Hypertensive crisis in the elderly
Introduction
Introduction to hypertension crisis in the elderly Hypertensive crisis refers to the primary and secondary hypertension in the process of disease development, under certain incentives, the peripheral arterioles are temporarily strong, causing a sharp rise in blood pressure and a sharp deterioration of the disease. And complications of severely impaired function of the main target organs such as the heart, brain, and kidney caused by hypertension. In addition, if the diastolic blood pressure is higher than 18.3 to 19.6 kPa (140 to 150 mmHg) and/or the systolic blood pressure is higher than 28.8 kPa ( 220mmHg), regardless of symptoms, should be considered a hypertensive crisis. basic knowledge The proportion of sickness: 0.01% Susceptible people: the elderly Mode of infection: non-infectious Complications: Hypertensive encephalopathy
Cause
The cause of hypertension in the elderly
Mental stress (20%):
If the elderly are exposed to strong external stimuli for a long time, they are prone to hypertension. That is to say, when the elderly are nervous, emotional, sad, sad and other unhealthy factors that are not stimulated for a long time, the cerebral cortex will be disordered and the process of excitability will be disordered, and the cortical dysfunction will be lost, thus losing the subcortical blood vessels. The regulation of central and sacral function causes an increase in systemic arteriolar spasm and peripheral vascular resistance, resulting in elevated blood pressure.Endocrine disorders (10%):
The organ regulation disorder in the elderly increases the adrenaline and norepinephrine secreted by the adrenal medulla. These two substances can make the peripheral arterioles in the body contract, the lumen narrows, and the blood flow resistance increases, thus making the blood pressure rise. High, deoxycorticosterone, aldosterone, cortisol and other hormones secreted by the adrenal cortex cause blood pressure to rise by allowing sodium and water to be stored and affecting vasomotor function.Increased renin secretion (28%):
Renal source is also known as renin-angiotensin-aldosterone theory. Renin is a renal endocrine hormone that is secreted when renal vascular functional or organic changes cause renal ischemia. After renin enters the blood circulation, angiotensin I and angiotensin II and III are formed through the action of a series of biochemical substances in the liver and lung. The latter two can cause paralysis of the surrounding small arteries and increase blood pressure. Angiotensin II and III act on the spheroidal band of the adrenal cortex, which promotes the increase of aldosterone secretion, causing sodium retention and blood volume, edema of the blood vessel wall, and increased peripheral resistance, which also promotes blood pressure. Elderly hypertensive patients with low renins may be a physiological response to increased blood pressure. Renal arteriosclerosis in the elderly impairs sodium-sparing ability, causing sodium retention and increased blood volume, and the decrease in the number of beta receptors reduces the sensitivity of circulating catecholamines, which is caused by feedback of arterial pressure to inhibit renin release.Genetic factors (25%):
Hypertension has a certain relationship with heredity. According to statistics from relevant scholars, one in the parents has hypertension, and 28% of the children have the disease; both parents have hypertension, and about 40% to 45% of their children may have essential hypertension.Excessive salt (10%):
It is currently believed that excessive intake of salt per day is prone to hypertension. The reason is that sodium ions in the salt can penetrate into the small arteries, causing the small arterial lumen to shrink, and the blood flow resistance to increase, thereby causing paralysis of the small arteries and raising blood pressure. Clinical and epidemiological data have also confirmed the prevalence of people with high prevalence in areas with high salt intake (such as Japanese) and those with low salt intake (such as Eskimos in Alaska). It is very low.Pathogenesis
The mechanism of occurrence of hypertensive crisis is considered by most scholars to be due to the influence of predisposing factors, such as renin, angiotensin II, norepinephrine and arginine vasopressin in blood circulation. A sudden and sudden increase in the active substance causes the kidney to swell and the small arteries of the ball to contract or expand. If this condition persists, in addition to a sharp increase in blood pressure, it can also lead to stressful polyuria, which in turn causes a decrease in circulating blood volume. The decrease in volume and reflexivity cause angiotensin II, an increase in the production and release of norepinephrine and arginine vasopressin, which leads to dangerous levels of vasoactive substances and vasotoxic substances in the circulating blood, thereby aggravating renal artery contraction. Due to the contraction of the arterioles and the dilation of the dilatation zone, it is a "sausage string"-like change, causing damage to the intima of the arterioles and platelet aggregation, resulting in the further release of harmful substances such as thromboxane, the formation of platelet thrombosis, causing tissue ischemia, lack of Oxygen, increased capillary permeability, accompanied by microvascular coagulation, punctiform hemorrhage and necrotizing arteriitis, to the brain and Visceral damage is most obvious, arteriosclerotic blood vessels are particularly prone to spasm, and exacerbate small intima hyperplasia, thus forming a pathological vicious circle (Figure 1), in addition, sympathetic hyperactivity and excessive secretion of vasopressor active substances Not only causes contraction of the renal arterioles, but also causes spasm of the small arteries around the whole body, resulting in a sudden increase in peripheral vascular resistance, which further raises blood pressure, and a hypertensive crisis occurs at this time.
Pathophysiology: Vascular injury of hypertensive hypertension mainly includes intimal hyperplasia and fibrinoid necrosis. The degree of intimal hyperplasia is related to the severity and time of hypertension. In the past, hypertensive encephalopathy was mainly due to progressive cerebral vasospasm and deficiency. Blood, currently considering the breakthrough of cerebral arterioles, leading to excessive perfusion, increased cerebral blood flow and body fluids through the blood cerebrospinal fluid barrier into the perivascular tissue, in patients with chronic hypertension, due to long-term adaptation to higher pressure, through sympathetic Neuromodulation thickens the wall. When MAP reaches a dangerous level of 23.8 kPa (180 mmHg), the previously contracted cerebral vessels suddenly expand due to the inability to withstand high pressure, first occurring in areas of lower muscle tone and then generally expanding. Under high pressure, cerebral vascular hyperperfusion, tissue fluid leaked into the perivascular tissue leading to cerebral edema, followed by hypertensive encephalopathy clinical syndrome.
The above studies can explain some clinical signs:
1 Those with normal blood pressure and sudden high blood pressure often have hypertensive encephalopathy such as acute glomerulonephritis and pregnancy-induced hypertension syndrome at relatively low blood pressure levels. It may be that the cerebral blood vessels of these patients have not formed like chronic In the hypertensive patients, the arterial wall is thickened, and at this time, the upper limit of the automatic regulation has not risen.
2 patients with chronic hypertension are not prone to hypertensive encephalopathy unless their blood pressure is high.
3 Chronic hypertension patients often can not tolerate rapid hypotension and dizziness, fatigue and other symptoms of severe orthostatic hypotension.
4 Further increase in cerebral blood flow methods such as inhalation of CO2 will aggravate the clinical symptoms of hypertensive encephalopathy.
5 Animal experiments have shown that the autoregulatory function of cerebral blood vessels is lost during cerebral thrombosis. With the increase of blood pressure, the damaged brain tissue is over-perfused, causing cerebral edema and compressing normal brain tissue. The above is caution for patients with hypertensive stroke. Antihypertensive provides an important clinical basis. In short, hypertensive encephalopathy is the consequence of progressive hypertension, which is caused by the failure of the blood-brain barrier and cerebral blood flow regulation and protection measures. Hypertensive encephalopathy can occur in any type of hypertension. However, it is more common in patients with normal blood pressure and sudden onset of hypertension, such as acute glomerulonephritis, when accompanied by renal dysfunction, prone to hypertensive encephalopathy.
Prevention
Elderly hypertensive crisis prevention
1, to avoid animal fat, high sugar, high salt, excessive drinking and so on.
2, must lose weight. In addition to controlling diet, you should also pay more attention to walking and proper exercise.
3, must quit smoking, because smoking can cause arteriosclerosis.
4, from the prevention of hyperlipidemia, to adjust the diet structure.
5. When you feel emotionally excited in your daily life, your blood pressure will suddenly rise. In order to make your blood pressure stable, you should pay attention to the psychological balance and emotional adjustment.
6, the middle and old people remember four principles: reasonable diet, moderate exercise, smoking cessation, alcohol, mental health. This can effectively prevent the occurrence of hypertension.
Complication
Hypertensive crisis in the elderly Complications hypertensive encephalopathy
Acute left heart failure can be combined, and hypertensive encephalopathy can be complicated in severe cases.
Symptom
Hypertensive crisis symptoms in the elderly Common symptoms Increased intracranial pressure, intracranial hemorrhage, fatigue, drowsiness, dyspnea, sudden death, increased heart rate, coma, irritability, anxiety
These diseases are collectively referred to as hypertensive emergencies. In 1984, the International Joint Commission divided them into two categories, requiring immediate treatment and allowing them to fall to the required target level in the short term. In 1997, JNCVI was unified as a hypertensive crisis. Hypertensive crisis is classified into hypertensive emergency and sub-acute according to target organ damage and whether immediate antihypertensive therapy is required.
Hypertensive emergencies: Hypertension with acute progressive target organ lesions, diastolic blood pressure 18.3 kPa (130 mmHg), requiring immediate antihypertensive therapy (but does not need to fall to the normal range) to prevent or reduce the target Organ damage, often need intravenous medication, mainly including: 1 hypertensive encephalopathy.
2 rapid/malignant hypertension with heart, brain, kidney, and fundus damage.
3 hypertension combined with intracranial hemorrhage / subarachnoid hemorrhage.
4 hypertension combined with acute renal failure.
5 hypertension combined with acute left heart failure / pulmonary edema.
6 hypertension combined with unstable angina and acute myocardial infarction.
7 acute aortic dissection aneurysm.
8 eclampsia.
9 pheochromocytoma, etc., as shown in Table 1.
Hypertensive urgencies: also known as hypertensive urgency, refers to a sharp increase in blood pressure without acute target organ damage, allowing blood pressure to be reduced within a few hours, does not necessarily require intravenous medication, may allow oral medication, Mainly include:
1 rapid advance / malignant hypertension without heart, brain, kidney, fundus damage.
2 pre-eclampsia.
3 perioperative hypertension and so on.
Common elderly hypertensive emergencies are as follows:
Hypertensive encephalopathy
(1) Hypertensive encephalopathy is defined as a series of clinical manifestations of acute blood circulation disorder, which causes cerebral edema and increased intracranial pressure during the course of hypertension. As long as blood pressure is significantly increased in any type of hypertension, Can cause hypertensive encephalopathy, but clinically more common in patients with normal blood pressure and sudden onset of hypertension, such as acute glomerulonephritis, pregnancy-induced hypertension syndrome, etc., also occur in acute or severely progressive hypertension Patients with obvious cerebral arteriosclerosis, in addition to sudden increase in blood pressure, often accompanied by severe headache and changes in consciousness, and sometimes physical activity disorders, fundus examination has localized or diffuse retinal arteriospasm, but not necessarily bleeding, exudation Or edema, rapid recovery after antihypertensive treatment, hypertensive encephalopathy is a serious complication in the course of hypertension, is one of the common emergency of internal medicine, should be diagnosed and positive immediately before the occurrence of irreversible brain damage is on the verge of death Rescue treatment, otherwise it will lead to death.
(2) Etiology and pathogenesis: The occurrence of hypertensive encephalopathy mainly depends on the height and the speed of blood pressure. The former is the condition, the latter is an important contributing factor. Hypertensive encephalopathy can be caused by a variety of diseases with hypertension. It is characterized by a long history of hypertension, and hypertension patients with obvious cerebral arteriosclerosis are more likely to occur, it occurs in patients with acute hypertension and severely progressive hypertensive patients, the latter is generally seriously ill, blood pressure Significantly increased blood pressure, which occurs only around 250/150mmHg, but hypertensive encephalopathy can also occur when the blood pressure of patients with acute hypertensive disease does not reach 200/130mmHg. In addition, according to reports in the literature, pregnancy-induced hypertension syndrome, kidney Small ball nephritis, renal artery stenosis, pheochromocytoma and other secondary hypertension as long as the blood pressure is moderately increased, there is also the possibility of hypertensive encephalopathy, rare causes of aortic stenosis and primary aldosteronism and other diseases.
The mechanism of hypertensive encephalopathy is quite complicated, and it is still not very clear. Most scholars believe that its occurrence is related to the dysfunction of the cerebral circulation itself. Under normal circumstances, cerebral blood flow remains constant within a considerable range of blood pressure fluctuations. The size of the cerebral artery is dynamic and has its own characteristics. It does not depend on the regulation of the autonomic nervous system. Instead, the cerebral artery wall directly responds to the relaxation and contraction of blood pressure. When the blood pressure drops, the cerebral arteriole expands to ensure the blood of the brain. The supply will not decrease. When the blood pressure is increased, the cerebral arteries will contract, so that the blood flow in the brain will not be overfilled. This will keep the cerebral blood flow relatively stable, and the fluctuation range is also within the physiological range. There is a limit to the adjustment ability. When the mean arterial pressure exceeds the upper limit of 160 mmHg or lower than the lower limit of 60-70 mmHg, this regulation function of the cerebral arterioles is lost. Hypertensive patients often change the limit of this blood pressure amplitude. There are two kinds of theories about the mechanism of hypertensive encephalopathy:
1 "over-regulatian" or arteriolar sputum theory: animal experiments show that when brain symptoms occur, it is common to have a strong contraction of the small arteries of the brain, and cerebral edema occurs after the sputum. According to this theory, patients An excessive small arterial response to elevated blood pressure, "excessive self-regulation", reduces blood flow to the capillary bed, leading to ischemia of the brain tissue, causing increased capillary wall permeability and rupture of the capillary wall , cerebral edema and punctiform bleeding.
2 Automatic adjustment of "breakthrough" or failure theory: Some people have pointed out that hypertension regulation can not maintain a constant cerebral blood flow, and when the blood pressure reaches a certain upper limit, the automatic adjustment mechanism "breaks", resulting in Increased cerebral blood flow, small arteries can not contract, resulting in increased capillary area, increased osmotic flow through the capillary wall, cerebral edema occurs, in addition, increased capillary pressure, can degeneration and necrosis of the blood vessel wall, and spotted bleeding And microinfarction, it is believed that the occurrence of hypertensive encephalopathy is not mainly the spasm of cerebral arterioles, but the passive or mandatory expansion of the above-mentioned arteries caused by the loss of cerebral blood flow autoregulation, resulting in excessive cerebral blood flow. of.
There are different opinions on the above two kinds of doctrines. At present, there are many small thrombi found in autopsy. It is still the result of cerebral vasoconstriction or other reasons. It is still unclear. Clinical data indicate that some hypertensive encephalopathy In patients with visual impairment or focal epilepsy, the fundus arterioles can be seen at the same time. However, after treatment, the vasospasm is eliminated and the symptoms disappear. This indirectly indicates that cerebral vasospasm exists in this disease. In recent years, most scholars The study concluded that the automatic regulation of cerebral blood circulation or mandatory vasodilation is the main mechanism for the development of hypertensive encephalopathy, and pointed out that cerebral arteriolar spasm is the initial manifestation of autoregulation. When blood pressure rises above the upper limit of mean arterial pressure, the brain The small arteries can no longer contract, and passive or forced expansion will automatically regulate the collapse, so the cerebral blood flow increases, and the brain is over-perfused to produce cerebral edema.
(3) Clinical manifestations:
Symptoms and signs: Hypertensive encephalopathy can be seen as a hypertensive crisis that occurs in the brain. It usually occurs on the basis of the original hypertension, and the blood pressure is further increased suddenly. The blood pressure can reach 200-260/140-180mmHg. The clinical features are mainly a series of manifestations of cerebral edema, increased intracranial pressure and localized brain damage. The course of the disease varies, the elders can last for several days, the short is only a few minutes, the first Symptoms are often diffuse severe headaches. At least a few hours after a headache, or even 1-2 days later, irritability, excitement or lack of consciousness, lethargy or stupor and other disturbances of consciousness, and then further development of confusion, eventually coma, but large Most patients are mainly irritated, such as coma, the degree is not deep, cerebral edema and increased intracranial pressure in addition to headache, often accompanied by jet vomiting, neck stiffness and visual impairment, the latter manifested as hemianopia, black Mongolian, severe cases may have temporary blindness, such as transient brain damage, transient or migratory, localized mental and neurological symptoms and signs, often temporary Sexual hemiplegia, localized convulsions, muscle spasm of the extremities, aphasia and irritations, etc., severe cases of respiratory and circulatory failure such as bradycardia and dyspnea.
2. Intracranial bleeding
(1) intracranial hemorrhage including brain parenchyma, intraventricular and subarachnoid hemorrhage: hypertension is one of the most important causes of intracranial hemorrhage. The relationship between hypertension and cerebral hemorrhage is more related to hypertension and atherosclerosis. Close, high blood pressure cerebrovascular disease may not rule out the possibility of cerebral infarction, on the contrary, if there is no high blood pressure, it is unlikely to be cerebral hemorrhage, the cause of intracranial hemorrhage:
1 vasospasm or vascular occlusion causes brain softening, reducing the supporting force of the perivascular tissue, making the blood vessels easy to rupture.
2 Nourishing blood vessels rupture, forming a small dissection aneurysm in the wall of the small artery. Under high pressure, the blood ruptures into the outer wall and enters the surrounding brain tissue.
3 rupture of miliary aneurysm, but in patients without cerebrovascular disease, miliary aneurysms are rarely found in the brain.
4 vascular functional disorders cause vasospasm of blood vessels, necrosis of the wall of the tube and even capillary and venous bleeding.
(2) cerebral hemorrhage and infarction should be identified before treatment. CT in the brain is helpful for diagnosis. Arterial angiography confirms that there is vasospasm in the bleeding site. Decompression can lead to a decrease in blood perfusion. In this case, it is controversial whether or not blood pressure is reduced. If the local nervous system symptoms are caused or aggravated during blood pressure reduction, the blood pressure should not be lowered too fast or too low.
3. Acute heart failure
Hypertension is one of the most common causes of heart failure. There are two main aspects of hypertension damage to the heart, namely cardiac hypertrophy and coronary artery disease.
(1) Hemodynamic changes in hypertension increase peripheral resistance and excessive ventricular pressure overload, causing ventricular hypertrophy.
The effects of neuroendocrine also play an important role in the development of ventricular hypertrophy. For example, catecholamine, norepinephrine, isoproterenol, and renin-angiotensin system can cause cardiomyocyte hypertrophy, other active substances. Such as serotonin, bradykinin, vasopressin, endothelin and growth regulator are also the causative factors of myocardial cell growth, in addition, proto-oncogene, increased blood viscosity, insulin resistance, etc. are also related to left ventricular hypertrophy, left Ventricular hypertrophy causes diastolic dysfunction and systolic dysfunction. The tolerance to hypertension is significantly different. The cardiac hypertrophy can be compensated for a long time. Once the failure occurs, the blood pressure will gradually decrease.
(2) hypertensive cardiac hypertrophy significantly reduced the coronary circulation reserve, and promoted the thickening of the small coronary artery or coronary artery vascular wall, which caused the diastolic function and systolic function of hypertrophic ventricle, cardiac dysfunction, and hypertension In addition to the sharp increase in blood pressure, the cause of heart failure is infection, overwork, agitation, arrhythmia and electrolyte imbalance. It should be pointed out that in severe heart failure, blood pressure drops due to a significant decrease in cardiac output, so it is often misdiagnosed as Dilated cardiomyopathy.
Hypertension with diagnosis of heart failure: first, according to the symptoms of labor, shortness of breath, nighttime paroxysmal dyspnea, sitting breathing, cough, hemoptysis and fatigue, cerebral hypoxia, with acute left heart failure with lungs The performance of edema, physical signs have increased heart rate, apical diastolic galloping, systolic murmur, both lungs have wet and dry voice, clinical examination has chest X-ray showing left heart enlargement, pulmonary interstitial or alveolar edema, but also Have pleural effusion.
The treatment of hypertensive heart failure is to control blood pressure, reduce stress load; reduce excessive volume load during heart failure, increase cardiac output, and reduce organ congestion.
4. Acute coronary insufficiency, unstable angina and acute myocardial infarction.
Hypertension is one of the main risk factors for coronary heart disease. Atherosclerosis can accelerate development due to hypertension, and promote coronary occlusion faster. Hypertension reduces the reserve function of coronary arteries, mainly due to vascular proliferation. Can not meet the needs of increased left ventricular mass, in addition to atherosclerosis and small arterial wall thickening and stenosis, can also cause myocardial insufficiency, hypertension is the main reason for the formation of coronary atherosclerotic lesions is increased pressure Caused by damage of the intima, lipid deposition, hypertrophic smooth muscle infiltration from the middle layer of the blood vessel to the intima of the injury, causing arterial fibrosis, hypertension can also have a mechanical effect on the structure and metabolism of the arterial wall, in addition, vasoactive substances and The chemical mediators of injury or inflammation also play a role in promoting atherosclerosis and vascular disease of hypertension. Most uncomplicated hypertensive patients can find left atrium and left ventricular enlargement during echocardiography. Clinical manifestations of angina pectoris, myocardial infarction and sudden death, Framingham study showed that the above abnormalities can lead to the risk of coronary heart disease The risk has increased significantly.
Unstable angina or acute coronary insufficiency with or without acute myocardial infarction, sometimes with severe hypertension, SBP up to 240mmHg, DBP>140mmHg, its clinical manifestations resemble pheochromocytoma, after coronary insufficiency Hypertension may be caused by pain or anxiety, and elevated blood pressure increases myocardial load and increases oxygen consumption, aggravating coronary insufficiency, forming a vicious circle, regardless of hypertension triggering coronary insufficiency or post-coronary The trigger of high blood pressure and the extremely high blood pressure will cause the myocardial ischemia or the area of the myocardial infarction to rapidly expand and cause serious complications. Therefore, the blood pressure should be reduced to a safe level as soon as possible.
Accelerated hypertension refers to a sudden increase in blood pressure due to a certain cause, diastolic blood pressure > 17.3 kPa (130 mmHg), retinal lesions in addition to small arteries contraction and sclerosis, as well as retinal hemorrhage and exudation, Keith-Wagener (KW) fundus classification is grade III, acute hypertension is further worsened or rapidly developed by hypertension, diastolic blood pressure 18.7kPa (140mmHg), optic disc edema appears in the fundus, KW fundus grade is grade IV, and the kidney has severe functional damage. It is called malignant hypertension.
Both primary and secondary hypertension can progress to rapid and malignant hypertension, and the renal artery stenosis caused by proximal atherosclerosis of the renal artery should be noted in the etiology of acute and malignant hypertension in the elderly. It can cause renal vascular hypertension, renal artery stenosis leads to renal atrophy, two-dimensional ultrasound can confirm, if necessary, renal angiography can be performed for percutaneous renal angioplasty or revascularization.
Examine
Examination of hypertensive crisis in the elderly
A small amount of protein and red blood cells appear in the urine during the attack, blood urea nitrogen, creatinine, and blood sugar rise.
Fundus examination has retinal hemorrhage and exudation.
Hypertensive encephalopathy auxiliary examination:
Fundus examination
It shows the characteristics of hypertensive fundus, showing that the retinal artery is diffuse or localized with strong sputum, hardening or bleeding, exudation and optic disc edema.
2. EEG examination
There may be localized abnormalities or bilateral synchronous sharp waves, sometimes showing poor rhythm. Due to cerebral edema, extensive slow waves often occur.
3. Cerebrospinal fluid examination
The pressure was significantly increased, and the test results were mostly normal. Occasionally, several red blood cells or white blood cells showed a slight increase in protein content.
Diagnosis
Diagnosis and diagnosis of hypertensive crisis in the elderly
Kaplan proposes the following diseases: acute left ventricular failure, uremia, cerebrovascular accident, subarachnoid hemorrhage, brain tumor, head injury, post-seizure, lupus erythematosus, encephalitis, acute anxiety associated with hyperventilation syndrome, Except for the above-mentioned diseases that cause high blood pressure before the diagnosis of acute and malignant hypertension.
