Clinical manifestations
According to the onset and progression of the disease, it can be divided into the slowly progressive type and the acutely progressive type, with the slowly progressive type being the most common.
I. Slowly progressive hypertension
(I) Early manifestation Early stage is mostly asymptomatic, or after nervousness, emotional excitement or exertion, dizziness, headache, blurred eyes, tinnitus, insomnia, weakness, lack of concentration and other symptoms, with the progress of the disease blood pressure continues to rise, organ involvement. Wang Mengjie, Department of Cardiovascular Medicine, People’s Hospital of Guangxi Zhuang Autonomous Region
(II) Brain manifestations Headache and dizziness are common.
Hypertensive crisis, mostly induced by emotional excitement, excessive fatigue, climate change or discontinuation of antihypertensive drugs. Acute increase in blood pressure, severe headache, blurred vision, palpitations, shortness of breath, pallor, tinnitus, vertigo, excessive sweating and acute cardiac, cerebral and renal insufficiency may occur, which should be treated rapidly by lowering blood pressure. If the sudden increase in blood pressure causes acute cerebral circulatory dysfunction, resulting in cerebral vasospasm, cerebral edema, and increased intracranial pressure, it is called hypertensive encephalopathy, which is a subacute attack, and it takes about 24-48 hours from the onset to the obvious symptoms. Severe headache, visual impairment, nausea, vomiting, convulsions, coma, transient hemiparesis, aphasia, etc. Small arterial spasms, optic nerve papillary edema, hemorrhage and exudate are seen in the fundus. The cerebrospinal fluid pressure is elevated, and the headache and impaired consciousness may improve significantly after 1-2 hours of antihypertensive treatment.
(C) Cardiac manifestations Causes of cardiac hypertrophy. Formation of hypertensive heart disease. In the early stage, the heart function is compensated and the symptoms are not obvious; in the later stage, the heart function is not compensated and heart failure occurs.
(iv) Renal manifestations Long-term hypertension causes small renal artery sclerosis. When renal function is reduced, it can cause nocturia, polyuria, urine containing protein, tubular and red blood cells. Low urinary concentration function, phenol red excretion and urea contouring disorders. Azotemia and uremia appear.
(v) Arterial changes An aortic coarctation aneurysm may form. It is one of the rare but serious comorbidities of hypertension.
(vi) Fundus changes Early retinal artery spasm and arterial thinning. Later, it develops into retinal artery stenosis and sclerosis, and arteriovenous cross-compression. Fundus hemorrhage or cotton wool exudate. Optic nerve papillary edema is a grade IV change.
Acute hypertension, also known as malignant hypertension, can be suddenly transformed from the slow-onset type, or it can start as a malignant type.
It can occur at any age, but is most common in the 30-40 age group. Blood pressure is significantly elevated, with diastolic blood pressure mostly above 17.3 Kpa (130 mmHg), with symptoms such as weakness, thirst, and polyuria. Visual acuity decreases rapidly, and there are retinal hemorrhages and exudates in the fundus of the eye, often with bilateral optic nerve papillary edema. Proteinuria, hematuria and renal insufficiency appear rapidly. Heart failure, hypertensive encephalopathy and hypertensive crisis may also occur, and the disease progresses rapidly and most die from uremia.
The diagnosis of malignant hypertension can be divided into two groups: Group A should have four conditions that
①Diastolic blood pressure persistently above 17.3Kpa (130mmHg).
②Fundus changes grade IV.
③Sharply progressive renal dysfunction (progression to renal failure at six months).
④Blood pressure and renal function deterioration were mostly accompanied by brain symptoms and heart failure. group B
①Diastolic blood pressure of 16 Kpa (120-130 mmHg).
② Grade III fundus of the eye.
③Renal dysfunction. The rest of the conditions are the same as group A.
Stages of hypertension
Stage I Blood pressure reaches the level of confirmed hypertension, without clinical signs of heart, brain or kidney damage.
Stage II Blood pressure reaches the level of confirmed hypertension, and one of the following is present
(1) Physical examination, X-ray, electrocardiogram or echocardiogram shows enlarged left ventricle.
(ii) Fundus examination with generalized or localized narrowing of the arteries in the fundus.
③Proteinuria or mildly elevated plasma creatinine concentration.
Stage III Blood pressure reaches the level of confirmed hypertension with one of the following;
①Brain hemorrhage or hypertensive encephalopathy.
②Heart failure.
③Renal failure.
④ Bleeding or exudation from the fundus of the eye with or without optic nerve papillary edema.
⑤ angina pectoris, myocardial infarction, cerebral thrombosis.
Diagnosis and differential diagnosis
I. Determine the presence or absence of hypertension
II. Identify the causes of hypertension Exclude symptomatic hypertension
(A) renal disease
1. renal parenchymal lesions
2. Renal artery stenosis
(Pheochromocytoma 90% occurs in the adrenal medulla, the rest occurs in the sympathetic ganglion and chromophobic tissues in other parts of the body. Due to the secretion of catecholamines by tumor cells, it can cause high blood pressure and metabolic disorders, manifested as paroxysmal or persistent hypertension with paroxysmal aggravation. It may be characterized by a rapid rise in blood pressure, severe headache, palpitations, shortness of breath, excessive sweating, pallor, tachycardia, elevated blood glucose, nausea, and weakness for several minutes or days, with intervals of normal blood pressure. Urinary epinephrine, norepinephrine or its metabolite 3-methyl-4 hydroxy bitter amygdalin (VMA) is measured during the period of increased blood pressure, and a significant increase is suggestive of pheochromocytoma.
A phentolamine blood pressure test may be performed during the period of increased blood pressure. A decrease in systolic blood pressure of more than 4.66 Kpa (35 mmHg) and diastolic blood pressure of more than 3.33 Kpa (25 mmHg), diluted with phentolamine 5 mg and 90 ml of glucose solution, and maintained for 3-5 minutes is considered positive. In normal subjects and patients with hypertension, the drop in blood pressure with phentolamine generally does not exceed 4 Kpa (30 mmHg). Interictal, normal blood pressure, can do histamine excitation test, with histamine phosphate 0.01-0.02mg intravenous injection, if no response, can increase the dose.
After injection, blood pressure is measured every minute for 15 minutes. The blood pressure of patients with this disease can rise within 2 minutes after injection. If the systolic blood pressure rises more than the original level of 8Kpa (60mmHg) or more, and the diastolic blood pressure rises more than 5.3Kpa (40mmHg) and lasts more than 5 minutes, it is positive, suggesting the possibility of this disease, also can do glucagon test, fasting in the morning, intravenous injection of glucagon 1mg, after that, blood pressure is measured once every minute for 15 minutes, the judgment criteria are the same as the tissue test. This method has fewer side effects and fewer false positives. Intravenous pyelogram and retroperitoneal inflatable angiography can show the tumor site, and ultrasound or computed tomography (CT) scan has the value of determining the diagnosis and tumor localization.
2.Primary aldosteronism This disease is mostly seen in adult women with chronic elevated blood pressure accompanied by intractable hypokalemia. Hyperkalemia occurs due to hypertension caused by increased secretion of aldosterone by adrenal cortical hyperplasia or tumor, and hypokalemia occurs due to massive potassium excretion by the kidneys. Neuromuscular dysfunction, paroxysmal or persistent muscle weakness or paralysis. Long-term massive potassium loss can lead to tubular vacuole-like degeneration, renal concentration dysfunction, polyuria, nocturia, irritability, and polyhydramnios. Blood potassium ≤ 33.24 mmol/24h (12ug/24h), normal 17 hydroxysteroids, reduced plasma renin activity, positive anisotropic test, adrenal scan or CT examination, which can reveal occupying lesions in the adrenal area, give objective evidence for the diagnosis of this disease.
3.Cortisolism Due to adrenal cortex hyperplasia or tumor, excessive secretion of glucocorticoid hormone, water and sodium retention resulting in increased blood pressure, centripetal obesity, full-moon face, hairiness, thin skin and purple lines, and elevated blood sugar. With the following special manifestations, the general diagnosis is not difficult. To confirm the diagnosis of the disease, further evidence of excessive cortisol secretion or loss of its normal circadian rhythm, i.e., higher than normal secretion in the morning and no lower than normal or higher than afternoon secretion levels in the evening and midnight.
The 24-hour urinary 17 hydroxysteroids and 17 ketosteroids are increased, the dexamethasone suppression test and the adrenocorticotropic hormone excitation test are positive, and the pteronamine is enlarged on X-ray cranial examination in some hyperplastic cases. Perinephric inflatable angiography is also available to aid in the diagnosis.
(iii) Toxemia of pregnancy Occurs in the second trimester of pregnancy (3-4 months) or during labor and delivery and within 48 hours after delivery. It is characterized by hypertension, edema and proteinuria. In severe cases, convulsions and coma. If increased blood pressure is detected early in pregnancy, it may be hypertensive disease or secondary hypertension combined with pregnancy. Most often a history of hypertension with milder urinary protein can be distinguished. However, in patients with hypertension, hypertension and urinary alterations can often worsen during pregnancy, and there are also statistics that show that in patients with hypertension combined with pregnancy, about 30%, gestational toxemia occurs, which can be considered in the diagnosis.
(iv) Vascular lesions Congenital aortic constriction, mostly seen in adolescents, more in males than females. Clinical manifestations are high blood pressure in the upper extremities and lower blood pressure in the lower extremities, creating a paradoxical upper high and lower low phenomenon. Due to insufficient blood supply to the lower extremities, there may be weakness and coldness in the lower extremities. A vascular murmur can be heard in the aortic auscultation area and interscapular region. Chest X-ray may show cut marks on the ribs due to erosion of arteries from the intercostal collateral circulation. Aortogram may clarify the diagnosis.
Multiple aortitis is a nonspecific inflammation of the aorta and its branches, which can lead to narrowing of the lumen of the diseased vessel. If the lesion affects the aorta, high blood pressure in the upper extremities and low blood pressure in the lower extremities may also be seen. If the lesion spreads to the renal artery, it leads to renal vascular hypertension, and a vascular murmur can be heard in the corresponding part of the stenosed vessel, and angiography can clarify the diagnosis.
(E) Cranio-cerebral diseases Intracranial tumor, encephalitis, cranio-cerebral trauma and other causes of increased intracranial pressure, can cause hypertension, due to the manifestations of the nervous system, generally not difficult to diagnose.