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OverPrimary respiratory acidosis that led to the increase of pH, PaCO2 decreased. Clinically, the disease can be kept separate health search, but also with other acid-base balance disorders exist based on the speed of onset can be divided into acute and chronic respiratory acidosis respiratory acidosis in two categories. Epidemiology: No information is currently
Causes: respiratory acidosis is the primary factor in the accumulation of CO2, arterial PCO2 increased, so that [BHCO3] / [HHCO3] larger the denominator of which led to decreased blood pH value. 1. Alveolar ventilation with the outside air of the poor (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 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 health search: for example, potassium deficiency, poliomyelitis, acute infectious 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. 2. The


blood and alveolar gas exchange between the poor (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. Pathogenesis: 1. Respiratory center inhibition of acute respiratory acidosis ventilation common clinical disorder are: central lesions, including brain trauma, brain lesions, etc., causing respiratory rhythm adjustment disorder; the formation of brain stem herniation, encephalitis, or use too much The drugs inhibit the respiratory center respiratory center directly caused by the brain stem rhythm less sexual dysfunction in patients with chronic hypercapnia upon the improper use of O2 can significantly relieve the respiratory center stimulation, acute respiratory acidosis; after cardiac arrest But more often such cases and metabolic acidosis in combination. Part of the extremely obese patients can be expressed as ventilation barriers to health search, respiratory acidosis or Pickwickian syndrome. 2. Respiratory muscles or chest wall barriers to acute respiratory acidosis seen in myasthenia gravis, periodic paralysis of acute onset, severe hypokalemia or hypophosphatemia, Guillain - Barre syndrome, and a small part of the aminoglycoside antibiotic poisoning. Chronic respiratory acidosis seen after polio, amyotrophic lateral sclerosis, multiple sclerosis, severe mucous edema, severe thoracic deformity. 3. Acute upper airway obstruction by foreign body, acute throat spasms caused. 4. Those who may be acute pulmonary disease with acute respiratory distress syndrome, acute pulmonary edema, severe bronchial asthma or pneumonia, pneumothorax, hemothorax, and other causes. Were the most common chronic obstructive pulmonary disease or chronic lung extensive fibrosis and so on. CO2 under normal circumstances, the metabolic process in the organization continuously generated, equal to the speed of the lung Zeyi the discharge, so PaCO2 constant. When all causes CO2 emission barrier, the blood CO2 levels can rise very quickly cause severe acidosis. Because extracellular fluid is mainly carbonate buffer system, too much CO2 and therefore can not afford to buffer the high CO2 mainly by cells of non-HCO3-buffer system and the buffer, leading to increased HCO3-and some can be transferred from cell to cell In addition, the blood HCO3-increased. In addition, high PaCO2 increase in cases of renal row H, HCO3-reabsorption also increased. Although the latter can be compensated Chi, but for a period to be 3 to 4 days to complete. Each in the acute phase generally increased PaCO2 1.3kPa (10mmHg), HCO3-increased 1mmol / L; the chronic phase is increased PCO2 per 1.3kPa (10mmHg) HCO3-increased 3.5mmol / L.
Laboratory tests: 1. Blood gas analysis and detection health search, CO2 binding detection health search. 2. Serum electrolytes potassium, sodium, chloride, calcium, magnesium testing. 3. Liver and kidney function tests. Other auxiliary examination: 1. Electrocardiogram arrhythmias can occur 2. According to the clinical manifestations, symptoms elected to do B-, X line. Related tests:> carbon dioxide combining p base ex arterial CO2 partial pres Inorganic phosp alveolar ventila Pulmonary Func Blood Gas Anal anion gap
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 is possible No 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 increased Chi 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 function of the kidney). 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. Pulmonary emphysema late in brain syndrome (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. 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 health search. 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 health search. 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, arrhythmia and other Chi hypoxia can occur, increase lactate production, metabolic acidosis occurs 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: 1. According to the original disease symptoms of respiratory acidosis. 2. Laboratory tests such as blood gases electrolytes potassium, sodium and magnesium chloride determination results. Differential Diagnosis: There are currently no relevant information
Treatment: 1. The treatment of acute respiratory acidosis is mainly the effective discharge of CO2, and treat hypoxemia. One must first rule out airway obstruction clearance within the mouth and trachea secretions, do endotracheal intubation, if necessary, can be used for tracheostomy, and use breathing machines or other methods of mechanical ventilation monitoring blood gas analysis, to serve as a basis for diagnosis and treatment . 2. Chronic respiratory acidosis (1) to control infection: broad-spectrum antibiotics given to strong reduction of pulmonary rales, purulent sputum disappeared after reducing the amount of withdrawal. (2) the elimination of CO2 build up and improve the anoxia: The ventilator can significantly improve the chronic symptoms of respiratory acidosis without breathing machine, when the arterial PO2 less than 6.7 ~ 7.3kPa (50 ~ 55mmHg), arterial oxygen saturation of less than 85%, can be sustained low-flow nasal cannula oxygen, or oxygen with intermittent nasal tube, each stop smoking 1h 1h. When 9.3kPa (70mmHg), AB higher than 35 ~ 37mmol / L that is close to C02 anesthesia, oxygen should be stopped. Do not allow the use of breathing machine PCO2 decreased too quickly, so as to avoid compensation has been made [BHCO3] / [HHCO3] suddenly larger molecules to smaller denominator, causing pH values have increased by respiratory acidosis alkalosis into would convulsions or coma (3) respiratory stimulants: the tube using a ventilator or nasal continuous oxygen or combined lung brain syndrome may use a variety of exciting drugs, such as the respiratory center dimethyl nikethamide Flynn , methylphenidate and so on. (4) bronchial spasm and expectorant agents: aminophylline 0.1 ~ 0.2g orally, 3 times / d, if necessary, and aminophylline 0.25g of 25% glucose solution by adding 20ml of slow intravenous injection. Salbutamol can be used such as 2-adrenergic receptor stimulant inhalation; or beclomethasone (becotide) aerosol inhalation. (5) tracheostomy: a serious condition, sputum viscosity, the above treatment does not improve the condition, you can do tracheotomy on respiratory dead space can be reduced to 70% reduction in the residual gas and then inhaled to improve the ventilation , easy to clear respiratory secretions also facilitate the implementation of intermittent or longer-term ventilator assisted breathing (6) simple chronic respiratory acidosis presented low chlorine, is the phenomenon of renal compensatory lung kidney multi-row H, and more recovery of sodium bicarbonate, to increase the molecule to adapt to increasing the denominator, thus obtained [BHCO3] / [HHCO3] to 20 / 1 HCO3-close and because increased renal multi-row Cl-, to maintain the balance between positive and negative ions, then Reduced chlorine. More conducive to play a low chlorine compensatory renal function, therefore, need to correct the low chlorine, with the improvement of respiratory acidosis, Cl-can be adjusted.
Prognosis: No information is currently Prevention: an active treatment of primary disease and prevent complications


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