All images in this article taken from the Nice guidelines on Hypertension, and reproduced in accordance with the terms on conditions of the author.
WHO criteria for defining hypertension:
  • Under 50 – should try to get it under 140/90
  • Over 50 – should try to get it under 160/95

NICE guidelines

Offer treatment to patients with:
  • Blood pressure >160/100 – on a one-off occasion
  • Blood pressure >140/90 – one two consecutive visits to the GP
  • Systolic of greater than 160
  • Blood pressure >140/90 – and 10 year CVD risk of >20%, OR, existing CVD organ damage
The aim of treatment is to get BP to less than 140/90.
Remember:
  • Cardiovascular risk increases with BP, even in the ‘normal limit’
  • Using the WHO criteria, up to 25% of the population have hypertension
  • Hypertension produces structural changes in the heart and cardiovascular system. This causes complications that are referred to as target organ damage.
  • Be wary of white coat hypertension – the phenomenon is real! It exists with doctors, and to a lesser extent, nurses. You may weed out many cases of this by taking several readings on different occasions – in cases of white coat hypertension, the readings will gradually approach the normal level. You could also try a 24 hour BP monitor. If white coat hypertension is treated, as ‘real hypertension’, then the patient can suffer serious hypotension when away from the GP’s surgery – and this can be dangerous!
  • When you start somebody on antihypertensive medication, it is likely they will be on it for life! Thus you shouldn’t make the decision lightly, and should ensure you have sounds readings as a basis.
  • Up to 20% of individuals suffer white coat hypertension
  • The risk of cardiovascular complications of those with white coat hypertension is much less than those with ‘proper’ hypertension, but still greater than those that exhibit no white coat hypertension.
  • 24 hour BP measurements are chronically lower than those in a clinical setting – by approximately 12/7mmHg, and as such, they must be adjusted. Also, note that you take an average of the BP during the day not during the night
  • The ‘ideal blood pressure’ is 120/80 – however, the actual distribution of blood pressures is like a bell curve, so ‘normal’ for some people is very low (or perhaps even very high!)
  • You cant take a BP of a person with atrial fibrillation with an electronic machine! The machine just comes up error.

 

When taking a reading
  • Patient should be relaxed, but not talking
  • Read to the nearest 2mmHg
  • Repeat after 5 minutes if the first reading is raised
  • Repeat on at least 2 separate visits to the GP if still raised
  • Remove tight clothing from the arm
  • Support the arm at the level of the heart
  • Use an appropriate size cuff – the bladder in the cuff must be at least 2/3 the circumference of the arm
  • Use phase 5 of the korotkoff sounds to measure diastolic BP
    • Phase 4 – this is where the sounds become muffled
    • Phase 5 – this is where the sounds completely disappear
  • Adults should have their BP measured at least every 5 years up the age of 80
  • You should take sitting and standing readings in those with diabetes and the elderly to exclude orthostatic hypotension
  • You need at least 2 consistently high results (on separate occasions), or 3+ high results (when numbers vary between each reading) to diagnose hypertension.

Epidemiology

  • BP rises with age (up to the 7th decade). This rise is more pronounced in the systolic pressure, and more common in men
  • Hypertension is present in roughly 30-40% of the population
  • Hypertension is more common in black Africans – 40-45% of adults

Classification

It is important to distinguish the tow types because in secondary hypertension you can treat the cause but in essential hypertension, you cannot.
Essential hypertension
This is where no underlying cause can be found, and it accounts for 90-95% of cases of hypertension.

It has multifactorial aetiology
Genetic factors – high blood pressure tends to run in families. 40%-60% have a genetic component
Foetal factors – low birth weight is associated with hypertension (and also CVD) in later life. This could be due to adaptive changes the foetus makes in the uterus to under nutrition. These changes could change the structure of arteries, resulting in hypertension later in life. Hormonal systems may also be altered
Environmental factors:

  • Obesity – fat people have a higher blood pressure than thin people. However – there is also a tendency to overestimate the BP when it is measured with a small cuff. Sleep disordered breathing is also seen with obesity, and may be an additional risk factor
  • Alcohol intake – there is a very strong correlation between alcohol intake and blood pressure. However – people who consume small amounts of alcohol tend to have a lower BP than those who consume none at all – the ‘one glass of red wine a day’ thing
  • Sodium intake – this is controversial. There is currently no strong evidence that consuming a high sodium diet is causal  in hypertension, only that it exacerbates existing hypertension. Nevertheless, those with a high sodium diet have a higher BP than those with a low sodium diet. High sodium diet is also associated with a western, urbanised lifestyle.
    • It is thought that a high potassium diet may be protective against a high sodium intake
  • Stress – acute stress and pain obviously raise BP, but the association of chronic stress and BP is uncertain (there probably isn’t much association)
  • Insulin intolerance – the metabolic syndrome(aka metabolic syndrome X)this is a syndrome that greatly increases the risk of heart disease and diabetes. The syndrome is said to exist when there is hyperinsulinaemia (i.e. insulin resistance), glucose intolerance, reduced levels of HDL cholesterol, hypertension, and central obesity.
Secondary hypertension
This accounts for 5-10% of cases. Causes include:
You can also class hypertension in respect to its progression
  • Benign hypertension – this is a stable elevation of blood pressure over many years. It is most common in those over 40
  • Malignant hypertension this is an acute, severe elevation of BP. It is rare, but if undiagnosed, can lead to death within 2 years, as a result of renal failure, heart failure or stroke. It is usually diagnosed due to the presence of retinal signs; Papilloedema, flame-shaped haemorrhages, hard exudates, and cotton wool spots. More on the retinal signs below

Clinical features

  • Usually asymptomatic
  • May be headaches (not that common)
  • Nosebleeds – but only if the BP is very very very high! This is not a particularly common cause of nodebleeds
  • Signs

Pathophysiology

Basically, there is an increase in peripheral vascular resistance as a result of vasoconstriction, and hypertrophy of the arterial wall.
  • There may also be endothelial dysfunction – whereby there is decreased EDRF release (NO).
Blood vessels
Not only does hypertension cause atherosclerosis, but it also changes the arterioles and small arteries. These changes essentially cause narrowing of the lumen.
Changes in benign hypertension include:

In arteries (over 1mm in diameter)muscular hypertrophy of the media, reduplication of the external lamina, intimal thickening. The walls of the arteries often become less compliant.

  • There is also a general widespread atheroma.

In arterioles – hyaline arteriosclerosisthis is protein deposition in the arterial wall. The lumen of the artery narrows, and aneurysms may develop.
In the vessels in the brain – microaneurysms (called Charcot-Bouchard aneurysms, and also sometimes miliary aneurysms)can appear

  • These aneurysms only occur in very small blood vessels (<300micrometers in diameter), and should not be confused with berry aneurysms.
  • They are usually located in the brainstem
  • As with any aneurysm, once formed they tend to expand, and possible eventually rupture. When they do rupture, they cause haemorrhagic stroke.
Other changes generally occur in malignant hypertension, but they can also sometimes occur in benign hypertension:
  • Hyperplastic arteriosclerosis – this is where there is muscular hypertrophy and reduplication of the basement membrane in arteries. This only occurs in the basement membrane, and thus is different from the changes that occur in benign hypertension. These changes are also often associated with fibrin deposition, in which case the condition is known as necrotising arteriolitis.
    • These changes most commonly affect the renal arteries, causing nephrosclerosis which can affect renal function, as well as exacerbating hypertension through the activation of the renin-angiotensin system.
Don’t forget, that the baroreceptors will ‘reset’ themselves to the high pressure – so if you reduce pressure really quickly, you get cerebral ischaemia!
Complications & risk factors
Basically these can be divided into cardiovascular risks, and cerebrovascular risks. These complications are more likely if the patient smokes, and if the patient has high cholesterol.

Cardiovascular events are twice as likely in hypertensive patients as those with normal BP. Examples include:

  • Atherosclerosis
  • Aortic  aneurysm
  • Cardiac failure – this is the cause of death in 1/3 of hypertensive patients
  • Atrial fibrillation

Cerebrovascular events – i.e. haemorrhage or clot

Renal failure, and other renal problems. Kidneys are more likely to be small than large
Visual disturbance – caused by papilloedema and retinal haemorrhages

Target organ damage
Retina
Fundoscopy is a very useful tool in determining the damage caused by hypertension all over the body – not just in the retina. by viewing the retina, you get an excellent view of the arteries that supply it – and this sort of view of the arteries cannot be seen anywhere else.
The retinal signs are most commonly seen in malignant hypertension
There are 4 grades of hypertensive retinopathy that can be distinguished:
  • Grade 1 – arteriolar thickening, increased tortuosity (twisty-ness), and increased reflectiveness – silver wiring
  • Grade 2 – grade 1 + venous narrowing at arterial crossing– arteriovenous nipping
  • Grade 3 – grade 2 + evidence of retinal ischaemia – flamed shaped, or blot haemorrhages, and cotton wool exudates (cotton wool spots are associated with areas of infarct. They fade within a few weeks, and thus their continued appearances suggest ongoing pathology)
  • Grade 4 – grade 3 + papilloedema (optic disc swelling)
‘hard exudates’ – are small white, hard, dense deposits of lipid. These, along with dot haemorrhages (micro aneurysms) are more commonly associated with diabetic retinopathy, than hypertension
Heart
Systemic (left sided) hypertensive heart disease
In this condition, changes that were initially adaptive to cope with the hypertension, lead to cardiac dilatation, congestive heart failure, and even sudden death.
  • Adaptive changes – the left ventricular wall hypertrophies (to increase the CO in the face of increased peripheral resistance), and initially, there is no reduction in left ventricular volume. Histologically there is enlargement of myocytes and their nuclei (hypertrophy). However, in the long term, the myocytes will atrophy, and the ventricle will dilate, and have a reduction in muscle volume, causing the complications of left ventricular dilatation and congestive heart failure.
Pulmonary hypertensive disease
Once the left side of the heart fails, then pulmonary hypertension can lead to congestive heart failure.
Ischaemic heart disease
Enlargement of the ventricle, combined with the artery effects, can lead to ischaemic heart disease
Brain
  • Hypertension is responsible for ½ of all strokes
  • Microaneurysms
Investigations
  • Glucose
  • Urinalysis (proteinuria, creatinine and urea (for eGFR)
  • Measure Hb
  • If suspect endocrine causes, then test these levels (e.g. hypokalaemia for Conn’s syndrome)
  • CXR (look for coarctation)
  • ECG – for left ventricular hypertrophy
  • Aldosterone – for primary aldosteronism

Management

Compliance is a big issue in hypertension, because often patients have no symptoms (particularly in essential hypertension) and as such they often feel like they don’t need treatment.

Lifestyle interventions

  • Discourage the intake of coffee and other high-caffeine products
  • Ask about diet and exercise and advise on a different pattern of these if appropriate
  • Ask about alcohol intake and advise of the risks of this
  • Encourage patients to reduce salt intake, or use a salt substitute
  • Offer smoking cessation advice
  • Tell the patient about local initiatives that provide support and promote lifestyle change
  • Do not:
    • Offer calcium, magnesium or potassium supplements to reduce BP
    • Offer relaxation therapies. Patient’s can chose to do them if they wish, but they are nor recommended by the NHS

Drug therapies

The old management pattern used to be: ABCD
  • A – ACE inhibitor (or angiotensin-II receptor antagonist if ACE not well tolerated)
  • B – beta-blocker
  • C – calcium channel blocker
  • D – diuretic (thiazide)
Start at ‘A’ for patients under 55, and start at D for those over 55, or of African origin. However, this management plan has now been modified slightly; and beta blockers are no longer recommended.

These are less effective than the other drugs at reducing cardiovascular risk factors – particularly stroke.
They do not reduce the risk of diabetes – especially in those patients also taking a diuretic, and may, in fact, increase the risk of diabetes. –  a diuretic, a 
They are no longer routine therapy, by may be considered in:

  • Women of child-bearing age
  • Patients with evidence of increased sympathetic drive
  • Patients who find it hard to tolerate ACE inhibitors and angiotensin-II receptor antagonists
  • If a patient already taking beta-blockers needs a second drug, give them a calcium channel blocker and not a thiazide diuretic. This reduces the risk of developing diabetes
  • If the blood pressure is well controlled on a beta-blocker (<140/90), it is not absolutely recommended to change it, however you should consider other options
  • Beta-blockers should not be withdrawn, if the patient has another suitable indication for being on one; e.g. symptomatic angina, MI

More management tips

  • Treatment is still worthwhile if it lowers the BP, even if it doesn’t reach the target of 140/90mmHg
  • If patients are particularly keen to try lifestyle interventions, and their cardiovascular risk is low, then you can try withdrawals of the drug treatment to see if the lifestyle interventions are making a difference.
  • Patients should have an annual review – you need to check BP, discuss lifestyle, discuss symptoms and medication.

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