High Blood Pressure

TL;DR. Blood pressure is the force your blood exerts on artery walls. Run it too high for years and it damages the arteries themselves, then everything they supply: heart, brain, kidneys, eyes. It produces no symptoms until it has already caused harm, which is why it is called the silent killer and why roughly half the people who have it do not know. It is the largest single contributor to death worldwide, ahead of smoking. It is also cheap to detect, cheap to treat, and among the most thoroughly proven treatments in medicine: lowering it prevents strokes and heart attacks in direct proportion to how much you lower it.

Key takeaways

• About 1.28 billion adults aged 30 to 79 have hypertension. Roughly 46 percent do not know, and only about 1 in 5 have it under control.
• Two numbers: systolic (the peak, when the heart contracts) over diastolic (the trough, when it refills). Systolic matters more after about age 50.
• Risk rises smoothly from around 115/75 upward. The diagnostic line at 130/80 (US) or 140/90 (most other guidelines) is a treatment decision, not a biological edge.
• The damage is mechanical and cumulative: pressure injures the artery lining, thickens and stiffens vessel walls, forces the heart to work against resistance, and destroys the kidney's filtering units.
• Lowering systolic pressure by 10 mmHg cuts major cardiovascular events by roughly 20 percent, stroke by about 27 percent, and death by about 13 percent.
• Salt reduction, weight loss, potassium, exercise, and less alcohol each lower pressure measurably, and combined they rival a single drug.

What it is

In short: Two numbers, routinely measured badly in clinics, marking a risk that rises smoothly with no natural cut-off.

Each heartbeat pushes blood into the arteries, and the pressure inside them rises and falls with the cycle. Systolic pressure is the peak during contraction; diastolic is the resting level between beats. Both are quoted in millimetres of mercury (mmHg), a unit inherited from the mercury columns of early instruments.

Pressure is determined by two things: how much blood the heart pumps per minute (cardiac output) and how hard it is to push blood through the small arteries (peripheral resistance). Anything that raises either raises blood pressure.

Most of the world outside the United States still uses 140/90 as the diagnostic threshold, with treatment decisions modified by overall cardiovascular risk. Both approaches are defensible; the 2017 US change reclassified tens of millions of people without changing anyone's arteries, which is the clearest illustration of the threshold point made in Chapter 12.

How it is measured matters as much as the number. Blood pressure varies minute to minute with posture, talking, caffeine, bladder fullness, and anxiety. A single reading in a clinic proves little. Two artefacts are common enough to have names: white-coat hypertension (high in clinic, normal elsewhere, present in perhaps 15 to 30 percent of raised clinic readings) and masked hypertension (normal in clinic, high at home, which is the more dangerous error). This is why guidelines now recommend home or 24-hour ambulatory monitoring before committing someone to lifelong treatment.

Don't be confused: high blood pressure is not the same as feeling stressed, and it does not cause headaches at ordinary levels. Acute stress raises blood pressure temporarily; chronic hypertension is a sustained baseline elevation. And the belief that you can tell when it is high is not just wrong but dangerous, because people use it to decide when to take their tablets. Symptoms appear at crisis levels, and by then the disease has usually been present for years.

The history

In short: High blood pressure was thought to be a necessary compensation until trials in 1967 and 1970 were stopped early because the untreated group was having strokes.

Stephen Hales first measured arterial pressure in 1733 by inserting a brass tube into a horse's artery and watching blood rise nine feet in a glass column. The method was accurate and unrepeatable in patients.

The practical instrument came in stages: Scipione Riva-Rocci's inflatable arm cuff in 1896 gave systolic pressure, and in 1905 the Russian surgeon Nikolai Korotkov discovered that listening over the artery while deflating the cuff produced sounds whose appearance and disappearance marked systolic and diastolic pressure. The sphygmomanometer in every clinic is the direct descendant.

For the next fifty years, high blood pressure was widely considered essential, meaning necessary: physicians believed elevated pressure was a compensation required to push blood through stiffened arteries, and that lowering it would be harmful. The term "essential hypertension" survives as a fossil of that belief.

The turning point was political as well as medical. Franklin D. Roosevelt's blood pressure was recorded above 180/100 by 1937 and above 260/150 in 1945; he died of a cerebral haemorrhage that April, having received no effective treatment, because none existed and because his readings were regarded as unremarkable for his age.

Three things then changed everything. The Framingham Heart Study, started in 1948, followed a whole town for decades and established hypertension as a measurable predictor of stroke and heart disease, introducing the term "risk factor" itself. Effective drugs arrived from the 1950s onward. And the Veterans Administration Cooperative trials (1967 and 1970) randomised men with high blood pressure to treatment or placebo and were stopped early because the untreated group was having so many strokes and deaths. That settled it: treating high blood pressure saves lives.

What actually goes wrong

In short: Kidney salt handling, the renin-angiotensin cascade, sympathetic overdrive, and stiffening arteries, plus a specific curable cause in 5 to 10 percent of cases.

In roughly 90 to 95 percent of cases the cause is not a single identifiable lesion. This is primary (essential) hypertension, and it emerges from several interacting systems.

The kidney and salt handling. The kidney regulates long-term blood pressure by adjusting how much sodium and water it excretes. If the kidney requires a higher pressure to excrete a given salt load (the pressure-natriuresis relationship shifted rightward), pressure settles at a higher point. Sodium intake matters because of this relationship, and populations with very low sodium intake show almost no rise in blood pressure with age, unlike industrialised populations where a rise with age is so universal it was long assumed to be natural ageing.

The renin-angiotensin-aldosterone system (RAAS). When the kidney senses low perfusion, it releases renin, which converts a liver protein into angiotensin I, which the angiotensin-converting enzyme (ACE) converts to angiotensin II, a potent vessel constrictor that also triggers aldosterone release, causing the kidney to retain sodium and water. This cascade evolved to protect against blood loss and dehydration. In hypertension it runs inappropriately high, and it is the target of two of the most-used drug classes.

The sympathetic nervous system. The fight-or-flight system raises heart rate and constricts vessels. Chronic activation, driven by stress, obesity, and untreated sleep apnoea, keeps pressure elevated.

Arterial stiffening. With age, elastin in large arteries fragments and is replaced by stiffer collagen. A stiff aorta cannot cushion each heartbeat, so systolic pressure rises and diastolic often falls. That is why isolated systolic hypertension dominates after 60 and why a wide gap between the two numbers (pulse pressure) is itself a risk marker.

Secondary hypertension is the 5 to 10 percent with a specific cause, and finding it matters because it can be cured: primary aldosteronism (the commonest, and much underdiagnosed), kidney artery narrowing, chronic kidney disease, obstructive sleep apnoea, thyroid disease, phaeochromocytoma, coarctation of the aorta, and drugs including oral contraceptives, NSAIDs, decongestants, steroids, and stimulants. Clues are onset before 30 or after 55, very high pressure, sudden change, resistance to three drugs, or low blood potassium.

What it does to the body

In short: Pressure damages the arteries first and then everything they supply: heart, brain, kidneys, and eyes.

Sustained high pressure damages the arteries first, then the organs they feed. Every consequence below is a plumbing consequence.

Arteries. Pressure injures the endothelium (the single-cell lining), which accelerates atherosclerosis (Chapter 21). Vessel walls thicken and narrow. Weak spots balloon into aneurysms, most dangerously in the abdominal aorta and the brain. The aortic wall can split (aortic dissection), which is catastrophic and for which hypertension is the leading risk factor.

Heart. Pumping against higher resistance thickens the left ventricle (left ventricular hypertrophy). Thicker muscle needs more oxygen while its blood supply does not grow proportionally, and it becomes stiff, so the chamber fills poorly. The result is heart failure with preserved ejection fraction, plus a higher risk of atrial fibrillation and of heart attack.

Brain. Hypertension is the single largest risk factor for stroke, both ischaemic (a blocked artery) and haemorrhagic (a burst one). Deep small vessels in the brain are particularly vulnerable, and their gradual damage produces vascular dementia and contributes to mixed dementia (Chapter 37).

Kidneys. High pressure damages the glomeruli, the tiny filters. Damaged kidneys regulate pressure worse, which raises pressure, which damages more kidney. Hypertension is the second leading cause of end-stage kidney disease after diabetes (Chapter 23).

Eyes. Retinal arteries can be seen directly through the pupil, which makes them a window onto what is happening everywhere else. Hypertensive retinopathy progresses from narrowed arterioles to haemorrhages and, at crisis levels, swelling of the optic disc.

Hypertensive emergency is pressure above roughly 180/120 with evidence of acute organ damage: chest pain, breathlessness, neurological deficit, or visual loss. It requires immediate hospital treatment, with pressure lowered in a controlled way rather than abruptly.

Is it deadly?

In short: It is the largest single contributor to death worldwide, and each 10 mmHg reduction in systolic pressure cuts strokes by about a quarter.

It is the leading contributor to death on earth. High systolic blood pressure is consistently ranked by the Global Burden of Disease study as the single largest attributable risk factor for mortality, associated with on the order of 10 million deaths a year, mostly through heart disease and stroke.

The benefit of treatment is quantified better than almost anything in medicine. A meta-analysis of over 300,000 participants across many trials found that each 10 mmHg reduction in systolic pressure produced approximately:

The SPRINT trial went further, randomising higher-risk patients without diabetes to a systolic target below 120 rather than below 140, and found fewer cardiovascular events and deaths, at the cost of more low blood pressure, fainting, electrolyte abnormalities, and kidney function decline. That trade-off is the reason targets are individualised, tighter in a robust 60-year-old and looser in a frail 85-year-old at risk of falls.

Is it contagious?

No. Blood pressure is a property of your own circulation. Nothing about it can be transmitted.

Families share it for two reasons that both look like transmission: genetics (hypertension is polygenic and heritable) and a shared salt-heavy diet, since everyone eating from the same kitchen consumes the same sodium load.

Who gets it

In short: 1.28 billion adults, nearly half unaware they have it, in patterns that track salt, age, and living conditions far more than ancestry.

Age. Prevalence rises steeply: uncommon below 30, present in the majority of people over 65 in most countries. Arterial stiffening makes this partly a function of ageing, though not an inevitable one, as low-sodium populations demonstrate.

Sex. Higher in men until about age 55 to 60, then higher in women, whose pressure rises faster after menopause.

Ancestry and geography. Hypertension is more common, appears earlier, and causes more organ damage in people of African descent in the United States, the Caribbean, and the United Kingdom. The explanation is frequently oversimplified into genetics. The better supported picture combines salt sensitivity (higher on average, mechanism debated), socioeconomic conditions, food environment, healthcare access, and the measurable physiological effects of chronic exposure to racial discrimination, which raises blood pressure in longitudinal studies. Notably, blood pressure in West African populations is generally lower than in African-descended populations in the United States, which argues strongly against a purely genetic account.

Salt intake. Global average sodium consumption is roughly double the WHO recommended maximum of 2 grams of sodium (about 5 grams of salt) a day. Most of it, in industrialised diets, comes from processed and restaurant food rather than the salt shaker.

Other risk factors: obesity, alcohol, physical inactivity, low potassium intake, sleep apnoea, chronic kidney disease, and family history.

Control rates are the scandal. Of the 1.28 billion adults with hypertension, roughly 46 percent are unaware, about 42 percent are diagnosed and treated, and only around 21 percent are controlled. This is not a technology problem. The drugs are generic and cost pennies.

Treatment, and how each drug works

In short: Four cheap first-line classes, each blocking a different mechanism, and adding a second at low dose beats doubling the first.

Four first-line classes, each interrupting a different part of the pressure system.

Second-line and specific-indication drugs: beta blockers (slow the heart and reduce its output; no longer first line for uncomplicated hypertension but essential after a heart attack or in heart failure), spironolactone (blocks aldosterone; the single most effective add-on for resistant hypertension), alpha blockers, and hydralazine.

Three principles govern how they are used.

Combination beats escalation. Adding a second drug at a low dose lowers pressure roughly five times more than doubling the first, because you are blocking a second mechanism instead of pushing harder on one. This is why single-pill combinations are increasingly the starting point.

Match the drug to the patient. Someone with diabetes and protein in the urine gets an ACE inhibitor or ARB for kidney protection. Someone after a heart attack gets a beta blocker. Someone of African descent without those indications typically starts with a calcium channel blocker or thiazide, which work better on average in that group.

Resistant hypertension means pressure above target on three drugs including a diuretic. The first step is not a fourth drug: it is checking adherence, confirming with home readings, reviewing NSAIDs and other pressure-raising drugs, and screening for secondary causes, particularly primary aldosteronism and sleep apnoea.

Renal denervation, a catheter procedure burning sympathetic nerves in the renal artery walls, has a mixed trial history. Early enthusiasm collapsed when a properly sham-controlled trial found no benefit; better-designed later trials show modest reductions, and it is now approved for selected patients rather than as a general solution. It is a clean case study in why sham controls matter.

What treatment costs

In short: Side effects are mostly minor and class-specific, and are usually solved by switching drug rather than by stopping treatment.

The general point: first-line antihypertensives are cheap, generic, and well tolerated by most people, and side effects are usually solved by switching class rather than by abandoning treatment. The most common real-world problem is not toxicity, it is people stopping a drug that makes them feel no better because the disease it prevents is invisible.

What the person can do

In short: Diet, salt, potassium, weight, exercise, and alcohol each move blood pressure measurably, and combined they rival a drug.

Lifestyle change is not a token gesture here. The measured effects are large enough to delay or avoid medication in mild cases and to improve control in everyone.

Two practical additions. Measure at home, with a validated upper-arm cuff, seated, back supported, feet flat, arm at heart level, after five minutes of rest, twice in the morning and twice in the evening for a week. Home readings predict outcomes better than clinic readings and give you and your clinician something real to work with. Take the tablets, including on days you feel well, which is all of them.

Salt substitutes deserve a specific mention because the evidence is unusually strong. The SSaSS trial in rural China randomised nearly 21,000 people at high stroke risk to a potassium-enriched salt substitute (75 percent sodium chloride, 25 percent potassium chloride) instead of regular salt, and found significant reductions in stroke, cardiovascular events, and death. Swapping one product in the kitchen produced an outcome benefit. The caution is that people with advanced kidney disease or on potassium-raising drugs must not use them.

Living with it

The defining difficulty is that hypertension is a disease of numbers rather than sensations. Adherence to antihypertensives at one year runs at roughly 50 percent, and the reasons people give are consistent: no symptoms to relieve, side effects that are noticeable when the disease is not, cost, complexity, and no sense of progress. The countermeasures that work are equally consistent: single-pill combinations, once-daily dosing, home monitoring so the person can see their own numbers move, and an explanation of what is actually being prevented.

What's next

• Twice-yearly injectable therapy. Zilebesiran, an siRNA that silences the liver's production of angiotensinogen, the precursor of the whole RAAS cascade, has produced sustained pressure reduction from a single injection in phase 2 trials. If outcome trials confirm it, adherence stops being a daily problem.
• Polypills, combining a statin and two or three antihypertensives in one cheap tablet, have shown large event reductions in trials in low-resource settings.
• Population salt reduction, through mandatory reformulation targets, which is the intervention with the best cost-per-life-saved of anything in this chapter.
• Cuffless continuous monitoring in wearables, currently not accurate enough for diagnosis, but improving.

Sources and notes

Prevalence, awareness, and control figures are from WHO's Global report on hypertension (2023), which gives 1.28 billion adults aged 30 to 79 with hypertension, about 46 percent unaware, and around 21 percent controlled, based on NCD-RisC pooled analyses. Diagnostic categories are the 2017 ACC/AHA guideline; the 140/90 threshold is ESC/ESH and WHO. Treatment effect sizes per 10 mmHg: Ettehad et al., The Lancet, 2016. SPRINT: NEJM, 2015. Lifestyle effect sizes are from the 2017 ACC/AHA guideline's summary of trial evidence and are averages, not guarantees. SSaSS salt substitute trial: Neal et al., NEJM, 2021. Renal denervation: SYMPLICITY HTN-3 (NEJM, 2014) was the negative sham-controlled trial; SPYRAL HTN-OFF MED and RADIANCE trials were later positive. Zilebesiran: KARDIA-1 phase 2 results, 2024. Roosevelt's blood pressure history is documented in Bruenn's clinical notes and subsequent historical analyses. Blood pressure in West African versus African-American populations: the ICSHIB studies (Cooper et al.).

Open questions. The optimal systolic target in the very old and the frail is unsettled. Whether population-wide sodium reduction benefits everyone equally, given individual variation in salt sensitivity, is still argued, though the population-level case is strong.

Next: what that pressure, plus cholesterol, plus time, does to the arteries feeding the heart. 👉