high blood pressure
Introduction
Introduction The blood pressure of normal people fluctuates within a certain range with the changes of internal and external environment. In the whole population, the blood pressure level gradually increases with age, and the systolic blood pressure is more obvious. However, after 50 years old, the diastolic blood pressure shows a downward trend, and the pulse pressure also increases. . In recent years, people's understanding of the multiple risk factors of cardiovascular disease and the protection of heart, brain and kidney target organs has been deepened, and the diagnostic criteria for hypertension have been constantly adjusted. It is currently considered that patients with the same blood pressure have different risk of cardiovascular disease. Therefore, with the concept of blood pressure stratification, that is, patients with different cardiovascular risk, the appropriate blood pressure level should be different. When the doctor faces the patient, based on the reference standard, the patient's most suitable blood pressure range is judged according to his specific situation, and targeted treatment measures are adopted.
Cause
Cause
genetic factors:
About 75% of patients with essential hypertension have a genetic predisposition, and hypertensive patients in the same family are often concentrated. Essential hypertension is believed to be a polygenic genetic disease. It has been reported that hypertensive patients and patients with a family history of hypertension and normal blood pressure have transmembrane electrolyte transport disorders, and there is a hormone-like substance in the serum that inhibits Na+/K+-ATPase activity, resulting in a decrease in sodium-potassium pump function. The concentration of Na+ and Ca2+ in the cells increased, the contraction of SMC in the arterial wall was strengthened, the density of adrenergic receptors increased, and vascular reactivity was enhanced. These all contribute to the increase in arterial blood pressure. Recent studies have found that angiotensin (AGT) gene may have 15 defects, and normal blood pressure is dysfunctional, while hypertensive patients have the same variation in three specific parts of the AGT gene. A brother or sister with high blood pressure can obtain the same copy of the parent's AGT gene. In patients with hypertension with this genetic deficiency, plasma angiotensinogen levels were higher than those in the control group.
Dietary electrolytes:
In general, people with high daily salt intake have a higher percentage of blood pressure or an average blood pressure higher than those with low salt intake. In the WHO measures to prevent hypertension, it is recommended that the daily salt intake per person should be controlled below 5g. A study of the relationship between electrolytes and blood pressure in a total of 53 centers in 32 countries showed that the average urine sodium level in Chinese population was 206 mmol/24 h, 43 mmol/24 h higher than other centers, and the urinary sodium/potassium ratio reached 6.7. More than twice the center. The highest sodium urate is Tianjin (242mmol/24h). This is related to the high sodium and low potassium of Chinese diet. Potassium can promote sodium excretion, and eating a lot of vegetables can increase potassium intake, which may protect the arteries from the adverse effects of sodium. Calcium can alleviate the effect of sodium on the pressurization. The general diet in China is low calcium, which may aggravate the effect of sodium/potassium on blood pressure. Intervention studies that increase dietary calcium intake have shown that an increase in calcium causes blood pressure to decrease in some patients.
Social psychological stress:
According to the survey, psychosocial stress is closely related to the onset of hypertension. Stressful life events include: early death, loss of love, widowhood, death of family members in car accidents, sickness, family breakdown, economic and political shocks, etc. The prevalence of hypertension in people who were motivated by life events was higher than that in the control group. It is believed that psychosocial stress can alter the hormone balance in the body and thus affect all metabolic processes.
Kidney factor:
Renal medulla interstitial cells secrete antihypertensive lipids such as prostaglandins, antihypertensive neutral renal medullary lipids and other secretion disorders, and sodium dysfunction may be related to the onset of hypertension.
Neuroendocrine factors:
It is generally believed that the excitability of the sympathetic nerve fibers of the arterioles is an important neurological factor in the pathogenesis of this disease. However, there are two types of sympathetic ganglion fibers:
1 vasoconstrictor fiber, the neurotransmitter is neuropeptide Y (NPY) and norepinephrine.
2 vascular fiber, the transmitter is calcitonin gene related peptide (CGRP) and substance P. The imbalance of these two fibers, that is, the former is more powerful than the latter, causes blood pressure to rise. In recent years, the relationship between central neurotransmitters and neuropeptides, as well as various regulatory peptides and hypertension, has become a very active research field. It has been reported that CGRP may inhibit the release of norepinephrine in the hypothalamus of rats, and it may inhibit the release of norepinephrine when stimulated by adrenal nerves in the periphery. It has been reported that the isolation of natriuretic peptides (types A, B and C) from mammalian hearts and brains suggests that there is a family of natriuretic peptides in the human body. Recent advances in the local renin-angiotensin system (RAS) have made new progress. The mouse renin gene (Ren-2 gene) was injected into rat egg cells through a microinjection device to form a transgenic rat germline TGR (mREN2) 27, which has extremely high blood pressure. Northern blot hybridization confirmed that the Ren-2 transgene was expressed in the adrenal gland, blood vessels, gastrointestinal tract and brain, and could be expressed in the thymus, reproductive system and kidney. Due to its expression in the blood vessel wall, angiotensin formation in blood vessels may be increased, resulting in hypertension and vascular SMC hypertrophy.
Examine
an examination
Related inspection
Blood pressure, urine routine blood atrial natriuretic peptide (ANP), spironolactone test, systolic blood pressure
First, determine whether there is high blood pressure: measuring blood pressure should be measured several times for several consecutive days of blood pressure, more than two times higher blood pressure, can be said to be high blood pressure.
Second, the reasons for the identification of high blood pressure: Where patients with hypertension, should be asked in detail about the medical history, comprehensive systemic examination to rule out symptomatic hypertension.
Laboratory tests can help diagnose and classify essential hypertension, understand the functional status of target organs, and are also conducive to the correct choice of drugs during treatment, hematuria, kidney function, uric acid, blood lipids, blood sugar, electrolytes (especially potassium ), ECG, chest X-ray and fundus examination should be used as routine examinations for patients with hypertension.
(A) blood routine: red blood cells and hemoglobin generally no abnormalities, but acute hypertensive patients may have Coombs test negative microvascular hemolytic anemia, with abnormal red blood cells, high hemoglobin increased blood viscosity, prone to thrombosis complications ( Including cerebral infarction) and left ventricular hypertrophy.
(2) Urine routine: the urine of normal patients is normal, the urine specific gravity is gradually decreased when the renal concentrating function is impaired, and there may be a small amount of urinary protein, red blood cells, and occasional cast type. As the renal lesion progresses, the amount of urine protein increases, and benign renal sclerosis For example, if the 24-hour urine protein is above 1g, the prognosis is poor, and the red blood cells and casts can also be increased. The tube type is mainly transparent and granules.
(3) Renal function: blood urea nitrogen and creatinine are used to estimate renal function. There is no abnormality in early patient examination. The renal parenchyma can be increased to a certain extent, and adult creatinine is >114.3mol/L. Elderly and pregnant. >91.5mol/L suggests renal damage, phenol red excretion test, urea clearance rate, endogenous creatinine clearance rate, etc. can be lower than normal.
(4) Chest X-ray examination: visible aorta, especially liter, bow flexion prolonged, its ascending, arch or descending can be expanded, there is left ventricular enlargement in hypertensive heart disease, left left heart failure Room enlargement is more obvious. When the heart is exhausted, the left and right ventricles are enlarged, and there are signs of pulmonary congestion. When the pulmonary edema is seen, the lungs are obviously congested with a butterfly-shaped blurred shadow. Comparison.
(5) Electrocardiogram: ECG in left ventricular hypertrophy may show left ventricular hypertrophy or both strains. The criteria for electrocardiogram diagnosis of left ventricular hypertrophy are not the same, but the sensitivity and specificity are not much different. The false negative is 68% to 77%. , false positive 4% ~ 6%, visible ECG diagnosis of left ventricular hypertrophy is not very sensitive, due to left ventricular diastolic compliance decreased, left atrial diastolic load increased, ECG can appear P wave widening, concave, Pv1 The negative value of the terminal potential increases, etc., the above performance may even appear before the left ventricular hypertrophy found in the electrocardiogram, there may be arrhythmia such as ventricular premature beats, atrial fibrillation and so on.
(6) Echocardiography: It is currently considered that compared with chest X-ray examination and electrocardiogram, echocardiography is the most sensitive and reliable means for diagnosing left ventricular hypertrophy. M-mode ultrasound curves can be recorded on the basis of two-dimensional ultrasound localization or directly from Two-dimensional images were measured. The ventricular septum and/or ventricular wall thickness >13 mm was left ventricular hypertrophy. In hypertensive patients, left ventricular hypertrophy was mostly symmetrical, but about 1/3 was mainly ventricular septal hypertrophy. (The ratio of ventricular septum and left ventricular posterior wall thickness > 1.3), ventricular septal hypertrophy often appears first, suggesting that the left ventricular outflow tract is the first to affect hypertension, and other cardiac chambers, valves and aortic roots can be observed by echocardiography. The condition can be used for heart function testing. Although the overall function of the heart such as cardiac output and left ventricular ejection fraction is still normal in the early stage of left ventricular hypertrophy, there is a decline in left ventricular systolic and diastolic compliance, such as myocardium. The maximum rate of contraction (Vmax) decreased, the isovolumic diastolic phase was extended, the mitral valve was delayed, and so on. After left heart failure, echocardiography revealed left ventricle, enlarged left atrium, and decreased left ventricular wall contractile activity.
(7) Fundus examination: The measurement of arterial pressure in the central retina is observed to increase, and the following fundus changes can be seen at different stages of the development of the disease:
Grade I: Retinal artery spasm
Grade II A: mild retinal artery sclerosis
Grade II B: Significant sclerosis of the retinal artery
Grade III: Grade II plus retinopathy (bleeding or exudation)
Grade IV: Grade III plus optic papilledema
(8) Other examinations: Patients may be accompanied by an increase in serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, and a decrease in high-density lipoprotein cholesterol, and a decrease in apolipoprotein A-I, and often have an increase in blood glucose. Hyperuricemia, plasma renin activity, and angiotensin II levels are elevated in some patients.
Diagnosis
Differential diagnosis
According to the recommendations of the World Health Organization (Who), the blood pressure standard is: normal adult systolic blood pressure should be less than or equal to 140mmHg (18.6kPa), and diastolic blood pressure is less than or equal to 90mmHg (12kPa). That is, the systolic blood pressure is between 141-159 mmHg (18.9-21.2 kPa) and the diastolic blood pressure is between 91-94 mmHg (12.1-12.5 kPa), which is a critical hypertension. When diagnosing high blood pressure, blood pressure must be measured multiple times. At least two consecutive two consecutive diastolic blood pressures of 90 mmHg (12.0 kPa) or more can be diagnosed as hypertension. Only one elevated blood pressure can not be diagnosed, but need to be followed up.
According to the difference in blood pressure, hypertension is divided into 3 levels:
Grade 1 hypertension (mild): systolic blood pressure 140~159mmHg; diastolic blood pressure 90~99mmHg.
Grade 2 hypertension (moderate): systolic blood pressure 160~179mmHg; diastolic blood pressure 100~109mmHg.
Grade 3 hypertension (severe): systolic blood pressure 180 mmHg; diastolic blood pressure 110 mmHg.
Simple systolic hypertension: systolic blood pressure 140mmHg; diastolic blood pressure <900mmHg.
Staging of hypertension:
The first phase: blood pressure to diagnose the level of hypertension, clinical unintentional, brain, kidney damage signs.
The second phase: blood pressure to determine the level of hypertension, and one of the following:
1 physical examination, X-ray, electrocardiogram or echocardiogram showing left ventricular enlargement;
2 fundus examination, general or partial stenosis of the fundus artery;
3 proteinuria or plasma creatinine concentration increased slightly.
The third phase: blood pressure to determine the level of hypertension, and one of the following;
1 cerebral hemorrhage or hypertension encephalopathy;
2 heart failure;
3 renal failure;
4 fundus hemorrhage or exudation, with or without optic nerve head edema;
5 angina pectoris, myocardial infarction, cerebral thrombosis.
Differential diagnosis
Primary hypertension, secondary hypertension, renal vascular hypertension, white coat hypertension, and pregnancy-induced hypertension are identified.
