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(D) morning porridge
Chinese health experts to promote solar terms in the fall 6 porridge every morning, especially in early autumn, in many places is still steaming hot and humid to pay, resulting in domestic demand, the spleen and stomach, decreased immunity, if then eat warm food, especially the drink very good ones for the body, the reason is as important components of medicated rice or glutinous rice, are excellent spleen and stomach, fill in the function of the gas, the previous lot of praise for this. 6 solar terms in the fall, now more respected porridge with sugar porridge, porridge odoratum, Adenophora porridge, porridge and other Polygonatum.
(E) balanced nutrition
Nutritionists point out that only the diversity of food available to the human body can be full of nutrition. Such as cereals, the main supply of energy and vitamin B1; beans and bean products, the main supply of vegetable protein; vegetables and fruits, the main supply of vitamin C, salts and food fiber. Fall should pay attention to the diversity of foods in the diet, nutritional balance, can be added in summer due to hot weather, loss of appetite caused by nutritional deficiencies, in particular, should eat chewy, rich in fiber foods.
Autumn diet regimen should be based on the flavors balanced diet, according to the specific circumstances of the individual, appropriate increase in sweet, bland, sour, eating nourishing food, but not too much.
Food should be slowly, both the full benefit of food digestion and absorption of nutrients completely, but also by intestinal fiber foods to maintain the role of water and chewing, the Student body fluid, to control the fall dry throat, dry bowel The purpose of constipation and other adverse reactions.
(F) should avoid hard dry
In medicine, pain of dry, hard dry goods easily disability allowance of gas consumption. "Q - the five organs produce articles" in the words: "eat bitterness, the paper is issued and hair pulling." Dry autumn seasonal evil, lung as Jiao dirty, dry autumn air with the same, easy to feel Qiuzao evil. Many chronic respiratory disease often start from the autumn of recurrence or gradually increased. Therefore, the "Golden Chamber - animals, fish and insects, and taboos governing the twenty-fourth" in the internal organs of the disease, flavors and the restraint of seasons relationship between the students, asked: "Autumn lung ban not eat hard . lung" point of view. Therefore, health should avoid bitter autumn weather dry diet.
301 Medical Court, Beijing: Beijing 301 Hospital Court Road, Maternal and Child Health Line Court, do people do that is embroidered, Luo Guangbin scissors neither they nor needle work. They are ground with an iron "little knife", the toilet paper carved five yellow five-pointed star . (more) Three
First, the acid-base balance and electrolyte disturbance
Second, changes in the respiratory system
Outside the respiratory dysfunction caused by hypoxemia and hypercapnia in different ways from the impact of respiratory function. PaO2 decreased to stimulate the carotid body and aortic body chemoreceptor reflex increased respiratory movement, a response to the PaO2 below 8kPa (60mmHg) was significantly, causing breathing deepened to speed up; Pa O2 was 4kPa (30mmHg) when the maximum pulmonary ventilation . However, hypoxia has a direct inhibitory effect on the respiratory center, when the Pa O2 less than 4kPa, this effect can be greater than leaving the role of sexual arousal reflex respiratory depression. PaCO2 increased to some extent is an important factor leading to respiratory excitement, PaCO2 major role in the central chemoreceptor and respiratory center caused reflex excitation and accelerated breathing deepened. PaCO2 each additional 0.133kPa (1mmHg), ventilation increased 2L/min. But when the PaCO2 10.7 kPa (80mmHg), then the inhibition of the respiratory center (caused by CO2 Ma * drunk), this time mainly by respiratory motion in patients with low arterial oxygen tension on vascular chemoreceptor stimulation can be maintained. At this point, if the oxygen can only be 24% -30% of inhaled oxygen, so as not to cause a hypoxic fully corrected respiratory depression, hypercapnia increase the leaving condition to worsen.
Respiratory failure caused by respiratory disease itself may lead to changes in the form of respiration. If central respiratory failure, breathing shallow and slow and can demonstrate and rhythm abnormalities (tidal breathing, intermittent breathing, sobbing like breathing, sighing like breathing, etc.). The most common of which is tidal breathing, may be due to a serious decline in the sensitivity of the respiratory center caused by apnea, must rely on blood PaCO2 increased to a certain extent, the respiratory center was caused by short-term cyclical excitement. Increased respiration, increased pulmonary CO2 emitted, when the PaCO2 can be reduced to a certain extent, lead to apnea, so the formation of periodic breathing exercise. In restrictive ventilatory disorders caused by reduced lung compliance leading to breathing shallow and fast, mainly due to stretch receptors or receptors by pulmonary capillary side (juxtapulmonary-capillary receptor, J-receptors) to stimulate the reflex induced . Obstructive ventilatory disorders, the different parts due to obstruction, manifested as difficulty breathing or breath inspiratory dyspnea. Respiratory failure, such as the existence of enhanced respiration long campaign to increase respiratory muscle oxygen consumption, coupled with lack of oxygen supply may lead to respiratory muscle fatigue, decreased respiratory muscle contraction, breathing becomes shallow and fast, was nodding or provide shoulder breathing. Shallow breathing causes further reduction in alveolar ventilation, and increased respiratory failure.
Third, the cardiovascular system
Although hypoxemia and hypercapnia on the heart and blood vessels is inhibited heart activity directly, and to blood vessels to dilate (pulmonary vascular exception). However, mild to moderate lower Pa O2 and Pa CO2 increased by exciting the central cardiovascular exercise, the heart rate, myocardial contractility enhanced peripheral vasoconstriction, with increased respiration to increase venous return, resulting in increased cardiac output . In addition, cardiovascular exercise excitability can be sympathetic to the skin, abdominal visceral vasoconstriction, cerebral and coronary vascular adenosine in local metabolic products such as the expansion under the regulation, which leads to blood flow redistribution to ensure that the vital organs of blood supply. This is particularly evident during acute respiratory failure, and has compensatory significance.
Severe hypoxia and hypercapnia can directly inhibit the cardiovascular center and heart activity, leading to dilation of blood vessels, blood pressure, decreased cardiac contractility, arrhythmia and other serious consequences.
Chronic respiratory failure caused by the consequences of involving the right heart hypertrophy and heart failure, that is, pulmonary heart disease. The pathogenesis of pulmonary heart disease can be summarized as follows: â‘ oxygen and carbon dioxide retention caused by high blood hydrogen ion concentration, through different channels, causing pulmonary vascular endothelium-derived contraction factor (EDCF) and relaxing factor (EDRF) secretion of abnormal contraction of small pulmonary arteries (CO2 itself from the expansion of the role of pulmonary vessels), pulmonary hypertension; â‘¡ long-term contraction of small pulmonary arteries, hypoxia can cause muscle-free muscle of pulmonary arterioles, pulmonary vascular smooth muscle cells and adult fiber cell hypertrophy and hyperplasia, collagen and elastin synthesis, leading to pulmonary vascular wall thickening and hardening, luminal narrowing, resulting in stable chronic persistent pulmonary hypertension; â‘¢ compensatory long-term hypoxia caused an increase in red blood cells disease can increase blood viscosity, increases the pulmonary vascular resistance and increased right heart load; â‘£ some pulmonary inflammatory diseases such as pulmonary artery, pulmonary capillary bed of the extensive damage, pulmonary embolism and other pulmonary hypertension can be reasons; â‘¤ myocardial hypoxia and acidosis to generate energy barrier, the formation of intracellular calcium overload and impede myocardial excitation - contraction coupling process of myocardial Shu, reduced function; â‘¥ breathing difficulties, chest makes the forced expiratory abnormally high pressure, cardiac compression, the diastolic function of the heart, forced inspiratory intrathoracic pressure anomaly is reduced, increasing the negative pressure outside the heart, increase the contraction of right heart load, prompting right heart failure.
Respiratory failure, left heart may also be involved, leading to left ventricular diastolic dysfunction. Pulmonary heart disease patients with decompensated heart function when half of the pulmonary artery wedge pressure increased, indicating that associated with left ventricular dysfunction, which may also be associated with some cases of coronary heart disease; acute respiratory distress syndrome also has half of the deaths occurred left ventricular failure. Thus, the present is generally believed that lung disease involving the left heart can be, and its mechanism is as follows: â‘ hypoxemia and acidosis can also reduce left ventricular contractility; â‘¡ the level of intrathoracic pressure also affect the left heart diastolic function; â‘¢ right heart to expand and push the right ventricular septal thickening of the heart to the left side of the left ventricle can reduce compliance and lead to left ventricular diastolic dysfunction.
Fourth, changes in the central nervous system
Central nervous system most sensitive to hypoxia, when Pa O2 fell 8kPa, may appear slightly impaired intelligence and vision. Such as the Pa O2 decreased rapidly to 5.33 ~ 6.67kPa the following, it will cause a series of neuropsychiatric symptoms such as headaches, anxiety, orientation and memory impairment, mental confusion, drowsiness, resulting in convulsions and coma. PaO2 of patients with chronic respiratory failure is still low as 2.67kPa mind clear, while the PaO2 of patients with acute respiratory failure 3.53kPa to coma. Carbon dioxide retention can be a variety of central nervous system, neuropsychiatric disorders, CO2 retention can cause cerebral vasodilation, increased cerebral blood flow, causing persistent headaches, particularly at night and early morning staggering. When PaCO2 than 10.7kPa, can cause headaches, dizziness, irritability, slurred speech, flapping wing-like tremors, mental confusion, drowsiness, convulsions, respiratory depression, known as carbon dioxide, Ma * drunk.
Respiratory failure caused by a brain dysfunction known as pulmonary encephalopathy (pulmonary encephalopathy). Patients showed conscious indifference, muscle tremors or flapping wing-like tremors, occasional convulsions, lethargy and even coma, may appear reduced or lost tendon reflexes, positive pyramidal tract signs and so on. Type â…¡ respiratory failure as an example, the pathogenesis of pulmonary encephalopathy were:
1. Cerebral vascular effects of cerebral vasodilation â‘ : either acidosis or carbon dioxide retention are the cerebral vasodilation. Pa CO2 increased 1.33kPa (10mmHg) cerebral blood flow increased approximately 50% can. Hypoxic cerebral vasodilation also. â‘¡ the formation of cerebral edema: hypoxia and acidosis but also to vascular endothelial hyperpermeability, leading to the brain interstitial edema; hypoxic cerebral vascular cells to generate ATP decrease of Na-K pump function, which can cause cell Na and water increased, the formation of cell edema; Naochong Xue, edema to increased intracranial pressure, cerebral compression, cerebral anoxia more weight, thus creating a vicious cycle, in severe form can lead to brain herniation. â‘¢ cerebral vascular endothelial injury can still cause intravascular coagulation, which is the incidence of pulmonary encephalopathy one of the factors.
2. â‘ the brain cells of acidosis: the role of the normal cerebrospinal fluid than the blood of the weak buffer, the pH is low (7.33-7.40), P CO2 higher than the arterial blood. Because the blood is not easy by HCO-and H blood-brain barrier into the cerebrospinal fluid, so the latter took longer to adjust pH. Respiratory failure, pH changes in cerebrospinal fluid is more obvious than in the blood. When the cerebrospinal fluid pH below 7.25, the brain wave activity slows down, pH lower than 6.8 the complete cessation of brain electrical activity. The one hand, neurons increase cerebral acidosis activity of glutamate decarboxylase, the inhibitory neurotransmitter Î³-aminobutyric acid formation increased, resulting in central inhibition; the other hand, increased activity of brain phospholipids, the lysosomal enzyme release, causing nerve cells and tissue damage. â‘¡ hypoxic hypoxia on brain cells, see chapter.
Part of the patients showed pulmonary encephalopathy nervous excitement, restlessness, may occur due to metabolic alkalosis. However, acidosis patients were also 1 / 3 of the performance of the neural excitability, the mechanism is unclear.
Fifth, changes in blood system
Occur in patients with chronic respiratory failure erythrocytosis. Due to chronic hypoxia, hypoxia stimulate blood flow through the kidneys and the release of stromal cells to produce erythropoietin, to promote differentiation and maturation of red blood cells, red blood cells increased.
Sixth, changes in renal function
Hypoxia and hypercapnia through reflex sympathetic to the renal vasoconstriction, renal blood flow was severely reduced, the light appears in the urine protein and red blood cells, white blood cells and casts, etc., can occur in severe acute renal failure, there oliguria, azotemia and metabolic acidosis. If no significant changes in renal structure, functional renal failure, as long as the external respiratory fun
Seven changes in the digestive system
Respiratory failure can occur when the gastrointestinal mucosa erosion, necrosis, hemorrhage and ulceration and other diseases, mainly seen in patients with chronic respiratory failure. The mechanism are: â‘ severe hypoxia can stomach blood vessels, can reduce the gastric mucosal barrier function; â‘¡ carbon dioxide retention can enhance the activity of carbonic anhydrase in gastric parietal cells, so that an increase in gastric acid secretion; â‘¢ If patients have disseminated intravascular coagulation, shock, etc., will further aggravate the digestive system ischemia and hypoxia.
Respiratory failure (all) | Overview | Causes and mechanisms | metabolism, functional changes
August 26, 2007 Sunday, 12:01 PM