP is 100-110 mm Hg.

Selection of antihypertensive medication

Although reducing maternal risk is the goal of treating chronic hypertension in pregnancy, it is fetal safety that largely directs the choice of antihypertensive agent. Methyldopa is generally the preferred first-line agent because of its safety profile.[1] Other drugs that may be considered include labetalol, beta-blockers, and diuretics. Data are limited regarding the use of clonidine and calcium antagonists in pregnant women with chronic hypertension; however, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor (ARB) antagonists should be avoided because of the risk of fetal toxicity and death.[1]

For further information, see the Medscape Reference articles Hypertension and Pregnancy, Preeclampsia, and Eclampsia.

Medications to treat high blood pressure Thiazide diuretics. Diuretics, sometimes called water pills, are medications that act on

your kidneys to help your body eliminate sodium and water, reducing blood volume. Thiazide diuretics are often the first — but not the only — choice in high blood pressure medications. If you're not taking a diuretic and your blood pressure remains high, talk to your doctor about adding one or replacing a drug you currently take with a diuretic.

Beta blockers. These medications reduce the workload on your heart and open your blood vessels, causing your heart to beat slower and with less force. When prescribed alone, beta blockers don't work as well in blacks or in older adults — but they're effective when combined with a thiazide diuretic.

Angiotensin-converting enzyme (ACE) inhibitors. These medications help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels.

Angiotensin II receptor blockers (ARBs). These medications help relax blood vessels by blocking the action — not the formation — of a natural chemical that narrows blood vessels.

Calcium channel blockers. These medications help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for blacks and older adults than do ACE inhibitors or beta blockers alone. A word of caution for grapefruit lovers, though. Grapefruit juice interacts with some calcium channel blockers, increasing blood levels of the medication and putting you at higher risk of side effects. Talk to your doctor or pharmacist if you're concerned about interactions.

Renin inhibitors. Aliskiren (Tekturna) slows down the production of renin, an enzyme produced by your kidneys that starts a chain of chemical steps that increases blood pressure. Tekturna works by reducing the ability of renin to begin this process. Due to a risk of serious complications, including stroke, you shouldn't take aliskiren with ACE inhibitors or ARBs.

If you're having trouble reaching your blood pressure goal with combinations of the above medications, your doctor may prescribe:

Alpha blockers. These medications reduce nerve impulses to blood vessels, reducing the effects of natural chemicals that narrow blood vessels.

Alpha-beta blockers. In addition to reducing nerve impulses to blood vessels, alpha-beta blockers slow the heartbeat to reduce the amount of blood that must be pumped through the vessels.

Central-acting agents. These medications prevent your brain from signaling your nervous system to increase your heart rate and narrow your blood vessels.

Vasodilators. These medications work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.

Once your blood pressure is under control, your doctor may have you take a daily aspirin to reduce your risk of cardiovascular disorders.

To reduce the number of daily medication doses you need, your doctor may prescribe a combination of low-dose medications rather than larger doses of one single drug. In fact, two or more blood pressure drugs often work better than one. Sometimes finding the most effective medication — or combination of drugs — is a matter of trial and error.

Lifestyle changes to treat high blood pressureNo matter what medications your doctor prescribes to treat your high blood pressure, you'll need to make lifestyle changes to lower your blood pressure. These changes usually include eating a healthier diet with less salt (the Dietary Approaches to Stop Hypertension, or DASH, diet), exercising more, quitting smoking and losing weight.

Resistant hypertension: When your blood pressure is difficult to controlIf your blood pressure remains stubbornly high despite taking at least three different types of high blood pressure drugs, one of which should be a diuretic, you may have resistant hypertension. Resistant hypertension is blood pressure that's resistant to treatment. People who have controlled high blood pressure but are taking four different types of medications at the same time to achieve that control also are considered to have resistant hypertension.

Having resistant hypertension doesn't mean your blood pressure will never get lower. In fact, if you and your doctor can identify what's behind your persistently high blood pressure, there's a good chance you can meet your goal with the help of treatment that's more effective.

Your doctor or hypertension specialist can evaluate whether the medications and doses you're taking for your high blood pressure are appropriate. You may have to fine-tune your medications to come up with the most effective combination and doses.

In addition, you and your doctor can review medications you're taking for other conditions. Some medications, foods or supplements can worsen high blood pressure or prevent your high blood pressure medications from working effectively. Be open and honest with your doctor about all the medications or supplements you take.

If you don't take your high blood pressure medications exactly as directed, your blood pressure can pay the price. If you skip doses because you can't afford the medication, because you have

side effects or because you simply forget to take your medications, talk to your doctor about solutions. Don't change your treatment without your doctor's guidance.