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Hypertension

Dr Tom Leach

Introduction

Hypertension is one of the most common medical diagnoses, and also one of the most well studied. Hypertension rarely causes any symptoms in its own right, but is clinically significant because it increases the risk of cardiovascular disease (heart attack and stroke), and to a lesser extent, kidney disease.
The textbook ‘normal’ blood pressure is 120/80 mmHg. Many patients, particularly young adults (more common in women) have a lower baseline blood pressure than this. Providing they are not symptomatic (e.g. light headed, syncopal symptoms), this is normal.
Hypertension is defined as a BP >140 systolic or >90 diastolic.
Some guidelines grade hypertension as mild, moderate and severe:

Diagnosis should involve measurement of BP in both arms during a consultation, and if it is raised, then the diagnosis should be confirmed with either ambulatory home blood pressure monitoring (ABPM) or home blood pressure monitoring (HBPM). 

Once the diagnosis is confirmed, the patient should be investigated for target organ damage, and they should be assessed for their risk of cardiovascular disease with a cardiovascular disease risk assessment tool, such as QRISK3 (UK) or cvdcheck (Australia).

The mainstay of management involves lifestyle interventions (encouraging exercise, modifications to diet), and pharmacological treatments.
The main classes of drugs used in medical management are:

They are broadly equally effective. It is thought that the reduction in cardiovascular disease risk is mainly related to the reduction in blood pressure, regardless of the mechanism used. Up to 70% of patients will not have adequately controlled BP with a single agent. It is very common to combine multiple medications to achieve an acceptable BP.

ACE inhibitors or ARBs are recommended as the first line drug, as it is thought they have slightly better long-term cardiovascular disease outcomes.

The first-line recommended combination is ACE-inhibitors (or ARB) with a calcium-channel blocker. This have been proven superior to combinations with thiazide diuretics.

Other drugs that can lower BP – such as alpha-blockers and beta-blockers are not routinely recommended for treatment of hypertension because they have been shown to be inferior at reducing the risk of cardiovascular disease.

Hypertension is rarely an emergency unless associated with signs of end organ damage, and thus is typically managed in the community. A hypertensive emergency (aka malignant hypertension) presents with acute signs and symptoms and needs urgent admission to hospital.

Epidemiology

Pathology

The vast majority of cases of hypertension have no identifiable underlying cause. We call this essential hypertension or sometimes primary hypertension. 
More rarely hypertension is due to an underlying identifiable disease process. We call this secondary hypertension. 
It is important to distinguish the two 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:

The J-curve of alcohol vs all cause mortality. Taken from the International Scientific Forum on Alcohol Research and AIM and reproduced in accordance with the Open Government License.
Secondary hypertension
This accounts for 5-10% of cases. Causes include:
You can also class hypertension in respect to its progression

Pathophysiology

In hypertension 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 (essential) 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 arteriosclerosis – this 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

Sometimes also referred to as target organ damage. 
These complications are more likely if the patient smokes, and if the patient has high cholesterol.
  • Cardiovascular events
    • 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
    • Stroke
  • Renal effects
    • Renal failure, and other renal problems. Kidneys are more likely to be small than large
  • Eye effects
    • Visual disturbance – caused by papilloedema and retinal haemorrhages
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 cardiac output 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

Clinical features

Diagnosis

Diagnosis is not aa straightforward as a one-off reading. Blood pressure varies greatly from minute to minute and day to day. To confirm a diagnosis of hypertension, some form of home monitoring is required.

If hypertension is suspected (e.g. from a one-off clinic reading):

Its at about this point that I tell my patients to “take a couple of deep breaths, and think some relaxing thoughts…”

 

When taking a reading in the clinic

Investigations

Every patient with hypertension should be tested for evidence of target organ damage. This should include:

Other tests to consider if clinical suspicion

Patients should also have the following baseline observations recorded:

Management

The aim of treatment is (usually) to get BP to less than 140/90.

Once the diagnosis of hypertension is established, you should estimate the cardiovascular risk score, with either QRISK (UK) or the cvdcheck tool (Australia). This can help to guide treatment choices. For example, a patient with mild hypertension and a low risk score might opt for lifestyle interventions first, whereas an individual with a high risk score and the same BP might be more inclined to start medication sooner.

Guidelines from various countries are quite similar, but if you want the specifics (as of November 2019):

Lifestyle interventions

The effect of lifestyle interventions on blood pressure. This is a printout I made to give to my patients in an attempt to give them some motivation! Summarised from: Frisoli TM, Schmieder RE, Grodzicki T, Messerli FH. Beyond salt: Lifestyle modifications and blood pressure. European Heart Journal. 2011;32(24).

Drug therapies

The main drugs used for management are:

In cases that are resistant to treatment, other agents that my be considered include:

Generally it is more effective, and has fewer side effects to use multiple agents at a smaller dose, rather than a single agent at a larger dose.

Guidelines

  1. In most patients – start with an ACE inhibitor or ARB
    • If over 55 (or of African origin at any age) and don’t have T2DM then start with a calcium channel blocker
    • If a calcium channel blocker is not tolerated, use a thiazide diuretic instead
    • In Australia, guidelines are simpler and recommend starting with the ACE inhibitor or ARB first regardless
  2. If hypertension remains uncontrolled
    • ACE or ARB PLUS CCB OR thiazide-like diuretic
  3. If still remains uncontrolled
    • ACE or ARB PLUS CCB PLUS thiazide-like diuretic
  4. If still uncontrolled – consider this resistant hypertnesion
    • Add a 4th agent, such as beta blocker, alpha blocker or spironolactone

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.

When is it an emergency?

Patients should be considered to have malignant hypertension and referred for emergency hospital management if:

Otherwise – it can be managed in the community.

As a doctor who works in the emergency department and general practice, I frequently see patients referred by their GP to emergency for asymptomatic hypertension, when the pressure is very high (typically >180/120 mmHg) without the signs of end organ damage. Usually, there is no need for this.

Info on beta-blockers

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.
They are no longer routine therapy, by may be considered in:

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.

Wrap-up pearls of wisdom

  • Cardiovascular risk increases with BP, even within 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 should 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 sound 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 threshold for diagnosing hypertension from home monitor readings is 135/85
  • Combinations of multiple drugs at lower doses is better than a single drug at a higher dose
    • More likely to be effective
    • Less likely to have side effects
    • The recommended combination is ACE-i/ARB + CCB
  • 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!)
  • Blood pressure measurements for patients with atrial fibrillation with an electronic devices are frequently inaccurate!

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