Chronic respiratory failure

Chronic respiratory failure
Chronic respiratory failure often bronchial - pulmonary disease caused by, such as chronic obstructive pulmonary disease, severe tuberculosis, interstitial pulmonary fibrosis, such as pneumoconiosis. Thoracic diseases and thoracic surgery, trauma, extensive pleural thickening, thoracic deformity can lead to chronic respiratory failure.


1 missing O2 and CO2 retention mechanism

(A) lack of ventilation in the resting breathing air, the alveolar ventilation is about 4 L / min, to maintain normal alveolar oxygen and carbon dioxide partial pressure. Reduce alveolar ventilation, alveolar oxygen pressure dropped, carbon dioxide partial pressure increased. Under the conditions of breathing air (oxygen concentration of respirable 20.93 percent, carbon dioxide close to zero).

(B) ventilation / flow ratio imbalance in the ventilation and pulmonary capillary blood perfusion around the ratio must be coordinated to ensure effective gas exchange. Every minute of normal alveolar ventilation (VA) 4L, pulmonary capillary blood flow (Q) 5L, both the ratio of 0.8. Such as pulmonary ventilation in the blood flow rate of greater than (> 0.8). Is a physiological dead space increases, which is invalid cavity effect; alveolar ventilation in the ratio of less than the blood flow (<0.8), so that the mixture of pulmonary blood oxygenation without full access to pulmonary vein, a kind arteriovenous shunt (Figure 2-6-2). Ventilation / flow ratio imbalance, a lack O2, without CO2 retention. The result of blood mixed with the blood of oxygen difference is much greater than CO2 partial pressure, the former for 7.98 kPa, while the latter only 0.79 kPa, difference of 10 times. It may, by the sound of alveolar hyperventilation, emit more CO2, inadequate ventilation to compensate alveolar retention of CO2, or even emit more CO2, a respiratory alkalosis. As hemoglobin oxygen dissociation of the characteristics of normal alveolar capillary blood oxygen saturation already in a flat, the increase even if ventilation, air suction, although the alveolar oxygen, but little increase in blood oxygen saturation, by Sound excessive alveolar ventilation can not compensate the lack of ventilation caused by the perturbation alveolar oxygen shortage and thus a lack O2.

Ventilation> normal blood flow> ventilation
(Dead space effect) (effective ventilation) (static artery diversion effect)

(C) pulmonary artery - because of pulmonary vein-like triage pulmonary diseases such as depression wilt, atelectasis, pneumonia and pulmonary edema and pulmonary real change may cause an increase like triage, so that blood no contact alveolar gas to gas exchange opportunities. Therefore, increasing oxygen concentration and can not be raised PaO2. The greater the flow, increase blood oxygen inhalation after the worse the effect of the partial pressure of oxygen, such as the flow of more than 30 percent of the oxygen partial pressure of oxygen on the limited impact.

(D) diffusion barriers oxygen diffusing capacity of carbon dioxide is only 1 / 20, is in the diffusion barriers, a simple hypoxia.

(5) oxygen consumption increased oxygen consumption is increasing missing one of the reasons for O2, fever, chills, breathing difficulties and convulsions are to increase oxygen consumption. Shivering oxygen consumption up to 500 ml / min, severe asthma, with the increased work of breathing, oxygen consumption for more than 10 times normal. Oxygen consumption increased, decreased alveolar oxygen, help increase the normal ventilation to prevent hypoxia. Breathing air, oxygen consumption in the partial pressure of oxygen and pulmonary alveolar ventilation of the impact. Map of the curve with the dotted line to the point of intersection of different oxygen consumption, the maintenance of normal alveolar oxygen for pulmonary ventilation, with the increase in oxygen consumption, has also increased significantly, oxygen consumption per minute, respectively For 200 ml, 400ml, 800ml, alveolar ventilation volume of 3 L, 6L, 12L.

Second, the lack O2, CO2 retention of the impact of the body

(A) the impact on the central nervous brain tissue oxygen consumption accounted for about systemic consumption of 1/5-1/4. Central cortex cells most sensitive to hypoxia, lack O2 and the extent of the central nervous Jihuan the middle of the highest bidders different effects on health. Such as a sudden interruption for O2, purity nitrogen absorption to be 20 seconds in deep coma and body convulsions. Gradually reduce the absorption of O2 concentration, slow onset of symptoms, can cause mild missing O2 attention is not focused, intelligence may be directed obstacles with the increasing lack O2, PaO2 (PaO2) below 6.66 kPa can induce irritability, Trance consciousness, delirium; below 3.99 kPa, would lose consciousness, and even coma; below 2.66 kPa will be irreversible brain damage.

CO2 cerebrospinal fluid retention so that the concentration of hydrogen ions, the impact of brain cell metabolism, reduce excitatory brain cells and inhibit cortex; With the increase in CO2, stimulate the strengthening of the lower cortex, the cortex caused excitement; if CO2 continue to rise, the lower deck of the cortex inhibit So that the central nervous system in a state of anesthesia. In a pre-anesthesia patients often suffer from insomnia, mental excitement, irritability symptoms of the threatened excited.

Missing O2 and CO2 retention will have cerebral vascular expansion, reduced resistance to blood flow, to compensate the血流量增加. O2 will be seriously lacking in brain cells, edema, increased permeability of blood vessels, caused brain interstitial edema, leading to increased intracranial pressure, squeezing brain tissue and oppression of blood vessels, thereby increasing brain missing O2, a vicious cycle.

(B) of the heart, circulation of missing O2 can stimulate the heart to speed up the heart rate and stroke volume increase, high blood pressure. Coronary blood flow in the lack O2, a marked increase in heart blood flow far exceeds the brain and other organs. O2 myocardial lack of sensitivity, early mild O2 that is lacking in the electrocardiogram appeared on the show, a serious lack of O2 can lead to ventricular fibrillation or cardiac arrest. Missing O2 and CO2 retention can cause pulmonary vasoconstriction small increase in pulmonary vascular resistance, leading to increased pulmonary hypertension and right heart burden.

Inhalation of gas in the concentration of CO2, will speed up the heart rate, stroke volume increased, cerebral, coronary vasodilation, subcutaneous superficial capillaries and veins expansion due to the muscles of the spleen and blood vessels to contract, coupled with increased stroke volume, the Blood pressure is still elevated.

(C) lack of respiratory effects of breathing O2 impact than the impact of CO2 retention for small. O2, mainly through lack of carotid sinus and aortic reflection of the role of chemical receptors to stimulate ventilation, such as the slow increase the degree of lack O2, the reflective slow.

CO2 is a strong respiratory center stimulants, inhalation of increased CO2 concentration, ventilation multiplied, the retention of CO2 in deep rapid breathing, but when inhaled超过12% CO2 concentration, ventilation will not increase in the respiratory center Was inhibited. And chronic hypercapnia, there is no corresponding increase in ventilation, but has declined, and respiratory center reaction of the slow, through the kidneys to absorb and bicarbonate from H +, so that no blood pH value decreased, and patients Gas resistance increased, a serious lung damage, the thorax movement dysfunction related to ventilation.

(D) of the liver, kidney and blood system of missing O2 can be direct or indirect damage to the liver ALT increased, but with the lack of corrective O2, liver function gradually returned to normal.

Reduce arterial blood oxygen, kidney blood flow, the volume of glomerular filtration, urine output and sodium from the increase of both, but when PaO2 <5.3kPa, reduce kidney blood flow, kidney function was inhibited.

Low oxygen erythropoietin to increase red blood cell proliferation. Kidney and liver produce an enzyme, the blood of the Central African erythropoietin, the predecessor of a generation of active substances to stimulate the bone marrow caused secondary erythrocytosis. To increase the carrying capacity of blood, but also increased blood viscosity, pulmonary circulation and increase the burden on the right heart.

CO2 retention mild renal vascular expansion will increase renal blood flow, increase the amount of urine when PaCO2超过8.64 kPa, blood pH decreased significantly, kidney vasospasm, reduced blood flow, HCO3-and Na + absorption to increase urine output reduction .

(5) of electrolyte and acid-base balance the impact of severe energy shortage O2 cells inhibited the middle of the process and radio, such as三羧酸循环, and the role of oxidative phosphorylation-related activities. This will not only have lower energy efficiency, but also due to produce lactic acid and inorganic phosphorus from metabolic acidosis. As the energy shortage, in-transit damage by the sodium pump, so that cells within the potassium transferred to the blood, and Na + and H + into the cells, causing cells acidosis and hyperkalemia. Metabolic acidosis the fixed buffer acid and bicarbonate in the system work, a carbonate, the organization increased carbon dioxide tension.

PH value of carbonate and bicarbonate depends on the ratio of the former regulation on the kidney (1-3 days), while carbonated regulation on the lung (hours). Healthy people every day from lung carbonate of as many as 15000 mmol, the acute respiratory failure CO2 retention impact on the pH very quickly, often with metabolic acidosis exist, due to acid poisoning caused serious decline in blood pressure, arrhythmia, and even cardiac arrest . And chronic respiratory failure due to the slow development of CO2 retention and kidney from reduced bicarbonate, does not result in significantly lower pH. Because of blood in the main anion HCO3-and CI-in and is a constant, when HCO3-increase, the CI-corresponding lower, a low chlorine hyperlipidemia.

In addition to chronic respiratory failure caused the primary symptoms, is missing O2 and CO2 retention caused by multiple organ dysfunction performance.

First, breathing difficulties

Manifested in the frequency and magnitude of changes in rhythm. Such as the hub of a wave of respiratory failure, intermittent or Chouqi respiration; COPD is slow and deep breathing to rapid shallow breathing, auxiliary respiratory muscle strengthening activities, was nodding his head or shoulder to breathe. Central nervous system for the performance of drug poisoning absorbed ease breathing, drowsiness, severe pulmonary heart disease complicated by respiratory failure of carbon dioxide anesthesia, a slow shallow breathing.

Second, cyanosis

O2 is the lack of typical symptoms. When arterial blood oxygen saturation below 85%, the blood flow in the larger lips nail in cyanotic the other should pay attention to red blood cells, increasing cyanosis more obvious, anemia who are not obvious or cyanotic not appear serious shock endings Patients with poor circulation, even if PaO2 is still normal, may also appear cyanotic. Cyanosis also by the skin pigment and cardiac function.

Third, the spirit of neurological symptoms

The spirit of acute respiratory failure symptoms of slower to clear, acute shortage of mental disorder can appear O2, manic, coma, convulsions and other symptoms. O2 has more chronic lack intellectual orientation or dysfunction.

CO2 retention appear before the central curb the excitement of symptoms such as insomnia, irritability, restless, but this must not use sedation or sleeping pills to avoid increasing CO2 retention, a pulmonary encephalopathy, for the performance of consciousness indifferent, muscle tremors, occasional convulsions, drowsiness And even coma. pH compensation, was able to day-to-day life of the individual activities of CO2 retention, pH <7.3, will appear psychiatric symptoms. Serious CO2 retention can occur tendon reflexes weakened or disappeared, pyramidal tract, such as positive sign.

4, symptoms of the circulatory system

A serious lack O2 and CO2 retention caused pulmonary hypertension, heart failure can occur right, with signs of systemic congestion. CO2 retention so that peripheral venous filling surface, skin Hongrun, wet warm sweating, elevated blood pressure, stroke volume increased pulse of Hong Tae result; due to cerebral vascular expansion, a pulsating headache. Late due to serious lack O2, myocardial damage from acid poisoning, a peripheral circulatory failure, blood pressure dropped, arrhythmias, heart arrest.

5, digestive and urinary symptoms

Severe respiratory failure of liver and kidney functions are affected, such as GPT and non-protein nitrogen increased, proteinuria, urine and a tube of red blood cells. Gastrointestinal mucosa due to congestion and edema, erosion, bleeding, stress ulcer or upper gastrointestinal bleeding caused. These symptoms may lack the O2 and CO2 retention corrective disappear.

Chronic respiratory failure decompensated period, according to patients with chronic respiratory diseases or other respiratory dysfunction leading to the history, missing O2 and (or) CO2 retention of clinical manifestations, with the relevant signs, the diagnosis is not difficult. Arterial blood gas analysis of respiratory failure can objectively reflect the nature and extent of the guidance of oxygen therapy, mechanical ventilation various parameters of the regulation, and correct pH balance and electrolytes are important values.

1. PaO2 (PaO2)

Refers to the physical dissolved in the blood oxygen molecules generated by the pressure. PaO2 healthy growth decreased gradually with age, and physiological effects of receptor. According to partial pressure of oxygen and oxygen saturation of the relationship between oxygenated hemoglobin dissociation curve was S shape, when PaO2> 8kPa (60mmHg) above, the flat of the curve, the oxygen saturation of more than 90%, PaO2 change 5.3 kPa (40mmHg ), But little change in oxygen saturation that much oxygen saturation of oxygen-sensitive, but when PaO2 <8kPa below, the steep curve, the slight decline in oxygen pressure, oxygen saturation sharp decline, the PaO2 Less than 8 kPa (60mmHg) as the diagnosis of respiratory failure indicators.

Second, the arterial blood oxygen saturation (SaO2)

Hemoglobin is the oxygen percentage of units, the normal value is 97 per cent. When PaO2 less than 8 kPa (60mmHg), hemoglobin oxygen dissociation curve in a steep section, the oxygen saturation only reflects the state of hypoxia, the severe respiratory failure in the rescue, with the pulse of oxygen saturation detector to help evaluate missing O2 level, adjust the absorption of O2 concentration SaO2 more than 90%, to reduce the trauma of pumping blood for blood gas analysis, which is a reasonable assessment effect of oxygen therapy and play an active role.

3, arterial blood oxygen content (CaO2)

100 ml of blood is the number of oxygen-ml. Including the combination of hemoglobin and oxygen dissolved oxygen in plasma physics combined. CaO2 = 1.34 × SaO2 × Hb +0.003 × PaO2. Healthy CaO2 reference value of 20 ml%. Mixed blood oxygen saturation (SVO2) to 75 percent, its oxygen content CVO2 for 15 ml%, per 100 ml blood by the organization after about 5 ml of oxygen for the organization to use. Hemoglobin reduction, SaO2 lower than normal, blood oxygen content can still be the normal range.

4. PaCO2 (PaCO2)

Refers to the physical dissolved in the blood of the CO2 produced by the pressure. PaCO2 normal for the 4.6 kPa-6kPa (35-45mmHg), more than 6 kPa for inadequate ventilation, less than 4.6 kPa for ventilation may be excessive. Acute lack of ventilation, PaCO2> 6.6kPa (50mmHg), according to Henderson-Hassellbalch formula, pH below 7.20, it will affect circulation and cell metabolism. Chronic respiratory failure due to the body compensatory mechanisms, PaCO2> 6.65kPa (50mmHg) as an indicator of respiratory failure.

5, pH value

For the hydrogen ion concentration in the blood of a negative value. The normal range of 7.35-7.45, an average of 7.40. Below 7.35 for decompensated acidosis, higher than the 7.45 for decompensated alkalosis, but could not explain what is the nature of the acid-base poisoning. Clinical symptoms and the pH is closely related to migration.

6, base excess (BE)

In 38 ℃, CO2 pressure 5.32 kPa (40mmHg), oxygen saturation measured 100 percent condition, blood titration to the pH of pH7.4. It is human metabolic acid-base balance of quantitative indicators, plus acid to BE positive of the metabolic alkalosis; Canadian base of EB was negative, of metabolic acidosis. The normal range of 0 ± 2.3mmol / L. In the correct metabolic acid-base imbalance, it can be used as estimated by acid or Kangjian dose drug reference.

7. Buffer base (BB)

Various buffer in the blood of the total content of alkali, including bicarbonate, phosphate, plasma protein salt, salt and other hemoglobin. It reflects human interference buffer against acid-base capability, and acid-base imbalance in the body of the specific circumstances of compensation. Normal for the 45 mmol / L.

8, the actual bicarbonate (AB)

AB is in the actual partial pressure of carbon dioxide and oxygen saturation of human plasma bicarbonate contained in the content. Normal for the 22-27 mmol / L, an average of 24 mmol / L. HCO3-related content and PaCO2, as PCO2 increased plasma HCO3-content has also increased. On the other hand HCO3-alkali plasma one of the buffer, when too much acid in fixed, by HCO3-buffer and pH stability, and HCO3-content reduction. So AB double by respiratory and metabolic effects.

9, the standard bicarbonate (SB)

Means isolated from the blood samples of air in 38 ℃, PaCO2 to 5.3 kPa, oxygenated hemoglobin 100 percent under the conditions, measured by the plasma bicarbonate (HCO3-) content, for the normal 22 - 27mmol / L, An average of 24 mmol / L. SB from respiratory factors, to reflect the increase or decrease its value in HCO3-the number of reserves, so that metabolic factors and extent of the trend. Metabolic acidosis, SB decreased metabolic alkalosis, SB increased. AB> SB, expressed CO2 retention.

10, the combination of carbon dioxide (CO2CP)

Normal for the 22-29 mmol / L, the main base in the reserves. Metabolic acidosis, or respiratory alkalosis, CO2CP lower metabolic alkalosis or respiratory acidosis, while CO2CP increased. However, respiratory and metabolic acidosis with acid poisoning, CO2CP not necessarily increased, due to respiratory acidosis, kidney or to NH4 + H + form from the H +, to compensate for HCO3-absorption, alkali reserve increase, the increase in the CO2CP Certain extent, respiratory acidosis reflect the seriousness of the blood but can not reflect the dramatic changes in CO2, but also by the metabolism of the base or acid poisoning effect, it has its one-sidedness CO2CP, must be integrated with clinical and electrolyte for full consideration.

These indicators to PaO2, PaCO2 and pH most important, reflecting the lack respiratory failure at the O2, CO2 retention, in an acid-base imbalance, such as adding BE will be able to reflect the body compensatory, or without metabolic acid or alkaline Poisoning, and electrolyte imbalance.


Chronic respiratory failure more than a certain diseases, but in acute decompensated respiratory failure, can be directly life threatening, must take timely and effective rescue. Respiratory failure is to maintain the principle of respiratory smooth conditions, improve and rectify O2 missing CO2 retention, and metabolic dysfunction, which is based on disease and treatment-induced factors for time and create the conditions, but the specific measures should be combined with the actual situation Set.

First, the establishment of the airway patency

In improving the ventilation and oxygen therapy before, we must take various measures to maintain smooth enable respiratory tract. Such as porous catheter through the mouth, throat, or secretion of gastric reflux aspiration. Kechu viscous phlegm difficult, the new spray of bromine has been inhaled, can also retain a ring of plastic membrane puncture, the injection of saline diluted secretions, or bronchial spasm of bronchial β2 doping expansion, if necessary, to adrenal cortex Inhaled steroid ease bronchospasm; bronchoscopy can be used to suction secretions. If the effect of the poor, the use of nasal intubation or tracheotomy, the establishment of artificial airway.

Second, oxygen therapy

By enhancing alveolar oxygen (PaO2), an increase O2 diffusing capacity, improve PaO2 and oxygen saturation, increasing the use of oxygen.

(A) hypoxia without carbon dioxide retention of the low-oxygen therapy oxygen therapy alveolar ventilation, oxygen consumption increased, and the diffusion of dysfunction can be better to correct missing O2; ventilation / imbalance in the ratio of blood flow in patients with increased concentration of oxygen after inhaling , To increase ventilation alveolar oxygen shortage, improve its surrounding capillary blood oxygen intake so that the PaO2 increased. The site of chronic pulmonary interstitial pneumonia, interstitial pulmonary fibrosis, pulmonary edema, alveolar cell carcinoma of the lymphatic cancer and inflammation of the patients, mainly for the diffusion damage, ventilation / flow ratio imbalance caused by hypoxia And stimulate the carotid sinus, the aorta of chemical receptors cause excessive ventilation, PaCO2 low absorption can be given a higher oxygen concentration (35% -45%), to correct missing O2, then improve ventilation. But late in patients with high concentrations of oxygen absorption less effective.

The pneumonia is caused by the change, pulmonary edema and atelectasis caused by ventilation / flow ratio imbalance and lack of pulmonary artery shunt O2, and can not increase due to oxygen therapy diversion of blood oxygenation, such as the flow is less than 20 hours %, Inhaled high concentrations of oxygen (> 50%) corrected missing O2; if more than 30 percent of its bad effects, such as long-term inhalation of high concentrations of oxygen will cause oxygen poisoning.

(B) hypoxia with the obvious carbon dioxide retention of its oxygen therapy oxygen therapy should be given to the principle of low concentration (<35%) continued to oxygen, its principles are as follows.

Decompensated chronic respiratory failure, lack O2 with CO2 retention is the consequences of inadequate ventilation, because of hypercapnia of patients with chronic respiratory failure, the respiratory center of chemical receptors on the CO2 response of the poor, relying mainly on the maintenance of respiratory O2 hyperlipidemia on the low-neck Sinus artery, the aorta of chemical receptors in the driving role. If inhaled high concentrations of oxygen, PaO2 rising rapidly, so that the loss of peripheral chemical receptors to stimulate low O2 hyperlipidemia, patients with the slow and shallow breathing, PaCO2 go up, when a serious CO2 anesthesia, which often change consciousness and PaCO2 Increase the speed; inhaled high concentrations of low-O2 lifting O2 pulmonary vasoconstriction, allowing high pulmonary ventilation and blood flow than the (VA / QA) units in the lung blood flow to the low-VA / QA than lung units, increase ventilation and blood Flow ratio imbalance caused physiological dead space and tidal volume ratio (VD / VT) increase, thereby reducing alveolar ventilation, PaCO2 further increased in accordance with hemoglobin oxygen dissociation of the characteristics of the serious shortage O2 when, PaO2 and SaO2 The relationship between oxygen in the dissociation of the steepness of the curve, PaO2 slightly higher, SaO2 will be more, but there are still missing O2, can stimulate the chemical receptors, the ventilation to reduce the impact of low concentration of O2 therapy to correct low alveolar Ventilation (VA) of the alveolar oxygen tension (PaO2), and this inhaled oxygen concentration at different alveolar oxygen and alveolar ventilation of the curve, has earlier steep, after the characteristics of the flat, see Figure 2-6 -4. When inhaled oxygen concentration in more than 30 percent, although the alveolar ventilation is less than 1.5 L / min, alveolar oxygen maintained at 10.67 kPa (80mmHg), and alveolar partial pressure of carbon dioxide (PaCO2) will exceed 13.3 kPa (100mmHg). Generally low concentration of respirable O2, PaCO2 rise no more than 17/21, PaO2 rose 2.8 kPa (21mmHg), while PaCO2 rise no more than 2.26 kPa (17mmHg).

(C) the method commonly used oxygen therapy oxygen therapy for nasal catheter or nasal oxygen, the oxygen concentration of respirable (F1O2) and the inhaled oxygen flow was broadly following relations: F1O2 = 21 +4 × inhaled oxygen flow (L / min). It should be noted the same flow, with nasal inhalation of oxygen concentration of respirable per minute ventilation volume changes and changes. As to the low ventilation inhalation, the actual oxygen concentration higher than the calculation of the value of the high ventilation when inhaled oxygen concentration than the calculated values to lower.


Chronic respiratory failure more than a certain diseases, but in acute decompensated respiratory failure, can be directly life threatening, must take timely and effective rescue. Respiratory failure is to maintain the principle of respiratory smooth conditions, improve and rectify O2 missing CO2 retention, and metabolic dysfunction, which is based on disease and treatment-induced factors for time and create the conditions, but the specific measures should be combined with the actual situation Set.

First, the establishment of the airway patency

In improving the ventilation and oxygen therapy before, we must take various measures to maintain smooth enable respiratory tract. Such as porous catheter through the mouth, throat, or secretion of gastric reflux aspiration. Kechu viscous phlegm difficult, the new spray of bromine has been inhaled, can also retain a ring of plastic membrane puncture, the injection of saline diluted secretions, or bronchial spasm of bronchial β2 doping expansion, if necessary, to adrenal cortex Inhaled steroid ease bronchospasm; bronchoscopy can be used to suction secretions. If the effect of the poor, the use of nasal intubation or tracheotomy, the establishment of artificial airway.

Second, oxygen therapy

By enhancing alveolar oxygen (PaO2), an increase O2 diffusing capacity, improve PaO2 and oxygen saturation, increasing the use of oxygen.

(A) hypoxia without carbon dioxide retention of the low-oxygen therapy oxygen therapy alveolar ventilation, oxygen consumption increased, and the diffusion of dysfunction can be better to correct missing O2; ventilation / imbalance in the ratio of blood flow in patients with increased concentration of oxygen after inhaling , To increase ventilation alveolar oxygen shortage, improve its surrounding capillary blood oxygen intake so that the PaO2 increased. The site of chronic pulmonary interstitial pneumonia, interstitial pulmonary fibrosis, pulmonary edema, alveolar cell carcinoma of the lymphatic cancer and inflammation of the patients, mainly for the diffusion damage, ventilation / flow ratio imbalance caused by hypoxia And stimulate the carotid sinus, the aorta of chemical receptors cause excessive ventilation, PaCO2 low absorption can be given a higher oxygen concentration (35% -45%), to correct missing O2, then improve ventilation. But late in patients with high concentrations of oxygen absorption less effective.

The pneumonia is caused by the change, pulmonary edema and atelectasis caused by ventilation / flow ratio imbalance and lack of pulmonary artery shunt O2, and can not increase due to oxygen therapy diversion of blood oxygenation, such as the flow is less than 20 hours %, Inhaled high concentrations of oxygen (> 50%) corrected missing O2; if more than 30 percent of its bad effects, such as long-term inhalation of high concentrations of oxygen will cause oxygen poisoning.

(B) hypoxia with the obvious carbon dioxide retention of its oxygen therapy oxygen therapy should be given to the principle of low concentration (<35%) continued to oxygen, its principles are as follows.

Decompensated chronic respiratory failure, lack O2 with CO2 retention is the consequences of inadequate ventilation, because of hypercapnia of patients with chronic respiratory failure, the respiratory center of chemical receptors on the CO2 response of the poor, relying mainly on the maintenance of respiratory O2 hyperlipidemia on the low-neck Sinus artery, the aorta of chemical receptors in the driving role. If inhaled high concentrations of oxygen, PaO2 rising rapidly, so that the loss of peripheral chemical receptors to stimulate low O2 hyperlipidemia, patients with the slow and shallow breathing, PaCO2 go up, when a serious CO2 anesthesia, which often change consciousness and PaCO2 Increase the speed; inhaled high concentrations of low-O2 lifting O2 pulmonary vasoconstriction, allowing high pulmonary ventilation and blood flow than the (VA / QA) units in the lung blood flow to the low-VA / QA than lung units, increase ventilation and blood Flow ratio imbalance caused physiological dead space and tidal volume ratio (VD / VT) increase, thereby reducing alveolar ventilation, PaCO2 further increased in accordance with hemoglobin oxygen dissociation of the characteristics of the serious shortage O2 when, PaO2 and SaO2 The relationship between oxygen in the dissociation of the steepness of the curve, PaO2 slightly higher, SaO2 will be more, but there are still missing O2, can stimulate the chemical receptors, the ventilation to reduce the impact of low concentration of O2 therapy to correct low alveolar Ventilation (VA) of the alveolar oxygen tension (PaO2), and this inhaled oxygen concentration at different alveolar oxygen and alveolar ventilation of the curve, has earlier steep, after the characteristics of the flat, see Figure 2-6 -4. When inhaled oxygen concentration in more than 30 percent, although the alveolar ventilation is less than 1.5 L / min, alveolar oxygen maintained at 10.67 kPa (80mmHg), and alveolar partial pressure of carbon dioxide (PaCO2) will exceed 13.3 kPa (100mmHg). Generally low concentration of respirable O2, PaCO2 rise no more than 17/21, PaO2 rose 2.8 kPa (21mmHg), while PaCO2 rise no more than 2.26 kPa (17mmHg).

(C) the method commonly used oxygen therapy oxygen therapy for nasal catheter or nasal oxygen, the oxygen concentration of respirable (F1O2) and the inhaled oxygen flow was broadly following relations: F1O2 = 21 +4 × inhaled oxygen flow (L / min). It should be noted the same flow, with nasal inhalation of oxygen concentration of respirable per minute ventilation volume changes and changes. As to the low ventilation inhalation, the actual oxygen concentration higher than the calculation of the value of the high ventilation when inhaled oxygen concentration than the calculated values to lower.
Through oxygen masks Venturi principle, the use of oxygen jet produced negative pressure, inhaled air to dilute oxygen, into the air-conditioning control of oxygen concentration in 25 to 50 percent range, face masks, oxygen concentration and stability, free from the respiratory rate and tidal Of the impact. Is the consumption of its shortcomings, expectoration inconvenience.

Oxygen therapy to the general physical and clinical needs to regulate the concentration of oxygen inhalation, PaO2 of more than 8 kPa, or SaO2 for more than 90 percent. Oxygen consumption increases, such as fever can increase the concentration of oxygen inhalation. Reasonable oxygen therapy increased the effect of respiratory failure, respiratory failure in patients with COPD such as long-term low concentrations of oxygen therapy (especially at night) can reduce pulmonary circulation of resistance and pulmonary artery pressure, increased cardiac contraction, with activities to enhance and extend the survival time of endurance .

Third, increase ventilation and reduce CO2 retention

Alveolar CO2 retention is caused by inadequate ventilation, only to increase alveolar ventilation to effectively discharge CO2. Mechanical ventilation in the treatment of respiratory failure effect has affirmed and the application of respiratory stimulants, because of their different effect, the surviving in the controversy. Profile is as follows:

(A) a reasonable application of respiratory stimulants, respiratory stimulants stimulate the respiratory center or around the chemical receptors, through enhanced respiratory center of excitement, increased respiratory rate and tidal volume to improve ventilation. At the same time, patients with oxygen consumption and CO2 output also increased, and ventilation and a positive correlation. Because of its use of simple, economic, and a certain effect, it was still widely used in clinical, but should have their clinical indications. Patients with low ventilation mainly because of the central inhibition, respiratory stimulant effect of better chronic obstructive pulmonary disease, respiratory failure due to bronchial - lung disease, the response of the central or lower respiratory muscle fatigue caused by low ventilation, at this time of breath Doping should be the pros and cons of the three factors of primary and secondary may be. In nerve conduction system and the respiratory muscle lesions, and pneumonia, pulmonary edema and pulmonary fibrosis of the extensive ventilation dysfunction, respiratory stimulants are no disadvantages benefit and should not be used.

In the application of respiratory stimulants at the same time, should attach importance to reduce the chest, lungs and airway mechanical load, such as the secretion of drainage, the application of bronchial spasm, the elimination of pulmonary edema and other factors affecting the chest compliance. Otherwise, ventilation drive will add to short breath and breathing to increase power, and the need to increase the concentration of oxygen inhalation. In addition, we must make full use of some stimulants respiratory consciousness back to the Soviet Union, to encourage patients to cough, sputum elimination, and maintain the airway open. If necessary, nose or mouth and nose mask with mechanical ventilation support.

Nikethamide is the common respiratory center stimulants, increase ventilation, have a certain role Su-Ti. Patients can sleepiness of the first slow intravenous injection 0.375 g-0.75g, then to 3-3.75 g adding 500 ml of liquid, drop by 25-30 / min infusion. Close observation of patients lashes response to change consciousness, and respiratory rate, the rate and rhythm, the follow-up of arterial blood gas, in order to regulate dosage. If a skin itching, irritability and other side effects, must be slowed down Disu. If the 4 h-12h did not bear fruit, or a muscle twitch serious reactions, should be suspended, if necessary, a change of mechanical ventilation support.

(B) a reasonable application of mechanical ventilation with respiratory physiology and pathophysiology of the development, nose and mouth masks, artificial airway, breathing and respiratory-care properties of continuous improvement, mechanical ventilation will enable patients with respiratory failure to grow. Practice has proved that mechanical ventilation for the success or failure of respiratory failure, in addition to the breathing machine and related properties, is more important to the medical staff to keep respiratory failure in patients with pathological changes in physiological and reasonable application of mechanical ventilation. By increasing ventilation and provide appropriate oxygen concentration, to a certain extent, improve the ventilation function and reduce the power consumption of breath, respiratory failure in patients with missing O2, CO2 retention and acid-base balance disorders can be different degrees of improvement and corrected, General will not die of respiratory failure. Attention should be paid to prevention and treatment may be lethal infection of the airway, obstructive airway secretions, high-pressure pulmonary complications such as trauma. Even in some serious respiratory failure complicated by multiple organ failure patients, after treatment by mechanical ventilation, because of improved patient heart, brain, kidney, liver and other organs of oxygen the body and internal environment, and then to nasal feeding or intravenous Nutritional support, create the conditions for the resumption of patients, save a lot of dying patient's life.

Shang-qing consciousness of mild to moderate, in line with the patients with respiratory failure, nose or mouth and nose mask for mechanical ventilation; serious condition, although the consciousness-but uncooperative, coma or respiratory secretions of the large number of patients, the timely establishment of gas Road, such as the nose (or mouth) intubation mechanical ventilation, the choice of organizations with good compatibility of high-capacity low-pressure air bags (<3.3 kPa) of PVC or silicone catheter, the catheter can retain more than half a month, to avoid Low capacity use latex rubber high-pressure balloon catheter, because of their reaction, can cause the airway mucosa clear congestion, edema, erosion, and ulcers. In very poor lung function, recurrent respiratory failure, secretions, the body extremely weak, malnutrition, need long-term support of patients with mechanical ventilation, for tracheotomy, the long-term retention of mechanical ventilation trachea casing.

In the use of breathing machine before the medical staff must understand the pathophysiology of patients with respiratory, to suit the tidal volume, respiratory rate and breathing, such as the ratio of various parameters, such as a blockage of the ventilation to be too large tidal volume, frequency slow breath longer Breathing, and restrictive ventilated patients is the opposite. Through simple hand pinch capsule breathing respirator for the transition, followed by a mechanical ventilation and monitoring of patients with clinical manifestations, such as the activities of the thorax, airway pressure and oxygen saturation changes in the general follow-up after 20 min blood gas again Further adjustments breathing machine parameters. In the different periods of mechanical ventilation, ventilation should use different approaches, such as respiratory or manual control capsule ventilation or assisted intermittent positive pressure ventilation (IPPV), PEEP ventilation (PEEP), synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation (PSV). Ventilation can also be different forms of composition, such as PEEP + PSV for the integration of bi-level positive airway pressure (BiPAP). PEEP improve the ventilation function, SIMV and PSV benefit from the breathing machine, so as to achieve avoid excessive ventilation or inadequate ventilation. Reduce the impact of the heart cycle. During the mechanical ventilation should strengthen management of respiratory and breathing machine. As to the wetlands of the respiratory tract, secretions to attract and maintain respiratory unobstructed; breathing machine disinfection and maintenance of clean, avoid cross-infection. Particularly want to emphasize is the need to strengthen the respiratory and cardiovascular care, early detection of problems, analyse problems and to properly resolve to give full play to mechanical ventilation in the treatment of respiratory failure of the active role so that a reasonable and effective application of mechanical ventilation, improve Its efficacy and reduce complications.

40, to correct acid-base balance disorders and electrolyte imbalance

Diagnosis and treatment of respiratory failure in the process, there are several common types of acid-base balance disorders.

(A) of respiratory acidosis due to lack of pulmonary ventilation, CO2 produced in the body retention hypercapnia, changed the BHCO3/H2CO3 the normal ratio of 1 / 20, acute respiratory acidosis. Patients with chronic respiratory failure, blood-buffer system and the role of the kidney adjustment (secretion of H +, Na + absorption and HCO3-integration into NaHCO3), to near normal pH. Respiratory failure stolen generation acid poisoning can use alkaline agent (5% NaHCO3) temporarily to correct the pH value, but will reduce the ventilation to further increase the CO2 retention, there is no acid poisoning have removed the root causes. Only increase alveolar ventilation can be corrected respiratory acidosis.

(B) respiratory acidosis merger metabolic acidosis due to low O2 levels, insufficient blood volume, cardiac output and reduce cycle around obstacles, such as lactic acid in fixed, such as increased renal damage impact from acid metabolites. Therefore, on the basis of respiratory acid can be complicated with metabolic acidosis.