Respiratory acidosis in the elderly

Introduction to respiratory acidosis in the elderly Respiratory acidosis (hook acid) is often caused by CO2 retention. The compensation of the kidney in the acute phase is not great, and the bicarbonate buffer system does not work. Therefore, the acidosis progresses quickly and the severity can be reached within ten minutes. And the retention of CO2 is very easy to enter the cell, leading to acidosis in the cell, if not corrected in time, the mortality rate is very high. Its main feature is an increase in plasma PaCO2 and a compensatory increase in HCO3-level in the chronic phase. basic knowledge The proportion of illness: 0.002% Susceptible people: the elderly Mode of infection: non-infectious Complications: coma, optic disc edema, brain edema, heart failure

The cause of respiratory acidosis in the elderly

(1) Causes of the disease

1. Respiratory central inhibition: drugs (various sedatives or anesthetics), central diseases, extreme obesity, etc.

2. Respiratory muscles or chest wall disorders: such as respiratory muscle weakness, paralysis or restriction, inadequate ventilation or ventilation problems when using the ventilator.

3. Upper airway obstruction: acute tracheal foreign body, acute throat and so on.

4. Pulmonary diseases: such as chronic obstructive pulmonary disease, pulmonary edema, atelectasis, ARDS, etc.

5. Others: such as high fever or hyperthyroidism.

(two) pathogenesis

Disorders of CO2 excretion, including CO2 diffusion disorder and hypopnea, are the main pathogenesis. If lung function is normal, CO2 production (such as hyperthermia or hyperthyroidism) often does not occur.

Elderly respiratory acidosis prevention

Diuretics such as acetazolamide can temporarily increase the urinary HCO3- excretion, but this leads to low potassium, and the decrease in capacity sometimes causes hypokalemia and metabolic alkali to occur, and must be used with caution.

Complications of respiratory acidosis in the elderly Complications coma optic disc edema cerebral edema heart failure

Concurrent convulsions, coma, optic disc edema, cerebral edema, ventricular fibrillation, heart failure, cardiac arrest, etc.

Respiratory acidosis symptoms in the elderly Common symptoms Respiratory acidosis, shortness of breath, dyspnea, irritability, edema, edema, tremor, arrhythmia, confusion

1. Acute severe acid reflux manifests as shortness of breath, difficulty breathing and obvious neurological symptoms such as headache, blurred vision, irritability, and even tremors, confusion, paralysis and coma, physical examination can detect optic disc edema, increased cerebrospinal fluid pressure and Arrhythmia and so on.

2. The symptoms of chronic acid reflux are often masked by primary disease.

Examination of respiratory acidosis in the elderly

Blood gas analysis and examination can be diagnosed as respiratory acidosis according to pH reduction and PCO2 increase, but respiratory acidosis can be mixed with metabolic acidosis and/or metabolic alkalosis, and simple respiratory acidosis There are acute and chronic points, the changes of blood gas analysis indicators of acute and chronic respiratory acidosis are different, and the acute respiratory acidosis can be combined with the onset of acute respiratory acidosis. Therefore, accurate identification of respiratory acidosis is more metabolic. The identification of acid-base disorders is more difficult.

Identifying acute and chronic respiratory acidosis from the results of laboratory tests, ie blood gas analysis, should mainly consider the limits of HCO3-increased and the time required to achieve HCO3-increased, ie the time required for the body to compensate, acute breathing The incidence of acidosis is fast, and the increase of HCO3- is mainly achieved by intracellular buffering. Therefore, for every increase of PCO2 of 1.33 kPa (10 mmHg), HCO3- is increased by 1 mmol/L, and the compensation limit of acute respiratory acidosis is generally not more than 5 mmol. /L, hypercapnia in chronic respiratory acidosis occurs slowly, and the compensation of HCO3-increased is mainly achieved by the absorption of HCO3- by the kidney. The increase of PCO2 is 1.33 kPa (10 mmHg), and HCO3- can be increased by 3.5 mmol/ L, the limit of HCO3-increased in chronic hypercapnia can reach 25mmol/L. If the increase of PCO2 is not compatible with the increase of HCO3- or is not compatible with the change of pH, non-simple respiratory acidosis should be considered. Therefore, Laboratory findings must be analyzed in combination with the etiology and various factors associated with the patient's combination (eg vomiting, diarrhea, metabolic disease, heart, kidney function, medication, asthma, lung infection, mechanical ventilation applications, etc.).

In addition, the calculation of the alveolar-arterial blood (Aa) oxygen gradient can help to identify whether hypercapnia is caused by intrapulmonary disease or extrapulmonary disease. The atmospheric oxygen partial pressure (PiO2) is 20 kPa (150 mmHg), normal. In the case, the PCO2 in the alveolar gas is equal to the PCO2 in the arterial blood, because the CO2 in the blood can rapidly diffuse through the pulmonary capillaries, causing the partial pressure of carbon dioxide in the arterial blood (PaCO2) and the partial pressure of carbon dioxide in the alveolar gas ( PACO2) quickly reaches equilibrium, so PACO2 is normally 5.33 kPa (40 mmHg). The carbon dioxide in arterial blood is mainly derived from metabolism in the body. The respiratory quotient is 0.8, which is to generate 1 molecule of carbon dioxide and enter the alveoli to use 1.25 molecules of oxygen. Therefore, the partial pressure of oxygen in the alveolar gas (PACO2) is the partial pressure of oxygen in the inhaled air minus the partial pressure of oxygen consumed by the body's metabolism, ie, the partial pressure of oxygen to be utilized and consumed to generate CO2, according to the following formula: PACO2= PiO2-PACO2 0.8=150-0.8=150-50=100 (mmHg), that is, PAO2 is normally 100mmHg (13.33kPa), in fact, the oxygen in the alveolar gas does not all diffuse into the blood, young alveoli under the age of 30 - Arterial blood (Aa) oxygen gradient averages 0.66 to 1.33 kPa (5 ~ 10mmHg), this age (Aa) O2 gradient will gradually increase to 2.00 ~ 2.67kPa (15 ~ 20mmHg), this change may be due to increased arteriovenous shunt and alveolar ventilation to reduce the proportion of ventilated blood flow Due to dysregulation, the oxygen gradient in patients with hypercapnia (Aa) with pulmonary disease should be increased, and some patients with extrapulmonary disease may also increase, but (Aa) oxygen gradient can basically exclude lungs. The disease suggests that it may be caused by abnormalities in the central or chest wall and respiratory muscles.

Alveolar-arterial oxygen gradient [P(Aa)O2], which is useful for the identification of acidosis due to differential disease caused by intrapulmonary disease and extrapulmonary disease.

Diagnosis and diagnosis of respiratory acidosis in the elderly

In addition to the need to identify acute and chronic, and in addition to chronic respiratory acidosis, respiratory acidosis requires a metabolic acid-base balance disorder and a mixed acid-base balance disorder with metabolic acid-base poisoning. Phase identification, generally through blood gas detection combined with etiological analysis and diagnosis is not difficult, but the acid and alkali in the body is constantly changing under normal conditions, acid and alkali maintain dynamic balance, the factors affecting acid-base changes in disease conditions are more complicated, such as pathological changes, Drugs and treatments, changes in the body's compensatory capacity, etc., especially respiratory acidosis, develop and change rapidly, so in some cases, the diagnosis and differential diagnosis of respiratory acidosis can also occur, due to respiratory The compensatory form of the acidosis body is mainly the increase of renal secretion H+ and reabsorption of HCO3-, especially in patients with chronic hypercapnia, the increase of PCO2 in the blood, and the increase of HCO3-, when taking any effective treatment of enhanced ventilation, PaCO2 Can be rapidly reduced and HCO3- can not be rapidly reduced, resulting in metabolic alkalosis after hypercapnia That transition from respiratory acidosis metabolic alkalosis.

In addition, according to the history of respiratory acidosis and the analysis of etiology, the main cause of respiratory acidosis is determined, and the identification will help the choice of clinical correct treatment.

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