19:10,12,Mar,2006 | (364/0/0) | Original

system compensates for respiratory alkalosis


(4), adrenal insufficiency (Addison's disease): one due to renal blood flow decreased, reducing filtration buffer substance, the formation of titratable acid less; the other hand, the reduction of Na reabsorption, NH3, and H of the excretion is reduced, because the Na reabsorption and excretion of NH3 and H there is an exchange relationship between the.
3. Extrarenal loss of alkaline intestinal juice, pancreatic juice and bile in the [HCO3-] were higher than in plasma [HCO3-] levels. Therefore, when diarrhea, intestinal fistula, intestinal decompression attract such, it can be lost due to a large number of [HCO3-] caused by the normal class of high blood chloride AG metabolic acidosis. Sigmoid anastomosis of ureter can also lose a lot of HCO3-which led to this type of acidosis, the mechanism may be passive reabsorption of Cl-and HCO3-lot discharge, that is, Cl - HCO3-exchange result.
4. Acid or medication intake or enter into too much acid chloride formation in the liver can break down ammonia and hydrochloric acid, expectorant course of time with this large amount can cause acidosis. NH4Cl → NH3 + H + Cl-. For the normal class of high blood chloride AG metabolic acidosis. Prolonged use of calcium chloride can also cause such a large amount of acid poisoning, the mechanism is less Ca absorption in the intestine, and accompanied by Cl-and H were absorbed more than the amount of Ca, Ca in the intestines and can buffer One of the HPO4 = base combine to make HPO4 = absorption decreased. Ca can also be combined with the H2PO4-generation does not absorb the Ca3 (PO4) 2 and H, and H with Cl-and is absorbed.
Salicylic acid preparations such as aspirin (acetylsalicylic acid) in the body can quickly break down into salicylic acid, which is a organic acids, consumption of plasma HCO3-, induced increase in class normal serum chloride AG metabolic acidosis.
Methanol poisoning because formic acid generated in vivo metabolism of methanol, can cause severe acidosis, and some case reports of blood pH can be reduced to 6.8. Drinking or industrial alcohol, methanol or methanol as the alcohol consumption may cause poisoning. Of 1987, there had been a large number of poisoning cases. In addition to methanol poisoning hazard to other outside, AG increased chlorine type normal blood metabolic acidosis of acute poisoning is one of the important causes of death. NaHCO3 active role in this rescue the truth.
Acidic foods such as protein metabolism eventually form sulfuric acid, keto acids and, of course, no problem in normal subjects. But when the renal dysfunction, high-protein diet may lead to metabolic acidosis. This is kind of normal blood chloride increased AG metabolic acidosis.
Amino acid infusion solution or hydrolyzed protein solution is excessive, may cause metabolic acidosis, especially in amino acid hydrochloride, in the metabolism to break down the HCl. Preparation of these solutions when the pH values were adjusted to 7.4, but its
hydrochloride salt can be decomposed in hydrochloric acid metabolism that still require attention. Clinically, the patient under the circumstances to add a certain amount of truth in this NaHCO3.
5. Dilution acidosis, a large number of input saline can dilute the body Cl-HCO3-and to increase, thus causing the normal class of high blood chloride AG metabolic acidosis.
(B) regulate the body's compensatory
Body metabolic acidosis, the aforementioned set of regulatory agencies will play a compensatory regulation. Such as to maintain the pH value within the normal range called compensatory metabolic acidosis, pH value was lower than the normal limit of decompensated metabolic acidosis.
1. Buffer extracellular fluid extracellular acidosis [H] increases, immediate reaction buffer. The buffer base in the largest number of HCO3-in this example, the reaction is as follows:
H + HCO3-→ H2CO3 → H2O + CO2 ↑
CO2 by breathing to enhance the discharge, HCO3-reduced.
2. Respiratory compensation [H] increases, the Laji medullary respiratory center, carotid body and aortic body chemoreceptors, cause breathing deepened to speed up, increase alveolar ventilation, and expel more CO2.
3. Extracellular ion exchange H into the cell, K out to the cell. H-ion cells with the buffer substance in the Pr-, HPO4 =, Hb-binding and so are buffered. H also cation exchange with bone buffering.
4. Kidneys of non-compensatory metabolic acidosis caused by renal dysfunction, who, by renal compensation. Row of three forms of renal acid are enhanced.
(1) row of H increased, HCO3-reabsorption strengthen: acidosis, renal tubular epithelial cells increased carbonic anhydrase activity, generating an increase in H and HCO3-, H secretion into the lumen, Na and HCO3-exchange accompanied by the re-absorption. Obviously this is a row of acid base security process.
(2) NH4 excretion increased: acidosis, renal tubular epithelial cells increased NH3, NH3 may be produced at this time of substrate, such as easy access to the mitochondrial glutamine metabolism in sake. NH3 diffusion into the lumen, combined with H generated NH4, combined with anion from the urine. This is the main form of renal row of H, so the compensatory role of big. This process is accompanied by an increase in NaHCO3 reabsorption.
(3) increase in titratable acid excretion: renal tubular acidosis, increased secretion of epithelial cells in H, can form more acid phosphate.
Na2HPO4 H → NH2PO4 + Na
(Discharge) (with HCO3-reabsorption)
Na2HPO4 and more with a H discharge, but also have increased reabsorption of sodium bicarbonate. Na2HPO4 that is, the amount of titratable acid.
Decompensated metabolic acidosis, acid-base balance of the index to reflect changes as follows:
pH ↓ CO2C.P. ↓
S.B. ↓ B.B. ↓
A.B. ↓ B.E. increased negative
AG AG is not measured by an increase of negative ions increased
No increase in negative ions were not determined not to increase BG
(C) the impact on the body
Metabolic acidosis on the cardiovascular and nervous system affected. In particular, severe acidosis, the rapid development of these two important because when dysfunction of the system and cause death. Chronic acidosis also affect the skeletal system.
1. Cardiovascular system dysfunction: H-ion concentration, the cardiovascular system can occur following changes:
(1) before capillary sphincter in [H] increases, the response of catecholamines decreased, and thus relaxation expansion; but venules and small veins are not so sensitive, so still some [H] remain within the limits of the original caliber. Song after song before this micro-vascular non-state, resulting in capillary volume expanding, change thy blood less, blood pressure, severe shock can occur.
(2) reduced cardiac contractility, stroke volume decreased. Ca normal receptor binding and troponin calcium is an important step in myocardial contraction, but in H and Ca acidosis inhibits Ca competition of this combination, it decreased myocardial contractility. Can increase the microcirculation, can also be aggravated due to lack of oxygen existing acidosis.
(3) arrhythmia: When the extracellular [H] is increased, H into the cell for the K, the potassium concentration and hyperkalemia, causing arrhythmia. In addition acidosis renal tubular epithelial cells increased row H, competitively inhibits the row K, is also one of the mechanisms of hyperkalemia. Then there are renal failure caused by acidosis, hyperkalemia is more serious. Performance of such arrhythmia heart block and ventricular fibrillation.
2. Nervous system dysfunction; metabolic acidosis nervous system dysfunction, mainly for depression, severe drowsiness or coma can occur. Its pathogenesis may be related to the following factors: (1) acidosis in the brain glutamic acid decarboxylase activity increased, so the increase in γ-aminobutyric acid generation, the substance can inhibit the central nervous system: (2) acidosis reduced biological activity of oxidative enzymes, oxidative phosphorylation is thus reduced, ATP generation are reduced, and thus brain energy supply.
3. Skeletal system changes: chronic metabolic acidosis, such as chronic renal failure, renal tubular acidosis, there can be prolonged for several years, due to the constant release of calcium from the bones, bone growth and development of children and can cause rickets and osteitis fibrosa. Osteomalacia may occur in the adult disease.
In addition to these three main areas of impact, other issues such as respiratory function has also changed. In metabolism due to inhibition of the activity of many enzymes and metabolic disorders.
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system compensates for respiratory alkalosis

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Traditional Chinese Medicine
Respiratory alkalosis names of diseases: respiratory alkalosis respective areas: the systemic treatment department: Department of Endocrinology, Department of Hematology, Department of Emergency Surgery, symptoms and signs: headache, coma, sensory disturbances, respiratory disorders, respiratory alkalosis respiratory alkalosis Introduction
Respiratory alkalosis is the primary of the PCO2 decreased (<4.67kPa) and higher pH values (> 7.45) characterized by respiratory alkalosis and hypocapnia, respiratory alkalosis cause of knowledge: one, the spirit of hyperventilation This is a common cause of respiratory alkalosis, respiratory alkalosis, but the symptoms of a .: clinical manifestations】 【PCO2 as reduced inhibition of the respiratory center, . respiratory alkalosis in the examination: PH value of blood gas analysis increased, PaCO2 decreased. The differential diagnosis of respiratory alkalosis: a clear diagnosis of the disease, without identification. Prevention of respiratory alkalosis: The best preventive measure is to be actively seized of the primary disease. Covering the nose and mouth with a paper bag . the complications of respiratory alkalosis: a common complication of the disease is acute respiratory distress syndrome. The treatment of respiratory alkalosis: treatment 【】 1, positive control of the original disease. 2, lower sick children . Expert Q & Gynecology Oncology Medicine Men Mental eye surgery medicine more>> similar symptoms and respiratory alkalosis disease desquamative interstitial pneumonia with chronic lead poisoning, strychnine poisoning the water of aortic dissection excessive rabies trachea, bronchial stenosis of carotid body tumor surgical trauma cryptococcosis nasal septum perforation of nasal septum perforation stone disease I have visited Peking University expert interviews about FINDING Men Zhi Xiuyi prevention of prostatitis, Professor Professor Xiao Dan talk about how science Professor Shen Lin quit smoking about c
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