Pregnancy with essential hypertension
Introduction
Introduction to pregnancy with essential hypertension There is no special prevention method for pregnancy with essential hypertension. After the illness, avoid cold, local physiotherapy and joint local anesthesia to protect the hands, feet and hypertension (hypertension) is the clinical manifestation of increased systemic arterial pressure. The sign can cause a series of symptoms, which can reduce the patient's life and work quality, and even severe cases can lead to death. The prevalence of essential hypertension increases with age, and generally increases after 35 years of age. Before the age of 60, the prevalence of men is higher than that of women, but after 60 years, women are higher than men. Essential hypertension can be divided into two types according to the onset of disease and the progress of the disease and the length of the disease. The former is also called benign hypertension. The majority of patients belong to this type, and the latter It is called malignant hypertension, which accounts for only 1% to 5% of patients with essential hypertension. basic knowledge Sickness ratio: 0.5% Susceptible population: pregnant women Mode of infection: non-infectious Complications: Hypertensive crisis Hypertensive encephalopathy Coma
Cause
Pregnancy with the cause of essential hypertension
(1) Causes of the disease
The etiology of this disease has not yet been fully elucidated. At present, it is generally believed that on the basis of certain genetics, due to the combined effects of various acquired factors, the normal blood pressure regulation mechanism of the body is decompensated. The following factors may be related to the onset.
Genetic (15%):
Epidemiological investigations, twin studies and animal experiments have shown that there is a clear genetic predisposition to essential hypertension. Studies have shown that siblings (also known as identical twins) are more siblings than twins (also known as fraternal twins). The blood pressure consistency is more obvious; epidemiology shows that there is significant family aggregation of essential hypertension; it is estimated that 20% to 40% of blood pressure variability in the population is genetically determined, but now it is speculated that this ratio may be higher In recent years, molecular biology studies have shown that angiotensinogen gene, angiotensin II receptor type I gene, renin gene, aldosterone synthase gene, etc. may be candidate genes for essential hypertension, and currently tend to be primary Hypertension is a polygenic genetic disease whose genetic characteristics are the cumulative effects of multiple minor genes and the decisive role of a major causative gene.
Diet (30%):
(1) Dietary high salt, low potassium, low calcium, low animal protein: Chinese people have higher salt intake than Western countries, 12 to 18 g per day in the north, 7 to 8 g per day in the south, dietary sodium intake and blood pressure There was a significant correlation between the levels. After controlling the total calories, the correlation coefficient between dietary sodium and systolic blood pressure and diastolic blood pressure reached 0.63 and 0.58, respectively. The 14 populations showed that the average dietary intake per person per day increased by 2g. The mean systolic and diastolic blood pressure increased by 0.267 kPa (2.0 mmHg) and 0.16 kPa (1.2 mmHg), respectively. The study of Tianjin residents and the three groups of people in China showed that the daily sodium intake or 24h urinary sodium excretion of the individual was related to their blood pressure. There was a significant positive correlation. The INTERSALT study analyzed data from three populations in China (Beijing, Tianjin, Guangxi). The urinary sodium/potassium ratio in Chinese population was higher than that in other study populations. The slope of systolic blood pressure increased with age was 45. %, which led to a rise in blood pressure between the ages of 25 and 55 compared with other populations, suggesting that the exposure of Chinese people to high sodium intake has a greater impact on blood pressure than other populations. In the population with lower intake than the median, the dietary sodium/potassium ratio was significantly positively correlated with blood pressure, while in the population with higher dietary calcium intake than the median, the association was not significant, indicating that the diet was in China. Low calcium may promote the blood pressure of sodium. The 14 populations showed that the average percentage of animal protein intake per person per day increased by 1 percentage point, and the mean systolic and diastolic blood pressure decreased by 0.12 kPa (0.9 mmHg) and 0.093 kPa, respectively. (0.7mmHg), these studies suggest that dietary high salt is an important risk factor for hypertension in Chinese population, and the dietary structure of low potassium, low calcium and low animal protein aggravates the adverse effects of sodium on blood pressure. (2) Drinking: If drinking at least once a week is used for drinking, the drinking rate of middle-aged males in China is 30% to 66%, and the drinking rate of females is 2% to 7%. Chinese and American cardiovascular epidemiology Cooperative studies have shown that male continuous drinkers have a 40% increased risk of developing hypertension within 4 years than non-drinkers.
Overweight and obesity (30%):
The average body mass index (kg/m2) of Chinese people is 21 to 24.5 for middle-aged men and 21 to 25 for middle-aged women. The difference in body mass index has a significant effect on blood pressure levels and the prevalence of hypertension in the population, such as blood pressure levels in Chinese population. The prevalence of hypertension and high blood pressure in the north is low in the north, and the regional difference is very large. Parallel to the difference in body mass index, prospective studies in 10 groups of patients in China show that hypertension is determined every 1 to 5 years after the increase of body mass index at baseline. The risk of [SBP 21.3 kPa (160 mmHg) or DBP 12.7 kPa (95 mmHg)] increased by 9%. The Sino-US Cardiovascular Epidemiology Collaborative Study showed that hypertension occurred every 3 to 4 years after the increase in body mass index at baseline [SBP Women who are 18.7 kPa (140 mmHg) or DBP 12.0 kPa (90 mmHg), or taking antihypertensive drugs, increase the risk by 57% and men by 50%, indicating that the Chinese population has a lower body mass index than the Western population, but overweight and obesity remain It is a risk factor for the onset of hypertension, and the mean body weight index and overweight rate of the population have increased in the past 10 years.
Occupation and environment (10%):
Engage in a highly concentrated occupation, long-term mental stress, long-term environmental noise and poor visual stimuli are prone to essential hypertension.
(two) pathogenesis
1. Pathophysiology of hypertension
(1) Hemodynamic changes: The main factors affecting arterial blood pressure are left hemodynamics, peripheral vascular resistance and other hemodynamic variables, so any factors that can directly or indirectly affect cardiac output or increase peripheral resistance, Can lead to an increase in arterial blood pressure.
1 Primary hypertension and cardiac output: The study observed an increase in cardiac output in patients with early essential hypertension or critical hypertension. The causal relationship between this increase and hypertension is still unclear. Some people think that cardiac output The increase precedes the rise in blood pressure, which is the result of increased cardiac output, but some facts do not support this view. For example, in anemia, hyperthyroidism and other diseases, cardiac output increases, but blood pressure tends to be normal. And in patients with essential hypertension, after the use of -blocker propranolol, cardiac output decreased rapidly, but did not affect arterial blood pressure, so the increase in cardiac output itself is not enough to maintain high blood pressure, but in The initiation mechanism of elevated blood pressure may play an important role.
2 changes in peripheral resistance: the so-called peripheral resistance refers to the blood flow resistance of small arteries and arterioles, a large number of clinical observations show that in young patients with essential hypertension, high flow - normal resistance type, and In elderly patients, low-flow-high-resistance type is the main study. It is found that a variety of hypertension have an early increase in cardiac output, and then the peripheral resistance increases, and the systemic blood flow returns to normal.
With the development of the disease, left ventricular hypertrophy may occur under long-term stress, the total peripheral resistance increases in the patients with essential hypertension, and the cardiac output is relatively reduced, while those without heart failure are centripetal hypertrophy and the ventricular cavity is small. On the contrary, high cardiac output is eccentric hypertrophy, ventricular cavity is large, in addition, the viscosity of whole blood is also the ventricular afterload, is one of the main determinants of peripheral resistance, and therefore, is also an important cause of left ventricular hypertrophy .
(2) RAA system and hypertension: The renin-angiotensin-aldosterone (RAA) system is one of the most important blood pressure control systems in the body. It has long been considered that the renin-angiotensin system is a circulating endocrine system. System, recent studies have found that not only in the kidney, but also in some extrarenal tissues such as the adrenal gland, heart, blood vessel wall, etc., there are also renin-like substances. Using molecular biology techniques, we discovered the messenger ribose of renin and its substrate in the above organs. Nucleic acid (mRNA), further confirming that renin and its substrate can be synthesized in local tissues, locally produced renin, angiotensin can strongly regulate tissue function through autocrine and paracrine , including the function of blood vessels.
1RAA system composition and its metabolic changes: renin is secreted by the paraglomeral cells, and an inactive angiotensin I (ATI) is produced by glomerular circulation in the circulation with the plasma substrate angiotensinogen. The latter is converted to angiotensin II (ATII) by the invertase, and the ATII is then converted to angiotensin III (ATIII) by ammoxidase, and finally decomposed into inactive substances and excreted by the kidneys.
The role of the 2RAA system: The physiological effect of ATII is the most important function of the RAA system. ATII is the most potent hormone in the known endogenous booster substance, and its pressurization effect is 5-10 times stronger than norepinephrine. It plays a key role in maintaining blood pressure and blood volume balance. The main functions of ATII are: A. The effect on the cardiovascular system. ATII is a powerful vascular smooth muscle contraction agent, which is the most important cause of hypertension. The role of the adrenal gland, ATII is the main hormone that stimulates and controls the secretion of aldosterone. It also stimulates the adrenal medulla to secrete catecholamines. C. The role of the kidneys, ATII can cause strong contraction of the renal arteries, reducing renal blood flow and reducing urine output.
3 In the case of ischemia and hypoxia: the kidney can secrete a variety of hormones that increase blood pressure, mainly the secretion of a large amount of renin by the cells of the glomerulus. Through the activity of the RAA system, a large amount of ATII and ATIII are produced, which is secreted by the kidney. Angiotensinase, which can destroy ATII, is greatly reduced. Excessive ATII and ATIII cause systemic small arteriolar spasm, increased aldosterone secretion, and sodium and water retention, which form high blood pressure, which in turn causes renal fine arterial lesions, aggravating Renal ischemia, such interaction, and blood pressure continue to increase, recent studies suggest that the pathogenesis of hypertension caused by renal disease is not entirely through the activities of the RAA system, and may also secrete prostaglandin A2 in the renal medulla. The lack of E2 is associated with a decrease in the amount of blood vessels that dilate blood vessels such as kallikrein and bradykinin.
(3) NO system and hypertension: In recent years, the nitric oxide (NO) system has played a role in the development of hypertension, and NO is an important molecule regulating vascular basal tone and blood pressure, Malinski et al. (1993) in experimental animals. A NO synthase (NOS) inhibitor was found, and L-NAME arginine methyl ester (L-NAME) inhibited the NOS-induced pressor response in the brain; calcium chloride stimulated NOS to induce a hypotensive response, Dubey et al. (1996) reported in large In the early stage of rat renal hypertension (week 2), the content of NO2-/NO3-(NO metabolites) in the blood was higher than normal, and then gradually decreased to the level before the fifth week, Krukoff et al. (1995) reported. At the 3rd week of renal artery stenosis in renal hypertensive rats, the expression of NOS mRNA in the hypothalamus decreased, while the expression of the ventrolateral medulla of the medulla increased and the expression in the medulla oblongated. These results indicate that the NO system changes and hypertension in hypertensive rats. The length of occurrence has a certain relationship. The increase of NO synthesis in early stage of hypertension may be a compensatory response to elevated blood pressure to delay the development of blood pressure. The decline of NO synthesis in the late stage may be due to the gradual adaptation to high blood pressure or persistently high Blood pressure causes endothelial cell damage, Yal Lampalli et al. (1993) also confirmed in the pregnant mouse experiment that the NO synthase inhibitor L-NAME can cause an increase in systolic blood pressure in pregnant mice.
2. Relationship between pregnancy and essential hypertension
(1) The effect of pregnancy on high blood pressure: Pregnancy has no effect on hypertension, because women with primary hypertension and pregnancy are mostly younger and have a shorter course of disease. Heart, brain and kidney lesions are not very obvious. During pregnancy, due to the effect of progesterone levels, smooth muscle relaxation, peripheral vascular resistance decreased, one third of patients in the second trimester of blood pressure dropped to normal, but generally increased to the pre-pregnancy level in the last few weeks, although the blood pressure drop in the second trimester is beneficial to the mother, However, due to the lowering of blood pressure, the perfusion of the uterus placenta is reduced, so it is unfavorable to the fetus. The cardiovascular system changes due to pregnancy in the third trimester, such as an increase in blood volume (an average increase of about 35%), an increase in cardiac output, and an increase in the burden on the heart. Increased blood pressure.
(2) The effect of hypertension on pregnancy: mild to moderate essential hypertension has little effect on the mother during the whole pregnancy, but the increase in blood pressure is not good for the fetus, and some even endanger the mother's life.
1 Intrauterine growth retardation, abortion and stillbirth: The effect of primary hypertension combined with pregnancy on the fetus is related to blood flow through the uterus placenta, intrauterine growth retardation and maternal hypertension, decreased blood volume, changes in uterine placental blood vessels Related, the heavier the hypertension, the smaller the placenta, the more severe the intrauterine growth retardation. If the pregnancy-induced hypertension is more serious, the fetal morbidity and mortality are 5 times higher than those without the comorbidity. Essential hypertension The incidence of intrauterine growth retardation in gestational pregnancy is about 9%, which is caused by changes in placental function. The placenta is usually smaller than expected, due to the supply of the corpus callosum in the decidual space, which hardens and enters the interstitial blood flow. Decreased, the ability of the placenta to maintain normal function, fetal growth is affected, causing miscarriage, premature delivery or fetal death, the prognosis of the fetus is related to the mother's blood pressure, the higher the blood pressure before pregnancy, the higher the blood pressure during the second trimester, the higher the blood pressure at the end of pregnancy High, urine protein appears, and pregnancy-induced hypertension or fundus vascular changes have reached level 2 or above, fetal prognosis is poor, live baby chances are small, blood Abortion is less likely to occur when the pressure is lower than 21.3/13.3 kPa (160/100 mmHg). For example, if the blood pressure is higher than 21.3/13.3 kPa (160/100 mmHg), the fetal mortality is significantly increased, and the blood pressure is higher than 26.7 kPa/14.7 kPa (200/110 mmHg). The chance of a baby is no more than 50%.
2 placental abruption: about half of patients with placental abruption have vascular disease, primary hypertension with pregnancy, vasospasm, sclerosis, decreased uteroplacental perfusion, increased risk of placental abruption, increased fetal and maternal mortality The incidence of placental abruption depends on the course of hypertension and the severity of the disease. In patients with mild comorbid hypertension, the incidence of placental abruption is 0.45% to 1.9%. Patients with severe hypertension with comorbidities, placenta The incidence of early exfoliation is 2.3% to 10%. Patients with primary hypertension and pregnancy complained of abdominal pain, which should be paid attention to. Exclusion of placental abruption by clinical strict monitoring and ultrasound-assisted examination.
3 pregnancy-induced hypertension: primary hypertension with pregnancy, the incidence of pregnancy-induced hypertension is about 25%, which is more serious than normal pregnant women with pregnancy-induced hypertension, symptoms appear early, rapid progress, rapid deterioration of renal function, treatment Ineffective.
4 primary hypertension combined with pregnancy also increased the risk of cerebrovascular accident, postpartum hemorrhage, renal failure and so on.
Prevention
Pregnancy with prevention of essential hypertension
Work and rest, maintain adequate and good sleep, sleep 10 ~ 12h at night, rest for 1 ~ 2h at noon, to avoid and eliminate tension, appropriate use of a small amount of tranquilizer (such as diazepam 2.5mg, oral). Avoid excessive mental and physical loads. For patients with moderate or severe hypertension or those with persistent target organ damage, competitive sports should be avoided, especially for isometric exercise. Reduce sodium intake (sodium chloride is limited to 1.5 to 3.0 g / d), maintain adequate potassium, calcium and magnesium intake in the diet. Weight-controlled, obese mild hypertensive patients often reduce blood pressure to normal by reducing body weight, and can reduce weight and antihypertensive medications for obese patients with moderate or severe hypertension. Other risk factors for controlling arteriosclerosis, such as smoking, increased blood lipids, etc.
Complication
Pregnancy with complications of essential hypertension Complications hypertensive crisis hypertensive encephalopathy coma
complication:
1. Hypertensive crisis (hypertensivecrisis).
2. Hypertensive encephalopathy (hypertensive encephalopathy).
Symptom
Pregnancy with symptoms of essential hypertension Common symptoms Pregnancy-induced hypertension edema vertigo blood pressure high dizziness more drink head swelling dull pain polyuria hair
Essential hypertension can be divided into two types according to the onset of disease and the progress of the disease and the length of the disease. The former is also called benign hypertension. The majority of patients belong to this type, and the latter It is called malignant hypertension, which accounts for only 1% to 5% of patients with essential hypertension.
Slow-onset hypertension
Most of them are onset after middle age. The age of onset of family history can be lighter, most of the onset is hidden, the disease progresses slowly, the course of disease is long, the blood pressure of early patients fluctuates, the blood pressure is high when normal, and it is stage of fragility hypertension. Mental stress, emotional fluctuations are prone to increase blood pressure, rest, after removing the above factors, blood pressure can often fall to normal, with the development of the disease, blood pressure can gradually increase and tend to persist or fluctuations, primary The symptoms of high blood pressure often vary from person to person, depending on the stage of the disease. Most of the early symptoms are asymptomatic or the symptoms are not obvious. Even when physical examination or blood pressure is measured for other reasons, there is no consistent relationship between the symptoms and the elevated blood pressure. This may be related to advanced neurological dysfunction, and a small number of patients are diagnosed with primary hypertension when complications occur in the heart, brain, and kidneys.
(1) Brain performance: headache, dizziness and head swelling are common neurological symptoms of essential hypertension, and may also have heavy head or neck tightening. Headache is a common symptom of hypertension, which occurs mostly in the morning, washing your face. Or after breakfast, relieved, increased after exercise or mental exhaustion, located in the forehead, occipital or ankle, and is beating, mostly persistent dull or pulsating pain, and even bursting pain, these patients have diastolic blood pressure How much is high, headache can be relieved after antihypertensive drug treatment, dizziness is the most common symptom of hypertension, some are transient, often appear suddenly when squatting or standing up, some are persistent, dizziness is patient's The main pain lies in the persistent dull discomfort in the head. In severe cases, it hinders thinking, affects work, and loses interest in surrounding things. When there is hypertensive crisis or vertebrobasilar insufficiency, it can occur with inner ear vertigo. Similar symptoms can be alleviated after antihypertensive drugs, but be aware that sometimes too much blood pressure can cause dizziness.
Acute cerebrovascular disease complicated by essential hypertension is collectively called cerebrovascular accident (stroke, also known as stroke), which can be divided into two categories:
1 ischemic infarction, including atherosclerotic thrombotic cerebral infarction, lacunar infarction, cerebral embolism, transient ischemic attack and untyped.
2 bleeding, according to the bleeding site basal ganglia hemorrhage, cerebral hemorrhage, brain stem hemorrhage, cerebellar hemorrhage and ventricular hemorrhage, most cerebrovascular accidents only involve one side of the hemisphere and affect the contralateral body activity, about 15% can occur in The brain stem affects both sides of the body. The light ones only have dizziness, dizziness, blindness, aphasia, difficulty in swallowing, slanting of the mouth, and limbs are not working or even hemiplegia, but can gradually recover within a few minutes to several days. Hemiplegia of the limbs, skewed mouth, vomiting, incontinence, followed by coma, deep breathing with a voice, pupil size, slow or disappeared response, loose sputum or pathological signs, increased neck resistance in some patients It can also only appear coma without central nervous system localization, severe cases of coma rapidly deepen, blood pressure drops, irregular breathing, tidal breathing (Reyne-Stokes breathing), etc., can die within hours to days, coma is not deep It can be gradually awake in a few days to several weeks, but some clinical symptoms can not be fully recovered, leaving different degrees of sequelae, cerebral hemorrhage is urgent, often Emotional, forced lifting or bowel movements, sudden rise due to sudden rise in blood pressure, the condition is generally heavier, the incidence of cerebral infarction is also urgent, cerebral arterial thrombosis is slow, mostly occurs during rest or sleep Often, there are dizziness, numbness, aphasia and other symptoms, and then gradually hemiplegia, generally no coma or only shallow coma.
(2) Cardiac performance: The heart is the first to be affected by left ventricular diastolic function, diastolic compliance decreases in left ventricular hypertrophy, active relaxation and filling function are affected. Hypertensive heart disease with clinical symptoms occurs frequently After the onset of hypertension for several years to more than ten years, in the heart function compensation period, in addition to feelings of heart palpitations, other cardiac symptoms may not be obvious, when the compensatory dysfunction, there may be left heart failure symptoms, the earliest performance For paroxysmal dyspnea at night, then an acute urgency during heavy physical activity, and finally dyspnea in a lighter physical activity or even resting state, sitting position, severe swell, or sudden increase in blood pressure, pulmonary edema, repeated or Sustained left heart failure can affect right ventricular function and develop into whole heart failure. There are symptoms such as oliguria, edema, loss of appetite, etc. Before the heart is enlarged, there is no special finding in the physical examination, or only pulse or apex beat. Strong, the second heart sound in the aortic valve area is hyperthyroidism. After the heart is enlarged, the physical examination can find the heart to the left and expand downward. The apex beats strong and powerful, and is lifted. The apical period and/or aortic valve area can hear the systolic murmur of grade II-III systolic murmur. The apical area murmur is caused by left ventricular enlargement leading to relative mitral regurgitation or dysfunction of mitral papillary muscle. Aortic valve area murmur is caused by aortic dilatation, resulting in relative aortic stenosis. The second heart sound in the aortic valve area can be metallic tones due to hard changes of the aorta and valve. It can have a fourth heart sound. Heart rate increases during heart failure. Fast, there is a cyanosis, the apex area can smell the galloping, the second heart sound of the pulmonary valve area is enhanced, the wet sounds of the lungs appear at the bottom of the lungs, and there are alternating veins. When the right heart failure is combined, the jugular vein is engorged and the liver is large. Positive jugular vein regurgitation, lower extremity edema, ascites and cyanosis.
Because high blood pressure can promote atherosclerosis, some patients may have angina pectoris and myocardial infarction due to coronary atherosclerotic heart disease (CHD).
(3) Kidney performance: Uncontrolled patients with essential hypertension have renal lesions, and there is no clinical manifestation in the early stage. Proteinuria occurs first with the progress of the disease, such as heart failure and diabetes. The total amount of 24h urine protein rarely exceeds 1g. When the blood pressure is high, the amount of protein in the urine increases, but generally does not exceed 3.5g. There may be a small amount of red blood cells and granular casts in the urine, and the renal tubules are sensitive to ischemia, kidney. Impaired concentrating function, polyuria, nocturia, thirst, polydipsia, etc., the urine specific gravity gradually decreased, and finally fixed at 1.010 or so, said isotonic urine, when the renal function is further reduced, the amount of urine can be reduced, blood Non-protein nitrogen, creatinine, and urea nitrogen are often increased, and the urea clearance rate or creatinine clearance rate can be significantly lower than normal. The above changes are aggravated with the increase of renal lesions, and eventually uremia occurs.
2. Rapidly advanced hypertension
In the untreated patients with essential hypertension, about 1% can develop into rapid hypertension, the incidence can be more rapid, or a history of slow-onset hypertension with different disease duration before the onset, the ratio of male to female is about 3: 2, more common in 40 to 50 years old, patients with obvious visual impairment, severe headache, beating, often located in the occipital or forehead, more common in the morning, blood pressure increased significantly, diastolic blood pressure continued at 17.3 ~ 18.7kPa (130 ~ 140mmHg ) or higher, various symptoms are obvious, fibrin-like necrotic lesions of small arteries progress rapidly, often severe brain, heart, kidney damage, cerebrovascular accident, heart failure and uremia occur within a few months to 1-2 years Symptoms, due to the most significant kidney damage, often with persistent proteinuria, 24h urine protein up to 3g, hematuria and tubular urine, due to hemolysis and disseminated intravascular hemolysis in small arteries, may have hemolytic anemia and bleeding.
Examine
Pregnancy with examination of essential hypertension
Blood routine
Erythrocytes and hemoglobin are generally not abnormal, but rapid hypertensive patients may have Coombs test (antiglobulin test) negative microvascular hemolytic anemia, with abnormal red blood cells, increased hemoglobin blood viscosity.
2. Urine routine and renal function
Mild hypertension has no abnormalities in urine routine and renal function tests. In patients with hypertension, kidney function can be significantly affected during pregnancy. In the middle and late pregnancy, proteinuria can be observed. When the renal concentrating function is impaired, the urine specific gravity gradually decreases. Impaired to a certain extent, blood urea nitrogen and creatinine began to rise, phenol red excretion test, urea clearance rate, endogenous creatinine clearance rate, etc. can be lower than normal.
3. Other inspections
Hypertensive patients may be accompanied by serum total cholesterol, triglyceride (triglyceride), increased low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, and often have elevated blood glucose and hyperuricemia, some patients with plasma kidney The activity of angiotensin II is elevated.
4. Chest X-ray examination
Visible aorta, especially the ascending part, the aortic arch is prolonged, there may be dilation, the descending part can also be dilated, there is a left ventricular enlargement when there is hypertensive heart disease, and the left ventricular enlargement is more obvious when there is left heart failure, and see Signs of pulmonary congestion, when the heart failure, the left and right ventricles are enlarged, and when the pulmonary edema is seen, the hilar is obviously congested, showing a butterfly-shaped blurred shadow.
5. ECG
Electrocardiogram in left ventricular hypertrophy can show left ventricular hypertrophy or both strains, sometimes P wave widening, incision, Pv1 terminal potential potential increase, etc., may have arrhythmia such as ventricular premature contraction, atrial fibrillation, etc. .
6. Echocardiography
Echocardiography is the most sensitive and reliable means of diagnosing left ventricular hypertrophy. The ventricular septum and/or left ventricular posterior wall thickness >13 mm is left ventricular hypertrophy, or by measuring left ventricular mass index, male >134 g/m2, female > 110g/m2 is left ventricular hypertrophy. The left ventricular hypertrophy is mostly symmetrical in primary hypertension, but about 1/3 is mainly ventricular septal hypertrophy. The ventricular septal hypertrophy often appears first, suggesting that hypertension is the first. Influencing the left ventricular outflow tract, although the systolic function of the left ventricular hypertrophy is normal, but the left ventricular diastolic compliance has decreased, the left ventricular inflow tract Doppler spectrum E peak and A peak ratio inverted, after the emergence of left heart failure Echocardiography can detect the left ventricle, enlarge the left atrium, and weaken the contraction of the left ventricular wall.
7. Fundus examination
The central retinal arterial pressure was measured to increase, and the following fundus changes were observed at different stages of the disease progression. Grade I: retinal arterial spasm; grade II: retinal arteriosclerosis, arteriovenous cross compression; grade III: grade II plus retinopathy ( Fundus hemorrhage or cotton-like exudation); Grade IV: Grade III plus optic disc edema.
Diagnosis
Diagnosis and diagnosis of pregnancy complicated with essential hypertension
diagnosis
When the blood pressure continues to be higher than the normal range and can exclude symptomatic hypertension, it can be diagnosed as hypertension. It is necessary to be cautious in the diagnosis of early patients. It is necessary to review blood pressure several times to avoid stress, emotional or physical activity. The temporary increase in blood pressure is misdiagnosed as early hypertension. For patients with doubts, it should be diagnosed after a period of observation. In addition, refer to urine routine, cardiac X-ray, electrocardiogram, echocardiography, fundus Check and assist in the diagnosis of plasma renin activity.
Differential diagnosis
Pregnancy-induced hypertension
Because pregnancy with primary hypertension, about 30% of patients with pregnancy-induced hypertension, it is sometimes difficult to make a difference with pregnancy-induced hypertension, pregnancy-induced hypertension often occurs after 20 weeks of pregnancy, often accompanied by early lower extremity edema and Increased blood pressure; often accompanied by varying degrees of proteinuria, generally no cast; most of the fundus has arterial spasm; arteriovenous ratio can be changed from normal 2:3 to 1:2 or 1:4; often around the fundus artery floc Exudation, even retinal edema, retinal detachment, fundus hemorrhage and insomnia; blood pressure returned to normal 3 to 6 weeks after delivery, patients with primary hypertension are generally older, more common in 35 to 40 years old, have high blood pressure before pregnancy, or Early pregnancy has increased blood pressure, often with a family history of hypertension, blood pressure still does not drop 3 months after delivery, no proteinuria in urine test, no abnormal renal function, fundus examination mainly for arteriosclerosis, and severe tuberculosis can be found in urine.
2. Renal hypertension
Primary cases of nephropathy, such as diabetes, polycystic kidney disease, glomerulonephritis, etc., since childhood, there have been eyelid edema, proteinuria and hypoproteinemia, etc., primary hypertension without the above history, onset Older age, fundus examination has primary hypertension, fundus vascular disease, urine culture, urine test can also be identified.
3. Primary aldosteronism
It is caused by adrenal tumor or adrenal hyperplasia, with sodium retention and hypokalemia, long-term blood pressure, hypokalemia, high blood sodium, and reduced urine specific gravity.
Cushing syndrome
For adrenal hyperfunction, increased blood pressure caused by excessive secretion of cortisol, determination of plasma cortisol, urinary 17-hydroxycorticosteroid levels can help diagnose.
5. Pheochromocytoma
Tumors of the chromaffin cells of the adrenal gland can be identified by B-ultrasound, CT and hematuria, and catecholamine examination.
6. Aortic coarctation
Pregnancy with congenital aortic coarctation is a rare case, and its clinical manifestations and auxiliary examination are not difficult to distinguish from primary hypertension. Congenital aortic coarctation is characterized by high blood pressure in the upper limbs and low or low blood pressure in the lower limbs. And the upper limb blood pressure is higher than the lower limbs, forming an abnormal upper and lower limb blood pressure difference [normal lower limb position lower limb blood pressure 2.7 ~ 5.4kPa (20 ~ 62mmHg) higher than the upper limb], lower limb arterial pulsation weakened or disappeared, there is a sense of cold and fatigue, Upper body hypertension can cause headache, dizziness, tinnitus, insomnia and other symptoms, systolic vascular murmur can be heard in the chest and back, in the interscapular region, the sternum, the ankle and the middle and upper abdomen, there may be collateral circulation The thick arteries compress the symptoms of nearby organs, such as compression of the spinal cord and cause paralysis of the lower extremities. Chest X-rays may show that the ribs are notched by the circumflex artery erosion, and pre-pregnancy aortic angiography can establish a diagnosis.
7. Renal artery stenosis
The etiology is congenital, inflammatory, atherosclerotic, inflammatory is more common in women under the age of 30, diastolic blood pressure is present, severe fixation is increased, high-pitched contraction can be heard at the upper abdomen or back rib angle - Diastolic or continuous murmur, venous pyelography showed delayed delivery of contrast agent on the affected side.
