Elderly respiratory failure

　　1. Etiology

　　There are many causes of respiratory failure, which are commonly summarized into the following 7 categories:

　　1. Respiratory tract diseases

　　Diseases affecting any part of the upper and lower respiratory tract, which cause obstruction, insufficient ventilation, and uneven distribution of gases, leading to imbalance in ventilation and blood flow ratio, can all cause respiratory failure. For example, laryngeal edema, bronchospasm caused by various reasons, obstruction of respiratory tract secretions or foreign bodies, etc.

　　2. Lesions of pulmonary tissue

　　There are many causes of diffuse pulmonary parenchymal lesions, the most common being various pneumonia, severe pulmonary tuberculosis, emphysema, diffuse pulmonary fibrosis, silicosis; pulmonary edema and atelectasis caused by various reasons, leading to reduced pulmonary ventilation volume and effective area, imbalance in ventilation and blood flow ratio, increased right-to-left shunting in the lungs, and hypoxia.

　　3. Pulmonary vascular diseases

　　Pulmonary embolism, fat embolism, pulmonary vasculitis, multiple microthrombosis, impairing pulmonary gas exchange function, leading to hypoxia.

　　4. Chest wall diseases

　　Including diseases of the chest wall and pleura. Severe chest deformities, chest trauma, pulmonary contusion, surgical trauma, large amounts of pneumothorax, or pleural effusion, thickening of the pleura, spontaneous or traumatic pneumothorax affecting chest movement and lung expansion, leading to reduced ventilation and uneven distribution of inhaled air, affecting gas exchange function.

　　5. Neuro-muscular diseases

　　Such patients often have completely normal lungs, with the primary disease mainly affecting the brain, neural pathways, or respiratory muscles, leading to direct or indirect suppression of the respiratory center; neuro-muscular junction blockage affects conduction function; the respiratory muscles lack the strength to perform normal ventilation. It is common in cerebrovascular diseases, encephalitis, brain trauma, electric shock, drug poisoning, poliomyelitis, and myasthenia gravis, among others.

　　6. Diseases leading to pulmonary edema

　　Including pulmonary edema caused by cardiac and non-cardiac factors. Non-cardiac pulmonary edema is often caused by increased capillary permeability, and its representative disease is adult respiratory distress syndrome (ARDS).

　　7. Sleep apnea

　　Normal people may have short periods of apnea during deep sleep, but it has been proven that extreme obesity, chronic high-altitude illness, tonsillar hypertrophy, and many other diseases can significantly prolong the duration of sleep apnea and cause severe hypoxemia.

　　II. Pathogenesis

　　Human respiratory activity can be divided into four functional processes: ventilation, diffusion, perfusion, and respiratory regulation. Each of these processes plays an important role in maintaining normal levels of arterial blood PO2 and PCO2. If any process occurs abnormally and is quite severe, it will lead to respiratory failure. In the common respiratory diseases seen in clinical practice, it is often the case that several abnormalities coexist simultaneously.

　　1. Ventilation insufficiency

　　Ventilation refers to the movement of air from the outside to the inside, and distribution to the lung gas exchange units through the trachea and bronchial system, which means the process of air reaching the alveoli. When PaCO2 increases, there is insufficient alveolar ventilation. At this time, the patient can only breathe in gas with a higher concentration of oxygen; otherwise, PaO2 will decrease with the increase of PaCO2. Although the changes in PaO2 and PaCO2 during insufficient ventilation are in opposite directions, the quantities are basically the same, so it can be easily determined where insufficient ventilation stands in the patient's hypoxemia. Arterial hypoxemia caused solely by insufficient alveolar ventilation does not accompany an increase in the alveolar-arterial PaO2 difference, so pure oxygen can correct it. Conversely, if it cannot be corrected, it is considered that other causes exist.

　　2. Diffusion impairment

　　Diffusion refers to the movement of O2 and CO2 across the alveolar capillary wall between the gas in the alveolar cavity and the blood in the pulmonary capillaries, which is the process of gas exchange.

　　The CO2 diffusion capacity is 20 times greater than that of O2. Unless the diffusion function is extremely severe, it will not cause arterial hypercapnia in a resting state. A reduction in diffusion area (such as lung parenchymal disease, emphysema, atelectasis, etc.) and an increase in diffusion membrane thickness (such as interstitial fibrosis, pulmonary edema, etc.) can cause simple hypoxemia.

　　3. Ventilation-perfusion imbalance

　　If the blood obtained by the gas exchange unit is more than the ventilation volume, hypoxemia of arterial blood will occur. Ventilation-perfusion mismatch is the most common cause of arterial hypoxemia, and it can be confirmed by improving the hypoxemia by administering 100% oxygen to the patient. Such patients rarely have CO2 retention.

　　4. Right-to-left shunting

　　The blood diversion from right to left can occur in cases with abnormal anatomical channels in the lungs, such as pulmonary arteriovenous fistulas. However, it is more common in atelectasis (pulmonary atrophy) or when the alveolar cavity is filled with fluid, such as pulmonary edema, pneumonia, or alveolar hemorrhage, causing physiological shunting and leading to hypoxemia. Such patients also do not show CO2 retention.

　　5. Hypercapnia

　　Hypercapnia can be said to be caused by a significant decrease in alveolar ventilation. The increase or decrease in PaCO2 in the blood directly affects the carbon content in the blood and has an opposite effect on pH. Acute changes in PaCO2 have a stronger impact on pH than chronic changes, due to the inability of plasma bicarbonate concentration to be supplemented in time. When the change in PaCO2 persists for 3 to 5 days, hypercapnia compensates through the renal mechanism, increasing bicarbonate; in cases of hypocapnia, it decreases. Both can promote the normalization of pH. Therefore, many patients with respiratory failure have a mixed respiratory and non-respiratory acid-base imbalance. If the course of the disease and the level of plasma bicarbonate are not understood, it is difficult to clarify its nature.

　　Hypoxia is an important manifestation of respiratory failure and is also a very common pathological process in various clinical diseases. Hypoxia in vital organs such as the brain and heart is also an important cause of death in the body. In addition, due to the significant decrease in arterial oxygen content, tissue oxygen supply is insufficient, leading to complications such as infection, gastrointestinal bleeding, shock, electrolyte imbalance, insufficient blood volume, heart failure, or respiratory failure, and CO2 retention, etc.

　　I. Clinical characteristics of respiratory failure in elderly patients

　　1. Prone to respiratory failure:An analysis of 1650 cases of respiratory failure shows that from the onset of the underlying disease to the development of respiratory failure, in the elderly, 63% at the 5th year, 77% at the 10th year, and 88% at the 15th year; while in young people, respectively, 57%, 68%, and 75%, indicating that the elderly are more prone to develop respiratory failure than young people.

　　2. No specific subjective symptoms and clinical manifestations:Once respiratory failure occurs in the elderly, only 45.5% of patients experience dyspnea, while the rest, although PaO2 shows abnormalities, do not necessarily experience any discomfort. The mucosal atrophy of the respiratory tract in the elderly leads to a decrease in clearance function, and the incidence of coughing, wheezing, and increased sputum volume is lower than that in young people, while the proportion of patients with consciousness disorders is significantly higher than that in young people.

　　3. Complications with other organ failure:The incidence of respiratory failure complicated with multiple organ failure in the elderly is significantly higher than that in the non-elderly group, especially in those with heart failure and renal failure; the incidence of DIC and gastrointestinal bleeding shows no significant difference between the two age groups.

　　II. Common clinical manifestations of respiratory failure

　　In addition to the symptoms of the primary disease leading to respiratory failure, it is mainly the signs caused by hypoxia and CO2 retention, but they are often mixed together, making it difficult to distinguish them clearly.

　　1. Dyspnea:It is the earliest symptom to appear in clinical practice and becomes more severe with the decline in respiratory function (but dyspnea does not necessarily indicate respiratory failure). In central respiratory failure, dyspnea is mainly manifested by changes in rhythm and frequency. Peripheral respiratory failure caused by respiratory organ damage, due to the involvement of accessory respiratory muscles, often presents with nodding, shrugging shoulders, or frowning-like breathing. Respiratory failure does not always accompany dyspnea, such as in cases of central nervous system drug intoxication and CO2 anesthesia during respiratory failure.

　　2. Cyanosis:When the absolute value of reduced hemoglobin (Hb) in the blood exceeds 50g/L, cyanosis is generally obvious. However, when anemia occurs, the Hb concentration decreases significantly, and even with obvious hypoxia, cyanosis does not appear.

　　3. Neurological and mental symptoms:The severity of the symptoms is closely related to the degree of hypoxia, CO2 retention, and the body's adaptation and compensation. Acute severe hypoxia can immediately cause confusion, excitement, coma, and convulsions, while chronic hypoxia may have symptoms such as apathy, muscle tremors, drowsiness, somnolence, and coma.

　　4. Symptoms of the circulatory system:When there is hypoxia and CO2 retention, the heart rate increases, blood pressure rises, myocardial ischemia, various arrhythmias; severe hypoxia can lead to decreased myocardial contractility, decreased blood pressure, leading to circulatory failure. Long-term pulmonary hypertension will induce right heart failure, and symptoms of systemic circulation congestion will appear.

　　5. Symptoms of digestion and urinary systems:Nausea, increased GPT, gastrointestinal bleeding, increased blood urea nitrogen, proteinuria, red blood cells and casts in urine may occur.

　　6. Diffuse intravascular coagulation (DIC):Infections, hypoxia, acidosis, shock, and other factors during the course of the disease can be triggering factors for DIC. Improper treatment can lead to the occurrence of DIC.

　　Third, Classification

　　1. Classification according to the course of the disease:

　　(1) Acute respiratory failure: patients have no history of respiratory disease, due to sudden factors, inhibiting respiration, or sudden failure of respiratory function, because the body is difficult to compensate well, if not diagnosed and treated early, it may threaten the patient's life, such as ARDS.

　　(2) Chronic respiratory failure: commonly seen in chronic respiratory diseases, such as chronic obstructive pulmonary disease, severe pulmonary tuberculosis, pulmonary diffuse fibrosis, etc. The respiratory function damage gradually worsens. Although there is hypoxia or CO2 retention, through the compensation and adaptation of the body, it is still possible to carry out personal life activities, which is called compensatory chronic respiratory failure.

　　(3) Acute onset of chronic respiratory failure: once a patient with chronic respiratory failure develops respiratory tract infection or other reasons increase the respiratory physiological burden, then compensation failure occurs, and clinical manifestations such as severe hypoxia, CO2 retention, and acidosis appear, which is called decompensated chronic respiratory failure.

　　2. Classification according to blood gas changes:

　　(1) Type I respiratory failure: mainly due to dyspnea dysfunction leading to hypoxia, with blood gas analysis showing simple PaO2

　　(2) Type II respiratory failure: mainly due to insufficient alveolar ventilation, with blood gas analysis showing PaO2 of 50mmHg.

　　1. Reduce energy consumption

　　Relieve bronchospasm, eliminate bronchial mucosal edema, reduce bronchial secretions, expel tenacious phlegm, decrease airway resistance, and reduce energy consumption.

　　2. Improve the nutritional status of the body

　　Enhance nutrition to increase the intake of sugar, protein, and various vitamins. In necessary cases, intravenous infusion of complex amino acids, plasma, and albumin can be administered.

　　3. Persist in exercise

　　Perform respiratory exercises every day to enhance the activity function of the respiratory muscles.

　　4. Use an extracorporeal diaphragmatic pacemaker

　　When respiratory muscle fatigue occurs, an extracorporeal diaphragmatic pacemaker can be used to improve alveolar ventilation, exercise the diaphragm, and enhance the activity function of the diaphragm.

　　1. Arterial blood gas analysis

　　PaO2 6.67 kPa or not high pH can decrease; chronic respiratory failure, AB compensation increases.

　　2. Electrolyte measurements

　　There is often hyperkalemia due to compensation for respiratory acidosis, and due to metabolic acidosis, it can be high, low, or normal.

　　3. Electrocardiogram

　　There may be sinus arrhythmia, conduction block, atrial and ventricular arrhythmias, and non-specific changes in S-T segment and T wave.

　　In addition to conventional treatment, attention should also be paid to the following aspects of diet for elderly patients with respiratory failure: diet should be light, with an emphasis on vegetables and fruits, a reasonable diet, and attention to adequate nutrition. Avoid smoking, alcohol, and spicy foods.

　　First, treatment:

　　The treatment of acute respiratory failure should be aimed at quickly identifying the cause and precipitating factors and providing appropriate treatment.

　　1. Establishing a clear airway:Before oxygen therapy and improving ventilation, it is necessary to keep the airways clear, aspirating secretions from the airways and reflux from the stomach. Patients with bronchospasm should be given bronchodilator drugs; for sputum that is thick and difficult to cough up, nebulized inhalation can be used, or a fiberoptic bronchoscope can be used to aspirate secretions. If the above treatments are ineffective, different methods such as tracheal intubation through the mouth or nose or tracheotomy can be used. The choice of method depends on the available equipment, personnel, the site and severity of airway obstruction.

　　2. Oxygen therapy:Oxygen therapy can be carried out using several different methods. The choice of method depends on the cause and severity of hypoxemia, as well as the convenience of use for the patient. While administering oxygen, the efficacy of oxygen therapy should be monitored through arterial blood gas analysis, and the oxygen concentration should be adjusted according to the condition to prevent oxygen toxicity.

　　① Oxygen therapy with a nasal cannula or nasal clip: A nasal cannula or nasal clip can be used to provide a higher concentration of O2, and it also has a good effect even if the patient breathes through the mouth. However, if an oxygen flow rate of 5 to 6 L/min or more is required to achieve a satisfactory arterial blood oxygen level, then other methods of oxygen therapy should be used.

　　② Oxygen therapy with a face mask: If a patient who has not been intubated requires high-concentration oxygen (40% to 80%), oxygen therapy with a face mask can be used. To ensure optimal efficacy, the mask must be airtight with no leaks. This often leads to discomfort in patients, making it difficult to provide high-concentration oxygen for a long time through a reservoir mask.

　　③ Mechanical ventilation with pressure oxygenation via tracheal intubation or tracheotomy: This is the most reliable method of oxygenation.

　　3. Differentiate and treat underlying diseases:Acute respiratory failure always has a precipitating cause. Therefore, while taking emergency measures to stabilize the patient's condition, it is necessary to actively treat the primary disease and remove the precipitating factors. Diagnosis can usually be made easily after a detailed medical history, a thorough physical examination, and blood, urine, and chest X-ray examinations. Checks on the central nervous system and heart function, as well as tests for the presence of drugs, toxins, and bacteria in secretions and blood, are all extremely helpful for diagnosis.

　　4. Monitor changes in the condition and prevent complications:Correcting acid-base balance disorders and electrolyte imbalances is also an important guarantee for the success of respiratory failure rescue.

　　II. Treatment of chronic respiratory failure

　　1. Keep the respiratory tract unobstructed

　　Chronic respiratory failure has a certain underlying disease, such as elderly COPD, which has varying degrees of airway obstruction, and airway obstruction is the main link that aggravates respiratory failure. The most life-threatening to patients is upper airway obstruction (upper respiratory tract, trachea, and main bronchus). For patients who are unable to cough or are unconscious, the first step should be to clear the secretions and gastric reflux from the oral cavity, pharynx, and stomach; for patients with atelectasis due to secretions or blood clots blocking the bronchus, fiberoptic bronchoscopy can be used to clear the secretions. All patients should use mucus solubilizers and antispasmodics for adjuvant treatment. If the above methods still cannot improve airway obstruction, artificial airways should be established.

　　2. Oxygen therapy

　　(1) Simple hypoxia: For patients with diffuse interstitial pneumonia, interstitial lung fibrosis, pulmonary interstitial edema, alveolar cell carcinoma, and cancerous lymphangitis, the main manifestation is chronic hypoxia caused by diffusion damage and imbalances in ventilation and blood flow ratio, often exacerbated by pulmonary infection. Generally, high oxygen concentration can correct hypoxia, but the effect of high concentration oxygen in late-stage patients is poor.

　　(2) Hypoxia with CO2 retention: The principle of chronic obstructive pulmonary disease should be low concentration (

　　(3) Long-term oxygen therapy during the remission period of chronic respiratory failure: In recent years, some developed countries have widely applied long-term home oxygen therapy to treat COPD patients. When PaCO2 is 6.7 kPa (50 mmHg), oxygen is inhaled at a low flow rate (1-2 L/min) for 12-15 hours a day, and the oxygen concentration can be appropriately increased during activity, which can improve the survival rate of patients, reduce pulmonary artery pressure, and high erythrocytosis. To avoid an increase in PaCO2, arterial blood gas analysis should be performed regularly to adjust the appropriate oxygen concentration.

　　II. Prognosis

　　The mortality rate of elderly patients with chronic respiratory failure is 40% to 76%. Respiratory muscle fatigue is an indicator of poor prognosis. The main cause of death is lung encephalopathy, followed by infection, acid-base and electrolyte disorders, and multiple organ failure.