Classification Systolic Pressure mmHg Diastolic Pressure mmHg

Classification | > Systolic Pressure (mmHg | > Diastolic Pressure (mmHg ) | > ) | Normal High Pressure | > < 120 and | > < 80 Normal High Value | > 120139 and | > 8089 | > /or | Hypertension | > ≥ 140 and /or | > ≥ 90 Grade 1 Hypertension ( | > 140159 and | Grade 2 Hypertension ( Moderate | > 160179 and | Grade 3 Hypertension ( | > ≥ 180 and /or | Isolated Systolic Hypertension | > ≥ 140 and | > < 90 Note: When systolic and diastolic pressures fall into different categories, the higher category shall prevail; the above standards apply to adult men and women.
Hypertension is a preventable and controllable disease. For those in the normal high value stage (130139)/(8589) mmHg, as well as for overweight/obese individuals, those with long-term high-salt diets, and excessive drinkers, targeted interventions should be carried out, regular health check-ups should be performed, and risk factors should be actively controlled. For hypertensive patients, regular follow-up visits and blood pressure measurements are necessary, with particular attention paid to managing morning blood pressure. Active treatment of hypertension (combining medication and lifestyle interventions) should be pursued to slow down target organ damage, prevent complications affecting the heart, brain, and kidneys, and reduce disability and mortality rates.
Due to the relatively infrequent measurement of clinic blood pressure and the obvious fluctuations in blood pressure, when 24-hour dynamic blood pressure monitoring is not feasible, multiple measurements over several weeks are required to determine whether blood pressure is elevated, especially in cases of mild to moderate increases. If conditions permit, 24-hour dynamic blood pressure monitoring or household blood pressure monitoring should be conducted.
Causes (---) Genetic Factors
Hypertension exhibits a clear familial clustering pattern: if parents have hypertension, the probability of their children developing the condition is high. (2) Environmental Factors

1. Diet
   (1) The prevalence of hypertension is significantly correlated with average sodium intake; the more salt consumed, the higher the blood pressure level and the prevalence of the disease, particularly among salt-sensitive populations. On average, for every additional 2 grams of salt consumed per day, systolic and diastolic pressures increase by 2.0 mmHg and 1.2 mmHg, respectively.
   (2) Potassium intake is negatively correlated with blood pressure.
   (3) Low calcium intake is associated with the occurrence of hypertension.
   (4) High protein intake is a contributing factor to elevated blood pressure; both animal and plant proteins can raise blood pressure.
   (5) A diet high in saturated fatty acids or a high ratio of saturated to unsaturated fatty acids is also a contributing factor to elevated blood pressure.
   (6) Alcohol consumption is linearly correlated with blood pressure levels, especially with systolic pressure. 2. Psychological Stress Mental workers, individuals engaged in high-stress occupations, and those with hearing sensitivity loss due to long-term exposure to noisy environments are more likely to develop hypertension. (3) Other Factors
2. Body Weight Overweight or obesity is an important risk factor for elevated blood pressure.
3. Contraceptive Pills The incidence and degree of blood pressure elevation in women taking contraceptive pills are related to the duration of use.
4. Sleep Apnea-Hypopnea Syndrome (SAHS) SAHS refers to recurrent episodes of respiratory arrest during sleep. It can be classified as central or obstructive; the latter is mainly caused by pathological narrowing of the upper airway, particularly the nasopharynx, such as adenoid and tonsillar hypertrophy, soft palate relaxation, elongated uvula, fat infiltration at the base of the tongue leading to drooping, and mandibular deformities. The severity of blood pressure elevation in SAHS patients is related to the course of the disease. II. Pathogenesis The etiology and pathogenesis of primary hypertension result from a combination of multiple acquired factors acting on a background of certain genetic susceptibility. Although many hypotheses have been supported by laboratory and clinical data, the exact mechanisms remain unclear. (1) Currently, it is believed that the pathogenesis of this disease is unknown; hypertension is not a uniform, homogeneous condition, and the etiology and pathogenesis vary among individuals. (2) Hypertension has a long course and generally progresses slowly, with different stages involving initiating, maintaining, and accelerating mechanisms. (3) The mechanisms involved in normal physiological regulation of blood pressure are not equivalent to the pathogenesis of hypertension; abnormalities or defects in one mechanism are often compensated by other mechanisms. (4) The pathogenesis of hypertension is difficult to clearly separate from the pathophysiological changes caused by hypertension. The fluctuation of blood pressure, the artificial nature of the definition of hypertension, and the ambiguity of the onset time also make it challenging to determine the initiating mechanism. From a hemodynamic perspective, blood pressure is primarily determined by cardiac output and peripheral vascular resistance in the systemic circulation, where mean arterial pressure (MBP) = cardiac output (CO) × total peripheral vascular resistance (PR). The hemodynamic characteristic of hypertension is mainly an increase in total peripheral vascular resistance, either relative or absolute. (---) Genetics
5. This disease exhibits a clear familial aggregation tendency. Children (or adolescents) of parents with hypertension show significantly higher plasma concentrations of norepinephrine and dopamine compared with the control group without a family history of hypertension, and they also have a higher incidence of developing hypertension in adulthood. Domestic surveys have found that compared with individuals without a family history of hypertension, those with one parent having primary hypertension have a 1.5 times higher prevalence of hypertension; while those with both parents having primary hypertension have a 2–3 times higher prevalence. Biological and adopted children of patients with this disease live in the same environment, but the former are more prone to hypertension.
6. In recent years, several gene mutations (such as those related to angiotensin, glucocorticoid receptors, lipoprotein lipase, etc.) have been found to be associated with hypertension. Observational studies on candidate genes for primary hypertension have reached 150, covering areas such as the sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS), endothelin, growth hormone, prostaglandins, natriuretic peptides, insulin resistance, hypothalamic-pituitary hormones, and many others. However, the specific genes associated with hypertension have yet to be definitively identified. At present, it is believed that this disease is a polygenic hereditary disorder. (2) Psychological and Neurological Effects
7. Psychogenic Theory Individuals who frequently work under stress, require intense concentration, experience prolonged mental tension, or are exposed to noise or adverse visual stimuli are more susceptible to this disease. Under long-term or repeated external stressors, patients may exhibit noticeable emotional changes such as mental tension, anxiety, and irritability. At this point, pathological signals transmitted by various sensory receptors increase, disrupting the balance between excitation and inhibition in the cerebral cortex and impairing its ability to properly regulate and control subcortical activities. Sympathetic nervous activity increases, with impulses sent from the vasomotor center favoring vasoconstriction, thereby causing small arteries to constrict, peripheral vascular resistance to rise, and blood pressure to increase.
8. Neurogenic Theory The nervous system can respond to cardiovascular needs and environmental stimuli, enabling rapid and precise regulation of blood pressure, and also influencing chronic, long-term blood pressure levels. Compared with the parasympathetic nervous system, the sympathetic nervous system and its associated neurohumoral factors play a more significant role in the onset and progression of hypertension through their effects on peripheral vessels and the heart. The actions of the sympathetic nervous system are carried out under the control of the medulla oblongata and other higher centers. The cardiovascular motor center in the medulla integrates incoming signals from pressure receptors, chemoreceptors, and the hypothalamus and other higher centers, continuously regulating this mechanism. Meanwhile, the cerebral cortex can influence blood pressure by regulating the blood pressure center based on changes in human emotions and physical activity. For example, when the number of vasoconstrictive impulses issued by various centers increases, or when vasoconstrictive signals received from various sensory receptors intensify, or when resistance vessels overreact to neurotransmitters, all these situations can lead to the development of hypertension. (3) Imbalance in the Renin-Angiotensin-Aldosterone System (1) Renin secreted by juxtaglomerular cells in the kidney can convert angiotensinogen synthesized in the liver into angiotensin I (AT I), which is then converted into AT II under the catalytic action of angiotensin-converting enzyme (ACE, also known as kininase I) as it passes through organs such as the lungs and kidneys. AT II can further lose aspartic acid under enzymatic action to become AT III, and ACE can also promote the breakdown of bradykinin. AT I can also form through non-ACE pathways—for example, pepsin can convert AT I into AT II, while tissue proteases can directly convert angiotensinogen into AT I and aldosterone. In addition, organs such as the brain, heart, kidneys, adrenal glands, and arteries can locally synthesize AT I and aldosterone, forming what is known as the tissue RAA system. (2) Within the RAA system, AT I is the most important active component, and its pathophysiological effects are mainly produced through binding to receptors. Through this pathway, it can induce vasoconstriction, increase aldosterone secretion, cause water and sodium retention, enhance sympathetic nervous activity, ultimately leading to elevated blood pressure. The pressurizing effect of AT I's strong vasoconstrictive action is about 10–40 times that of adrenaline, and excessive activity of the RAA system will lead to the development of hypertension. AT I and aldosterone also serve as stimulants for tissue growth, so it can be said that AT I plays an important role in the onset and progression of hypertension, tissue remodeling of target organs, and the occurrence of complications. (4) Metabolic Syndrome
9. One of the main manifestations of metabolic syndrome is hypertension. Approximately 50% of patients with primary hypertension exhibit insulin resistance, which is closely related to hyperinsulinemia, metabolic syndrome, and type 2 diabetes—some even believe it is the root cause. The incidence of hypertension among patients with type 2 diabetes is 2–3 times higher than that of non-diabetic individuals. Genetic research has found that individuals with PPARγ gene mutations first develop hyperinsulinemia, followed by hypertension and low HDL-C, further confirming the interrelationship between them and suggesting that hypertension may be associated with metabolic diseases.
10. Mechanism of Blood Pressure Elevation During Insulin Resistance It is possible that elevated insulin levels affect Na⁺-K⁺ ATPase and other ion pumps, leading to increased intracellular sodium and calcium concentrations, heightened sympathetic nervous activity, enhanced renal tubular reabsorption of water and sodium, increased sensitivity of blood pressure to salt, reduced nitric oxide production by endothelial cells, stimulation of growth factors (especially smooth muscle), and increased endothelin secretion. (5) Excessive Sodium Intake Sodium metabolism is closely related to this disease. (1) There is a positive correlation between population blood pressure levels and the prevalence of this disease and average sodium intake; limiting sodium intake can improve hypertension conditions. (2) In patients with renovascular hypertension, high blood sodium can worsen the condition, while reducing sodium intake can improve it. (3) Among patients and animals who died from hypertension, the sodium content per unit volume of dry matter in renal arteries was higher than in those without hypertension. (4) Sodium retention increases extracellular fluid volume, leading to increased cardiac output; increased water content in small arterial walls leads to increased peripheral resistance; and changes in the ratio of intracellular to extracellular sodium concentrations can also increase small arterial tension—all of which may be contributing mechanisms. (5) However, laboratory and clinical studies have found that altering salt intake and blood sodium levels can only affect some individuals' blood pressure, not all. The pathogenic effect of dietary salt is conditional: it only causes hypertension in individuals with genetic defects in sodium transport who are sensitive to salt intake. (6) Obesity Obese individuals are more prone to hypertension. (1) For every 1.7 kg/m² increase in male body weight and every 1.25 kg/m² increase in female body weight, systolic blood pressure rises by 1 mmHg. Conversely, weight loss can lead to a corresponding decrease in blood pressure. (2) Experiments have shown that in animal models of obesity induced by a high-fat diet (DIO), blood pressure remains persistently elevated, possibly due to fat accumulation within the kidneys, proliferation of mesenteric cells and capillary endothelial cells, obstruction and deformation of the collecting ducts at the renal papilla resulting in urinary flow obstruction and increased intrarenal pressure. (3) Obesity is part of metabolic syndrome, often accompanied by hyperinsulinemia, increased sympathetic nervous activity, and excessive production of angiotensinogen by adipocytes—these factors may all contribute to the development of hypertension. (7) Other (1) The prostaglandin system is closely related to the RAA system; some believe that hypertension may be linked to insufficient synthesis of vasodilatory prostaglandins A or E in the renal medulla. (2) ACE can promote the degradation of kinins, thereby eliminating their vasodilatory effects and causing blood pressure to rise. (3) In recent years, the relationship between vasopressin, endothelin, and other peptide substances and this disease has also attracted widespread attention, but no clear causal link has yet been established. (4) Smoking and excessive alcohol consumption also increase the risk of hypertension. III. Pathology (---) Arteries
11. Small Arteries Lesions of small arteries are the most important pathological changes in this disease. (1) In the early stages, there is generalized spasm of small arteries; prolonged, recurrent spasms cause hyalinization of the intima due to increased pressure load and ischemia/hypoxia, while the media thickens due to proliferation and hypertrophy of smooth muscle cells, leading to vascular wall remodeling and eventually fibrosis of the vessel wall and stenosis of the lumen, resulting in irreversible lesions. (2) In patients with rapidly progressing primary hypertension, the walls of small arteries may undergo fibrinous necrosis in a relatively short period of time. (3) Lesions of small arteries at any stage can lead to luminal stenosis, promoting the maintenance and progression of hypertension. Small arteries in surrounding tissues and organs can all develop similar lesions, but the small arteries in the kidneys are the most prominent, and these lesions ultimately lead to ischemic damage to tissues and organs.
12. Large Arteries As people age, large arteries gradually harden and their compliance decreases, which is an important cause of systolic hypertension in the elderly. (1) In the later stages of hypertension, the aorta may experience cystic necrosis of the media and dissection. Dissection commonly occurs at the junction of the aortic arch and descending aorta, but can also occur in the ascending aorta and abdominal aorta. At this point, high-pressure blood tears the aortic intima, allowing large amounts of blood to enter the media and separate the intima from the media, forming a false channel. (2) Hypertension promotes the development of atherosclerosis; in addition to large arteries, there may also be thickening of the carotid intima, coronary artery disease, and other vascular lesions in peripheral vessels. (2) Heart Hypertension primarily causes left ventricular hypertrophy and dilation. (1) The long-term narrowing of small arterial lumens throughout the body, leading to sustained increases in peripheral vascular resistance, is one of the causes of left ventricular hypertrophy. However, myocardial hypertrophy does not always correlate positively with the degree of blood pressure elevation. (2) Long-term increased pressure load, along with catecholamines and angiotensin I and other growth factors, can stimulate myocardial cell hypertrophy and interstitial fibrosis. When the sympathetic nervous system is excited, the released catecholamines can stimulate protein synthesis in myocardial cells, while circulating RAA system components such as AT I and aldosterone can not only stimulate myocardial cell hypertrophy but also promote collagen production between myocardial cells, which is another reason for myocardial hypertrophy in patients. In the early stages, left ventricular hypertrophy is mainly concentric; however, with long-term disease progression, the myocardium undergoes degenerative changes, including myocardial cell atrophy, interstitial fibrosis, thinning of the ventricular wall, and enlargement of the left ventricular cavity. (3) Based on the degree of left ventricular hypertrophy and dilation, it can be classified as symmetrical hypertrophy, asymmetric septal hypertrophy, and dilatative hypertrophy. (4) When long-term hypertension causes myocardial hypertrophy or dilation, it is referred to as hypertensive heart disease. (5) Hypertensive heart disease is often accompanied by coronary atherosclerosis and microvascular lesions, which can ultimately lead to heart failure. With myocardial hypertrophy, the coronary blood flow reserve decreases, and the presence of coronary atherosclerosis in hypertensive patients further exacerbates myocardial ischemia, worsening cardiac lesions. The changes in the myocardium during hypertension are very similar to those during heart failure, suggesting that myocardial hypertrophy in hypertension may be a process of cardiomyopathy; if left untreated, it will eventually lead to heart failure. Recent findings indicate that using certain antihypertensive drugs, especially those that block the RAA system, can reverse myocardial hypertrophy. (6) Elderly patients have fewer myocardial cells and relatively more collagen tissue, so their cardiac contractile and diastolic functions have already declined under normal circumstances. Under hypertension, they are even more prone to decompensation of cardiac function, and because the myocardium has already undergone physiological loss, myocardial hypertrophy is less likely to occur during hypertension. (3) Central Nervous System (1) Long-term hypertension causes ischemia and degeneration of cerebral blood vessels, making microaneurysms more likely to form and leading to cerebral hemorrhage. Cerebral small arteries may undergo a series of changes ranging from spasm to hardening, but the structure of cerebral blood vessels is relatively fragile; once hardened, they become even more vulnerable. Moreover, with long-term hypertension, microaneurysms often form in cerebral small arteries, making them prone to rupture and bleeding during vascular spasms or fluctuations in intravascular pressure. Small arterial ruptures often occur in the internal capsule and basal ganglia. (2) Hypertension promotes atherosclerosis in cerebral arteries, and rupture of atherosclerotic plaques can lead to cerebral thrombosis. On the basis of small arterial hardening, thrombi are easily formed, resulting in cerebral infarction; after infarction, the softened brain tissue may bleed around the infarct area. If the lesion occurs in medium-sized cerebral arteries, it can further aggravate cerebral ischemia. (3) Occlusive lesions in cerebral small arteries can cause pinpoint, small-area infarcts, known as lacunar infarcts. (4) Atherosclerosis inside and outside the skull can easily cause atherosclerotic plaque detachment from the arterial wall, leading to cerebral embolism. (4) Kidneys Kidney small artery lesions are the most obvious, mainly occurring in the afferent arterioles, with interlobar small arteries also potentially involved. If there is no concurrent diabetes, the efferent arterioles are less affected. Lesioned vessels may narrow or even become occluded, causing renal parenchymal ischemia, glomerular fibrosis, renal tubular atrophy, and interstitial fibrosis, gradually thinning the renal cortex. Relatively normal nephrons can compensate by hypertrophy. In the early stages, the kidneys appear unchanged, but as the disease progresses, the kidney surface becomes granular, and the kidney volume gradually shrinks with disease progression. These pathological changes are seen in slowly progressing primary hypertension, which is called benign renal sclerosis due to its slow progression, but ultimately leads to renal failure. In cases of rapidly progressing hypertension, the middle layer of the afferent arterioles develops fibrinous necrotic inflammation, and the lesion can directly extend to the glomerular capillary network, causing glomerular sclerosis. In interlobar and arcuate arteries, the intima shows cellular proliferation, with collagen and fibroblasts arranged in concentric circles like "onion skin." Due to the rapid disease progression, patients may experience renal failure in a short period of time, which is called malignant renal sclerosis. (5) Retina Retinal small arteries initially experience spasm, then gradually harden; in severe cases, retinal hemorrhage and exudation occur, along with optic disc edema. Clinically, observing changes in retinal arteries through fundus examination can reflect changes in other small arteries, especially those in the eye. Clinical Manifestations (1) Slowly Progressing Hypertension Most cases begin in young to middle age, and those with a family history may develop the disease at a younger age. The onset is often insidious, the disease progresses slowly, and the course is long.
13. Neuropsychiatric Manifestations Headache, dizziness, and head fullness, possibly accompanied by tightness in the head or neck. (1) Headache: Often occurs in the morning, localized in the forehead, occipital region, or temporal region. After treatment with antihypertensive drugs, the headache can be alleviated. (2) Dizziness: May be temporary or persistent, with few cases of vertigo. It is related to inner ear labyrinthine vascular disorders. Symptoms can be relieved after antihypertensive treatment, but note that sometimes too rapid or excessive blood pressure reduction can also cause dizziness. (3) Some patients also experience fatigue, insomnia, and decreased work capacity. (4) Cerebrovascular Accidents: A general term for cerebrovascular diseases complicated by hypertension, commonly known as stroke, which can be divided into two main categories: ① Ischemic cerebral infarction, including atherosclerotic thrombosis, lacunar infarction, embolism, transient cerebral ischemia, and various other types; ② Cerebral hemorrhage, including parenchymal and subarachnoid hemorrhage.
14. Cardiovascular System During hypertension, the main manifestations in the cardiovascular system include palpitations and symptoms following left ventricular dysfunction. (1) Symptoms: In the cardiovascular system during hypertension, the left ventricle's diastolic function is the first to be affected. When the left ventricle hypertrophies, its diastolic compliance decreases, and its relaxation and filling functions are impaired. Even in cases of borderline hypertension where clinical examinations fail to detect left ventricular hypertrophy, this may be due to increased collagen in the myocardial interstitium. But at this stage, patients may have no obvious clinical symptoms.
    Symptoms of clinical heart failure often appear several to more than ten years after the onset of hypertension.
    During the compensatory phase of cardiac function, apart from occasional palpitations, other cardiac symptoms may be mild or inconspicuous.
    When compensatory function fails, symptoms of left heart failure may occur, such as paroxysmal nocturnal dyspnea,
    shortness of breath, palpitations, and cough during physical exertion, overeating, or excessive talking; in severe cases or when blood pressure rises suddenly, pulmonary edema may develop.
    Recurrent or persistent left heart failure can impair right ventricular function, leading to global heart failure with symptoms such as oliguria and edema.
    Since hypertension can promote atherosclerosis, some patients may also present with angina pectoris or myocardial infarction due to concomitant coronary atherosclerotic heart disease.
    (2) Physical signs: ① Before cardiac enlargement, physical examination may reveal no specific findings, or only a strong and forceful pulse or apical impulse; the second heart sound in the aortic area may be accentuated due to elevated diastolic aortic pressure; ② After cardiac enlargement, the cardiac border expands to the left and downward, the apical impulse becomes strong and forceful, with a lifting sensation. A grade I–III systolic blowing murmur may be heard in the apical area and/or the aortic area.
    The aortic murmur is caused by aortic dilation, decreased aortic valve compliance, and accelerated blood flow, resulting in relative aortic stenosis. The second heart sound in the aortic area may take on a metallic tone due to hardening of the aorta and valves. The apical murmur is caused by left ventricular enlargement leading to relative mitral regurgitation or dysfunction of the mitral papillary muscles, and a fourth heart sound may be present.
15. Renal manifestations
    The degree of renal vascular lesions is closely related to the severity and duration of hypertension, often presenting as polyuria, nocturia, thirst, and polydipsia.
    (1) Proteinuria: In the early stages of hypertension, there may be no clinical manifestations; in fact, all patients with uncontrolled blood pressure have renal damage. As the disease progresses, proteinuria may first appear,
    but if there is no concurrent heart failure or diabetes, the total 24-hour urinary protein rarely exceeds 1 g; controlling hypertension can reduce proteinuria.
    (2) Hematuria: Mostly microscopic hematuria, with rare transparent and granular casts.
    (3) Polyuria and nocturia: When renal function decompensates and the kidney's concentrating ability is impaired, polyuria, nocturia, thirst, and polydipsia may occur, with urine specific gravity gradually decreasing until it stabilizes around 1.010, known as isosmotic urine. When renal function further declines, urine output may decrease, while blood urea nitrogen and creatinine levels rise; the phenol red excretion test shows a significant reduction in excretion, and the urea clearance rate or creatinine clearance rate may fall markedly below normal. These changes worsen as renal damage progresses, eventually leading to uremia. However, in patients with slowly progressive hypertension, most die from cardiovascular or cerebrovascular complications before developing uremia.
16. Other manifestations
    (1) Patients with acute aortic dissection may experience severe chest or abdominal pain depending on the location of the lesion.
    (2) Those with peripheral vascular disease in the lower extremities may develop intermittent claudication.
17. Physical signs
    (1) Blood pressure fluctuates considerably with seasons, time of day, and emotional state. Blood pressure is higher in winter and lower in summer; there are obvious diurnal fluctuations, with generally lower nighttime blood pressure and a rapid increase upon waking and activity, forming a morning blood pressure peak.
    (2) Cardiac auscultation may reveal an accentuated second heart sound in the aortic area, a systolic murmur, or an early systolic click.
    (II) Malignant or rapidly progressive hypertension
    The condition progresses rapidly, with diastolic pressure persistently ≥ 130 mmHg, accompanied by headache, blurred vision, retinal hemorrhage, exudation, and papilledema, along with prominent renal damage, including persistent proteinuria, hematuria, and urinary casts. Patients often die from renal failure, stroke, or heart failure.
    II. Complications
    (---) Hypertensive crisis 1. Causes
    Due to factors such as stress, fatigue, cold, paroxysmal hypertensive attacks caused by pheochromocytoma, or sudden discontinuation of antihypertensive medications, small arteries undergo severe spasm, causing a sharp rise in blood pressure that impairs blood supply to vital organs and results in critical symptoms.
18. Hypertensive crisis
    (1) Aggravated malignant hypertension. Diastolic pressure is often > 140 mmHg, accompanied by papilledema, hemorrhage, and exudation in the fundus; patients may experience headache, vomiting, somnolence, confusion, blindness, oliguria, and even convulsions and coma.
    (2) Marked elevation of blood pressure combined with severe lesions in the brain, heart, kidneys, and other urgent conditions, such as hypertensive encephalopathy, stroke, traumatic brain injury, acute myocardial infarction,
    acute heart failure, acute aortic dissection, acute nephritis, pheochromocytoma, postoperative hypertension, severe burns, eclampsia, etc.
19. Clinical manifestations
    Severe symptoms include headache, irritability, dizziness, nausea, vomiting, palpitations, shortness of breath, and blurred vision, as well as ischemic symptoms affecting target organs due to spasmodic arteries (vertebrobasilar artery, internal carotid artery, retinal artery, coronary artery, etc.).
    (II) Hypertensive encephalopathy
    Can occur in patients with either slowly progressive or rapidly progressive hypertension. When blood pressure rises above 180 mmHg, the cerebral vasculature’s ability to autonomously regulate its tone in response to blood pressure changes weakens or disappears, causing vessels to shift from constriction to dilation. Excessive blood flow under high-pressure conditions enters the brain tissue, leading to cerebral edema.
    (Overly high blood pressure exceeds the range of automatic regulation of cerebral blood flow, resulting in excessive perfusion of brain tissue and subsequent cerebral edema.)
20. Clinical manifestations
    Diffuse severe headache, vomiting, consciousness disturbance, mental confusion, and even coma, as well as focal or generalized seizures.
    Severe headache, dizziness, nausea, vomiting, irritability, slow but strong pulse, possible difficulty or slowing of breathing, visual impairment, blackouts, convulsions, confusion, and even coma; temporary hemiplegia, aphasia, or unilateral sensory disturbances may also occur.
21. Examination
    Papilledema, increased cerebrospinal fluid pressure, and elevated protein content.
    (1) Brief episodes last for a few minutes, while prolonged ones may last for hours or even days.
    (2) Patients experiencing hypertensive emergencies should receive intravenous medication as quickly as possible—measured in minutes or hours—to bring blood pressure down to an appropriate level; otherwise, they may die within minutes or hours.
    (3) Severe hypertension refers to cases where blood pressure is markedly elevated but there are no rapid deteriorations in vital organ function—for example, no changes in the fundus or any symptoms. For such patients, there is currently no evidence that emergency blood pressure reduction provides benefits; therefore, emergency intravenous medication is generally not required, but oral medication should be administered promptly to effectively control blood pressure, with close follow-up to prevent progression to hypertensive emergencies.
    (III) Other
    (1) Cerebrovascular diseases, including cerebral hemorrhage, cerebral thrombosis, lacunar infarction,
    and transient ischemic attack.
    (2) Heart failure.
    (3) Chronic renal failure.
    (4) Aortic dissection. Aortic dissection is a serious cardiovascular emergency in which blood seeps into the media of the aortic wall, forming a dissecting hematoma that extends and peels along the aortic wall, and is one of the causes of sudden death. Hypertension is an important contributing factor. Clinically, it presents as sudden, severe chest pain, with tachycardia and marked elevation of blood pressure during the pain episode, followed rapidly by various manifestations of dissection rupture or compression of major aortic branches.
    III. Auxiliary examinations (---) Complete blood count
    Red blood cells and hemoglobin are generally normal.
    In cases of rapidly progressive hypertension, there may be microangiopathic hemolytic anemia with negative Coombs test, accompanied by abnormal red blood cells; high hemoglobin levels increase blood viscosity, making thrombosis more likely (including cerebral infarction) and left ventricular hypertrophy.
    (II) Urinalysis
    Early-stage patients usually have normal urinalysis.
    As renal concentrating function declines, urine specific gravity gradually decreases, with trace amounts of protein, red blood cells, and occasional casts. As renal disease progresses, urinary protein increases; in patients with benign renal sclerosis, if 24-hour urinary protein exceeds 1 g, it indicates a poor prognosis. Red blood cells and casts may also increase, with casts mainly being transparent or granular.
    (III) Renal function
    Blood urea nitrogen and creatinine are commonly used to assess renal function. Early-stage patients show no abnormalities; however, once renal parenchymal damage reaches a certain degree, these values begin to rise. For adults, creatinine > 114.3 mol/L; for the elderly and pregnant women, > 91.5 umol/L indicates renal damage, and endogenous creatinine clearance rates may fall below normal.
    (IV) Chest X-ray
    The aorta is visible, especially the ascending and arch portions, which may be tortuous and elongated; the ascending, arch, or descending portions may dilate. Left ventricular enlargement may be observed, with more pronounced enlargement in cases of left heart failure and both left and right ventricles enlarging in cases of global heart failure, accompanied by signs of pulmonary congestion. In cases of pulmonary edema, the pulmonary hilum appears markedly congested, showing a butterfly-shaped blurred shadow. Routine radiography is recommended for follow-up comparison.
    (V) Electrocardiogram
    When left ventricular hypertrophy occurs, the ECG may show left ventricular hypertrophy combined with strain. Due to decreased diastolic compliance of the left ventricle and increased diastolic load on the left atrium, the ECG may show widening of the P wave, deepening of the notch, and an increase in the negative terminal potential of PV1, among other changes. This manifestation may even appear before left ventricular hypertrophy is detected on the ECG. Arrhythmias such as atrial or ventricular premature contractions and atrial fibrillation may also occur.
    (VI) Echocardiography
    Echocardiography is the most sensitive and reliable method for diagnosing left ventricular hypertrophy. Based on two-dimensional ultrasound localization, M-mode echocardiographic curves can be recorded, or measurements can be taken directly from the two-dimensional image. If the interventricular septum and/or the posterior wall of the left ventricle are thicker than 13 mm, it indicates left ventricular hypertrophy.
    In hypertension, left ventricular hypertrophy is symmetrical, but about one-third of cases are primarily characterized by interventricular septal hypertrophy (the ratio of interventricular septal thickness to left ventricular posterior wall thickness is > 1.3). Interventricular septal hypertrophy often appears first at the upper end, suggesting that hypertension initially affects the left ventricular outflow tract.
    Echocardiography can also observe other cardiac chambers, valves, and the aortic root, and perform cardiac function tests. Although early-stage left ventricular hypertrophy does not yet affect overall cardiac function—such as cardiac output and left ventricular ejection fraction—the compliance of the left ventricle during both systole and diastole has already declined, with reductions in maximum myocardial contraction velocity (vmax), prolongation of isovolumetric relaxation, and delayed mitral valve opening. After left heart failure develops, echocardiography can reveal enlargement of the left ventricle and left atrium, as well as weakened contractile activity of the left ventricular wall.
    (VII) Ambulatory blood pressure monitoring
    This allows observation of the subject’s 24-hour blood pressure changes, typically measuring blood pressure every 15–20 minutes during the day and every 20–30 minutes at night, then plotting the readings into a curve or calculating average values for different time periods.
    This examination helps to:
    (1) Clarify the diagnosis of hypertension, especially “white coat hypertension” (elevated blood pressure during physician examination) or “pseudo-normal blood pressure.” “Pseudo-normal blood pressure” is the opposite of “white coat hypertension”—it refers to situations where blood pressure is normal during physician examination, but ambulatory blood pressure monitoring or home self-measurement reveals blood pressure above normal, indicating greater target organ damage and metabolic abnormalities compared to the general population, thus increasing cardiovascular risk.
    (2) Understand diurnal blood pressure variations, allowing hypertension to be classified into structured and unstructured types. Structured hypertension still exhibits the characteristic of higher daytime and lower nighttime blood pressure, accounting for about 80% of hypertensive patients. Unstructured hypertension, on the other hand, shows less noticeable nighttime blood pressure decline (less than 10% of the daytime drop), and is generally considered to have a greater impact on target organs and a higher risk of cardiovascular events. Ambulatory blood pressure monitoring can also observe how blood pressure changes with emotions and activity levels, providing guidance for treatment.
    (3) Observe the efficacy and safety of medications, evaluate new antihypertensive drugs, calculate the trough-to-peak ratio and smoothness index of blood pressure reduction, and analyze reasons for drug resistance or hypotension during antihypertensive therapy.
    (4) Predict prognosis. The standard for diagnosing hypertension using ABPM is an average 24-hour ambulatory blood pressure > 130/80 mmHg, with daytime readings > 135/85 mmHg and nighttime readings > 120/75 mmHg; however, the implementation methods and some parameter standards for ambulatory blood pressure monitoring have not yet been unified. See Table 2-1.
    (8) Fundus examination
    Measurement of central retinal arterial pressure reveals elevation; at different stages of disease progression, the following fundus changes may be observed:
    Grade I: Retinal arterial spasm.
    Grade IA: Mild retinal arterial hardening; Grade IB: Significant retinal arterial hardening.
    Grade III: Grade I combined with retinal lesions (hemorrhage or exudation).
    Grade V: Grade III combined with papilledema.
    (9) Other examinations
    Patients may also exhibit elevated serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, and reduced high-density lipoprotein cholesterol, along with decreased apolipoprotein A1.
    Table 2-1 Factors influencing the prognosis of hypertensive patients