respiratory failure

Introduction

Introduction Respiratory failure is a serious disorder of respiratory function, so that normal breathing can not be performed at rest, and hypoxia or carbon dioxide retention occurs, causing a series of clinical and metabolic disorders. In the early stage of illness, only breathing is strong. When it is severe, it is not easy to breathe, sweating is dripping, nails and nails are prominent, mental function changes, directional dysfunction, headache, insomnia, sorrow, irritability, turmoil, and then lethargy, causing coma, convulsions , heart rate is accelerated, blood pressure is elevated, skin vasodilatation and the like. Some severe patients have oliguria, lower extremity edema or liver damage and gastrointestinal bleeding.

Cause

Cause

First, the cause

The causes of respiratory failure are many, and any factor that can damage respiratory function can lead to failure. For clinical work, it will be caused by the following three categories, namely, respiratory obstruction, pulmonary parenchymal lesions and abnormal breathing pump.

1. Respiratory obstruction: This type is divided into two categories according to the location:

1. Upper airway obstruction: The upper respiratory tract refers to the upper part of the throat, including the nose, pharynx and throat. In the entire respiratory anatomy dead space, the upper respiratory tract is about half, the respiratory tract resistance is 45% from the nose and pharynx, and the upper airway obstruction can lead to obstructive sleep apnea syndrome. The larynx is an important part of obstruction, usually due to infection, foreign body, sputum, trauma, tumor, congenital malformation.

2. Chronic obstructive pulmonary disease: including chronic bronchitis, emphysema and some asthma, airway obstruction continues to progress, becoming the main cause of chronic respiratory failure in the elderly, and often due to the influence of certain predisposing factors leading to acute respiratory failure To make the condition worse.

2, lung parenchymal disease

1. General pulmonary parenchymal disease: including various pulmonary infections, pneumonia, pulmonary edema, lung abscess, pulmonary embolism, pulmonary interstitial lesions, pulmonary vascular disease and various causes of lung parenchymal injury.

2. Acute respiratory distress syndrome: including neonatal respiratory distress syndrome and adult respiratory distress syndrome.

3. Abnormal breathing pump: including from the respiratory center, spinal cord to the respiratory center, resulting in hypoxia or carbon dioxide retention, and even respiratory arrest.

2. Peripheral nerve conduction system and respiratory muscle disease: acute infectious polyradiculitis, poliomyelitis, amyotrophic lateral sclerosis, cervical spine trauma, myasthenia gravis, progressive muscular dystrophy, anticholinesterase drugs Poisoning, hypokalemia, paralysis, etc. can cause the thoracic expansion and contraction of people to lose power, weaken ventilation, and cause respiratory failure.

3. Thoracic disorders: trauma, surgical trauma, malformation or thickening of pleural adhesions, massive pleural effusion, pneumothorax, etc. affect thoracic activity and lung expansion, resulting in reduced alveolar ventilation and/or uneven distribution of inhaled gas, degrading ventilation and ventilation Features.

Second, classification

According to the clinical manifestations of respiratory failure, there are two types of acute and chronic.

1, acute respiratory failure: refers to the original lung function is normal, due to sudden causes; such as drowning, electric shock, trauma, drug poisoning or physical and chemical stimulation and acute respiratory distress syndrome, such as the clinical manifestations of sudden failure of respiratory function. In patients with acute complete asphyxia or respiratory arrest, the patient mainly dies from hypoxia. If the breathing does not stop, but the ventilation is insufficient, the main risk is not in hypoxia, but in carbon dioxide tumors and the resulting severe acidosis. The duration of acute respiratory failure depends on the primary disease. If the primary disease can be cured, the modern respiratory failure rescue technique can save most patients. The key is to prevent a series of complications during the rescue, especially respiratory infections. In acute respiratory failure with a course of more than one week, the body can exert the maximum compensatory effect in the absence of other systemic complications, but it is not necessarily fully compensated, and gradually transitions to chronic, but there is no obvious time limit between the two.

2, chronic respiratory failure: mainly on the basis of the original chronic obstructive pulmonary disease, in the process of repeated acute attacks, respiratory dysfunction gradually worsened, the emergence of severe carbon deficiency tumor.

This classification method is affected by the cause, the slow course of the disease, the quality of the body, etc. As a diagnostic criterion or guiding treatment, it has its inadequacies. According to the pathophysiological characteristics, it has its advantages, which can be divided into two types.

Type I respiratory failure (also known as ventilation disorder type of respiratory failure); arterial blood gas changes are characterized by decreased arterial partial pressure, arterial carbon dioxide partial pressure is often reduced or normal. Mainly caused by lung parenchymal lesions, lung compliance decreased, ventilation dysfunction is the main pathophysiological changes, static arterial shunt, ventilation / blood flow imbalance is the main cause of decline in blood oxygen. Oxygen therapy is an indication.

Type II respiratory failure (also known as ventilatory failure type): Arterial blood gas is characterized by an increase in arterial carbon dioxide partial pressure and a decrease in oxygen content. It can be caused by the same cause of the lung (airway obstruction, increased physiological dead space) or extrapulmonary cause (abnormality of the respiratory center or thoracic cavity, etc.). The basic pathophysiological change is insufficient alveolar ventilation. This type of respiratory failure can only be resolved by increasing ventilation.

mechanism:

1. Insufficient ventilation: Under normal circumstances, the total alveolar ventilation needs about 4L/min to maintain the normal alveolar-capillary and carbon dioxide partial pressure difference, so that oxygen and carbon dioxide can be exchanged effectively. Insufficient alveolar ventilation, decreased alveolar oxygen partial pressure, increased carbon dioxide partial pressure, and decreased alveolar-capillary partial pressure difference induced respiratory failure.

2, ventilation / blood flow imbalance: effective gas exchange in addition to requiring adequate alveolar ventilation, but also depends on the coordination of alveolar ventilation and blood flow in the number of normal, the ratio between the two is about 0.8, the basic unit of alveoli Therefore, the ventilation/blood flow ratio of a single alveolus is maintained at 0.8 to maximize the ventilation efficiency of the lungs. In the pathological condition, if the ventilatory/blood flow ratio is lower than 0.8, part of the blood cannot fully take oxygen and excrete carbon dioxide and enter the artery, causing physiological arterial shunt; the alveolus with a ratio of ventilation/blood flow higher than 0.8 enters. Part of the gas in the alveoli cannot be fully ventilated with the blood, forming an ineffective ventilation or "dead cavity" effect. The main consequence of the imbalance of ventilation/blood flow is hypoxia.

3, diffusion barrier: The ability of oxygen and carbon dioxide to penetrate the alveolar membrane is very different, the diffusion of oxygen is only 1/20 of carbon dioxide, so in the pathological situation, the diffusion barrier mainly affects the exchange of oxygen, resulting in simple hypoxia. Recent studies have shown that thousands of ventilation/proportional imbalances change before pathological changes impair diffuse function.

4. Oxygen consumption: Increased oxygen consumption is one of the causes of aggravation of hypoxia when respiratory function is insufficient. Fever, chills, dyspnea and convulsions can increase oxygen consumption, increase oxygen consumption, and reduce alveolar oxygen partial pressure. . When the normal person exercise, the oxygen consumption can be increased to prevent the occurrence of hypoxia. If there is ventilatory dysfunction, the partial pressure of the alveolar oxygen can not be raised, and the hypoxia is difficult to relieve.

Examine

an examination

Related inspection

Peak expiratory flow (PEFR) chest CT examination lung function test chest flat carbon dioxide partial pressure (PCO2, PCO2)

1. Difficulty breathing, cyanosis and three concave signs.

2. Abnormal breathing rhythm, amplitude, or cycle.

3. Disorders of consciousness, such as dullness, lethargy, convulsions, convulsions, coma, etc.

4. Others: elevated or decreased blood pressure, arrhythmia, sweating, prominent eyeballs, conjunctival hyperemia, hypercoagulable state, acid-base imbalance or electrolyte imbalance.

5. Some scholars believe that under standard atmospheric pressure, when the sea level is at a high resting state, when the arterial blood oxygen partial pressure PaCO2<7.98kPa (60mmHg) or with the carbon dioxide partial pressure PaCO2<6.67kPa (50mmHg), as a breath Diagnostic blood gas diagnostic criteria. According to changes in blood gas, respiratory failure is divided into two types. Type I means that PoO2 decreases and PaCO2 decreases normal; Type II means PaO2 decreases and PaCO2> increases.

Diagnosis

Differential diagnosis

Difficulty breathing: It is an important symptom of respiratory insufficiency. It is subjectively characterized by insufficient air or difficulty in breathing, and objectively manifested as changes in respiratory frequency, depth, and rhythm.

Sleep apnea: refers to the temporary stop of breathing during sleep. The most common cause is obstruction of the upper airway, often ending with loud snoring, body twitching or arm twitching. Sleep apnea is associated with sleep defects, daytime snoring, fatigue, and bradycardia or arrhythmia and EEG wakefulness.

Cardiogenic respiratory distress: refers to cardiogenic dyspnea caused by factors such as increased hydrostatic pressure, common in cardiac edema caused by left ventricular dysfunction, and thus caused by respiratory failure. Cardiac dyspnea is mainly caused by left heart and/or right heart failure. The mechanism of the two is different. The dyspnea caused by left heart failure is more serious. In acute left heart failure, paroxysmal dyspnea often occurs, which occurs during nighttime sleep, which is called paroxysmal nocturnal dyspnea. Respiratory depression is more common in opioid poisoning:

1. The clinical manifestations of mild opioid poisoning are headache, dizziness, nausea, vomiting, excitement or inhibition. The patient has illusions, lost time and space.

2. In severe poisoning, there are three major signs of coma and dilated pupils such as needle tip size and severe respiratory depression. Patients may have convulsions, closed jaws, and angular arches. Breathing becomes shallower and slower, followed by sigh-like breathing or tidal breathing, often accompanied by pulmonary edema. Acute poisoning died of respiratory failure within 12 hours.

3. Chronic poisoning mainly manifests as loss of appetite, constipation, weight loss, aging and sexual dysfunction. Respiratory distress syndrome: A clinically dyspnea syndrome due to the lack of pulmonary surfactant in premature infants. Breathing increases, difficulty, respiratory sputum often occurs immediately after birth or within a few hours, the upper and lower sternum inspiratory depression, the nose flaps. The extent of atelectasis and the severity of respiratory failure gradually worsen. In severe respiratory distress syndrome, fatigue of the diaphragm and intercostal muscles leads to CO2 retention and respiratory acidosis. Because blood can't be exchanged for oxygen through the atelectasis (such as right to left shunt in the lung), infants develop hypoxemia, leading to metabolic acidosis.

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