Acute respiratory failure

Introduction to Acute Respiratory Failure Acute respiratory failure means that the patient's original respiratory function is normal. Due to some sudden causes, such as airway obstruction, drowning, drug poisoning, and central nervous system disorders, the body often has no time to compensate. If it is not diagnosed in time and effective control is taken as soon as possible. Measures can often be life-threatening. However, the original respiratory function of patients with this type of respiratory failure is often good. If timely and effective rescue, the prognosis is often better than chronic respiratory failure. However, patients with poor original respiratory function can also be common in the clinic. Due to some sudden causes, common airway infections cause airway obstruction, which can cause a sharp rise in PaCO2 and a sharp drop in PaO2. It is clinically accustomed to classify this type of respiratory failure to chronic breathing. Acute exhaustion is exacerbated. basic knowledge The proportion of illness: 0.025% Susceptible population: more common in patients with respiratory diseases Mode of infection: non-infectious Complications: respiratory infections atelectasis lung injury pulmonary edema

Causes of acute respiratory failure

Substantial lung lesions (10%):

Various types of pneumonia include pneumonia caused by bacteria, viruses, fungi, etc., aspiration of stomach contents into the lungs, drowning and the like.

Pulmonary edema (20%):

1 cardiogenic pulmonary edema: caused by a variety of severe heart disease heart failure; 2 non-cardiogenic pulmonary edema: the most common is acute respiratory distress syndrome, other recurrent pulmonary edema, acute mountain disease, etc. Diseases can often cause severe hypoxemia.

Pulmonary vascular disease (10%):

Acute pulmonary infarction is a common cause of acute respiratory failure, and such diseases are fierce and have a high mortality rate.

Chest wall and pleural disease (10%):

A large number of pleural effusions, spontaneous pneumothorax, chest wall trauma, chest surgery injury, etc., can affect thoracic movement and lung expansion, resulting in reduced ventilation and/or uneven distribution of inhaled gas, impairing ventilation and/or ventilation function, clinical Type I respiratory failure is common, but severe type 2 respiratory failure can also be used.

Airway obstruction (20%):

Respiratory tract infections, respiratory tract burns, foreign bodies, and laryngeal edema cause acute infarction of the upper respiratory tract are common causes of acute type II respiratory failure.

Neuromuscular disorders (10%):

Patients with such diseases have no obvious pathological changes in the lungs, but are caused by impaired respiratory regulation or respiratory muscle dysfunction, resulting in type II respiratory failure, such as Guillain-Barré syndrome, which can damage peripheral nerves, severe Muscle weakness, polymyositis, hypokalemia, periodic spasm and other respiratory muscle involvement; cerebrovascular accident, craniocerebral trauma, encephalitis, brain tumor, carbon monoxide poisoning, hypnotic poisoning caused by respiratory center inhibition.

It must be borne in mind that type II respiratory failure can occur in the late stage of type I respiratory failure, and type II respiratory failure can be cured after type I respiratory failure, respiratory failure caused by airway obstruction and neuromuscular disorders. All are type II respiratory failure.

Pathogenesis

Hypoxia and CO2 retention are the basic pathophysiological changes of respiratory failure. Figure 1 briefly illustrates the pathogenesis and pathophysiological characteristics of ARDS.

1. Mechanism of hypoxia

(1) Ventilation disorder: severely insufficient alveolar ventilation leads to hypoxia and CO2 retention. It is mainly caused by limited lung expansion or increased airway resistance. Normal lung expansion depends on respiratory center drive, nerve conduction, and inhalation. Muscle contraction, diaphragmatic dilation, thoracic and alveolar dilatation, any of the above-mentioned obstacles such as respiratory central inhibition, respiratory muscle fatigue, decreased thoracic and lung compliance, etc. can lead to limited lung expansion and limited alveolar ventilation. Insufficient obstructive alveolar ventilation is mainly caused by increased airway resistance.

(2) Ventilation disorders:

1 ventilated blood flow ratio imbalance: ratio <0.8 found in pulmonary edema, pneumonia, atelectasis, etc.; ratio > 0.8 seen in pulmonary embolism, extensive destruction of pulmonary capillary bed, partial pulmonary vasoconstriction.

2 Dispersion disorders: seen in thickening of the respiratory membrane (such as pulmonary edema) and area reduction (such as atelectasis, lung consolidation), or pulmonary capillary hypovolemia (emphysema) and blood oxygenation rate slow (anemia) Wait.

The characteristics of blood gas changes caused by simple ventilation disorder: only PaO2 decreased, PaCO2 was normal or decreased; alveolar gas-arterial oxygen partial pressure difference P(Aa)O2 increased.

(3) Increased oxygen consumption: fever, difficulty breathing, convulsions, etc. can increase oxygen consumption, which is an important reason for aggravating hypoxia.

2. The mechanism of CO2 retention PaCO2 depends on the amount of CO2 produced and discharged. The increase in CO2 production, such as fever, hyperthyroidism, etc., rarely causes an increase in PaCO2. CO2 retention is mainly caused by insufficient alveolar ventilation. Therefore, PaCO2 is the best indicator of alveolar ventilation, and its elevation must be insufficient for alveolar ventilation.

Acute respiratory failure prevention

First, prevention and treatment of primary disease for the prevention of primary disease caused by respiratory failure, or timely active treatment after the onset, including:

1. Actively prevent pneumonia and various infectious diseases.

2. Actively prevent various accidents.

3. Prevent drug poisoning or other poisoning.

Second, the role of prevention and removal of incentives

For diseases that may cause respiratory failure, it is also necessary to prevent the effects of the incentives. For example, in trauma patients, it is necessary to avoid inhaling high concentrations of oxygen, losing blood to the long-term blood bank or excessive infusion, so as to avoid adult respiratory distress syndrome. Patients with respiratory diseases must first check the patient's lung function reserve. Patients with impaired lung function or chronic respiratory failure should actively prevent and remove various causes to avoid acute respiratory failure. .

Third, open airway and improve ventilation

Common methods are:

1 clear airway contents or secretions;

2 relieve bronchospasm;

3 use anti-inflammatory treatment to reduce the swelling and secretion of the airway;

4 if necessary, for tracheal intubation or tracheotomy;

5 given a respiratory central stimulant;

6 Master the indications and use mechanical assisted ventilation correctly.

Fourth, improve hypoxia

There must be severe hypoxia in respiratory failure, so correcting hypoxia and increasing Pao2 levels are necessary for each patient. The aim is to increase Pao2 to 6.67-8.0 kPa (50-60 mmHg) and arterial oxygen saturation in the short term. The degree rose to around 85%.

Type I respiratory failure has hypoxia and no carbon dioxide retention, and can inhale a higher concentration of oxygen (generally no more than 50%). In chronic type II respiratory failure, due to changes in respiratory central reactivity, it is generally believed that oxygen supply is sustained in principle. Low concentration and low flow rate are suitable, so Pao2 should reach a safe level of 8.0 ~ 9.33kPa (60 ~ 70mmHg), in order to supply the necessary oxygen to the tissue without causing carbon dioxide anesthesia, and then adjust and gradually increase the concentration of inhaled oxygen according to the patient's condition. And the flow rate, such as the progressive increase in the partial pressure of carbon dioxide during oxygen supply, must be assisted by artificial ventilation to promote the discharge of carbon dioxide.

Fifth, close observation and monitoring, comprehensive treatment, pay attention to correct the acid-base balance disorder and water and electrolyte disorders; maintain the function of important organs such as heart, brain, kidney; prevention and treatment of serious serious complications.

Complications of acute respiratory failure Complications, respiratory infection, pulmonary atelectasis, pulmonary edema

Acute respiratory failure, generally no lung disease, sudden onset, prognosis is mainly related to on-site first aid, can be cured, but not timely rescue, can be life-threatening, its complications include respiratory failure, the normal function of the body's various systems and Hazards from various treatments (mainly ventilator treatment), such as: respiratory infections, atelectasis, ventilator and lung injury, complications of tracheal intubation and tracheotomy, pulmonary edema and water retention, circulatory system Complications, kidney and acid-base balance.

Symptoms of Acute Respiratory Failure Common Symptoms Fingernails Nail Depression Heart Function Sudden Decompensation Dyspnea Pulmonary Fibrosis Significant Twitch Heart Rate Increased Gas Dispersion Disorder Respiratory Failure Respiratory Alkalosis Cardiac Arrest

Rapid onset, many brain trauma, drowning, electric shock, spinal cord injury, neuromuscular joint lesions, and soon respiratory slowdown or stop, accompanied by purpura, convulsions, coma, the specific performance is:

1. Patients with dyspnea are subjectively aware of lack of air. The objective manifestation is respiratory exertion, accompanied by changes in respiratory rate, depth and rhythm. Sometimes nasal flaps are seen, sitting breathing, upper respiratory tract disorders often manifest as inspiratory dyspnea, and there are three Abdominal signs, expiratory dyspnea are more common in incomplete obstruction of the lower respiratory tract such as bronchial asthma, thoracic disorders, severe pneumonia, etc., manifested as mixed dyspnea, central respiratory failure is often characterized by irregular breathing rhythms, such as tidal breathing, etc. Respiratory muscle fatigue, manifested as shallow breathing, abdominal abnormal breathing, such as inhalation, abdominal wall retraction, respiratory failure does not necessarily have difficulty breathing, such as sedative poisoning, can express breathing is moderate, expression is indifferent or lethargy.

2. Hairpin is a typical sign of hypoxia. The arterial blood reduces hemoglobin, causing earlobe, lips, oral mucosa, and nails appear blue-purple.

3. Neuropsychiatric symptoms Neuropsychiatric symptoms of acute respiratory failure are more common than chronic ones, and may appear irritability, flapping tremors, convulsions, convulsions, coma, etc.

4. Circulatory symptoms Symptoms of hypoxia and CO2 retention can lead to increased heart rate, elevated blood pressure, severe hypoxia, various types of arrhythmias, and even cardiac arrest. CO2 retention can cause superficial capillary and venous dilatation. It is characterized by excessive sweating, conjunctival edema, and jugular vein filling.

5. Dysfunction of other organs severe hypoxia and CO2 retention can lead to liver and kidney dysfunction, clinical jaundice, abnormal liver function; blood urea nitrogen, creatinine increased, protein in the urine, cast; may also appear upper digestive tract Bleeding, etc.

6. Acid-base imbalance and water, electrolyte imbalance due to hypoxia and excessive ventilation can cause respiratory alkalosis, CO2 retention is manifested as respiratory acidosis, severe hypoxia is accompanied by metabolic acidosis and electrolyte imbalance.

Examination of acute respiratory failure

Laboratory tests can objectively reflect the nature and extent of respiratory failure, and have important value in guiding oxygen therapy, adjustment of various parameters of mechanical ventilation, and correcting acid-base balance and electrolytes.

1. pH is a pH indicator, the normal is 7.35 ~ 7.45, the average is 7.40, the venous blood pH is about 0.03 lower than the arterial blood, pH>7.45 indicates alkaliemia, pH <7.35 indicates acidemia, pH is normal Normal acid-base balance, compensatory acid (alkali) poisoning or complex acid-base balance imbalance, it is generally considered that it is difficult to survive when pH<6.8 or >7.8, human acid resistance is strong, [H] rises to normal 3 The ratio is still viable; the tolerance to alkali is poor, and [H] is life-threatening when it falls to half of normal, but if metabolic acidosis and respiratory alkalosis are present at the same time, the pH may be normal, so A single pH can only indicate whether there is acid or alkaliemia. It must also be combined with other acid-base indicators (such as PaCO2, HCO3-, BE, etc.), biochemical indicators (such as blood potassium, chlorine, calcium) and medical history to correctly judge. Whether it is acid (alkali) poisoning, or complex acid-base poisoning.

2. Standard bicarbonate (SB) and actual bicarbonate (AB) SB refers to whole blood specimens that are isolated from air. Under standard conditions (temperature 38 ° C, PaCO 2 5.33 kPa, hemoglobin complete oxygenation, ie oxygen saturation) The concentration of bicarbonate ion [HCO3-] measured by 100%) has been reduced to normal conditions due to the influence of PaCO2 and SaO2 of [HCO3-], so the effect of [HCO3-] caused by the imbalance of respiratory acid-base has been eliminated. Therefore, the increase and decrease of SB reflects the reserve amount of [HCO3-] in the body, reflecting the quantitative index of the metabolic acid-base balance of the body, and the normal value is 22-27 mmol/L.

AB is directly measured from plasma [HCO3-], which is a whole blood sample isolated from air. The value of bicarbonate ion measured without any treatment is affected by both metabolic and respiratory factors. Under AB=SB, the difference between AB and SB reflects the degree of influence of respiratory factors on acid-base balance. When AB>SB, it indicates that CO2 retention in the body is more common in respiratory acidosis or metabolic alkalosis caused by insufficient ventilation function; AB

3. Alkali surplus (BE) or base loss (-BE) Alkali residual or base loss means 1L under standard conditions (38 ° C, PaCO2 5.33 kPa, hemoglobin 150 g / L, blood oxygen saturation 100%) The amount of acid or base required for titration of blood to pH 7.4, such as pH > 7.40, requires acid titration, referred to as base residue (BE); if pH < 7.4, base titration is referred to as base loss (BD or -BE), its normal range: neonatal -10 ~ -2mmol / L, infants - 7 ~ -1mmol / L, children -4 ~ +2mmol / L, adults ± 3mmol / L, because of breathing The effects of factors usually reflect only changes in metabolism, and their significance is similar to SB.

BE is divided into two types: actual alkali surplus (ABE) and standard alkali surplus (SBE). ABE is the measured BE, which reflects the alkali residue of whole blood. SBE reflects the alkali residue of interstitial fluid because interstitial fluid is the body cell. The exact external environment is in place, so SBE is more ideal than ABE to reflect the alkali residue of the body.

4. Carbon dioxide binding capacity (CO2CP) CO2CP refers to the plasma CO2 content obtained by equilibrating venous plasma specimens with normal human alveolar gas (PaCO2 5.33 kPa), that is, the amount of carbon dioxide contained in plasma HCO3-, mainly refers to the amount of carbon dioxide contained in plasma. The amount of CO2 in the combined state is an approximation of HCO3-, the normal value is 23~31mmol/L (55-70Vo1%) for adults, and the lower is 20~29mmol/L (45-65Vo1%) for children. CO2CP is metabolized and The effects of two factors of respiration, CO2CP reduction, suggesting metabolic acidosis (HCO3-reduction) or respiratory alkalosis (excessive CO2 excretion), and vice versa, but no decisive significance in mixed acid-base disorders For example, in respiratory acidosis, the pH drops and CO2CP rises. Conversely, CO2CP decreases when respiratory alkalosis occurs. Therefore, CO2CP does not reflect the true acid-base balance in the body during respiratory acid-base balance.

5. Total amount of carbon dioxide (T-CO2) refers to the sum of carbon dioxide in various forms in plasma, including HCO3- in the ionized portion, in HCO3-, CO3- and RNH2COO, and non-ionized HCO3- and physically dissolved The sum of CO2 and the like is 24 to 32 mmol/L for normal adults and 23 to 27 mmol/L for children.

6. Arterial oxygen partial pressure (PaO2) refers to the pressure generated by physically dissolved O2 molecules in plasma. Arterial oxygen partial pressure can better reflect the function of the lungs, mainly used for respiratory hypoxia, PaO2, SaO2 (oxygen saturation), O2CT (oxygen content or CO2, which refers to the total amount of oxygen contained in every 100 ml of blood, including hemoglobin-carrying oxygen and dissolved oxygen) can reflect the body's hypoxia, but the sensitivity is not enough Consistently, SaO2 and O2CT are affected by hemoglobin. For example, children with anemia may be hypoxic even if SaO2 is normal, and PaO2 is not affected. Therefore, PaO2 is a good indicator for judging the presence or absence of hypoxia, but the results are analyzed. At the time, it is necessary to know whether or not to take oxygen, because oxygen is completely different from oxygen, so it is best to measure without oxygen.

The normal value of PaO2 is 10.6413.3.kPa (80100mmHg), the neonatal is 811.0kPa (6080mmHg), and the venous blood oxygen partial pressure is 5.3kPa (40mmHg). It is generally considered that PaO2 is 7.98kPa (60mmHg). The above does not cause hypoxia. At this time, SaO2 is 90%, which is the part where the oxygen dissociation curve begins to turn. Below this, with the decrease of oxygen partial pressure, SaO2 can be reduced to 75%, which is obvious in clinical practice. Bun.

7. Carbon dioxide partial pressure (PaCO2) refers to the pressure generated by carbon dioxide dissolved in arterial blood. Because CO2 has a large dispersion capacity, about 25 times that of oxygen, it can be considered that PaCO2 can basically represent the partial pressure of carbon dioxide in the alveoli. PaCO2 can reflect the size of alveolar ventilation and is a good indicator of alveolar ventilatory function. Therefore, in alveolar interstitial edema, congestion, exudation, oxygen exchange has been significantly reduced, but carbon dioxide exchange can still be normal, such as patient arterial blood Oxygen partial pressure is reduced, and the partial pressure of carbon dioxide is normal, which indicates that the ventilation function is impaired. However, if the partial pressure of arterial oxygen is decreased and the partial pressure of carbon dioxide is increased, the ventilation is insufficient.

The normal value of PaCO2 is 4.665.99kPa (3545mmHg), and the child is low, 4.55.3kPa (3440mmHg), which may be related to the metabolism of children and the rapid respiratory rate. The PCO2 of venous blood is more than that of arterial blood. 0.8 to 0.93 kPa (6 to 7 mmHg).

According to clinical needs, X-ray chest X-ray, electrocardiogram, B-ultrasound, brain CT and other examinations were selected.

Diagnosis and diagnosis of acute respiratory failure

diagnosis

1. Most of the patients have no respiratory diseases, brain trauma, drowning, electric shock, etc., and soon the breathing slows down or even stops.

2. Arterial blood gas analysis: PaO2 <8.0KPa, PaCO2 can be normal, reduced or increased.

3. Usually diagnosed according to medical history, physical examination, chest radiograph, etc.

Differential diagnosis

1. Identification of acute respiratory failure and chronic respiratory failure:

Acute respiratory failure: refers to the normal respiratory function, caused by various sudden causes, caused by ventilation, or severely damaged ventilation function, sudden clinical manifestations of respiratory failure, such as cerebrovascular accident, drug poisoning inhibits respiratory center, respiratory muscle paralysis , pulmonary infarction, ards, etc., because the body can not be quickly compensated, if not rescued in time, it will endanger the patient's life.

Chronic respiratory failure: more common in chronic respiratory diseases, such as chronic obstructive pulmonary disease, severe tuberculosis, etc., the respiratory function damage is gradually worsening, although there is a lack of 02, or with co2 retention, but through the body compensation, can still engage in personal life Activity, called compensatory chronic respiratory failure, once concurrent respiratory infections, or other factors that increase the respiratory physiology burden caused by decompensation, the emergence of severe lack of 02, c02 retention and acidosis clinical manifestations, known as decompensation Chronic respiratory failure.

2. Clinically, it is necessary to identify respiratory failure caused by various causes. Firstly, it is necessary to exclude the intracardiac anatomical shunt and the decrease of PaO2 and PaCO2 caused by the etiology of lower cardiac output; secondly, it is necessary to identify various acute respiratory diseases. The cause of failure can be diagnosed by means of medical history, clinical manifestations and a variety of auxiliary examinations, paying attention to the identification of two different types of respiratory failure, respiratory obstruction or extensive lung lesions.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.