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7.6 — Blood Pressure and How It Is Controlled
High blood pressure is the leading modifiable risk factor for death worldwide. It causes more deaths than smoking, and around 1.3 billion people have it. Roughly half of them do not know, because it produces no symptoms until it has already caused damage.
That combination — enormously common, entirely silent, and highly treatable — is why understanding it matters more than almost anything else in this volume.
What blood pressure is
Systolic pressure — the peak during ventricular ejection. About 120 mmHg. Diastolic pressure — the trough during ventricular relaxation. About 80 mmHg.
Mean arterial pressure (MAP) is not the arithmetic mean, because the heart spends about twice as long in diastole as in systole:
MAP \approx DBP + \tfrac{1}{3}(SBP - DBP)
For 120/80: 80 + \tfrac{1}{3}(40) \approx 93 mmHg.
MAP is the number that matters for organ perfusion, and it is what is monitored in intensive care. A MAP below about 60 mmHg means organs are not being adequately perfused, whatever the systolic reading says.
Pulse pressure is the difference, normally about 40 mmHg. A widening pulse pressure in older people indicates arterial stiffening (Chapter 7.5). A narrowing pulse pressure with a rising heart rate is an early sign of blood loss, because the body constricts arterioles to maintain diastolic pressure while stroke volume falls — and it appears before the systolic pressure drops, which makes it one of the earliest warnings in trauma.
Blood pressure is the product of two things:
BP = CO \times TPR
Cardiac output times total peripheral resistance. Everything that raises or lowers blood pressure does so through one or both, and every antihypertensive drug can be classified by which one it targets.
Measuring it, and getting it right
The classic method uses a cuff and a stethoscope, listening for the Korotkoff sounds. Inflate above systolic so flow stops and there is silence. Deflate slowly: the first sound appearing is systolic, as blood begins to jet through the partly compressed artery turbulently. The point where sound disappears is diastolic, as flow becomes smooth again.
Errors in measurement are common and clinically significant.
A cuff that is too small over-reads, sometimes by 10 to 30 mmHg, because more pressure is needed to compress a large arm through a narrow cuff. This systematically over-diagnoses hypertension in people with larger arms.
Talking during measurement raises it by around 10 mmHg.
A full bladder raises it by around 10 to 15 mmHg.
Crossed legs, an unsupported arm, or an arm below heart level all raise the reading.
White coat hypertension — raised in the clinic, normal at home — affects perhaps 15 to 30 percent of people diagnosed in a clinic. Masked hypertension is the reverse and is arguably more dangerous, because it goes untreated.
This is why diagnosis now relies on ambulatory or home monitoring rather than a single clinic reading. A diagnosis of a lifelong condition requiring lifelong medication should not rest on one measurement taken in a stressful setting with a possibly wrong cuff.
The fast control: the baroreceptor reflex
Stretch receptors in the carotid sinus and the aortic arch measure the pressure and report to the brainstem continuously.
When pressure rises, they fire more, the brainstem reduces sympathetic output and increases vagal output, so the heart slows, contractility falls and arterioles dilate. Pressure falls.
When pressure falls, the reverse. This is a classic negative feedback loop (Chapter 4.7).
It operates within one or two heartbeats, and it is what stops you fainting when you stand up. On standing, about 500 to 700 ml of blood pools in the legs immediately, venous return falls, stroke volume falls, and pressure would drop sharply — except the reflex fires within a beat and increases heart rate and vascular tone.
When that reflex is impaired, you get orthostatic hypotension — a fall of more than 20 mmHg systolic or 10 mmHg diastolic on standing, causing dizziness and falls.
Causes are common and mostly treatable: dehydration, blood loss, many antihypertensive drugs, alpha-blockers used for prostate symptoms, tricyclic antidepressants, autonomic neuropathy from diabetes, Parkinson's disease, and prolonged bed rest.
It is a leading cause of falls in older people, and checking lying and standing blood pressure in anyone who has fallen is one of the highest-yield simple tests in geriatric medicine — and one of the most frequently omitted.
The crucial limitation of the baroreflex is that it resets. Within days it adapts to whatever pressure it experiences and begins defending that. So the baroreflex has essentially no role in long-term blood pressure control, and this is why it cannot be targeted to treat hypertension.
The slow control: the kidney
Long-term blood pressure is set by the kidney, through the volume of fluid it retains. Arthur Guyton's work established that if the kidney's pressure–natriuresis relationship is normal, blood pressure returns to normal regardless of what else is done to it; and if it is shifted, blood pressure follows.
The basic mechanism is direct. When arterial pressure rises, the kidney excretes more salt and water, blood volume falls, and pressure falls. When pressure falls, the kidney retains salt and water. This loop has no adaptation ceiling and no reset, so it wins over time.
The renin–angiotensin–aldosterone system
This is the most therapeutically important hormone system in cardiovascular medicine, and it is targeted by three separate drug classes.
The trigger. Cells in the kidney's afferent arterioles sense low pressure, low sodium delivery, or sympathetic stimulation, and release renin.
The cascade.
- Renin cleaves angiotensinogen, made by the liver, into angiotensin I.
- Angiotensin-converting enzyme (ACE), mostly in the lungs, converts angiotensin I into angiotensin II.
- Angiotensin II is the active hormone, and it does four things, all raising pressure:
- Powerful arteriolar constriction — raising resistance.
- Stimulates aldosterone release from the adrenal cortex, which makes the kidney retain sodium and therefore water.
- Stimulates ADH (vasopressin) release, retaining water.
- Stimulates thirst.
And it has a fifth effect that matters over years: it promotes fibrosis and thickening of the heart and blood vessels. This is why blocking the system improves outcomes in heart failure by more than the blood pressure reduction alone would predict.
The drugs, and why each has its characteristic side effect:
ACE inhibitors (names ending in -pril) block the converting enzyme. The characteristic side effect is a dry persistent cough, in around 10 to 20 percent of users, and the reason is specific: ACE also breaks down bradykinin, so blocking it lets bradykinin accumulate in the airways. The cough is not a sign of anything harmful, but it is a common reason for switching. Rarely, the same mechanism causes angioedema — sudden swelling of the lips, tongue or airway — which can be life-threatening and requires permanent avoidance.
Angiotensin receptor blockers (names ending in -sartan) block the receptor instead. No effect on bradykinin, so no cough, which is exactly why they are the standard substitute.
Aldosterone antagonists — spironolactone, eplerenone. Block the final step. Spironolactone also blocks androgen receptors, causing breast tenderness and enlargement in men, which is why eplerenone is used when that is a problem.
And all three raise potassium, because aldosterone normally causes potassium excretion. Combining them, or combining any of them with a potassium supplement or a potassium-sparing diuretic, risks dangerous hyperkalaemia, and this is one of the commonest serious prescribing errors in general practice. Chapter 22.7.
Hypertension
Definitions vary between guidelines, which is itself worth knowing when reading conflicting advice. Broadly:
| Systolic | Diastolic | |
|---|---|---|
| Normal | under 120 | under 80 |
| Elevated | 120–129 | under 80 |
| Stage 1 | 130–139 | 80–89 |
| Stage 2 | 140 or more | 90 or more |
| Crisis | over 180 | over 120 |
Around 90 to 95 percent of cases are primary (essential) hypertension — no single identifiable cause, arising from an interaction of genetics, salt intake, obesity, alcohol, inactivity and age.
Secondary hypertension (5 to 10 percent) has an identifiable cause, and it is worth looking for in the young, in the severe, and in the treatment-resistant:
- Kidney disease — the commonest cause.
- Renal artery stenosis — narrowing of a kidney's artery, so the kidney senses low pressure and floods the system with renin.
- Primary hyperaldosteronism — an adrenal problem producing too much aldosterone. Increasingly recognised as far commoner than the textbook 1 percent, possibly 5 to 10 percent of hypertension, and important because it is often curable.
- Phaeochromocytoma — an adrenaline-producing tumour, causing episodic pressure surges with headache, sweating and palpitations.
- Obstructive sleep apnoea — a frequently missed and highly treatable cause.
- Drugs — the contraceptive pill, NSAIDs, steroids, decongestants, cocaine, and liquorice in quantity.
Why it matters: the damage is silent and cumulative.
Heart — the left ventricle thickens against the raised afterload, then stiffens, then fails. Coronary disease risk rises. Brain — stroke, both from vessel rupture and from accelerated atherosclerosis. Hypertension is the single largest risk factor for stroke.Kidneys — damage to the small vessels causes progressive kidney failure. And the kidney's own role in setting pressure means this becomes a vicious circle.Eyes — retinal damage, visible on examination. Arteries — accelerated atherosclerosis, aneurysm, dissection.
The relationship with risk 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 suddenly appears; the categories are administrative conveniences.
Treatment
Lifestyle first, and the effects are quantifiable rather than vague.
| Intervention | Typical systolic reduction |
|---|---|
| Weight loss | ~1 mmHg per kg lost |
| DASH-style diet | 8–14 mmHg |
| Reduced sodium | 5–8 mmHg |
| Regular aerobic exercise | 4–9 mmHg |
| Reduced alcohol | 2–4 mmHg |
Sodium reduction deserves a note. The average intake in most countries is around 8 to 12 grams of salt a day, against a recommended maximum of 5 to 6. Most of it — around 70 to 75 percent — is already in processed and restaurant food rather than added at the table, which is why individual advice to "use less salt" achieves less than reformulation policies do. The United Kingdom's voluntary salt reduction programme reduced average intake by around 15 percent over a decade, with a corresponding fall in average population blood pressure.
Drug classes, and each maps onto the physiology above:
ACE inhibitors and ARBs — block the renin–angiotensin system. Calcium channel blockers — relax arteriolar smooth muscle, reducing resistance. Thiazide diuretics — reduce sodium and volume. Beta-blockers — reduce cardiac output and renin release. No longer first-line for uncomplicated hypertension, because they perform less well for stroke prevention than the others, but first-line where there is also angina, previous heart attack or heart failure. Spironolactone — the standard fourth agent in resistant hypertension, largely because unrecognised aldosterone excess is so common.
Choice varies with age and ethnicity, and there is a physiological reason. Younger and white patients tend to have higher renin levels, so ACE inhibitors and ARBs work well. Older and Black patients tend to have lower renin and more volume-dependent hypertension, so calcium channel blockers and diuretics work better. This is one of the few places where ancestry genuinely guides prescribing, and it is based on measured differences in renin physiology rather than on category alone.
Most people need two or more drugs, and combination pills improve adherence substantially.
Hypertensive emergency — very high pressure with acute organ damage: chest pain, breathlessness, neurological signs, or visual changes with retinal haemorrhages.
The pressure is lowered with intravenous drugs — and deliberately 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 the brain's autoregulation has adapted to the high pressure (Chapter 4.7), and a "normal" pressure is now below what it can cope with.
Hypertensive urgency — very high pressure with no acute organ damage — is managed with oral medication over days, not hours. Treating an asymptomatic high reading aggressively in an emergency department causes more harm than the reading does.
What the next page fixes
The heart supplies the whole body, and it is itself an organ needing a blood supply. Chapter 7.7 covers the coronary circulation — the three arteries that supply it, why the left ventricle can only be perfused when the heart is relaxed, and why that single fact explains angina, heart attacks, and why a fast heart rate can be dangerous.