Blood pressure

• 1. Introduction

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  Blood pressure is something your body monitors every second of every day, adjusting itself with a speed and precision that no machine has yet fully replicated. Right now, inside your arteries, a force is pushing outward against vessel walls. That force has two numbers attached to it: a peak, reached each time the heart contracts, and a floor, held during the quiet between beats. Together they tell a story about the entire circulatory system.

  Normal resting blood pressure in an adult sits at approximately 120 millimetres of mercury over 80, written as 120/80 mmHg. Yet globally, the age-standardised average has hovered near 127/79 in men and 122/77 in women since 1975. Those averages, though, conceal striking regional differences that researchers are still working to explain.

• 2. Reading the Numbers

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  A standard blood pressure reading is measured in the brachial artery of the arm, and it is expressed as two values separated by a slash. The higher number, systolic pressure, records the peak force during a heartbeat. The lower number, diastolic pressure, captures the minimum force between beats. The difference between those two figures is the pulse pressure, and the average across a full cardiac cycle is the mean arterial pressure.

  For most of clinical history, a healthcare worker placed a stethoscope against the arm artery while a sphygmomanometer compressed it, listening for the characteristic sounds that mark the systolic and diastolic thresholds. Auscultation remains the accepted gold standard for non-invasive readings in clinical settings. Semi-automated and fully automated oscillometric devices have become common since 1981, driven partly by concerns about mercury toxicity and partly by the practical need for home and ambulatory monitoring.

  Ambulatory measurement - using an automated device across a full 24-hour period - has persuaded some authorities to reconsider how hypertension is diagnosed. The National Institute for Health and Care Excellence in the United Kingdom has advocated ambulatory blood pressure as the preferred method for that diagnosis. Night-time readings are particularly telling: the normal dip in pressure during sleep has emerged as a stronger predictor of future cardiovascular events than daytime readings, and people who lose that nocturnal fall face elevated long-term risk.

  Classification thresholds differ by the setting in which the measurement is taken and by the guidelines being applied. The 2017 American College of Cardiology and American Heart Association guidelines place a systolic reading of 130-139 with a diastolic of 80-89 at stage one hypertension. The European Society of Cardiology's 2024 guidance and the European Society of Hypertension's 2023 framework use slightly different cut-offs for office, home, and ambulatory contexts. What all frameworks agree on is that the risk of cardiovascular disease rises progressively above a systolic pressure of 90 mmHg.

• 3. How Pressure Is Made

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  The heart's pumping action is the primary engine of blood pressure. Cardiac output, the volume of blood the heart ejects each minute, is the product of two simpler quantities: the stroke volume pushed out with each beat, and the rate at which those beats occur. Stroke volume itself depends on how full the ventricle is at the end of filling, the contractile force of the heart muscle, and the resistance the circulation presents to outgoing flow.

  Systemic vascular resistance, the opposition that blood vessels offer to flow, is governed largely by the caliber of small arteries and arterioles. The Hagen-Poiseuille equation captures the relationship precisely: resistance is proportional to the inverse of the fourth power of a vessel's radius. Halving a vessel's radius therefore multiplies its resistance sixteen-fold. Length and blood viscosity also contribute, though less dramatically.

  Vasoconstrictors, substances that narrow vessels, raise blood pressure. Vasodilators such as nitroglycerin widen vessels and lower arterial pressure. Over longer periods, a process called remodeling changes the caliber of small blood vessels, and reductions in capillary density - termed capillary rarefaction - can add further resistance in some conditions.

  High dietary salt intake has been proposed to raise blood pressure by increasing blood volume and therefore cardiac output. The relationship is not simple, however: responses to added sodium vary between individuals and depend heavily on the autonomic nervous system and the renin-angiotensin system. Changes in plasma osmolarity may also play a role, and over the long term the connection between volume and pressure grows more complex still.

• 4. The Body's Pressure Governors

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  Baroreceptors, pressure-sensitive nerve endings located in the carotid sinuses and the aortic arch, sit at the front line of moment-to-moment blood pressure control. When they detect a change in arterial pressure, they relay signals to the rostral ventrolateral medulla in the brain stem. The medulla responds through the autonomic nervous system, adjusting both the force and speed of cardiac contractions and the degree of constriction in the peripheral vessels.

  For longer adjustments, the renin-angiotensin system is the dominant mechanism. When blood pressure drops, juxtaglomerular cells in the kidney sense the fall and release renin. Renin converts a circulating protein called angiotensinogen into angiotensin I. Angiotensin I travels to the lung capillaries, where angiotensin-converting enzyme transforms it into angiotensin II, a potent vasoconstrictor that also stimulates the adrenal cortex to release the steroid hormone aldosterone.

  Aldosterone drives the kidneys to retain sodium and excrete potassium. Water follows the retained sodium by osmosis, expanding plasma volume and raising arterial pressure. The macula densa of the kidney plays its own role: it senses falling sodium levels as a proxy for falling filtration rate, triggers further sodium reabsorption, and releases adenosine to constrict the afferent arterioles.

  Pharmacologists exploit each step of this cascade. ACE inhibitors block the conversion of angiotensin I to angiotensin II. Angiotensin receptor blockers prevent angiotensin II from acting on its targets. Aldosterone antagonists suppress the downstream fluid-retention effect. Diuretics reduce blood volume directly. The baroreceptor reflex, by contrast, is generally not targeted by antihypertensive drugs, because blocking it tends to produce orthostatic hypotension and fainting.

• 5. The Pulse Pressure Problem

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  A healthy pulse pressure - the gap between systolic and diastolic readings - sits near 40 mmHg. When that gap reaches 50 mmHg, the risk of cardiovascular disease and complications including eye and kidney disease begins to climb. At 60 mmHg or above, the gap is likely to signal active disease.

  A meta-analysis published in 2000 found that each 10 mmHg rise in pulse pressure was associated with a 20% increase in cardiovascular mortality and a 13% increase in risk across all coronary endpoints. The analysis also revealed a counterintuitive finding: at any given systolic pressure, risk rises rather than falls as diastolic pressure decreases. Interventions that lower diastolic pressure without also lowering systolic pressure widen the pulse pressure and may be counterproductive as a result.

  The widening of pulse pressure with age reflects increasing arterial stiffness. In adults, systolic pressure tends to rise from early adulthood through at least the age of 70. Diastolic pressure begins rising at the same time but starts to fall around age 55. Pulse pressure rises markedly after age 40. When systolic pressure in an older person exceeds normal limits while diastolic remains in range, the condition is called isolated systolic hypertension.

  No drugs are currently approved specifically to lower pulse pressure. Some antihypertensive agents reduce it modestly; others that successfully lower overall pressure can paradoxically raise the pulse pressure. In people with sepsis, pulse pressure can widen or narrow depending on the severity of circulatory compromise. A pulse pressure above 70 mmHg in sepsis correlates with better survival odds and a more favourable response to intravenous fluids.

• 6. When Pressure Falls

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  Hypotension, blood pressure too low to sustain adequate perfusion, carries no universally agreed diagnostic threshold. Readings below 90/60 mmHg are commonly treated as hypotensive, but in practice a blood pressure is considered too low only when it produces symptoms: dizziness, fainting, or in severe cases, circulatory shock. Causes range from sepsis and bleeding to hormonal disorders such as Addison's disease and eating disorders including anorexia nervosa and bulimia.

  Orthostatic hypotension is a specific and revealing form of low pressure. Standing up shifts roughly 500 millilitres of blood from the chest and upper body into the veins of the lower limbs. Central blood volume drops, ventricular filling falls, and stroke volume decreases. Normally the autonomic nervous system compensates within a minute or less: heart rate rises, myocardial contractility increases, and both arterial and venous vessels constrict to stabilise pressure. A complementary mechanism, the intrinsic myogenic response in venous smooth muscle, also stiffens the lower-body veins against the added hydrostatic load.

  Other stabilising mechanisms include the veno-arteriolar axon reflex, the skeletal muscle pump, and the respiratory pump. When these mechanisms fail - typically because of disease or drugs that suppress the sympathetic nervous system - perfusion to the brain drops below a critical threshold and the person faints. A closely analogous phenomenon occurs in aerobatic and combat pilots pulling high G-forces: the extreme hydrostatic pressures in the lower body exceed even a healthy nervous system's ability to compensate.

  Mean systemic pressure, or mean circulatory filling pressure, describes what remains if the heart stops completely. Blood redistributes throughout the circulation and settles at approximately 7 mmHg. This non-zero resting pressure reflects the elastic recoil of the vessels themselves, not any active pumping.

• 7. Pressure Across the Body

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  The number most people associate with blood pressure - the reading from the arm - captures only one type of pressure in one part of the circulation. Venous pressure in the right atrium averages around 5 mmHg; in the left atrium it averages around 8 mmHg. The portal vein, which carries blood from the intestines to the liver, normally carries 5-10 mmHg. The pulmonary artery, supplying the lungs, sits near 15 mmHg at rest. When lung capillary pressure climbs above 20 mmHg, interstitial fluid begins to accumulate; above 25 mmHg, pulmonary edema develops.

  Aortic pressure, also called central blood pressure, is the pressure at the root of the aorta. Research has found it to be a more accurate predictor of cardiovascular events, mortality, and structural heart changes than the peripheral reading taken at the brachial artery. The way antihypertensive drugs affect peripheral pressure can diverge substantially from how they affect central aortic pressure. Traditionally, measuring aortic pressure required an invasive arterial catheter; non-invasive indirect methods are now available.

  Among non-human mammals, blood pressure tracks with body size in distinctive ways. The giraffe stands as the most striking example: its arterial pressure runs near 190 mmHg, a level needed to push blood the two metres from the heart up through the neck to the brain. Arboreal snakes, which must also resist gravity's pull on their circulation, carry higher pressures than ground-dwelling relatives. In cats and dogs, hypertension is generally diagnosed when systolic pressure exceeds 150 mmHg, with a higher threshold of 180 mmHg applied to sight hound breeds.

  Blood pressure in fetal life is built entirely by the fetal heart, not the mother's. In the fetal aorta, pressure runs near 30 mmHg at 20 weeks of gestation and rises to approximately 45 mmHg by the 40th week.