The clinical manifestations of chronic respiratory failure include the clinical manifestations of primary disease and organ damage caused by hypoxia and carbon dioxide retention. The harm of hypoxia and carbon dioxide retention to the body depends not only on the degree of hypoxia and carbon dioxide retention, but also on the speed and duration of hypoxia and carbon dioxide retention. Therefore, in the acute attack of chronic respiratory failure, the clinical manifestations are often particularly serious because of the rapid occurrence of hypoxia and carbon dioxide retention. The damage of hypoxia and carbon dioxide retention is not the same, but there are many overlaps. For patients with 1 respiratory failure, the clinical manifestations are often the result of the interaction between hypoxia and carbon dioxide retention. Therefore, the following will comprehensively explain the clinical manifestations caused by hypoxia and carbon dioxide retention.
1. Respiratory dysfunction, hypoxia and carbon dioxide retention will all affect respiratory function. Dyspnea and increased respiratory rate are often the first important clinical symptoms. It is characterized by intense breathing, accompanied by increased breathing frequency, shallow breathing, flapping of the alar and accessory muscles involved in breathing activities, especially in COPD patients with airway obstruction and respiratory pump failure. Sometimes there may be respiratory rhythm disorder, such as tidal breathing and sighing breathing, mainly when the respiratory center is suppressed. Respiratory failure does not necessarily have dyspnea, but also has respiratory depression in severe cases.
2. Cyanosis is a reliable sign of hypoxemia, but it is not sensitive enough. In the past, the view that cyanosis occurred when the blood reduced hemoglobin exceeded 50g/L was denied. In fact, when the PaO2 is 50mmHg and the oxygen saturation (SaO2) is 80%, cyanosis will occur. Compared with lips and nail beds, cyanosis of tongue appears earlier and more obvious. Cyanosis mainly depends on the degree of hypoxia, and is also affected by hemoglobin, skin pigment and heart function.
3. Mild hypoxia of neuropsychiatric symptoms can lead to inattention and disorientation; Severe hypoxia, especially when accompanied by carbon dioxide retention, can cause headache, excitement, depression, lethargy, convulsions, loss of consciousness and even coma. Acute exacerbation of respiratory failure caused by chronic chest and lung diseases, rapid hypoxemia and carbon dioxide retention, so obvious neuropsychiatric symptoms can appear, which can be called pulmonary encephalopathy.
4. Severe carbon dioxide retention and hypoxia with cardiovascular dysfunction can cause palpitations, conjunctival congestion and edema, arrhythmia, pulmonary hypertension, right heart failure, hypotension, etc.
5. Symptoms of digestive system ① Ulcer symptoms; ② Upper gastrointestinal bleeding; ③ Abnormal liver function. These changes are related to carbon dioxide retention and severe hypoxia.
6. Renal complications can be renal insufficiency, but most of them are functional renal insufficiency, severe carbon dioxide retention and renal failure in the late stage of hypoxia.
7. Acid-base imbalance and electrolyte disorder Respiratory failure can often be complicated by acid-base imbalance and electrolyte disorder due to hypoxia and/or carbon dioxide retention, as well as clinical application of glucocorticoid and diuretic and loss of appetite. The common types of arterial blood gas abnormality and acid-base imbalance are:
(1) Severe hypoxia with respiratory acidosis.
(2) Severe hypoxia with respiratory acid and metabolic alkalosis (alkali replacement).
(3) Severe hypoxia accompanied by respiratory acid and metabolic acidosis (acid replacement).
(4) Hypoxia with respiratory alkalosis (respiratory alkalosis).
(5) Hypoxia is accompanied by alkali calling and alkali replacement.
(6) Hypoxia is accompanied by triple acid-base imbalance (TABD).
Two. diagnose
In the decompensated period of chronic respiratory failure, according to the patient's history of chronic respiratory diseases or other respiratory dysfunction, there are clinical manifestations of O2 deficiency and/or CO2 retention, and combined with related signs, the diagnosis is not difficult. Arterial blood gas analysis can objectively reflect the nature and degree of respiratory failure, and is of great value in guiding the adjustment of various parameters of oxygen therapy and mechanical ventilation, as well as correcting acid-base balance and electrolytes.
A, arterial oxygen partial pressure (PaO2)
Refers to the pressure generated by oxygen molecules physically dissolved in blood. In healthy people, PaO2 _ 2 gradually decreases with the increase of age, and is influenced by physiological factors such as receptor position. According to the relationship between oxygen partial pressure and oxygen saturation, the dissociation curve of oxygenated hemoglobin is S-shaped. When pao 2 >:8 kpa(60 mmhg), the curve is flat, the oxygen saturation is above 90%, PaO2 _ 2 changes by 5.3kPa(40mmHg), and the oxygen saturation changes little, indicating that the oxygen partial pressure is far more sensitive than the oxygen saturation. But when pao 2
Second, arterial oxygen saturation (SaO2)
Is the percentage of oxygen in hemoglobin, and the normal value is 97%. When PaO2 _ 2 _ 2 is lower than 8kPa(60mmHg), the oxygen dissociation curve of hemoglobin is in a steep section, and the oxygen saturation reflects the anoxic state. Therefore, in the rescue of severe respiratory failure, the pulse oxygen saturation analyzer is used to assist in evaluating the degree of hypoxia, and the oxygen concentration is adjusted to make the patient's SaO2 _ 2 reach more than 90%, so as to reduce the traumatic arterial blood sampling for blood gas analysis, which plays a positive role in rational oxygen therapy and curative effect evaluation.
Third, arterial oxygen content (CaO2)
Is 100ml of blood. It includes the sum of hemoglobin bound oxygen and physical dissolved oxygen in plasma. CaO2 =1.34× Sao 2× HB+0.003× pao 2. The reference value of Cao 2 in healthy people is 20ml%. The oxygen saturation (SVO2 _ 2 _ 2) of mixed venous blood is 75%, and its oxygen content (CVO2 _ 2 _ 2) is 65438±05ml%, so every 65438±000ml arterial blood passes through the tissue, the available oxygen of the tissue is about 5ml. Hemoglobin decreased, SaO2 was lower than normal, and blood oxygen content was still in the normal range.
Four. Partial pressure of arterial blood carbon dioxide
Refers to the pressure generated by CO2 molecules dissolved physically in blood. Normal PaCO2 _ 2 is 4.6kPa-6kPa(35-45mmHg), the value greater than 6kPa is hypoventilation, and the value less than 4.6kPa may be hyperventilation. Acute hypoventilation, PaCO2 & gt at 6.6 kPa (50 mHg), according to the Henderson-Hassellbalch formula, the pH is lower than 7.20, which will affect the circulation and cell metabolism. Chronic respiratory failure is due to the compensatory mechanism of the body, PaCO 2 >；; 6.65 kPa (50 nanograms) was used as the diagnostic index of respiratory failure.
Verb (abbreviation for verb) ph value
Is the negative logarithmic value of hydrogen ion concentration in blood. The normal range is 7.35-7.45, with an average of 7.40. Less than 7.35 is decompensated acidosis, and more than 7.45 is decompensated alkalosis, but it cannot explain the nature of acid-base poisoning. Clinical symptoms are closely related to pH deviation.
Six, alkali excess (BE)
Under the conditions of 38℃, CO2 partial pressure of 5.32kPa(40mmHg) and oxygen saturation 100%, the blood is titrated to pH7.4, which is a quantitative index of human metabolic acid-base imbalance, and the amount of acid added is positive, which is metabolic alkalosis. The alkaline dose EB is negative, which is metabolic acidosis. The normal range is 0 2.3 mmol/L, which can be used as a reference for estimating the dosage of antacids or antacids when correcting metabolic acid-base imbalance.
Seven. Buffer alkali (BB)
It is the total content of various buffer bases in blood, including bicarbonate, phosphate, plasma protein salt, hemoglobin salt and so on. It reflects the buffering ability of human body to acid-base interference and the specific situation of acid-base imbalance compensation. The normal value is 45 mmol/L.
Eight, the actual bicarbonate (AB)
AB is the content of bicarbonate in human plasma under actual partial pressure of carbon dioxide and oxygen saturation. The normal value is 22-27 mmol/L, and the average value is 24 mmol/L. The content of bicarbonate is related to the partial pressure of carbon dioxide. With the increase of PCCO 2, the content of HCO3- in plasma also increased. On the other hand, HCO3- one of the plasma buffer bases, when there is too much fixed acid in the body, the pH can be kept stable through HCO3- buffering, while the content of HCO3- is reduced. Therefore, AB is affected by both respiration and metabolism.
Nine, standard bicarbonate (SB)
Refers to the whole blood sample separated from the air. At 38℃, the partial pressure of carbon dioxide is 5.3 kPa, and hemoglobin is 65438 000% oxygenated, the content of bicarbonate (HCO 3-) in plasma is 22-27 mmol/L, with an average of 24 mmol/L. SB is not affected by respiratory factors, and its increase or decrease reflects the amount of HCO3- reserves in the body, thus indicating the trend and degree of metabolic factors. SB decreased in metabolic acidosis; SB increased during metabolic alkalosis. AB & gtSB stands for CO2 retention.
X. Carbon dioxide binding capacity
The normal value is 22-29mmol/L, which reflects the main alkali reserves in the body. CO2CP decreased in metabolic acidosis or respiratory alkalosis. When metabolic alkalosis or respiratory acidosis occurs, CO2CP will increase. However, when respiratory acidosis is accompanied by metabolic acidosis, CO2CP does not necessarily increase. Because of respiratory acidosis, the kidney excretes H+ in the form of NH4+ or H+, absorbs HCO3- for compensation, and the alkali reserve increases. Therefore, the increase of CO2CP reflects the severity of respiratory acidosis to some extent, but it cannot reflect the rapid change of CO2 in blood in time, and it is also affected by metabolic alkali or acidosis. So CO2CP has its one-sidedness.
Among these indicators, PaO2 _ 2, PaCO2 _ 2 and pH are the most important, reflecting insufficient O2 and CO2 retention and acid-base imbalance during respiratory failure. If BE is added, it can reflect the compensation of the body, whether it is complicated with metabolic acid or alkalosis and electrolyte disorder.
According to the etiology, medical history, inducement, clinical manifestations and signs, it can be clinically diagnosed as chronic respiratory failure. Arterial blood gas analysis is of great significance for definite diagnosis, classification, guiding treatment and judging prognosis. Diagnostic criteria are: ① PaCO2 _ 2 is normal or decreased, PaO _ 2 is normal or decreased when type I respiratory failure breathes air at sea level.