Clinical Review - GP management of hypertension

A clinical review of the diagnosis and management of hypertension, according to the latest NICE guidelines. By Dr Klaus Witte

BP at presentation was 158/98mmHg (Photograph: SPL)
BP at presentation was 158/98mmHg (Photograph: SPL)

Section 1: Epidemiology and aetiology

Hypertension is a major contributor to the development of cardiovascular disease and affects more than 25% of the UK population. The prevalence increases with age such that more than half of all people older than 65 years have a BP of >140/90mmHg.1

The prevalence, the fact that the attributable risk of stroke due to hypertension is >60% and that of coronary artery disease (approx) 40-50%, and that treating hypertension can prevent or postpone cardiovascular events2 has led to BP control becoming a major focus of primary and secondary cardiovascular disease prevention. Hypertension is now one of the most common conditions treated in primary care in the UK.

Although young adults with high BP are frequently referred for investigation to exclude high-profile but rare secondary causes (see box, below), most adult patients (>95%) with high BP have primary hypertension.

Hypertension risk factors
Smoking, obesity and metabolic syndrome are causally associated with high BP and the combination of several or all of these risk factors in the UK population is increasingly common.

Other risk factors for the development of hypertension include alcohol, family history and ethnic origin. For example, the prevalence of hypertension is greater in patients of African or Caribbean origin in whom it often appears earlier and is more difficult to treat.

Causes of secondary hypertension
Renal disease  

Parenchymal disease


Arterial disease

 - Chronic renal failure, acute and chronic glomerulonephritis polycystic disease, pyelonephritis, tumours (Wilm’s tumour), diabetes

- Atherosclerosis, fibromuscular dysplasia, embolism, polyarteritis nodosa

Endocrine disease         

Adrenal cortical overactivity

Adrenal medullary overactivity

Pituitary overactivity

Thyroid overactivity

 - Conn’s syndrome, Cushing’s syndrome, congenital adrenal hyperplasia


 - Phaeochromocytoma


 - Acromegaly, Cushing’s disease


 - Hyperthyroidism

Drug-induced  - Combined oral contraceptive pill, steroids
Congenital defects  - Aortic coarctation
Miscellaneous  - Porphyria (during attacks), lead poisoning (acute phase), raised intracranial pressure, aortic regurgitation, pre-eclampsia, polycythaemia rubra vera

Section 2: Making the diagnosis

Most patients have no symptoms or clinical findings on examination and their hypertension is identified incidentally, or as a result of the complications of essential hypertension, such as angina pectoris, MI, stroke and arrhythmias, such as AF.

Physical examination is nevertheless important since evidence of end-organ damage, such as a displaced apex beat due to left ventricular hypertrophy (LVH), or ocular changes, such as silver wiring and arteriovenous nipping, identifies patients at higher risk in whom there should be a lower threshold for treatment.

It is also useful to exclude radiofemoral delay (aortic coarctation), central obesity and abdominal striae (Cushing's syndrome) or skin thickening and bone changes (acromegaly).

Blood samples should be drawn for renal function, electrolyte levels and glucose. Blood should also be taken to exclude hyperuricaemia, hyperlipidaemia and anaemia.

A urine dipstick will identify proteinuria and haematuria, but in patients with diabetes mellitus or younger patients in whom secondary hypertension is suspected, a 24-hour urine collection for protein excretion or hormonal metabolites is useful.

In most cases an ECG should also be performed to exclude arrhythmia, and to document baseline heart rate and the presence or absence of LVH.

LVH or high resting heart rate are markers of worse outcome in patients with hypertension.3,4 An abnormal ECG should prompt a referral for consideration of echocardiography.

In young people or those with resistant hypertension, renal ultrasound with Doppler of renal arteries can identify renal artery stenosis, although renal arterial angioplasty does not reliably lead to better BP control or preservation of renal function.

NICE guidelines have focused on ambulatory BP monitoring (ABPM).5 Patients with a clinic BP of >140/90mmHg but <180/110mmHg on the second or third measurement at the consultation should undergo ABPM (or home BP monitoring (HBPM) for at least four days).

A diagnosis of hypertension is made when the mean BP is >135/85mmHg. Stage I hypertension is a mean BP of <150/95mmHg; stage II is a mean BP of ≥150/95mmHg.

Recent changes to guidelines
The latest NICE guidelines aim to improve the accuracy of making a diagnosis of hypertension6 and are proposed to be cost-saving by reducing the number of patients incorrectly labelled as hypertensive, or by limiting drug up-titrations in hypertensive patients who are already controlled.7

Patients with clinic systolic readings of (approx)155mmHg, for example, which equates to an ambulatory systolic reading of (approx)135mmHg,8 now fall outside diagnosis and treatment thresholds. It is difficult to reconcile this aim with recent data suggesting that patients throughout Europe, including the UK, are frequently undertreated or not treated at all.9

Cardiovascular risk increases from a BP of 120mmHg systolic10,11 and treatment down to 115mmHg systolic is of benefit,12 so overdiagnosing hypertension seems generally harmless, yet underdiagnosing it might not be.

Furthermore, although ABPM and HBPM readings are better at predicting cardiovascular events than clinic readings, all of the studies demonstrating improved outcome from antihypertensive therapy have been based on a diagnosis made in a clinic setting.

The guidelines are instead selecting patients assumed to be at highest risk.

Section 3: Managing the condition

Patients with severe hypertension (clinic reading ≥180/110mmHg), those with confirmed stage II hypertension (on ABPM) and those less than 80 years with stage i hypertension and target organ damage established cardiovascular disease renal diabetes mellitus or a 10-year risk 20 should be treated.5

Young patients without comorbidities fail to register on the risk tables, yet might have the most life gain from early treatment, so could be referred for specialist advice. The guidelines suggest that older patients (>80 years) with stage I hypertension should not receive treatment.

Lifestyle advice
Weight loss, exercise, alcohol and salt restriction are associated with a reduction in BP so patients should be counselled appropriately. Smoking is not directly associated with BP, but contributes significantly to overall cardiovascular risk and patients should be offered help and advice to stop.

Antihypertensive medication
The treatment target in most patients is 140/90mmHg, although this is lower (135/85mmHg) in patients with diabetes mellitus and higher in those ≥80years (150/90mmHg).

Many patients will require more than one agent, and it is important to discuss this when starting treatment.

A poor response to the first agent despite up-titration does not mean the drug has 'failed' and if this drug is well tolerated, a second, complementary agent should be added.

There has been controversy about the relegation of beta-blockers to fourth-line agents in the management of hypertension. It is incongruous that they should be fourth line for hypertension in patients with quiescent coronary artery disease, but then receive an upgrade to first line once coronary artery disease becomes overt, despite the fact that BP lowering is the most powerful way to control both primary and secondary risk.

There are suggestions that they might be less protective against stroke and might increase the rate of diabetes. However, two recent meta-analyses concluded that the protective effect of BP lowering was broadly similar for all classes of antihypertensive agents,13 with a significant advantage of beta-blockers following a coronary event.14

Antihypertensive combinations
Common antihypertensive agents are often prescribed concurrently and there are now many combinations available.

The term 'fixed dose combination' is no longer appropriate because most combination tablets come with a variety of doses of each agent.

Combination tablets improve compliance (see graph, below), which is itself associated with a greater reduction in BP but they are not mentioned in the 2011 version of the guidelines.

However, chlortalidone is recommended, which is only available at studied doses in combination tablets.

A patient stabilised but not controlled on an ACE inhibitor or ARB, for example, can take a single tablet containing two generic agents, moving to step two of the treatment algorithm while incurring only a single prescription charge. If side-effects develop subsequently, this is due to the second agent.

Section 4: Prognosis

BP is associated with cardiovascular risk. Lower systolic BP of around 20mmHg was associated with a halving of risk of death from stroke and IHD over 13 years.12

This relationship was consistent over a wide range of ages, for men and women and down to a BP of around 115mmHg.

The effects of treatment mirror these data. BP reduction by 5mmHg leads to a relative reduction in stroke and CHD of 42% and 14% respectively.15

Efficacy can be monitored using clinic readings unless there is a discrepancy between those and the ambulatory reading (20/10mmHg), in which case home or ambulatory monitoring might be an alternative.

Patients with hypertension on treatment should be followed up annually to ensure continued control and patients who are at risk should be reassessed every five years.

Section 5: Case study

A 52-year-old male patient fully employed as a heavy goods vehicle driver was seen for a cough found to be due to a chest infection.

The patient had a BMI of 34kg/m2 and smoked 15 cigarettes per day. Resting BP in the clinic at the time of presentation was 158/98mmHg.

He received treatment for his chest infection and was invited to return at one month for a repeat BP check.

At the second visit, the BP was 154/94mmHg. Blood was sampled for renal function, random glucose and lipids. Urine dipstick was clear and an ECG was performed. An ABPM was organised.

At one further week, the patient returned. His renal function, random glucose and ECG were normal. His LDL cholesterol was 4mmol/L. The ABPM revealed a mean daytime reading of 138/89mmHg.

Plans were made to start treatment with an ACE inhibitor (lisinopril 5mg), but the patient requested lifestyle advice and a further review at three months.

At his return at three months, he had lost weight (BMI now 29kg/m2), stopped smoking and was eating less fast food. He also admitted he had previously been drinking 20 pints of beer per week at weekends, which he had now cut to two bottles per week. He was disappointed that his clinic BP at that time was 146/92mmHg.

A further ABPM was organised and revealed a mean BP of 130/78mmHg. His LDL has also reduced to 2.9mmol/L.

The patient was delighted and a review at one year was planned.

Key guideline changes
  • ACE inhibitor should not be combined with ARBs.
  • Alternative thiazide or thiazide-like diuretics are preferred.
  • Beta-blockers are not advised as first(or second-) line therapy unless there are special circumstances (women of childbearing age, patients with contraindication to ACE inhibitor or ARB).
  • Second-line treatment should be a combination of calcium-channel blocker with ACE inhibitor or ARB (rather than a thiazide).
  • Third-line treatment should include calcium-channel blocker, ACE inhibitor or ARB, thiazide-like diuretic.
  • If BP remains over 140/90mmHg and compliance is reasonable, a fourth agent can be added, and referral for specialist advice considered.
  • Patients should be offered once-a-day agents.
  • Patients with isolated systolic hypertension should be managed similarly to those with raised diastolic and systolic readings.

Section 6: Evidence base

  • Czernichow S, Zanchetti A, Turnbull F et al. Blood Pressure Lowering Treatment Trialists' Collaboration. The effects of BP reduction and of different blood pressure-lowering regimens on major cardiovascular events according to baseline blood pressure: meta-analysis of randomized trials. J Hypertens 2011; 29: 4-16.

This paper pulls together the results of 32 trials showing that the effectiveness of BP lowering in prevention of cardiovascular events does not depend on starting BP and that additional efforts in those meeting existing targets will produce further benefits.

  • Kotseva K, Wood D, De Backer G et al; the Euroaspire Study Group. Euroaspire III. Management of cardiovascular risk factors in asymptomatic high-risk patients in general practice: cross-sectional survey in 12 European countries. Eur J Cardiovasc Prev and Rehab 2010; 17: 530-40.

These data come from a survey of 66 general practices in 12 European countries suggesting that BP remains poorly diagnosed and controlled, lipid and glucose control are inadequate and that lifestyle issues also remain a cause for concern with a high prevalence of persistent smoking and obesity.

This was a study in more than 24,000 patients demonstrating equivalence between telmisartan (an ARB) and ramipril (an ACE inhibitor) for cardiovascular outcomes. The combination of an ARB with an ACE inhibitor in this study was of no additional benefit but was associated with more side-effects.



Click here to take a test on this article and claim your certificate on MIMS Learning


These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.

  • Revise the potential causes of secondary hypertension and present a summary to colleagues in a clinical practice meeting.
  • Review patients with historically poor compliance on multiple antihypertensives and consider whether they are on the most appropriate combinations.
  • Check the diagnosis and management algorithms in the 2011 NICE guidelines and ensure you are aware of any changes.

1. DH. Health Survey for England - 2009. health-and-lifestyles-related-surveys/health-survey-for-england

2. Capewell S, Morrison CE, McMurray JJ. Heart 1999; 81: 380-6.

3. Okin PM, Kjeldsen SE, Julius S et al. Eur Heart J 2010; 31: 2271-9.

4. Okin PM. J Electrocardiol 2009; 42: 584-8.

5. Krause T, Lovibond K, Caulfield M et al. BMJ 2011; 343: d4891.

6. Hodgkinson J, Mant J, Martin U et al. BMJ 2011; 342: d3621.

7. Redon J, Campos C, Narciso ML et al. Hypertension 1998; 31: 712-18.

8. Mancia G, Sega R, Bravi C et al. J Hypertens 1995; 13(12 Pt 1): 1377-90.

9. Kotseva K, Wood D, De Backer G et al; the Euroaspire Study Group. Euroaspire III. Eur J Cardiovasc Prev and Rehab 2010; 17: 530-40.

10. Kokubo Y, Kamide K, Okamura T et al. Hypertension 2008; 52: 652-9.

11. Conen D, Ridker PM, Buring JE et al. BMJ 2007; 335: 432.

12. Lewington S, Clarke R, Qizilbash N et al. Lancet 2002; 360: 1903-13.

13. Turnbull F, Neal B, Ninomiya T et al. BMJ 2008; 336: 1121-3.

14. Law MR, Morris JK, Wald NJ. BMJ 2009; 338: b1665.

15. Collins R, Peto R, Macmahon S et al. Lancet 1990; 335: 827-38.

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