IELTS Academic Reading Practice Test 391

For most of human history, the force that drives blood around the body remained invisible. A physician could count the pulse at a patient's wrist, but the pressure inside the arteries could not be measured. The first person to obtain a direct reading was Stephen Hales, an English clergyman. In experiments described in his Statical Essays of 1733, Hales fastened a horse on its back, opened an artery in its leg and connected it to a brass tube leading to a long glass pipe. Blood rose in the pipe to a height of more than two metres above the heart.

Hales's apparatus was crude and destroyed the artery it measured, so the method could not be applied to a human patient. A practical instrument appeared only in the middle of the nineteenth century, when physiologists began trying to record the pulse from outside the body. The most successful device was the sphygmograph, invented by the German physiologist Karl von Vierordt in 1855 and improved a few years later by the Frenchman Étienne-Jules Marey. A small pad pressed against an artery at the wrist moved levers that traced a line on smoked paper. It was ingenious, but it recorded the shape of the pulse rather than the pressure that produced it.

The instrument that turned blood pressure into a routine clinical measurement came from Italy. Scipione Riva-Rocci, a physician working in Turin, published a description of his device in 1896. It consisted of a rubber cuff wrapped around the upper arm and inflated with a hand pump until the brachial artery was squeezed shut and the pulse at the wrist could no longer be felt. Air was then released slowly, and the pressure at which the pulse returned was read from a mercury manometer. The apparatus was cheap, robust and simple enough to be used at a bedside.

Riva-Rocci's method had two important limitations. Because it depended on feeling the pulse, it could reveal only the systolic pressure, the highest pressure in the arteries during each beat; the lower, diastolic pressure remained hidden. His cuff was also narrow, barely five centimetres wide, so the force it exerted was concentrated on a small area of the arm and readings came out too high in many patients. In 1901 the German physician Heinrich von Recklinghausen increased the width of the cuff to about twelve centimetres, and the accuracy of the technique improved accordingly.

The device might have remained a European curiosity had it not been for Harvey Cushing, an American surgeon who saw it while travelling in Italy in 1901. He recognised its value and helped to introduce it in the United States. Even so, the measurement still produced only one number, and physicians had no reliable way of identifying the diastolic pressure until a young Russian surgeon turned his attention to the problem.

In 1905 Nikolai Korotkov, working at the Imperial Military Medical Academy in St Petersburg, presented a very short report on a technique still taught to medical students. Rather than feeling the pulse, he placed a stethoscope over the artery just below the cuff and listened while the air was released. He described a sequence of sounds: a clear tapping as blood first forced its way through the narrowed artery, then louder and softer noise, and finally silence. The pressure at which the tapping began was taken as the systolic value, and the pressure at which the sounds disappeared as the diastolic.

Together, the cuff and the stethoscope gave doctors the familiar pair of numbers, written one above the other, that is still used to describe blood pressure: a reading such as 120 over 80 means 120 millimetres of mercury systolic and 80 diastolic. The instrument became known as the sphygmomanometer, and for decades the mercury column was the standard against which every other device was judged.

Mercury, however, is a toxic metal, and concern about spills and disposal has led to it being phased out of clinical use in many countries. Its place has been taken by aneroid gauges, and increasingly by automatic devices that need no stethoscope at all. These work on a different principle: as the cuff deflates, the artery opens and closes with each beat, and the resulting fluctuations in pressure inside the cuff are detected by a sensor. An algorithm then calculates the systolic and diastolic values from the pattern of those oscillations. Their readings may differ slightly from those obtained by listening.

For an individual, a single measurement may seem of little consequence, but small errors matter when they are repeated across a whole population. Blood pressure is one of the strongest predictors of heart attack and stroke, and the decision to offer treatment usually depends on whether a reading lies above or below a threshold. Guidelines therefore specify how the measurement should be taken: the patient should sit quietly for several minutes, the cuff must be the right size for the arm, and the average of two or more readings should be recorded.

Modern technology has not made the old difficulties disappear. Readings taken in a clinic may be higher than those taken at home, because being measured can itself raise the pressure, and devices differ in how they cope with an irregular heartbeat. The mercury column, whatever its drawbacks, had the virtue of being easy to trust.

Blood pressure, the push that blood applies to the artery walls, rises and falls from one moment to the next. It climbs when a person takes the stairs, argues with a colleague or drinks a strong coffee, and it falls during sleep. The aim is not a fixed number but a pressure adequate for whatever the tissues happen to be doing: the circulation must send more blood to working muscles and less to the skin during exercise, and it must keep the brain supplied when a person stands up. What a doctor measures in the clinic is therefore a snapshot of a variable, not a fixed property of the body.

The pressure depends on two quantities: the volume of blood the heart pumps out each minute, and the resistance offered by the small arteries, the arterioles, which can narrow or widen. Multiply the flow by the resistance and the result is the pressure. A heart that pumps more vigorously raises it; so does a set of arterioles that has tightened, even if the heart's output has not changed at all. Every mechanism that regulates blood pressure in the short term works by altering one or both of these quantities, and each mechanism has its own timescale, from a fraction of a second to the better part of a day.

The fastest of these mechanisms is a reflex built around stretch-sensitive nerve endings in the walls of two large arteries, the carotid arteries in the neck and the aorta just above the heart. These sensors, called baroreceptors, fire more rapidly when the artery wall is stretched by a rise in pressure and less rapidly when it slackens. Their signals travel along nerves to a region of the brainstem, which responds by adjusting the balance of the autonomic nervous system. If pressure is too high, the brainstem increases the activity of the parasympathetic nerve that slows the heart and reduces the sympathetic signals that constrict vessels; if pressure is too low, it does the opposite. The whole response takes a second or two.

The value of such speed becomes obvious when a person stands. Gravity collects blood in the veins of the legs, less of it returns to the heart, and the pressure at the head begins to fall within a second or two. The baroreceptors register the change, the heart beats faster and the arterioles tighten, and the pressure is restored before the brain notices. When the reflex is blunted — by age, by dehydration, or by drugs prescribed for high blood pressure — the result is dizziness on standing, and sometimes a faint. Older people are particularly vulnerable, because their arteries respond less readily and their reflexes are slower.

The second system is slower and works through chemistry. When the kidneys detect a fall in the pressure or flow of blood reaching them, they release an enzyme called renin into the bloodstream. Renin sets off a short chain of reactions that ends with a hormone, angiotensin II, which tightens the arterioles and prompts the adrenal glands to release aldosterone, a hormone that makes the kidneys hold on to sodium and water. The volume of blood in the body then increases, and with it the pressure. This response takes minutes to hours rather than seconds, which suits its purpose: it is a system for correcting sustained losses, such as bleeding or a day without enough to drink.

The kidneys are also the body's main route for getting rid of salt and water. When pressure rises, the kidneys filter more sodium out of the blood and into the urine, which reduces the volume of blood and brings the pressure down again; when pressure falls, they retain sodium instead. Because of this link, many physiologists regard the kidney as the central organ of long-term pressure control, and the renin-angiotensin system as one of its instruments rather than the whole story. This mechanism operates over hours, and it helps to explain why a diet heavy in salt raises pressure in people whose kidneys are less able to excrete it.

Alongside these body-wide systems, each tissue makes local adjustments. The inner lining of the blood vessels, the endothelium, releases nitric oxide, a gas that relaxes the muscle in the artery wall and allows the vessel to widen; it also produces substances that constrict. Nitric oxide was identified as a vessel-relaxing signal only in the 1980s, and the discovery transformed the study of the circulation. In a healthy person the two kinds of signal keep the vessel in balance and match blood flow to what the surrounding tissue is doing. In people with longstanding high blood pressure the endothelium is often damaged, and its ability to relax vessels is reduced.

Why pressure settles at a high level in some people and not others is still not fully understood. Genes clearly matter, and so do salt, body weight, alcohol and inactivity, but the size of each contribution varies from one person to another. In established hypertension the baroreceptors adapt to the raised pressure and come to defend it as though it were normal, so the reflex that should correct the problem protects it instead. Arteries also stiffen with age, which pushes the systolic figure up and may leave the diastolic figure unchanged or even lower. Because high pressure produces no symptoms, it is usually found only when someone measures it.

Every year in England, everyone who turns forty becomes eligible for an NHS Health Check, and remains so every five years until the age of seventy-four. The invitation comes from the local general practice. Those who accept are asked about their family history, smoking and drinking, have their height, weight and blood pressure measured, and usually give a blood sample so that cholesterol and glucose can be tested. Forty is not a biological turning point; it is an administratively convenient age at which to begin a conversation about risk. On paper, the logic is hard to fault. In practice, few preventive programmes have attracted such fierce criticism from researchers.

The critics' central piece of evidence is a review of general health checks carried out by the Cochrane Collaboration. Its most recent version, published in 2019, pooled seventeen randomised trials involving a quarter of a million people. The conclusion was uncomfortable. Inviting people to a check increased the number of diagnoses, including new cases of high blood pressure and diabetes, but it did not reduce deaths from any cause, deaths from cardiovascular disease, or the number of people who became ill. If the purpose of screening is to leave people healthier, the review found little sign that it does.

Several explanations have been offered. Most of the trials were conducted before statins and modern blood-pressure drugs came into routine use, so it is possible that a programme today does more good than those results suggest. Possible, however, is not the same as demonstrated, and the burden of proof lies with those who claim the benefit. A second explanation is that identifying a risk is not the same as reducing it: telling someone that their blood pressure is raised is a long way from changing what they do.

There is also the awkward matter of who attends. Those who come for a check are, on average, healthier and better off than those who stay away; a person who already visits the doctor regularly is the easiest to invite. A single appointment, meanwhile, is a fragile basis for judgement. Blood pressure in particular varies through the day, and a reading taken once, in an unfamiliar room, is not always representative.

None of this means the checks are worthless. Their defenders point out that the trials tested an older model of care, in which a check was an isolated event with little follow-up, and that treatment is now considerably more effective. A programme that finds undiagnosed diabetes, kidney disease or an irregular heartbeat is doing something that no other part of the health service is doing for that person. Analyses of the English scheme have reported that it identifies previously unknown cases of high blood pressure and diabetes in significant numbers.

The harms are less often discussed. Screening always produces false alarms: some people will be told they may have a problem that further tests show to be trivial or temporary, and the anxiety this causes is a real cost, not an imaginary one. Others will be given a label and a prescription for a condition that would never have troubled them. Every appointment also takes time from a nurse who could be seeing patients who are already ill.

Money is the least romantic objection and perhaps the most important. Inviting and assessing several million people every five years costs a great deal, and that money cannot be spent twice: it is not available for cancer treatment, mental health services or the consultations that patients actually come for. The question is not whether the checks cost anything, but whether what they buy is worth more than what the same resources would buy elsewhere. At present, the honest answer is that nobody knows.

Attendance is another weakness. Studies of the English programme have generally found that roughly half of those invited attend, and the figure falls well below that in some areas and among some groups. The reasons people give are overwhelmingly practical: appointments that clash with shift work, difficulty taking time off, caring responsibilities, and a lack of confidence about what the appointment will involve. An offer that is taken up unevenly will, by definition, do most for those who need it least.

Yet there is something valuable in the encounter itself. A check at forty is one of the few occasions when a healthy adult with no complaint sits down with a clinician and talks about the future. Done well, it is a conversation in which a person's own priorities — a parent's stroke, a wish to keep walking in the hills — are connected to measurements on a screen. Done badly, it is a series of instructions. A check that ends with a leaflet and no further contact is a wasted opportunity.

My own conclusion is that the programme should be kept — but as the beginning of continuing care rather than as an event. Its strongest feature is that it reaches people who would never otherwise have their risk assessed, and that is an argument no critic of the evidence can dismiss. Its weakest feature is that a single appointment, unsupported by follow-up, changes very little. The fix is not to abolish the check but to redesign it: shorter and more frequent contact, a smaller number of tests, and a system that records whether the people found to be at risk are actually treated.