CO2 retention

Introduction Carbon dioxide retention is a special pathology term. Various causes of respiratory dysfunction lead to hypoxia, which causes carbon dioxide to increase, accumulate, and retain, affecting normal cell metabolism and gas exchange, resulting in carbon dioxide retention and a series of clinical manifestations.

Cause

Respiratory dysfunction caused by various causes, resulting in hypoxia, resulting in carbon dioxide increase, accumulation, retention, affecting normal cell metabolism and gas exchange, resulting in carbon dioxide retention.

O2 in the blood exists in both dissolved and bound forms. The amount of dissolution is extremely small, accounting for only about 1.5% of the total O2 content of the blood, and the binding is about 98.5%. The binding form of O2 is oxyhemoglobin (HbO2). Hemoglobin (Hb) is a chromoprotein in red blood cells, and its molecular structure makes it an excellent tool for O2. Hb is also involved in the transport of CO2, so Hb plays an important role in blood gas transport.

an examination

Arterial blood gas analysis can objectively reflect the degree of CO2 retention, and has important value for guiding oxygen therapy, adjusting various parameters of mechanical ventilation, and correcting acid-base balance and electrolyte.

First, arterial blood carbon dioxide partial pressure (PaCO2)

Refers to the pressure generated by the physically dissolved CO2 molecules in the blood. The normal PaCO2 is 4.6kPa-6kPa (35-45mmHg). If the pressure is greater than 6kPa, the ventilation is insufficient. If the pressure is less than 4.6kPa, the ventilation may be excessive. The acute ventilation is insufficient. PaCO26.6kPa (50mmHg) According to the Henderson-Hassellbalch formula, the pH is lower than 7.20, which will affect circulation and cell metabolism. Chronic respiratory failure due to the body compensation mechanism, PaCO26.65kPa (50mmHg) as a diagnostic indicator of respiratory failure.

Second, the pH value

For the negative logarithm of the concentration of hydrogen ions in the blood, the normal range is 7.35-7.45, the average is 7.40, which is less than 7.35 for decompensated acidosis, and higher than 7.45 for decompensated alkalosis, but it is not indicative of the nature. Acid-base poisoning, clinical symptoms and pH shift are closely related.

3. Alkali excess (BE)

At 38 ° C, CO2 partial pressure 5.32 kPa (40 mmHg), blood oxygen saturation measurement 100% conditions, the blood titration to pH 7.4 required amount of acid and alkali, it is a quantitative indicator of metabolic acid-base imbalance in humans, acid The amount of BE is positive, is a metabolic alkalosis; the amount of alkali added EB is negative, is metabolic acidosis, the normal range is 02.3mmol / L, when correcting metabolic acid-base imbalance, it can be used as an estimated acid Or a reference to the dose of an anti-alkaline drug.

Fourth, buffer alkali (BB)

It is the total content of various buffer alkalis in the blood, including bicarbonate, phosphate, plasma protein salt, hemoglobin salt, etc. It reflects the buffering ability of the human body against acid-base interference, and the body's specific compensation for acid-base imbalance In the case, the normal value was 45 mmol/L.

V. Actual bicarbonate (AB)

AB is the content of bicarbonate contained in human plasma under actual carbon dioxide partial pressure and oxygen saturation. The normal value is 22-27mmol/L, the average value is 24mmol/L, and the HCO3- content is related to PaCO2. PCO2 is increased and plasma HCO3- content is also increased. On the other hand, one of HCO3-plasma buffer bases, when the acid is too much fixed in the body, the pH can be stabilized by HCO3-buffering, while the HCO3- content is decreased, so AB is breathed and The dual effects of metabolism.

Standard bicarbonate (SB)

Refers to whole blood specimens that are isolated from air. At 38 ° C, PaCO 2 is 5.3 kPa, and hemoglobin is 100% oxygenated, the measured plasma bicarbonate (HCO3-) content, the normal value is 22-27 mmol / L, The average 24mmol/L, SB is not affected by respiratory factors, the increase or decrease of its value reflects the amount of HCO3-reservoir in the body, thus indicating the trend and degree of metabolic factors, SB decreased in metabolic acidosis; SB in metabolic alkalosis Raised, ABSB, indicates CO2 retention.

Seven, carbon dioxide binding capacity (CO2CP)

The normal value is 22-29mmol/L, which reflects the main alkali reserve in the body. When the metabolic acidosis or respiratory alkalosis occurs, the CO2CP decreases. When the metabolic alkalosis or respiratory acidosis occurs, the CO2CP increases, but the respiratory acid When poisoning is accompanied by metabolic acidosis, CO2CP does not necessarily increase. Due to respiratory acidosis, the kidney discharges H+ in the form of NH4+ or H+, and absorbs HCO3- to compensate, and the alkali reserve increases. Therefore, the increase of CO2CP reflects to some extent. The severity of respiratory acidosis, but can not reflect the rapid changes of CO2 in the blood, is also affected by metabolic alkali or acidosis, so CO2CP has its one-sidedness, must be considered in combination with clinical and electrolyte.

Differential diagnosis

(1) Acid-base balance imbalance and electrolyte imbalance

Normal people have a certain amount of fixed acid excreted from the kidney every day, and H2CO3 (volatile acid) excreted through the lungs is quite large. Therefore, respiratory failure will seriously affect the regulation of acid-base balance and body fluid electrolyte content.

1, acid-base balance disorders: respiratory failure due to ventilatory disorders, due to a large number of CO2 retention, PaCQ2 increased, causing respiratory acidosis; at the same time due to severe hypoxia, oxidation process disorders, acidic metabolites increased, often concurrent , metabolic acidosis. If the patient has renal insufficiency or infection, shock, etc., the metabolic acidosis is aggravated by the increase in renal dysfunction or the increase in the amount of fixed acid in the body. Respiratory failure caused by ventilation disorders, due to lack of oxygen can cause excessive remission of ventilation, so that CO2 is excessively discharged, so metabolic alkalosis can occur concurrently with respiratory alkalosis. Metabolic alkalosis in some patients with respiratory failure, mostly iatrogenic, often occurs after treatment, such as improper use of artificial respirator in the treatment of chronic respiratory acidosis, excessive CO2 emission, so that blood H2CO3 is significantly reduced, and at this time, the increased HCO3 by compensatory regulation can not be quickly discharged with urine, so metabolic alkalosis can occur; in the case of correcting acidosis, excess alkali can also cause metabolic alkalosis, such as potassium intake. Insufficient and application of a large number of potassium-distributing diuretics and adrenocortical hormones can cause hypokalemia alkalosis.

2, electrolyte imbalance: respiratory acidosis, often caused by blood C lower and increased HCO3, which is due to: 1 renal tubular secretion of hydrogen, increased, NaHCO3 reabsorption increased, while more Cl- in the form of NH4Cl with urine Excretion; 2 long-term use of diuretics or increased intracranial pressure, vomiting can also lose too much Cl, 3 when the accumulation of CO2 in the blood, HCO3 in the red blood cells and plasma Cl- exchange caused by blood cl lower. Changes in serum potassium, blood sodium, and blood calcium are affected by acid-base balance disorders, treatment measures, and renal function, and their concentrations may be normal or elevated or decreased.

(B) changes in the central nervous system - pulmonary encephalopathy

1, CO2 retention: increase the concentration of hydrogen ions in the cerebrospinal fluid, affect brain cell metabolism, reduce brain cell excitability, inhibit cortical activity; with the increase of CO2, strengthen the subcortical stimulation, causing cortical excitability; if CO2 continues to rise, cortex The lower layer is inhibited, leaving the central nervous system under anesthesia. In patients who have had pre-anesthesia, there are often symptoms of insomnia, mental excitement, and irritability.

2. Pulmonary encephalopathy: refers to a syndrome characterized by central nervous system and dysfunction caused by respiratory failure. Clinically, due to the increased excitatory process in the early stage, the patient showed memory loss, headache, dizziness, irritability, hallucinations, and confusion. When PacO2 reached above 10,6 kPa (80 mmHg), the cerebral cortex was inhibited and the patient gradually turned into a lack of expression. Drowsiness, confusion, coma, etc. Pulmonary encephalopathy is mostly a functional disorder in the early stage, with cerebral vasodilatation and congestion. Late stage may have severe cerebral edema, cerebral hemorrhage and other serious lesions. Pulmonary encephalopathy is the result of a combination of hypoxia, hypercapnia, acidosis, and microthrombus formation in the brain.

3. Hypercapnia and acidosis: The elevation of PaCO2 not only inhibits the function of the central nervous system, but also directly acts on the cerebral blood vessels. When PaCO2 exceeds the normal level of 1.33 kPa (10 mmHg), the cerebral blood vessels dilate and the cerebral blood flow can be increased by 50. %. If PaCO2 is too high, the cerebral blood vessels can be obviously dilated and congested, and the capillary wall permeability is increased, causing vasogenic cerebral edema, increased intracranial pressure and optic nerve head edema. In severe cases, it can also cause cerebral palsy. The effect of CO2 accumulation on the central center can also be exerted by altering the pH of the cerebrospinal fluid and brain tissue. The buffering capacity of cerebrospinal fluid is lower than that of blood. The pH of normal cerebrospinal fluid is low (7.33~7.40), while PCO2 is about 1.0kPa (7.5mmHg) higher than arterial blood. Therefore, when PaCO2 is increased, CO2 in cerebrospinal fluid also increases. Lower pH of the blood, so it can aggravate brain cell damage, such as enhance phospholipase activity, damage cell membrane structure, increase permeability; lysosomal membrane stability is reduced, can release various hydrolases, decompose tissue components It promotes edema, degeneration and necrosis of brain cells.

(three) changes in the respiratory system

1. A certain concentration of PCO2 is an important physiological stimulus for maintaining respiratory movement. The stimulating effect of CO2 on breathing is achieved in two ways.

1 Stimulation of peripheral chemoreceptors: When PCO2 is elevated, it stimulates the peripheral chemoreceptors of the carotid body and aorta, increasing the afferent impulses of sinus nerves and aortic nerves, causing excitement to the medullary respiratory center, leading to accelerated breathing.

2 Stimulation of central chemoreceptors: Central chemoreceptors are located in the superficial part of the ventrolateral medulla, sensitive to H+. The extracellular cells around it are also cerebrospinal fluid. The blood-cerebrospinal fluid barrier and the blood-brain barrier are relatively impervious to H+ and HCO-3, while CO2 is easily passed. When PCO2 in the blood rises, CO2 enters the cerebrospinal fluid through the above barrier, and combines with H2O to form HCO3-, which then dissociates H+ to stimulate central chemoreceptors. Exciting the medullary respiratory central neurons through a certain neural connection, and enhancing breathing. Among the two pathways in which PCO2 regulates respiration, the pathway of central chemoreceptors is dominant. Within a certain range, elevated arterial blood PCO2 can strengthen the breathing, but beyond a certain limit, it can cause respiratory depression.

2. Hypoxemia and hypercapnia caused by respiratory failure can further affect respiratory function. PaO2 reduces the stimulation of the carotid body's primary aortic chemoreceptor, and the effect of PaCO2 on the central medullary chemoreceptor can accelerate the deepening of the respiration and increase the alveolar ventilation, which is compensatory. But Pao2, below 4kPa (30n1mHg) or Paco. Above 10.6KPa (80mmHg), it inhibits the respiratory center and weakens the breathing. Changes in respiratory function in patients with respiratory failure are also associated with many primary diseases. Such as obstructive ventilatory disorder, due to the obstruction of the obstruction, the lack of restrictive ventilation caused by decreased inspiratory dyspnea (upper respiratory tract obstruction) or expiratory dyspnea (lower respiratory tract obstruction), often Shallow and rapid breathing occurs; central respiratory failure often shows slow breathing, severe respiratory rhythm disorders, tidal breathing, medullary breathing, sigh-like breathing and soaking breathing.

Tidal breathing is more common. It is characterized by the fact that the breathing gradually changes from shallow to deep, and then gradually slows down. After a short breath stop, the above breathing process is repeated. This type of breathing is seen in elevated intracranial pressure, uremia, severe hypoxia, and damage or inhibition of the respiratory center. The mechanism is generally considered to be due to the decrease in excitability of the respiratory center. At this time, the normal concentration of CO2 in the blood can not cause the respiratory center to excite, so apnea occurs, and then the CO2 in the blood gradually increases, reaching a concentration sufficient to excite the respiratory center. Breathing occurs, CO2 is gradually discharged, the concentration of CO2 in the blood decreases, and apnea occurs. Repeatedly and repeatedly, the performance is like a tide, so it is called tidal breathing. Medullary respiration is a late manifestation of central respiratory failure. The rhythm and amplitude of breathing are irregular and have apnea. The respiratory rate is less than 12 beats/min. Sigh-like breathing and sobbing-like breathing are dying respiratory manifestations, which are characterized by breathing. : Dilute and irregular, there is an increase in mouth inhalation and respiratory assisted muscle activity, and finally the breathing is weakened and stopped. These two breaths indicate that the respiratory center is in a state of deep inhibition.

(4) Changes in the circulatory system

A certain degree of PaO2 reduction and elevated PaCO2 can stimulate peripheral chemoreceptors (carotid body and aortic body), accelerate heart rate, strengthen myocardial contractility, and increase blood pressure. It can also cause sympathetic excitation and adrenal gland. Increased secretion, resulting in rapid heartbeat, increased myocardial contractility, elevated blood pressure, skin and abdominal visceral vasoconstriction, and heart and cerebral vasodilation. These changes are compensatory. A certain degree of CO2 retention also has a direct effect on the peripheral small blood vessels, so that it expands (except for the lungs and renal arteries). The skin vasodilatation can make the limbs warm and rosy with sweating; the conjunctiva and cerebral vasodilatation are congested. Severe hypoxia and CO2 retention can directly inhibit cardiovascular center and heart activity, aggravate vasodilation, leading to decreased blood pressure, and decreased myocardial contractility. Lack of O2 and CO2 retention can cause small pulmonary vasoconstriction and increase pulmonary circulation resistance, leading to pulmonary hypertension and increased right heart burden.

Respiratory failure is often associated with heart failure, especially right heart failure, the main cause of which is pulmonary hypertension and myocardial damage. The mechanism of occurrence is closely related to severe hypoxia (see Pulmonary Heart Disease and Hypoxia). Hypercapnia can also be caused by acidosis, which aggravates damage to the heart.

(5) Changes in renal function

Mild CO2 retention will increase renal blood vessels, increase renal blood flow, and increase urine output. When PaCO2 exceeds 8.64 kPa, blood pH drops significantly, renal vasospasm, blood flow decreases, HCO3- and Na+ reabsorption increases, and urine output decreases. Respiratory failure due to hypoxia and CO2 accumulation can cause persistent arteriolar spasm, reduce renal blood flow, kidney small: ball filtration rate is reduced, light urine, protein, red blood cells, white blood cells and casts. In severe cases, acute renal failure can occur, with changes such as oliguria, azotemia, and metabolic acidosis.

(6) Gastrointestinal changes

CO2 retention can increase gastric acid secretion, so gastric mucosal erosion, necrosis and ulceration can occur during respiratory failure. Causes gastrointestinal bleeding.

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