Decreased venous oxygen saturation (SVO2)

Introduction Mixed venous oxygen saturation (SvO2) refers to oxygen saturation in the blood of the pulmonary arteries, which reflects the degree of oxygenation in the tissue and is affected by oxygen supply and oxygen consumption. Both oxygen supply reduction and increased oxygen consumption can result in a decrease in SvO2. The heart index is calculated from stroke volume and body surface area. It is an important indicator to measure circulation efficiency, cardiac contractility, and assessment of cardiac pump function. It can objectively and specifically reflect cardiac hemodynamic changes. Clinically, SvO2 is highly correlated with cardiac output (CO) and cardiac index (CI). SvO2 decline is caused by abnormal cardiovascular function and limited blood output.

Cause

Decreased oxygen output caused by various factors such as insufficient blood circulation, peripheral circulatory failure, sepsis, cardiogenic shock, hyperthyroidism, anemia, and degenerative hemoglobin, and lung disease. When SvO2 is less than 60%, it usually indicates an increase in tissue oxygen consumption or poor cardiopulmonary function.

Chronic respiratory failure occurs on the basis of existing lung diseases such as chronic obstructive pulmonary disease, severe tuberculosis, pulmonary interstitial fibrosis, pneumoconiosis, thoracic lesions and chest surgery, trauma, extensive pleural thickening, and thoracic deformity. Common diseases because of COPD, early manifestations of type I respiratory failure, as the condition gradually worsens, lung function is getting worse and worse, can be expressed as type II respiratory failure. In the stable phase of chronic respiratory failure, although PaO2 is lowered and PaCO2 is elevated, patients can be stabilized within a certain range by compensation and treatment, and patients can still engage in general work or daily life activities. Once the respiratory infection is aggravated or other causes, PaO2 can be significantly decreased, PaCO2 is significantly increased, which can be called acute exacerbation of chronic respiratory failure, which is the most common type of chronic respiratory failure in China.

an examination

Related inspection

Alveolar gas-arterial oxygen partial pressure difference lung ventilation function lung volume (TLC)

Clinical manifestations:

The clinical manifestations of chronic respiratory failure include the original clinical manifestations of the primary disease and various organ damage caused by hypoxia and carbon dioxide retention. The harm to the body caused by hypoxia and carbon dioxide retention is not only due to the degree of hypoxia and carbon dioxide retention, but also depends on the speed and duration of hypoxia and carbon dioxide retention, so when chronic respiratory failure is acutely intensified, due to hypoxia and carbon dioxide retention It occurs sharply, so clinical performance is often particularly severe. Hypoxia and carbon dioxide retention are not the same as the body damage, but there is a lot of overlap. For a patient with respiratory failure, the clinical manifestations are often the result of a combination of hypoxia and carbon dioxide retention. Therefore, the clinical manifestations caused by hypoxia and carbon dioxide retention are combined below.

1. Respiratory dysfunction Hypoxia and carbon dioxide retention can affect respiratory function. Dyspnea and increased respiratory rate are often the earliest clinically important symptoms. It is characterized by breathing effort, accompanied by accelerated breathing rate, superficial breathing, nasal fanning, and assisted muscle involvement in respiratory activities. In particular, patients with COPD have airway obstruction and respiratory pump failure, and breathing difficulties are more obvious. Sometimes respiratory rhythm disorders can occur, manifested as tidal breathing, sigh-like breathing, etc., mainly when the respiratory center is inhibited. Respiratory failure does not necessarily have difficulty breathing, and respiratory depression occurs in severe cases.

2. Hair bun is a reliable sign of hypoxemia, but not sensitive enough. In the past, the view that blood-reduced hemoglobin exceeds 50 g/L is considered to have been delayed. In fact, when PaO2 is 50 mmHg and blood oxygen saturation (SaO2) is 80%, cyanosis can occur. The color of the tongue is more pronounced and more obvious than the lips and nail bed. Hair blemishes are mainly determined by the degree of hypoxia and by the amount of hemoglobin, skin pigmentation, and cardiac function.

3. Neuropsychiatric symptoms Mild hypoxia may have inattention and disorientation; severe hypoxia, especially with carbon dioxide retention, may cause headache, excitement, depression, lethargy, convulsions, loss of consciousness, and even coma. Acute exacerbation of respiratory failure caused by chronic chest disease, hypoxemia and carbon dioxide retention occur rapidly, so there may be obvious neuropsychiatric symptoms. At this time, it may be called pulmonary encephalopathy.

4. Cardiovascular dysfunction, severe carbon dioxide retention and hypoxia can cause palpitations, conjunctival congestion and edema, arrhythmia, pulmonary hypertension, right heart failure, hypotension and so on.

Differential diagnosis

The disease must be differentiated from human atelectasis, spontaneous pneumothorax, persistent asthma state, upper respiratory airway obstruction, acute pulmonary embolism, cerebrovascular accident and cardiogenic pulmonary edema. By asking about medical history, physical examination and chest x-ray Apricot can be identified. Patients with cardiogenic pulmonary edema have difficulty breathing when they are in bed. Cough pink foamy sputum, wet lungs at the bottom of the lungs, better treatment for cardiac, diuretic, etc. If there are difficulties, can be identified by measuring PAwP, echocardiography.

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