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18.2 — High Blood Pressure

Around 1.3 billion people have high blood pressure. Roughly half do not know, and of those who do, only a minority are adequately controlled.

It is the leading modifiable risk factor for death worldwide — ahead of smoking — and it causes no symptoms at all until it has already damaged something.

Chapter 7.6 covered the physiology and the drug classes. This chapter is the practical version.

The numbers

SystolicDiastolic
Normalunder 120under 80
Elevated120–129under 80
Stage 1130–13980–89
Stage 2140+90+
Crisisover 180over 120

Thresholds differ between guidelines, which causes genuine confusion. The disagreement is about where to draw a line on a continuous relationship, not about the underlying biology.

And the relationship is continuous and steep. Above about 115/75, each 20 mmHg rise in systolic pressure roughly doubles cardiovascular mortality. There is no threshold below which risk appears.

Getting the measurement right

Because a diagnosis of a lifelong condition should not rest on one reading taken badly.

The errors, and their size (Chapter 7.6):

A cuff that is too small over-reads by 10 to 30 mmHg.Talking adds around 10.A full bladder adds 10 to 15.Crossed legs, an unsupported arm, or an arm below heart level all add.And the first reading is usually the highest, which is why several are taken and the first discarded.

White coat hypertension affects 15 to 30 percent of people diagnosed in a clinic. Masked hypertension — normal in clinic, high at home — is arguably more dangerous because it goes untreated.

Which is why diagnosis now relies on ambulatory or home monitoring.

Home monitoring, done properly: sitting quietly for five minutes first, arm supported at heart level, two readings a minute apart, morning and evening, for a week, discarding the first day.

And a validated upper-arm device. Wrist and finger devices are less reliable, and most smartwatch blood pressure features are not validated to clinical standards.

Who has it and why

Around 90 to 95 percent is primary — no single cause, arising from genetics, salt, weight, alcohol, inactivity and age together.

5 to 10 percent is secondary, and looking for it is worthwhile in specific circumstances: onset before 40, resistant to three drugs, sudden worsening, or accompanying features.

The causes (Chapter 7.6): kidney disease, renal artery narrowing, primary hyperaldosteronism — which is far commoner than the textbooks used to say, at 5 to 10 percent of hypertension, and is potentially curable, phaeochromocytoma, thyroid disease, obstructive sleep apnoea — common, treatable and frequently missed (Chapter 8.5), and drugs.

The drug list is worth knowing because it is easily corrected: the combined pill, NSAIDs, steroids, decongestants containing pseudoephedrine, some antidepressants, cocaine, and liquorice in quantity.

What it does

Silently, over years.

Heart — the left ventricle thickens against the raised afterload, then stiffens, then fails (Chapter 7.4). Coronary risk rises.

Brainhypertension is the single largest risk factor for stroke, both from vessel rupture and from accelerated atherosclerosis. It also causes vascular cognitive impairment, through damage to the small deep vessels.

Kidneys — progressive damage to the small vessels, and a vicious circle since the kidney sets long-term pressure (Chapter 10.6).

Eyes — retinal damage, gradeable on examination, and the only place the small vessels can be seen directly.

Arteries — accelerated atherosclerosis, aneurysm, dissection.

Treatment

Lifestyle first, and the effects are quantifiable rather than vague.

InterventionSystolic reduction
Weight loss~1 mmHg per kg
DASH-style diet8–14 mmHg
Reduced sodium5–8 mmHg
Regular aerobic exercise4–9 mmHg
Reduced alcohol2–4 mmHg
Increased potassium intake4–5 mmHg

Several of those, combined, match a drug.

On salt: average intake is 8 to 12 grams a day against a recommended maximum of 5 to 6, and 70 to 75 percent of it is already in processed and restaurant food rather than added at the table.

Which is why individual advice achieves less than reformulation policy. The UK's voluntary salt reduction programme reduced average intake by around 15 percent over a decade, with a corresponding fall in population blood pressure — an intervention nobody had to comply with individually.

Potassium matters as much as sodium and is discussed far less. Increasing dietary potassium — fruit, vegetables, pulses — lowers blood pressure, and salt substitutes containing potassium chloride have shown reductions in stroke and death in large trials. They must be avoided in kidney disease and with potassium-raising drugs (Chapter 10.3).

Drugs (Chapter 7.6):

ACE inhibitors and ARBs, calcium channel blockers, thiazide-like diuretics, and spironolactone as the standard fourth agent — because unrecognised aldosterone excess is so common.

Beta-blockers are no longer first-line for uncomplicated hypertension, and remain first-line where there is also angina, previous heart attack or heart failure.

Choice varies with age and ethnicity for a physiological reason (Chapter 7.6): renin levels differ, so ACE inhibitors and ARBs work better in younger and white patients, and calcium channel blockers and diuretics in older and Black patients.

Most people need two or more drugs, and single-pill combinations improve adherence measurably — which matters because adherence is the main determinant of control.

Targets

And they have moved, on the basis of trial evidence.

The SPRINT trial compared a systolic target of 120 with 140 in high-risk patients and found the tighter target reduced cardiovascular events and death — at the cost of more low blood pressure episodes, fainting and kidney effects.

So targets are now generally below 130/80 for most people, with individualisation in the frail elderly, where over-treatment causes falls.

And that trade-off is real rather than theoretical. In an 85-year-old, a fall causing a hip fracture carries a worse prognosis than a systolic pressure of 145 (Chapter 5.6), which is why targets are relaxed with frailty.

When it is an emergency

Hypertensive emergency — very high pressure with acute organ damage: chest pain, breathlessness, neurological signs, visual changes with retinal haemorrhages, or acute kidney injury.

And the treatment rule is counter-intuitive and important. Lower it slowly — by no more than about 25 percent in the first hour.

Dropping it to normal rapidly can cause stroke, blindness or kidney injury, because cerebral autoregulation has adapted upward (Chapter 4.7) and a "normal" pressure now underperfuses the brain.

Hypertensive urgency — very high pressure without organ damage — is managed with oral medication over days.

And treating an asymptomatic high reading aggressively in an emergency department causes more harm than the reading does, which is a well-documented pattern.

Low blood pressure

Briefly, because it is the other end.

Low blood pressure without symptoms needs no treatment.

Orthostatic hypotension — a fall of more than 20 systolic or 10 diastolic on standing — is a leading cause of falls in older people, is frequently drug-induced, and is one of the highest-yield simple tests in anyone who has fallen (Chapter 7.6).

The practical summary

Know your number. Most people have had it measured and could not state it.

If it is raised, confirm it at home rather than accepting one clinic reading.

The lifestyle measures are not a preliminary to real treatment — they are treatment, with quantified effects.

And if you are prescribed tablets, the main determinant of benefit is taking them. Around half of people prescribed antihypertensives are not taking them a year later, which is the largest single loss of benefit in this entire chapter.

It is a condition with no symptoms, cheap treatment, and enormous consequences — which is exactly the combination that produces poor adherence, and exactly why knowing why it matters is the intervention.

What the next page fixes

Chapter 18.3 covers what happens when a coronary plaque ruptures — the heart attack, how to recognise it, and why every minute matters.