Hypertension is a major risk factor for cardiovascular disease (CVD) - cerebrovascular events (CVEs) and ischaemic heart disease (IHD) - and is therefore one of the most important preventable causes of premature morbidity and mortality in developed and developing countries.

Normal control mechanisms

Kidney (fluid balance): when BP is low, renal blood flow drops. This stimulates renin and angiotensin production by the kidney. Angiotensin is converted to angiotensin II in the lung. This is controlled by angiotensin-converting enzyme. Angiotensin II is a vasoconstrictor - which will increase SVR. Angiotensin II also stimulates the adrenal cortex to produce aldosterone. Aldosterone causes sodium and water to be retained by the kidney. This will increase the extra cellular fluid (ECF) volume and therefore the circulating blood volume. This is also supported by antidiuretic hormone (vasopressin) which is produced by the hypothalamus and released by the posterior pituitary in response to angiotensin II. Angiotensin II also stimulates thirst, leading to increased fluid intake.

Autonomic nervous system: the autonomic nervous system receives continuous information from the baroreceptors (pressure-sensitive nerve endings) situated in the carotid sinus and the aortic arch. This information is relayed to the brainstem medulla to the vasomotor centre (VMC). A decrease in BP causes activation of the sympathetic nervous system resulting in increased contractility of the heart (beta receptors) leading to an increase in cardiac output. Also, vasoconstriction of both the arterial and venous side of the circulation (alpha receptors) increases SVR.

Hormonal control: in addition to the renin-angiotensin system (as above) adrenaline and noradrenaline are produced by the adrenal medulla in response to sympathetic nervous system activity. They also increase cardiac output and SVR quickly.

Capillary shift: this is the exchange of fluid across the capillary membrane between the blood and the interstitial fluid. This fluid movement is controlled by the capillary BP, the interstitial fluid pressure and the colloid osmotic pressure of the plasma. Low BP results in fluid moving from the interstitial space into the circulation helping to restore blood volume and BP.


Hypertension is often symptomless, so screening is vital - before damage is done. Many surveys continue to show that hypertension remains underdiagnosed, undertreated and poorly controlled in the UK.1
Overall, the prevalence of hypertension (at least ≥140/90 mm Hg or on treatment for hypertension) in those aged over 35 was 32% in men and 27% in women.2

The prevalence significantly increased with age in both sexes:

  • About 33% of men and 25% of women aged 45-54 years have hypertension.
  • About 73% of men and 64% of women aged ≥75 years or older have hypertension.

Screening for hypertension

All adults should have their BP measured, at least every five years up to the age of 80,3 and at least annually thereafter.

Measuring blood pressure3

  • Use a correctly calibrated and maintained machine (manual or automatic).
  • Seated BP is adequate except in elderly or diabetic patients who may have orthostatic hypotension (standing BP is needed as well - after at least one minute's standing).
    If standing systolic blood pressure (SBP) is 20 mm Hg or lower than when seated, review medication, measure all subsequent blood pressures with the person standing (consider specialist referral if postural hypotension symptoms persist).3
  • Remove tight clothing and support the arm with the hand relaxed and the cuff (of appropriate size) at heart level.
  • Initially, measure BP in both arms; if there is a persistent difference of >20 mm Hg between arms then ensure subsequent blood pressures are taken in the arm with the higher reading.

Use an automated machine or the following manual method (if the pulse is irregular (e.g. in atrial fibrillation), always use the manual method):

  • Inflate the cuff whilst palpating the brachial artery, until the pulse disappears. This provides an estimate of systolic pressure.
  • Inflate the cuff until 30 mm Hg above systolic pressure, then place a stethoscope over the brachial artery. Deflate the cuff at 2 mm Hg per second.
  • Systolic pressure: the appearance of sustained repetitive tapping sounds (Korotkov I). Diastolic pressure: usually the disappearance of sounds (Korotkov V). However, in some individuals (e.g. pregnant women) sounds are present until the zero point. In this case the muffling of sounds,(Korotkov IV), should be used.
  • Record to the nearest 2 mm Hg.
  • If initial BP is ≥140/90 mm Hg, take a second or even third reading and record the lowest as the clinic BP.

If BP in the GP surgery is ≥140/90 mm Hg then offer ambulatory blood pressure monitoring (ABPM) to confirm the suspected hypertension, or home blood pressure monitoring (HBPM) if ABPM is not available or not tolerated.3

  • If using ABPM - take ≥2 readings every waking hour, and average at least 14 measurements when deciding whether hypertension is present.
  • If using HBPM - on each occasion take two consecutive BP measurements (<1 minute apart), with the person seated. Take readings twice daily (morning and evening) over ≥4 days (ideally 7 days) - disregard the first day and then average the rest.

Those with high normal values (130-139/85-89 mm Hg) subsequently should be checked annually.

While waiting for further BP readings to confirm diagnosis of hypertension, look for target organ damage and assess cardiovascular risk assessment with a suitable assessment tool - look for hypertensive retinopathy, left ventricular hypertrophy on ECG, and perform blood tests (serum electrolytes, creatinine, eGFR, fasting glucose and lipids) and urinalysis for albuminuria, proteinuria or haematuria ± albumin:creatinine ratio.

Defining hypertension3

BP has a skewed normal distribution within the population and the currently accepted model assumes risk is continuously related to BP. The National Institute for Health and Clinical Excellence (NICE) recommends the following definitions:

  • Stage 1 hypertension - BP in surgery is ≥140/90 mm Hg and ABPM or HBPM is ≥135/85 mm Hg.
  • Stage 2 hypertension - BP in surgery is ≥160/100 mm Hg and ABPM or HBPM is ≥150/95 mm Hg.
  • Severe hypertension - BP in surgery is ≥180/110 mm Hg or higher.

Other considerations

  • Malignant (accelerated) hypertension: this is a syndrome characterised by severe hypertension (e.g. systolic >200 mm Hg, diastolic >130 mm Hg) accompanied by encephalopathy or nephropathy, or by papilloedema and/or angiopathic haemolytic anaemia. Accelerated hypertension needs urgent (same day) assessment and treatment.3
  • Suspected phaeochromocytoma: consider this diagnosis if there is labile or postural hypotension, headache, palpitations, pallor and profuse sweating - refer for urgent (same day) assessment.3
  • Hypertensive crisis: a systolic blood pressure (SBP) ≥180 mm Hg or a diastolic blood pressure (DBP) ≥120 mm Hg is considered a 'hypertensive crisis'. Treatment should safely reduce BP. Immediate reduction in BP is required only in patients with acute end-organ damage.4,5
  • Systolic or diastolic pressure: for many years diastolic pressure was considered to be more important than systolic pressure. However, evidence from the Framingham study6 and the Multiple Risk Factor Intervention Trial (MRFIT) study7 indicates that systolic pressure is the most important determinant of cardiovascular risk.
  • Hypertension in the elderly: although age-related, rise in systolic pressure can be considered part of the 'normal' ageing process, isolated systolic hypertension (ISH) in the elderly should not be ignored; the benefits of treatment are far greater than treating moderate hypertension in middle-aged patients.8,9



It is usually asymptomatic, except accelerated hypertension.

All patients need a full history and physical examination. Look hard for a cause (renal, endocrine, etc. - as above) in the young, severe hypertensive.11,12

Start by talking to the patient:

  • Take a full drug history (non-steroidal anti-inflammatory drugs (NSAIDs), oral contraceptives, steroids, licorice, sympathomimetics, i.e. cold cures).
  • Are they aware of the hypertension? Episodic feelings 'as if about to die' or headaches, or paroxysmal sweats or palpitations, suggest phaeochromocytoma.
  • Consider renal causes: is there a present, past or family history of renal disease? Are the kidneys palpable? Is there an abdominal or loin bruit (renovascular disease) or delayed or weak femoral pulses (coarctation).
  • Does the patient look Cushingoid or might he or she have Conn's syndrome (tetany, weak muscles, polyuria, hypokalaemia)?
  • Consider contributory factors: obesity, excess alcohol, salt intake and lack of exercise, environmental stress, and cardiovascular risk factors (smoking, diabetes, cholesterol and family history) ready for your management plan.

Assess the degree of end-organ damage or complications of hypertension; previous cerebrovascular event (CVE), transient ischaemic attack (TIA), dementia or known left ventricular hypertrophy (LVH)/left ventricular (LV) strain, ischaemic heart disease (IHD), peripheral vascular disease, renal impairment? Perform ophthalmoscopy; dilate with 1% tropicamide if there is poor view.


  • Routine investigation should be limited to:
    • Urine dipstick test for protein and blood.
    • Serum creatinine and electrolytes and eGFR.
    • Fasting blood glucose.
    • Fasting serum total and high-density lipoprotein (HDL) cholesterol.
    • 12-lead ECG (looking for LVH or signs of IHD).
  • Echocardiography is useful in young patients who commonly have ECGs with voltage criteria of LVH, without T-wave abnormalities.
  • Specific investigations for a suspected secondary cause:
    • Plasma calcium.
    • CXR.
    • Renal ultrasound.
    • Intravenous urogram (IVU).
    • Renal arteriography.
    • 24-hour urinary vanillylmandelic acid (VMA) x 3.
    • Urinary free cortisol.

Referral to a specialist may be appropriate for some of these tests.

Indications for specialist referral13

  • Urgent treatment needed: accelerated hypertension, severe hypertension (>220/>120 mm Hg) or impending complications (e.g. transient ischaemic attack (TIA), left ventricular (LV) failure).
  • Possible underlying cause: low K+, Na+ elevated (possible Conn's syndrome); elevated creatinine, proteinuria or haematuria; sudden onset or rapidly worsening or resistant hypertension (i.e. needs >3 drugs); young age: patient aged <20 years, or <30 years needing treatment.
  • Therapeutic problems: multiple drug intolerance or contra-indications, persistent noncompliance or treatment refusal (the reluctant hypertensive).
  • Special situations: hypertension in pregnancy,14 unusual BP variability.


For a full discussion on cardiovascular heart disease (CVD) risk assessment, treatment thresholds and their modification dependent on target organ damage and concurrent diseases, see separate related article Management of Hypertension.

Resources on hypertension:

Patient experiences

Document references

  1. Wolf-Maier K, Cooper RS, Kramer H, et al; Hypertension treatment and control in five European countries, Canada, and the United States.; Hypertension. 2004 Jan;43(1):10-7. Epub 2003 Nov 24. [abstract]
  2. Health Survey for England 2009, Volume 1 Health and Lifestyles; NHS Information Centre (16 December 2010)
  3. Hypertension: management of hypertension in adults in primary care, NICE Clinical Guideline (August 2011)
  4. Varon J; The diagnosis and treatment of hypertensive crises. Postgrad Med. 2009 Jan;121(1):5-13. [abstract]
  5. Perez MI, Musini VM; Pharmacological interventions for hypertensive emergencies. Cochrane Database Syst Rev. 2008 Jan 23;(1):CD003653. [abstract]
  6. Sytkowski PA, Kannel WB, D'Agostino RB; Changes in risk factors and the decline in mortality from cardiovascular disease. The Framingham Heart Study. N Engl J Med. 1990 Jun 7;322(23):1635-41. [abstract]
  7. Kannel WB, Neaton JD, Wentworth D, et al; Overall and coronary heart disease mortality rates in relation to major risk factors in 325,348 men screened for the MRFIT. Multiple Risk Factor Intervention Trial. Am Heart J. 1986 Oct;112(4):825-36. [abstract]
  8. Lewington S, Clarke R, Qizilbash N, et al; Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002 Dec 14;360(9349):1903-13. [abstract]
  9. Effectiveness Matters. Drug Treatment of Essential Hypertension in Older People; Vol 4 issue 2; October 1999
  10. Gibson P et al; Hypertension and Pregnancy, Medscape, Mar 2011
  11. Stergiou GS, Nasothimiou E, Giovas P, et al; Diagnosis of hypertension in children and adolescents based on home versus ambulatory blood pressure monitoring. J Hypertens. 2008 Aug;26(8):1556-62. [abstract]
  12. Falkner B; Hypertension in children and adolescents: epidemiology and natural history. Pediatr Nephrol. 2009 May 7. [abstract]
  13. Ezzati M, Lopez AD, Rodgers A, et al; Selected major risk factors and global and regional burden of disease. Lancet. 2002 Nov 2;360(9343):1347-60. [abstract]
  14. Hypertension in pregnancy, NICE Clinical Guideline (August 2010); The management of hypertensive disorders during pregnancy
© EMIS 2011Author: Dr Huw ThomasReviewer: Dr Hannah Gronow
Document ID: 2289Document Version: 25Last Reviewed: 8 Sep 2011
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