Systolic Pressure kPa mmHg Diastolic Pressure kPa mmHg

| > Systolic Pressure kPa (mmHg) | > Diastolic Pressure kPa (mmHg)

Normal Blood Pressure | > <17.3 (130) | > <11.3 (85) Upper Limit of Normal Blood Pressure | > 17.318.5 (130139) | > 11.311.9 (8589) Stage I Hypertension (Mild) | > 18.721.2 (140159) | > 12.013.2 (9099) Stage II Hypertension (Moderate) | > 21.523.9 (160179) | > 13.314.5 (100109) Stage III Hypertension (Severe) | > 24.027.9 (180209) | > 14.715.9 (110119) Stage IV Hypertension (Very Severe) | > ≥28.0 (210) | > ≥16.0 (120) Research has found that the cardiovascular disease mortality rate in the former group is 2.5 times higher than in the latter; moreover, a single blood pressure measurement cannot accurately reflect a person's typical daily blood pressure, so hasty antihypertensive medication for some individuals can be harmful. Clinically, when encountering mild cases of elevated blood pressure, repeated examinations at intervals are necessary to determine whether a diagnosis of hypertension can be made. Since 1979, China has adopted the World Health Organization's standards. Section 1: Epidemiological Characteristics In 1979–1980, a census of over 4 million people aged 15 and above across China clearly showed that the average prevalence of hypertension and borderline hypertension was 4.85% (age-standardized to 4.67%) and 2.88%, respectively. Prevalence was higher in urban areas than in rural areas, and higher in northern regions than in southern regions. Beijing's confirmed hypertension prevalence was 9.53%, ranking second nationwide, only behind Lhasa in Tibet; Guangdong had the lowest rate at 2.44%. In 1991, China conducted its third national sample survey on hypertension, covering 950,356 urban and rural residents aged 15 and above across 30 provinces, autonomous regions, and municipalities directly under the central government. According to WHO standards, systolic pressure ≥21.331 kPa (160 mmHg) and/or diastolic pressure ≥12.665 kPa (95 mmHg) were defined as confirmed hypertension; systolic pressure 18.798–21.198 kPa (141–159 mmHg) and/or diastolic pressure 12.132–12.532 kPa (91–94 mmHg) were classified as borderline hypertension. The confirmed hypertension prevalence was 4.13%, borderline hypertension 7.31%, totaling 11.44%. When standardized according to the 1964 population, the rates were 3.26%, 6.15%, and 9.41%, respectively. Compared with the 1979–1980 national standardized prevalence of 7.25%, the 1991 total standardized rate represents a 25.1% increase over ten years. In Guangdong Province, during the same period, the standardized prevalence rose from 4.73% to 8.99%, an increase of 47.4%, significantly higher than the national average growth rate. Hypertension prevalence increases with age; in cities, the rise generally begins around age 35, whereas in rural areas, the increase occurs about ten years later. Before age 35, there is no significant difference in prevalence between men and women; sometimes men have slightly higher rates, but after age 35, in high-prevalence areas, women tend to have higher rates than men, while in low-prevalence areas, women's rates fall below those of men after age 45. In China, both men and women's systolic pressures rise in a parabolic curve with age, with women's curves showing a much steeper slope than men's; before age 40, men's systolic pressures are slightly higher than women's, but after age 45, women's systolic pressures surpass men's, and the gap widens with age, reaching an average difference of 2.67 kPa (20 mmHg) for those over 70. Women's diastolic pressures also increase with age, but the rate of increase is much less pronounced than that of systolic pressures; in young and middle-aged women, diastolic pressures are slightly lower than men's, but after age 40, women's diastolic pressures become slightly higher than men's, and after age 60, the difference narrows to about 0.66–1.33 kPa (5–10 mmHg). Foreign data indicate that women's blood pressure rises more noticeably after age 50, with systolic pressures continuing to rise throughout life, while diastolic pressures often stop increasing around ages 55–60. Individuals with initially higher baseline blood pressure also experience more pronounced increases with age. In the United States, African Americans' blood pressure rises more sharply than that of whites, resulting in significantly higher prevalence rates among African Americans; however, in some isolated communities, blood pressure tends to be lower and does not increase with age. European and American countries have relatively high hypertension prevalence rates. According to the fifth report of the U.S. National Committee on Detection, Evaluation, and Treatment of Hypertension in 1993, as many as 50 million Americans may suffer from hypertension; however, since the implementation of the national hypertension education program in the early 1970s, the mortality rates from coronary heart disease and stroke—both major risks associated with hypertension—have declined markedly and continuously. The incidence of secondary hypertension varies depending on the population and the extent of further examination; in specialized hospitals, where difficult-to-diagnose hypertensive patients are concentrated, the prevalence of secondary hypertension is notably higher. Section 2: Etiological Factors Currently, the prevailing view is that hypertension is a disease caused by multiple factors acting on a genetic predisposition, leading to decompensation of the blood pressure regulatory mechanism.

1. Genetics: Among hypertensive patients, 40%–60% have a family history of the disease. Children or adolescents whose parents both have hypertension show significantly higher plasma levels of norepinephrine and dopamine compared with those from families without a history of hypertension. Even though biological and adopted children of hypertensive patients grow up in similar environments, the former are more likely to develop hypertension, highlighting the importance of genetic factors in the onset of hypertension.

2. Occupation: Mental workers tend to have higher blood pressure than physical workers. A 1973 Shanghai survey of prevalence rates across all age groups showed that urban mental workers had higher rates than urban physical workers, with a significant difference.

3. Salt and trace elements: Some epidemiological reports indicate that regions with high salt consumption have higher hypertension prevalence, while areas with low salt intake have lower rates. For example, a certain indigenous tribe in northern Brazil hardly consumes salt, excreting only 1 mmol of sodium per day; men aged 40–49 have blood pressure of 14.3/8.9 kPa (107/67 mmHg), while women have 12.4/8.3 kPa (93/62 mmHg). Similarly, on the Solomon Islands, six tribes live under identical conditions, yet their blood pressure correlates closely with salt intake. In Japan, fishermen in Hokkaido consume high amounts of salt, resulting in significantly higher rates of hypertension and stroke. Limiting daily salt intake to 60–90 mmol can reduce blood pressure for most people. However, even under the same environmental conditions and with the same high-salt diet, only some individuals develop hypertension, suggesting a genetic predisposition. In recent years, some scholars have reported that low calcium intake is a risk factor for hypertension. According to the U.S. National Health and Nutrition Survey, individuals consuming less than 300 mg of calcium per day have a 2–3 times higher risk of developing hypertension compared with those consuming 1,200 mg daily; yet other scholars have found different results, requiring further research. The trace element cadmium (Gd) is mainly derived from smoking and is associated with the onset of hypertension.

4. Vegetarianism and meat consumption: Reports indicate that vegetarians tend to have lower blood pressure than meat-eaters. When meat-eaters move to vegetarian-dominated areas and reduce their meat intake to match local residents, their blood pressure often drops to local levels; conversely, when vegetarians switch back to meat, their blood pressure rises. Regions with high fish consumption tend to have lower blood pressure.

5. Obesity and overweight: Obese and overweight individuals have a higher risk of hypertension than those who are thin. Reports suggest that obese patients are 2–6 times more likely to develop hypertension than those with normal weight. Overweight hypertensive patients can lower their blood pressure by controlling their diet and losing weight.

6. Psychological factors: Mental stimulation, adverse environments, and noise are all associated with the onset of hypertension.

7. Other factors: Smokers and heavy drinkers have a higher risk of hypertension. Section 3: Pathogenesis For a long time, people have hoped to find the root cause of hypertension and provide targeted treatment, just as they do with infectious diseases, in order to cure patients. Every time a new vasoactive substance is discovered, people place great hopes on it, believing it might solve the mystery of hypertension's etiology—but so far, this has not been achieved. Currently, most scholars have gradually come to realize that the causes of hypertension are complex and multifactorial; it remains unclear which factors are primary and which are secondary, whether it is a single disease presenting differently in clinical settings or a syndrome arising from multiple diseases manifesting clinically. Based on the evidence accumulated so far, the latter possibility seems more likely. Blood pressure is the force exerted by the heart as it pumps blood into the arteries and propels it through the vascular system, pressing against the vessel walls. The magnitude of this pressure depends on cardiac output and total peripheral vascular resistance. Cardiac output is determined by myocardial contractility, heart rate, and venous return, which in turn is influenced by blood volume and venous tone. Although the mechanisms underlying the onset of hypertension remain largely unexplained, numerous theories have been proposed to explain the disease's pathogenesis; the main ones are briefly outlined below: (1) Dysfunction of the autonomic nervous system. In healthy individuals, blood pressure is maintained within the normal range through regulation by the autonomic nervous system. However, strong external stimuli, mental stress, chronic depression, and chronic illnesses can all lead to impaired cortical function, resulting in autonomic dysfunction. Disorder, hyperfunction, and increased pressor hormones. For example, if preganglionic fibers directly stimulate the adrenal medulla, adrenaline and noradrenaline are secreted; postganglionic sympathetic fibers can also directly secrete noradrenaline. Adrenaline increases cardiac output, while noradrenaline causes constriction of peripheral arterioles. (2) Dysfunction of the renin-angiotensin-aldosterone system (RAA). Due to dysfunction of the hypothalamic center, the tone of the renal afferent arterioles changes, leading to decreased blood volume. Juxtaglomerular cells then release renin, which subsequently produces angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin III (Ang III). Ang II is a potent vasoconstrictor that directly raises blood pressure and also promotes aldosterone secretion by the adrenal cortex and catecholamine release from the medulla, further elevating blood pressure. Ang III has about 50% of the vasoconstrictive effect of Ang II but slightly stronger aldosterone-promoting effects. In addition, adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to produce aldosterone, increasing sodium reabsorption in the distal convoluted tubule and thereby increasing blood volume, which can also lead to elevated blood pressure. (3) Research on the pathogenesis of hypertension. In recent years, research in this area has been extensive and rapid. For instance, studies on bioactive substances of vascular endothelial cells suggest that these cells are not only physiological barriers to blood circulation but also metabolic and endocrine organs, capable of releasing a series of bioactive substances to regulate blood pressure levels. Studies on cardiac and endocrine functions indicate that cardiomyocytes secrete a powerful natriuretic hormone called atrial natriuretic peptide, also known as atrial natriuretic factor or atrial natriuretic hormone, which lowers blood pressure through its natriuretic and diuretic effects. With age, reduced secretion of atrial natriuretic peptide is also one of the causes of hypertension. Furthermore, research on calcium (Ca²⁺) channels reveals that excessive influx of Ca²⁺ into cells can cause smooth muscle contraction in blood vessels, thereby leading to hypertension. Section 4 Pathology In the early stages, there is spasm of small and arterioles throughout the body; over time, the vessel walls become hypoxic and undergo hyalinization. When arterial pressure remains persistently elevated, fibrous tissue and elastic fibers proliferate in the intima, narrowing the lumen and exacerbating ischemia. As small and arterioles harden and blood pressure rises, secondary changes occur in various organs, with the heart, brain, and kidneys being the most significant.

8. After blood pressure rises, the left ventricular workload increases, leading to myocardial hypertrophy and dilation; if the condition progresses, heart failure may develop. Prolonged hypertension facilitates lipid deposition in the intima of large and medium-sized arteries, resulting in atherosclerosis. If coronary atherosclerosis develops concurrently, myocardial ischemia will worsen, further aggravating the aforementioned cardiac changes.

9. Cerebral arteriosclerosis is common. If accompanied by vasospasm or thrombosis, it can cause cerebral softening; at the distal end of the spasmed vessels, nutritional necrosis may occur, forming tiny aneurysms, which, if ruptured, can lead to cerebral hemorrhage. Widespread and acute cerebral arteriosclerosis and hardening result in ischemia and increased permeability of capillary walls, causing acute cerebral edema.

10. Renal arteriosclerosis. Hyalinization and fibrosis of the glomerular afferent arterioles lead to atrophy and loss of nephrons; in severe cases, renal failure occurs. Chapter 2 Diagnosis Section 1 Clinical Manifestations (1) General Signs Primary hypertension has a slow onset, often asymptomatic in the early stages, typically discovered incidentally during physical examination. Most patients may experience dizziness, headache, blurred vision, tinnitus, insomnia, fatigue, and other symptoms, though these symptoms do not necessarily correlate with blood pressure levels. During examination, an accentuated second heart sound of the aortic valve may be heard; in older individuals, it may have a metallic quality. With prolonged hypertension, signs of left ventricular hypertrophy may appear. (2) Classification and Staging In 1993, the World Health Organization and the International Society of Hypertension (WHO/ISH) jointly proposed a new classification and staging system for hypertension.

11. Classification by blood pressure level (Table 2): Previously, classification was based on diastolic blood pressure (DBP) levels; now, the importance of elevated systolic blood pressure (SBP) has been recognized. A new category of isolated systolic hypertension has been introduced, defined as SBP elevation with DBP below 12 kPa (90 mmHg). Critical high blood pressure and critical isolated systolic hypertension are classified as subtypes of mild hypertension and isolated systolic hypertension, respectively. Mild hypertension accounts for 70% of all hypertensive patients. Table 2: Hypertension Classification (by Blood Pressure Level) (WHO/ISH, 1993)

SBP | | > DBP | | > kPa(mmHg) | | > kPa(mmHg) Normal18.7(140 | > and | > <12(90) Mild18.724(140180) subtype: | > and(or) | > 1214(90105) Critical18.721.3(140160) | > and(or) | > 1212.7(9095) Moderate to severe≥24(180) | > and(or) | > ≥14(105) Isolated systolic≥21.3(160) subtype： | > and | > <12(90) Critical isolated systolic18.721.3(140160) | > and | > <12(90)

2. Classification by target organ damage into three stages (Table 3): Unlike previous staging systems, the new classification includes detection of atherosclerotic plaques via ultrasound or X-ray, particularly in the carotid arteries, which can predict a higher likelihood of stroke and concurrent coronary artery disease. Table 3: Hypertension Staging (WHO/ISH, 1993)