For most patients, health care providers diagnose high blood pressure when blood pressure readings are consistently 140/90 mmHg or above. A blood pressure test can be done in a health care provider’s office or clinic. To track blood pressure readings over a period of time, the health care provider may ask the patient to come into the office on different days and at different times. The health care provider also may ask the patient to check readings at home or at other locations that have blood pressure equipment and to keep a written log of results. The health care provider usually takes 2–3 readings at several medical appointments to diagnose high blood pressure. Using the results of the blood pressure test, the health care provider will diagnose prehypertension or high blood pressure if:

- For an adult, systolic or diastolic readings are consistently higher than 120/80 mmHg.

- A child’s blood pressure numbers are outside average numbers for children of the same age, gender, and height.

Once the health care provider determines the severity, he or she can order additional tests to determine if the blood pressure is due to other conditions or medicines or if there is primary high blood pressure. Health care providers can use this information to develop a treatment plan.

Hypertension is diagnosed on the basis of a persistently high resting blood pressure. Traditionally, the National Institute of Clinical Excellence recommends three separate resting sphygmomanometer measurements at monthly intervals. The American Heart Association recommends at least three resting measurements on at least two separate health care visits.

For an accurate diagnosis of hypertension to be made, it is essential for proper blood pressure measurement technique to be used. Improper measurement of blood pressure is common and can change the blood pressure reading by up to 10 mmHg, which can lead to misdiagnosis and misclassification of hypertension. Correct blood pressure measurement technique involves several steps. Proper blood pressure measurement requires the person whose blood pressure is being measured to sit quietly for at least five minutes which is then followed by application of a properly fitted blood pressure cuff to a bare upper arm. The person should be seated with their back supported, feet flat on the floor, and with their legs uncrossed. The person whose blood pressure is being measured should avoid talking or moving during this process. The arm being measured should be supported on a flat surface at the level of the heart. Blood pressure measurement should be done in a quiet room so the medical professional checking the blood pressure can hear the Korotkoff sounds while listening to the brachial artery with a stethoscope for accurate blood pressure measurements. The blood pressure cuff should be deflated slowly (2-3 mmHg per second) while listening for the Korotkoff sounds. The bladder should be emptied before a person's blood pressure is measured since this can increase blood pressure by up to 15/10 mmHg. Multiple blood pressure readings (at least two) spaced 1-2 minutes apart should be obtained to ensure accuracy. Ambulatory blood pressure monitoring over 12 to 24 hours is the most accurate method to confirm the diagnosis.

An exception to this is those with very high blood pressure readings especially when there is poor organ function. 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. The United States Preventative Services Task Force also recommends getting measurements outside of the healthcare environment. 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 in abnormally high blood pressure readings with a blood pressure cuff while intra arterial measurements of blood pressure are normal. Orthostatic hypertension is when blood pressure increases upon standing.

Once the diagnosis of hypertension has been made, healthcare providers should 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 kidney disease. Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension. 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.

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). eGFR can also provide a baseline measurement of kidney function that can be used to monitor for side effects of certain anti-hypertensive 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.

In studies, white coat hypertension can be defined as the presence of a defined hypertensive average blood pressure in a clinic setting, although it isn't present when the patient is at home.

Diagnosis is made difficult as a result of the unreliable measures taken from the conventional methods of detection. These methods often involve an interface with health care professionals and frequently results are tarnished by a list of factors including variability in the individual’s blood pressure, technical inaccuracies, anxiety of the patient, recent ingestion of pressor substances, and talking, amongst many other factors. The most common measure of blood pressure is taken from a noninvasive instrument called a sphygmomanometer. "A survey showed that 96% of primary care physicians habitually use a cuff size too small," adding to the difficulty in making an informed diagnosis. For such reasons, white coat hypertension cannot be diagnosed with a standard clinical visit. It can be reduced (but not eliminated) with automated blood pressure measurements over 15 to 20 minutes in a quiet part of the office or clinic.

Patients with white coat hypertension do not exhibit the signs indicative of trepidation and their increased blood pressure is often not accompanied by tachycardia. This is supported by studies that repeatedly indicate that 15%–30% of those thought to have mild hypertension as a result of clinic or office recordings display normal blood pressure and no unusual response to pressure stimulus. These persons did not show any specific characteristics such as age that may be indicative of a higher susceptibility to white coat hypertension.

Ambulatory blood pressure monitoring and patient self-measurement using a home blood pressure monitoring device is being increasingly used to differentiate those with white coat hypertension or experiencing the white coat effect from those with chronic hypertension. This does not mean that these methods are without fault. Daytime ambulatory values, despite taking into account stresses of everyday life when taken during the patient's daily routine, are still susceptible to the effects of daily variables such as physical activity, stress and duration of sleep. Ambulatory monitoring has been found to be the more practical and reliable method in detecting patients with white coat hypertension and for the prediction of target organ damage. Even as such, the diagnosis and treatment of white coat hypertension remains controversial.

Recent studies showed that home blood pressure monitoring is as accurate as a 24-hour ambulatory monitoring in determining blood pressure levels. Researchers at the University of Turku, Finland studied 98 patients with untreated hypertension. They compared patients using a home blood pressure device and those wearing a 24-hour ambulatory monitor. Researcher Dr. Niiranen said that "home blood pressure measurement can be used effectively for guiding anti-hypertensive treatment". Dr. Stergiou added that home tracking of blood pressure "is more convenient and also less costly than ambulatory monitoring."

Use of breathing patterns has been proposed as a technique for identifying white coat hypertension.

In one Turkish study of 438 consecutive patients, 38% were normotensive, 43% had white coat hypertension, 2% had masked hypertension, and 15% had sustained hypertension. Even patients taking medication for sustained hypertension who are normotensive at home may exhibit white coat hypertension in the office setting.

In people aged 18 years or older hypertension is defined as a systolic or a diastolic blood pressure measurement consistently higher than an accepted normal value (this is above 129 or 139 mmHg systolic, 89 mmHg diastolic depending on the guideline). Other thresholds are used (135 mmHg systolic or 85 mmHg diastolic) if measurements are derived from 24-hour ambulatory or home monitoring. 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. The "Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure" (JNC7) published in 2003 uses the term prehypertension for blood pressure in the range 120–139 mmHg systolic or 80–89 mmHg diastolic, while European Society of Hypertension Guidelines (2007) and British Hypertension Society (BHS) IV (2004) 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. The ESH-ESC Guidelines (2007) The results also demonstrated a correlation of chronically low vitamin D levels with a higher chance of becoming hypertensive. Supplementation with vitamin D over 18 months in normotensive individuals with vitamin D deficiency did not significantly affect blood pressure.

In general, individuals with white coat hypertension have lower morbidity than patients with sustained hypertension, but higher morbidity than the clinically normotensive.

However, it should be remembered that all the established published trials on the consequences of high blood pressure and the benefits of treating are based on one-time measurement in clinical settings rather than the generally slightly lower readings obtained from ambulatory recordings.

The debate and conflicting ideas revolve around whether or not it would be feasible to treat white coat hypertension, as there still is no conclusive evidence that a temporary rise in blood pressure during office visits has an adverse effect on health.

In fact, many cross sectional studies have shown that "target-organ damage (as exemplified by left ventricular hypertrophy) is less in white-coat hypertensive patients than in sustained hypertensive patients even after the allowance has been made for differences in clinic pressure". Many believe that patients with "white coat" hypertension do not require even very small doses of antihypertensive therapy as it may result in hypotension, but must still be careful as patients may show signs of vascular changes and may eventually develop hypertension. Even patients with established hypertension that is well-controlled based on home blood pressure monitoring may experience elevated readings during office visits.

In a hypertensive urgency blood pressure should be lowered carefully to ≤160/≤100 mmHg over a period of hours to days, this can often be done as an outpatient. There is limited evidence regarding the most appropriate rate of blood pressure reduction, although it is recommended that mean arterial pressure should be lowered by no more than 25 to 30 percent over the first few hours. There is also limited evidence about the best drugs in hypertensive urgencies, oral, short-acting agent such as captopril, labetalol, or clonidine have been used. Sublingual nifedipine is contraindicated in hypertensive urgencies and should "not" be used. Acute administration of drugs should be followed by several hours of observation to ensure that blood pressure does not fall too much. Aggressive dosing with intravenous drugs or oral agents which lowers blood pressure too rapidly carries risk; conversely there is no evidence that failure to rapidly lower blood pressure in a hypertensive urgency is associated with any increased short-term risk.

Several classes of antihypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the usual blood pressure of the person before the hypertensive crisis. In most cases, the administration of intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect, is suitable (but in many cases not readily available). Besides, nitroprusside runs a risk of cyanide poisoning. Other intravenous agents like nitroglycerine, nicardipine, labetalol, fenoldopam or phentolamine can also be used, but all have a delayed onset of action (by several minutes) compared to sodium nitroprusside.

In addition, non-pharmacological treatment could be considered in cases of resistant malignant hypertension due to end stage kidney failure, such as surgical nephrectomy, laparoscopic nephrectomy, and renal artery embolization in cases of anesthesia risk.

It is also important that the blood pressure is lowered smoothly, not too abruptly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% (within minutes to 1 or 2 hours), and then toward a level of 160/100 mm Hg within a total of 2–6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.

The diagnosis of a hypertensive emergency is not based solely on an absolute level of blood pressure, but also on the typical blood pressure level of the patient before the hypertensive crisis occurs. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.

Regular physical exercise reduces blood pressure. The UK National Health Service advises 150 minutes (2 hours and 30 minutes) of moderate-intensity aerobic activity per week to help prevent hypertension.

Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.

The morbidity and of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good blood pressure control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.

The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increases. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

Several studies have concluded that African Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease than non-Hispanic whites. It appears that hypertensive crisis is also more common in African Americans compared with other races.

Although severe hypertension is more common in the elderly, it may occur in children (though very rarely). Also, women have slightly increased risks of developing hypertension crises than do men. The lifetime risk for developing hypertension is 86-90% in females and 81-83% in males.

Not much is known about the epidemiology of hypertensive urgencies. Retrospective analysis of data from 1,290,804 adults admitted to hospital emergency departments in United States from 2005 through 2007 found that severe hypertension with a systolic blood pressure ≥180 mmHg occurred in 13.8% of patients. Based on another study in a US public teaching hospital about 60% of hypertensive crises are due to hypertensive urgencies.

Risk factors for severe hypertension include older age, female sex, obesity, coronary artery disease, somatoform disorder, being prescribed multple antihypertensive medications, and non-adherence to medication.

Prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore those who also have renal dysfunction have a higher mortality risk.

However, the majority of renovascular diseases can be improved with surgery.

The diagnosis for renovascular hypertension is done by:

- Blood test (for renal function)

- Urinary test (tests for microalbuminuria)

- Serology (to exclude systemic lupus erythematosus )

- Lipid profile

- Urinalysis (to exclude presence of red blood cells)

Diagnostic methods for hypertensive encephalopathy include physical examination, blood pressure measurement, blood sampling, ECG, EEG, chest X-ray, urinalysis, arterial blood gas analysis, and imaging of the head (CAT scan and/or MRI). Since decreasing the blood pressure is essential, anti-hypertensive medication is administered without awaiting the results of the laboratory tests. Electroencephalographic examination detects the absence of alpha waves, signifying impaired consciousness. In people with visual disturbances, slow waves are detected in the occipital areas.

The initial aim of treatment in hypertensive crises is to rapidly lower the diastolic pressure to about 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in BP not exceeding 25 percent of the presenting value. This level of BP control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease).

Once the BP is controlled, the person should be switched to medication by mouth, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months. The initial reduction to a diastolic pressure of approximately 100 mmHg is often associated with a modest worsening of renal function; this change, however, is typically transient as the vascular disease tends to resolve and renal perfusion improves over one to three months. Antihypertensive therapy should not be withheld in this setting unless there has been an excessive reduction in BP. A change in medication, however, is indicated if the decline in renal function is temporally related to therapy with an angiotensin (ACE) converting enzyme inhibitor or angiotensin II receptor blocker, which can interfere with renal autoregulation and produce acute renal failure in patients with bilateral renal artery stenosis. (See "Renal effects of ACE inhibitors in hypertension".)

Several parenteral antihypertensive agents are most often used in the initial treatment of malignant hypertension.

- Nitroprusside – an arteriolar and venous dilator, given as an intravenous infusion. Nitroprusside acts within seconds and has a duration of action of only two to five minutes. Thus, hypotension can be easily reversed by temporarily discontinuing the infusion, providing an advantage over the drugs listed below. However, the potential for cyanide toxicity limits the prolonged use of nitroprusside, particularly in patients with renal insufficiency.

- Nicardipine – an arteriolar dilator, given as an intravenous infusion.

- Clevidipine – a short-acting dihydropyridine calcium channel blocker. It reduces blood pressure without affecting cardiac filling pressures or causing reflex tachycardia.

- Labetalol – an alpha- and beta-adrenergic blocker, given as an intravenous bolus or infusion. Bolus followed by infusion.

- Fenoldopam – a peripheral dopamine-1 receptor agonist, given as an intravenous infusion.

- Oral agents — A slower onset of action and an inability to control the degree of BP reduction has limited the use of oral antihypertensive agents in the therapy of hypertensive crises. They may, however, be useful when there is no rapid access to the parenteral medications described above. Both sublingual nifedipine and sublingual captopril can substantially lower the BP within 10 to 30 minutes in many patients. A more rapid response is seen when liquid nifedipine is swallowed.

The major risk with oral agents is ischemic symptoms (e.g., angina pectoris, myocardial infarction, or stroke) due to an excessive and uncontrolled hypotensive response. Thus, their use should generally be avoided in the treatment of hypertensive crises if more controllable drugs are available.

Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110—sometimes termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressure at this level confers 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) and dizziness than the general population. Other symptoms accompanying a hypertensive crisis may include visual deterioration due to retinopathy, breathlessness due to heart failure, or a general feeling of malaise due to kidney failure. Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.

A "hypertensive emergency" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. 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 papilledema and/or fundal bleeds 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 coughing up 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. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. 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. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.

The effects of high blood pressure during pregnancy vary depending on the disorder and other factors. Preeclampsia does not in general increase a woman's risk for developing chronic hypertension or other heart-related problems. Women with normal blood pressure who develop preeclampsia after the 20th week of their first pregnancy, short-term complications--including increased blood pressure--usually go away within about 6 weeks after delivery.

Some women, however, may be more likely to develop high blood pressure or other heart disease later in life. More research is needed to determine the long-term health effects of hypertensive disorders in pregnancy and to develop better methods for identifying, diagnosing, and treating women at risk for these conditions.

Even though high blood pressure and related disorders during pregnancy can be serious, most women with high blood pressure and those who develop preeclampsia have successful pregnancies. Obtaining early and regular prenatal care is the most important thing you can do for you and your baby.

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.

The ABCDE mnemonic can be used to help determine a secondary cause of hypertension

- A: Accuracy, Apnea, Aldosteronism

- B: Bruits, Bad Kidney

- C: Catecholamines, Coarctation of the Aorta, Cushing's Syndrome

- D: Drugs, Diet

- E: Erythropoietin, Endocrine Disorders

A major aim of treatment is to prevent, limit, or reverse target organ damage by lowering the person's high blood pressure to reduce the risk of cardiovascular disease and death. Treatment with antihypertensive medications may be required to control the high blood pressure.

Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach. Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.

Transjugular intrahepatic portosystemic shunt procedures, or TIPS involve decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy. Since it treats the root cause of portal hypertension gastropathy, it has been putatively used for the condition. The literature reports suggest both regression of portal hypertensive gastropathy on endoscopic images and improvement in bleeding after TIPS.

Finally, cryotherapy involves the use of pressurized carbon dioxide administered through the endoscope to freeze and destroy tissue in a focal area. It is being studied for the treatment of portal hypertensive gastropathy.

Several other diseases can result in retinopathy that can be confused with hypertensive retinopathy. These include diabetic retinopathy, retinopathy due to autoimmune disease, anemia, radiation retinopathy, and central retinal vein occlusion.

Congestion of the mucosa in other parts of the gastrointestinal tract can also be seen in portal hypertension. When the condition involves the colon, it is termed "portal hypertensive colopathy".

Blood pressure control can be accomplished before pregnancy. Medications can control blood pressure. Certain medications may not be ideal for blood pressure control during pregnancy such as angiotensin-converting enzyme (ACE) inhibitors and Angiotensin II (AII) receptor antagonists. Controlling weight gain during pregnancy can help reduce the risk of hypertension during pregnancy.

Increasing access to, and use of, genome profiling may provide opportunity for diagnosis based on presentation and genetic risk factors, by identifying ApoL1 gene variants on chromosome 22.

According to the United States Renal Data System (USRDS), hypertensive nephropathy accounts for more than one-third of patients on hemodialysis and the annual mortality rate for patients on hemodialysis is 23.3%.

Haemodialysis is recommended for patients who progress to end-stage kidney disease (ESKD) and hypertensive nephropathy is the second most common cause of ESKD after diabetes.

Patient prognosis is dependent on numerous factors including age, ethnicity, blood pressure and glomerular filtration rate. Changes in lifestyle factors, such as reduced salt intake and increased physical activity have been shown to improve outcomes but are insufficient without pharmacological treatment.