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Introduction to respiratory acidosis disease is increased in the primary of the PCO2 and pH values decrease as the characteristics of hypercapnia. Actual bicarbonate (AB) is greater than the standard bicarbonate (SB) prompted respiratory acidosis.
Pathogenesis of respiratory acidosis respiratory acidosis is the primary factor in the accumulation of CO2, arterial PCO2 increased, so that the denominator BHCO3/HHCO3 larger causing the blood pH value decreased. Between alveolar ventilation and outside air bad (1) airway obstruction: laryngeal edema, laryngospasm, such as diphtheria, foreign body obstruction, lymph node or tumor compression of the trachea, drowning, amniotic fluid obstruction and hypoventilation during anesthesia or mismanagement Chi breathing machine, may cause acute respiratory acidosis. (2) inhibition of the respiratory center: for example, morphine, barbiturates, narcotics, alcoholism, etc., can inhibit the respiratory center caused by respiratory acidosis (3) respiratory muscle paralysis: potassium deficiency, for example, polio, acute infection of multiple nerve root inflammation, myasthenia gravis, hyperthyroidism of hypokalemic paralysis, paraplegia and so on. (4) chest wall injuries: chest pain or chest wall after injury destabilizing effects of the ventilation, CO2 can not fully exhaled, resulting in respiratory acidosis. Alveolar gas exchange between blood and bad (1), pulmonary diseases: such as pneumonia, pulmonary edema, cardiopulmonary arrest


, etc., can cause acute respiratory acidosis. Emphysema and lung fibrosis, bronchiectasis, chronic bronchitis, due to reduced lung elasticity, decreased alveolar ventilation, not only, but also the lungs are not well mixed gases, often chronic respiratory acidosis. (2) congestive heart failure or pulmonary heart disease: slow down the CO2 emission due to slow circulation, accumulation in the body; another and pulmonary edema or lung disease, can cause respiratory acidosis. 3. Intrapulmonary right to left shunt increased after massive atelectasis, although alveolar collapse, but the alveolar capillary wall is still open to the blood from the pulmonary artery without gas exchange, that is, back to the left heart, arterial blood increased PCO2, PO2 decreased alveolar and arterial oxygen difference increased significantly. Symptoms Symptoms: As in the respiratory acidosis, increased blood H2CO3, lung function can not be compensated from the main row of the buffer system and the kidneys to regulate the acid base security. The main clinical manifestations are so a. difficulty breathing, hypoventilation, dyspnea, cyanosis, chest tightness and headache. b. increased acidosis, changes in consciousness occur, there are drowsiness, confusion, delirium, and coma. c. CO2 excess product storage, in addition to blood pressure decline, there may be sudden ventricular fibrillation (the Na into the cell, K out of cells, acute hyperkalemia). d. test results: those with acute or decompensated blood pH value decreased, PCO2 increased, CO2CP, BE, SB, BB normal or slightly increased; those with chronic respiratory acidosis, or compensatory, pH value decreased obvious, PCO2 increased, CO2CP, BE, SB, BB has increased; blood K can be increased. Clinical manifestations 1. Acute respiratory acidosis respiratory illness at the time, if acute respiratory acidosis, the better to speed up breathing, cyanosis, and tachycardia and other performance drugs or if the respiratory center due to CO2 accumulation was inhibited, it may not breathing deepened to speed up performance. If in surgery anesthesia with endotracheal intubation, inadequate ventilation can be due to the sudden acute respiratory acidosis. When 6.7kPa (50mmHg), the blood pressure increased significantly, PCO2 increased further, the decline in blood pressure but without timely detection, due to acidosis so that the transfer of extracellular K to the excessive and fast, the blood can be acute hyperkalemia disease or cardiac arrest caused by ventricular fibrillation. Therefore, endotracheal intubation anesthesia, if found blood pressure, should be careful to check whether there is bad ventilation may be required to replace the sodium lime. Arterial blood gas analysis showed elevated PCO2, blood pH value decreased, even down to pH 7.0, standard bicarbonate (SB) more than in the normal range, actual bicarbonate (AB) higher than the standard bicarbonate, BBb or BEb reduced (not yet had time to play a compensatory kidney function). Acute respiratory acidosis, mainly through blood and hemoglobin in the buffer is increased by PCO2 1.3kPa (10mmHg), plasma HCO3-increased by about 1mmol / L, limit its compensation formula is expected to: HCO3-= 0.1 PCO2. Even if the PCO2 rose 10.7kPa (80mmHg), plasma HCO3-also increased, but only 4mmol / L Therefore, acute respiratory acidosis, if 30mmol / L, you may as respiratory acidosis with metabolic alkalosis. If AB 24 0.35 PCO2 5.58, may be a chronic respiratory acidosis with metabolic alkalosis, or over-compensation system of the respiratory acidosis. 3. Lung brain syndrome: late in the emphysema (chronic respiratory failure) due to reduced arterial oxygen saturation and CO2 accumulation can cause various neurological symptoms, known as pulmonary syndrome in the clinical manifestations of the brain: headache , vomiting, optic disc edema (increased intracranial pressure) psychotic symptoms, such as excited delirium, drowsiness, coma. sports symptoms such as tremors, convulsions, facial paralysis, hemiplegia, or a brief. Etiology etiology and pathogenesis of dysfunction caused by alveolar ventilation system. A. respiratory center is common in depression, such as narcotics overdose; b. respiratory tract obstruction, such as laryngospasm, bronchospasm, respiratory tract burns, foreign bodies, drowning, neck hematoma, or mass compression of the trachea, etc.; c. lung disease, such as shock lung, pulmonary edema, atelectasis, pneumonia, etc.; d. thoracic injuries: such as surgery, trauma, pneumothorax, pleural effusions. Pathogenesis 1. Respiratory center inhibition of central nervous system diseases, such as extension of the brain tumor, extension of cerebral polio, encephalitis, meningitis, vertebral artery embolism or thrombosis, intracranial pressure, head injury, etc., respiratory center activity can be inhibited, so that ventilation to reduce the CO2 accumulation. In addition, some drugs such as narcotics, tranquilizers, sedatives (morphine, barbital sodium, etc.) have the role of inhibition of respiration, excessive doses can cause hypoventilation. Carbonic anhydrase inhibitors such as acetazolamide can cause metabolic acidosis mentioned before. It also inhibits carbonic anhydrase in red blood cells leaving CO2 released from red cells in the lung decreased, which led to increased arterial Pco2. The sick and wounded have a tendency to acidosis the drug should be used with caution. 2. Respiratory nerve and muscle dysfunction seen in polio, acute infectious polyneuritis (Guillain-barre syndrome) botulism, myasthenia gravis, hypokalemia, or familial periodic paralysis, spinal cord injury, etc. In severe cases, paralysis of respiratory muscles can be. 3. Thorax thoracic abnormalities of respiratory motion abnormalities are common after spinal, scoliosis, flail chest (Flail Chest), between ankylosing spondylitis (Ankylosing Spondylitis), cardiopulmonary obesity syndrome (Picwick syndrome) and so on. 4. The common airway obstruction foreign body obstruction, laryngeal edema and inhalation of vomit. 5. Diffuse lung disease is respiratory acidosis the most common cause. It includes chronic obstructive pulmonary disease, bronchial asthma, severe interstitial lung disease. These diseases can seriously impede the alveolar ventilation. 6. CO2 inhalation means high concentration of CO2 gas inhalation, such as trenches, tanks and other small space with poor ventilation of the environment. At this point does not reduce alveolar ventilation. Complications 1. Respiratory acidosis showed metabolic acidosis PaCO2, HCO3-was significantly increased and decreased. Because the two significantly increased the ratio of lead to severe acidosis. Common reasons are as follows: In cardiac arrest, severe pulmonary edema, the most typical. Excessive use of salicylate poisoning with sedatives and on the basis of existing lung disease or renal failure, septic shock can occur when. Cardiac arrest or acute pulmonary edema, the lungs can not be discharged when the CO2, the CO2 produced in vivo accumulation of a large number of respiratory acidosis Chi. Circular obstacles organizations can not perfusion, hypoxia resulted in substantial lactate production, the formation of metabolic acidosis and central nervous system disorders as ventilation PaCO2 value can not decrease disease, so treatment can significantly reduce the pH value of immediate cardiopulmonary resuscitation should be to restore airway patency, ventilation is not in the former can not be too smooth infusion NaHCO3, the reasons mentioned above. In addition, NaHCO3 injection of hypertonic induced hyperlipidemia and to facilitate the K into the cell from the extracellular and various other changes, can exacerbate the risk of disease. 2. Salicylate poisoning are mostly found in the elderly and those suffering from joint pain, can produce chronic acidosis. When the increase in pain intensity with sedatives or analgesics, can cause suppression of central produce metabolic acidosis plus respiratory acidosis. Chronic obstructive pulmonary disease can generally be increased by hematocrit, the total oxygen-carrying capacity increased oxyhemoglobin dissociation curve to the right, etc., the normal compensatory oxygen to tissues. When combined with severe anemia, such as sudden gastrointestinal bleeding, hypotension, cardiac arrhythmias can occur hypoxia, lactate production increases, there metabolic acidosis plus respiratory acidosis. If renal dysfunction, infections are more serious metabolic disorders, increasing the degree of acidosis. 3. Respiratory acidosis with metabolic alkalosis which is more common clinical acid-base balance of a mixed type disorder, seen in chronic obstructive pulmonary disease combined vomiting; chronic pulmonary heart disease, heart failure using row K of diuretic therapy and so on. At this point changes in blood pH, acidosis and alkalosis depends on the strength, such as the extent appropriate, then cancel each other, pH values remained unchanged; as one strong, the pH value is slightly higher or lower; PaCO2 and plasma HCO3- concentration was significantly increased, and exceeded the degree of change between the two should meet each other, the scope of compensation. 4. Acute respiratory acidosis hyperkalemia caused by ventricular fibrillation, can 5% sodium bicarbonate 60 ~ 100ml, within 5 ~ 10min in the intravenous infusion, the K transfer to the cells. Diagnosis of affected patients have a history of respiratory function, but also some of the symptoms of respiratory acidosis, that weakness should be suspected of having respiratory acidosis. Acute respiratory acidosis, blood gas analysis showed significantly decreased blood pH, PCO2 increased plasma HCO3- normal. Chronic respiratory acidosis, decreased blood pH value is not obvious, PCO2 increased plasma HCO3- increased. Treatment 1. To prevent and treat respiratory acidosis caused the original disease.
Methylphenidate 2. To improve alveolar ventilation, exhaust too much CO2. Feasible under the circumstances tracheotomy, artificial respiration, the lifting of bronchial spasm, expectorant, oxygen and other measures, the oxygen concentration when oxygen is not too high, so as not to suppress breathing. Artificial respiration should be appropriate, because the respiratory acidosis NaHCO3/H2CO3 increase in the primary H2CO3, NaH2CO3 showed a compensatory secondary increase. If hyperventilation is rapid decline in plasma Pco2, and NaHCO3 was still high, then the patient into the extracellular liquid caustic soda poisoning, the situation is so fluid. Can cause hypokalemia, decreased plasma Ca, central nervous system extracellular liquid caustic soda poisoning, coma and even death. 3. Generally do not give basic drugs, unless the pH decreased very drama, only temporarily due to the application of sodium bicarbonate to reduce acidosis, not long application. Patients with severe acidosis, such as coma, cardiac arrhythmia, treatment may be given THAM medium and high H. NaHCO3 solution can also be used, but must ensure adequate alveolar ventilation conditions can effect. As to correct the respiratory acidosis NaHCO3 body fluids high H, can generate CO2, such as not fully discharged, the depth will increase CO2. Common sense to prevent respiratory acidosis, airway obstruction mainly seen in the surgery and chest surgery or trauma. Therapy to relieve airway obstruction and improve pulmonary ventilation function-based. Chronic bronchitis, pneumonia and other respiratory insufficiency caused by internal diseases, respiratory acidosis is more common, as detailed in respiratory failure.


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