Obesity hypoventilation

Introduction Obesity-pulmonary hypoventination syndrome, also known as obesity-pulmonary hypoventination syndrome, obesity with cardiopulmonary failure, cardiopulmonary failure, idiopathic alveolar hypoventilation Syndrome, cardio-obesity syndrome, obesity-dyspnea-sleepiness syndrome, narcolepsy with diabetic hyperinsulin syndrome. This symptom is common in children with extremely obese body and is a clinical syndrome of severe obesity. It is associated with obesity to hypoventilation and is a type of alveolar hypoventilation syndrome. It is a special type of pulmonary heart disease and a common and serious complication in obesity patients. This symptom refers to a series of symptoms caused by poor alveolar ventilation in patients with extreme obesity without primary heart or lung disease. If the weight is reduced, the clinical symptoms can be significantly improved.

Cause

(1) Causes of the disease

Long-term consumption of energy exceeds consumption, resulting in excessive accumulation of body fat, and the weight is significantly higher than the standard of normal children of the same age and height. Obese people need more oxygen because of their weight gain, but obese people can not only increase their function, but their lung capacity is significantly lower than that of normal children. The main cause of cardiopulmonary insufficiency syndrome and the increase of adipose tissue in the thoracic cavity, intra-abdominal and systemic, leading to a reduction in the volume of the thoracic cavity, limited diaphragmatic movement, limited lung function, ventilation, and impaired heart function and nervous system. Wait for a series of changes.

(two) pathogenesis

Abdominal fat accumulation, increased intra-abdominal pressure, increased yaw pressure, increased chest pressure, massive fat accumulation in the mediastinum, thick chest wall, limited thoracic expansion and diaphragmatic movement, limiting lung respiratory function. Total chest compliance decreased, resulting in poor lung ventilation, decreased tidal volume, decreased lung ventilation, decreased lung function, and reduced lung capacity, reserve expiratory volume, functional residual capacity, and total volume. As the body weight continues to increase, the degree of uneven ventilation increases, so that the arterial blood carbon dioxide partial pressure rises while the oxygen partial pressure decreases.

People with severe obesity also have excess fat around the neck, hypertrophy of the tongue, and falling of the tongue root, which can lead to different degrees of upper airway obstruction. In addition, the reduction of ventilation is limited, and the ventilation is limited. The result is carbon dioxide retention and hypoxemia. disease. It is difficult to breathe, can not be supine, intermittent breathing during sleep, cyanosis, excessive carbon dioxide accumulation in the blood, causing respiratory acidosis, can appear unconscious and drowsiness. Causes periodic tracheal occlusion during sleep, insomnia or deprivation of sleep syndrome, sleep apnea (airway obstruction or central) syndrome, and the interval between each breath is prolonged after asleep. Long-term increase in arterial blood carbon dioxide partial pressure, the central nervous system's response to hypercapnia is low, the respiratory center induced by the increase of blood carbon dioxide is excited, in a state of loss, and is not sensitive to hypoxic respiratory response. Breathing, disturbing the rest of the patient, causing day and night sleepiness, lack of energy and so on.

Further, due to prolonged hypoxia, patients are prone to secondary polycythemia, increased blood viscosity, increased circulation resistance, early use of heart reserve during activities, and insufficient cardiac function. Patients with severe obesity are often accompanied by Left ventricular overload and venous return disorder caused by increased total circulating blood volume, elevated venous pressure, increased pulmonary hypertension and right heart load, edema, jugular vein engorgement and even cardiac insufficiency. Decreased ventilation function, decreased aerobic capacity, etc., resulting in shortness of breath, difficulty in breathing, hypoxia, cyanosis, obesity cardiopulmonary insufficiency syndrome in the terminal phase, prone to right ventricular hypertrophy, enlarged heart or congestive heart failure.

an examination

The main clinical manifestations of the patient are: symptoms that cannot be supine, palpitations, cyanosis of the lips, systemic edema, and difficulty breathing. As the disease progresses, the patient has intermittent or tidal breathing, confusion, lethargy, or lethargy.

1. Insufficient symptoms and signs of hypoventilation

There are a series of symptoms of respiratory failure, such as bruising and respiratory distress, blood gas examination see hypoxemia and carbon dioxide retention.

2. Respiratory symptoms and signs

Shortness of breath, frequent apnea episodes at night, peripheral or mixed sleep apnea, accompanied by upper airway obstruction and nighttime sleep snoring.

3. Cardiac symptoms and signs

Early symptoms include cough, shortness of breath, palpitations, edema of the lower extremities, and long-term dyspnea, which can lead to chronic pulmonary heart disease and heart failure.

When right heart failure is aggravated, dyspnea, bruising, oliguria, etc. may occur, and a small number of patients have symptoms of whole heart failure.

4. Neurological symptoms and signs

Hypoxia, fatigue, headache, dizziness, palpitations, excessive sweating, irritability, paralysis, convulsions, carbon dioxide retention, can cause hallucinations, mental disorders, daytime sleepiness, a small number of children with mental retardation or dullness.

Such patients do not respond well to the effects of general cardiotonic and diuretic treatments, giving intermittent oxygen or selective application of central respiratory excitement.

Those who weigh more than 20% of the same sex and normal height are obese, more than 30% to 39% of body weight is moderately obese, more than 40% to 59% are severely obese, and more than 60% are extremely obese. According to the obese people with reduced ventilation function, the clinical manifestations of the heart and nervous system symptoms and signs, combined with pulmonary function tests and blood gas analysis can be diagnosed.

Differential diagnosis

Obesity hypoventilation is distinguished from the following symptoms:

1. Inhibition of the respiratory center: With the drugs, encephalitis and other diseases, the respiratory center is inhibited, the respiratory motility is weakened, and the ventilatory dysfunction is caused, resulting in the identification of hypoxia and carbon dioxide retention.

2. Pulmonary lesions

(1) Physiological ineffective cavity increases ventilation: In the pneumonia, bronchiolitis, asthma and pulmonary edema, the breathing is shallow, the airway is paralyzed, narrowed or blocked, the ventilation is reduced, the physiological ineffective cavity is enlarged, and the respiratory efficiency is reduced. When respiratory muscle paralysis, such as infectious polyradiculitis and pleural effusion, the thoracic and lung expansion is limited, the alveoli can not expand normally, and the tidal volume decreases, resulting in decreased ventilation, resulting in an increase in PaCO2 and a decrease in PaO2.

(2) Ventilation/blood flow ratio (V/Q) imbalance: normal V/Q average is 0.8, V/Q ratio increases with ineffective cavity-like ventilation, ie alveolar ventilation but insufficient blood flow, seen when local blood perfusion is reduced . The available void volume (VD) and tidal volume (VT) ratio (VD/VT) is normally 0.3. VD/VT was significantly increased in pulmonary embolism, acute lung injury, and ARDS. ARDS can be increased to 0.75. V/Q decline is pathological pulmonary arteriovenous shunt, which refers to blood flow through unventilated or poorly ventilated alveoli, which is the cause of severe hypoxemia. The main manifestation is that PaO2 is significantly reduced. Increasing oxygen concentration does not improve arterial oxygenation. Partial pressure. More common in local ventilation abnormalities, such as pneumonia, atelectasis, pulmonary edema. Expressed by the shunt fraction, normal only 5%, greater than 15% will seriously affect oxygenation.

(3) Dispersion disorder: There is an abnormality in the diffusion of oxygen through the alveolar capillary membrane. Diffusions (such as pneumonia, atelectasis) or diffuse membrane thickening (such as pulmonary edema, pulmonary fibrosis) lead to diffusion disorders. Since the diffusion capacity of carbon dioxide is about 20 times greater than that of oxygen, the diffusion barrier mainly refers to oxygen, which is characterized by a decrease in PaO2 but no carbon dioxide retention. Usually, the ventilation disorder is judged by the difference of the alveolar arteriovenous oxygen pressure difference, which is more sensitive than PaO2, and it can react to oxygen intake earlier. The normal value of the alveolar arterial oxygen pressure difference [(Aa)DO2] is 0.67-2.0 kPa (5-15 mmHg). This difference is mainly due to some short-circuit in the normal anatomy and inconsistent V/Q values in various parts of the lung. (Aa) elevated DO2 suggests ventilation disorders, and one has proposed >6.7 kPa (50 mmHg) as one of the diagnostic criteria for acute respiratory failure. However, it should be noted that the cardiac output is reduced and the value can be increased when oxygen is absorbed. The consequences of insufficient ventilation function have the following three characteristics: PaO2 must decrease, PaCO2 generally does not increase; increasing oxygen absorption can not improve PaO2.

In conclusion, the most common cause of PaO2 decline in acute respiratory failure is V/Q imbalance, the most serious cause of increased arteriovenous shunt in the lung. The most fundamental cause of the increase in PaCO2 is insufficient alveolar ventilation. When children suffer from respiratory diseases, there may be ventilation disorders caused by different reasons. ARDS increased with intrapulmonary shunt, V/Q imbalance, which is more common in general lung lesions.

3. Simple and secondary obesity: Combined with medical history, physical signs and laboratory data, the first diagnosis is simple secondary depression. If there is hypertension, centripetal obesity, purple streak, amenorrhea, etc. with 24-hour urinary 17-hydroxysteroids, it should be considered as hypercortisolism, and low-dose (2mg) dexamethasone inhibition test should be used for identification. Those with low metabolic rate should further check T3, T4 and TSH and other thyroid function tests to determine whether there is hypothyroidism. Patients with hypopituitar dysfunction or hypothalamic syndrome should be tested for pituitary and target gland endocrine tests, scab, visual field, visual acuity, etc., if necessary, CT scan should be performed, and patients with enlarged saddle should consider pituitary tumors. Excluding the empty sella syndrome. Amenorrhea, infertility and masculinity should exclude polycystic ovaries. No obvious endocrine disorders, afternoon foot swelling, morning relief should be excluded from water, sodium retention obesity, vertical position water test is quite helpful. In addition, it is often necessary to pay attention to the presence of diabetes, coronary heart disease, atherosclerosis, gout, cholelithiasis and other concomitant diseases. As for other types of rare obesity, it can be combined with its clinical characteristics to judge.

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