Chronic respiratory failure mostly has certain underlying diseases, but acute attacks of decompensated expiratory failure can be directly life-threatening and must be rescued in a timely and effective manner. The principle of respiratory failure management is to maintain the airway under the condition of patency, improve O2 deficiency and correct CO2 retention, as well as metabolic dysfunction, so as to buy time and create conditions for the treatment of underlying diseases and triggering factors, but the specific measures should be combined with the actual situation of the patient.
I. Establishment of a patent airway
Before oxygen therapy and improvement of ventilation, various measures must be taken to keep the airway unobstructed. Such as using a porous catheter through the mouth and throat to suck out secretions or regurgitated material in the stomach. If the sputum is sticky and not easy to be coughed out, use bromhexine spray inhalation, or keep the cricothyroid membrane to puncture the plastic tube and inject saline to dilute the secretion, or use bronchial antispasmodic β2 stimulant to dilate the bronchus, and if necessary, give adrenal corticosteroid inhalation to relieve the bronchospasm; also use fibrinoscope to aspirate the secretion. If the effect of the above treatment is poor, then use transnasal tracheal intubation or tracheotomy to establish an artificial airway.
Oxygen therapy
It is to increase the oxygen available by raising the partial pressure of oxygen (PaO2) in the alveoli, increasing the O2 diffusion capacity, and raising the partial pressure of arterial blood and oxygen saturation.
(a) Oxygen therapy for hypoxia without carbon dioxide retention: oxygen therapy can better correct O2 deficiency in patients with low alveolar ventilation, increased oxygen consumption, and diffusion dysfunction; patients with ventilation/blood flow ratio imbalance can increase the partial pressure of oxygen in hyperventilated alveoli and improve the oxygen intake of capillary blood around it, resulting in an increase in PaO2 after increasing the concentration of inhaled oxygen. In patients with diffuse chronic interstitial lung pneumonia, interstitial pulmonary fibrosis, interstitial pulmonary edema, alveolar cell carcinoma and carcinomatous lymphangitis, mainly manifesting hypoxia due to diffusion damage, ventilation/blood flow ratio imbalance, and stimulation of carotid sinus and aortic body chemoreceptors causing hyperventilation and low PaCO2, higher oxygen concentration (35%-45%) can be given for inhalation. O2 deficiency is corrected and ventilation is subsequently improved. However, the effect of high oxygen concentration in advanced patients is poor.
For the real change caused by pneumonia, pulmonary edema and pulmonary atelectasis caused by ventilation/blood flow disorders and intrapulmonary arterial shunt O2 deficiency, because oxygen therapy can not increase the oxygenation of shunt venous blood, such as shunt flow is less than 20%, inhalation of high concentration oxygen (>50%) can correct O2 deficiency; if more than 30%, its efficacy is poor, such as long-term inhalation of high concentration oxygen will cause oxygen toxicity.
(B) oxygen therapy for hypoxia with obvious carbon dioxide retention: the principle of oxygen therapy should be given low concentration (<35%) continuous oxygen, the principle is as follows.
O2 deficiency with CO2 retention in chronic respiratory failure decompensated patients is a consequence of hyperventilation. Due to the poor responsiveness of the respiratory central chemoreceptors to CO2 in hypercapnic chronic respiratory failure patients, the maintenance of respiration mainly depends on the driving effect of hypo-O2emia on the chemoreceptors of carotid sinus and aortic body. If high concentration of oxygen is inhaled, PaO2 rises rapidly, so that the peripheral chemoreceptors lose the stimulation of low O2emia, the patient’s breathing becomes slower and shallower, PaCO2 then rises, and in severe cases, they can fall into CO2 anesthesia, and this change in mental status is often related to the rate of PaCO2 rise; inhalation of high concentration of O2 lifts the low O2 pulmonary vasoconstriction, so that the high alveolar ventilation to blood flow ratio (VA/QA) Inhaled high concentration of O2 release the low O2 pulmonary vasoconstriction, make the blood flow in the lung unit with high alveolar ventilation to blood flow ratio (VA/QA) to the lung unit with low VA/QA ratio, aggravate the imbalance of ventilation to blood flow ratio, cause the increase of physiological dead space to tidal volume ratio (VD/VT), thus reduce the alveolar ventilation and further increase the PaCO2; according to the characteristics of hemoglobin oxygen dissociation curve, in severe O2 deficiency, the relationship between PaO2 and SaO2 is in the steep and straight section of oxygen dissociation curve, PaO2 is slightly increased, SaO2 is increased, and PaCO2 is increased. According to the characteristics of the hemoglobin oxygen dissociation curve, the relationship between PaO2 and SaO2 is in the steep and straight section of the oxygen dissociation curve, with a slight increase in PaO2, SaO2 has more increase, but there is still a lack of O2, which can stimulate the chemoreceptors and reduce the effect on ventilation; low concentration of O2 therapy can correct the alveolar oxygen partial pressure (PaO2) of low alveolar ventilation (VA), which is the same as the relationship curve between alveolar oxygen partial pressure and alveolar ventilation when inhaling different oxygen concentrations, both have the characteristics of steep and straight in the front section and flat in the back section, see Figure 2-6-4. When the inhaled oxygen concentration is above The partial pressure of alveolar oxygen is maintained at 10.67 kPa (80 mmHg), while the partial pressure of alveolar carbon dioxide (PaCO2) will exceed 13.3 kPa (100 mmHg) when the concentration of inhaled oxygen is above 30%, although the alveolar ventilation is lower than 1.5 L/min. Generally inhaled low concentration of O2, PaCO2 rise not more than 17/21, that is, PaO2 rise 2.8kPa (21mmHg), then PaCO2 rise not more than 2.26kPa (17mmHg).
(C) the method of oxygen therapy: commonly used oxygen therapy for nasal catheter or nasal plugs oxygen, inhalation oxygen concentration (F1O2) and inhalation oxygen flow is roughly the following relationship: F1O2 = 21 + 4 × inhalation oxygen flow (L/min). However, it should be noted that the same flow rate, nasal inhalation oxygen concentration varies with the change of ventilation per minute of inhalation. If low ventilation is given to inhalation, the actual oxygen concentration is higher than the calculated value; when high ventilation is given, the inhaled oxygen concentration is lower than the calculated value.
Mask oxygen supply is through Venturi principle, using the oxygen jet to generate negative pressure, inhaling air to dilute oxygen, adjusting the air intake can control the oxygen concentration in the range of 25%-50%, the structure of the graded adjustment schematic diagram 2-6-5, the oxygen concentration in the mask is stable, not affected by the respiratory frequency and tidal volume. The disadvantage is the inconvenience of feeding and coughing up sputum.
Oxygen therapy generally takes the physiological and clinical needs to adjust the concentration of inhaled oxygen so that the partial pressure of arterial blood oxygen reaches above 8kPa, or SaO2 is above 90%. When the oxygen consumption increases, such as fever can increase the concentration of inhaled oxygen. For example, long-term low-concentration oxygen therapy (especially at night) can reduce pulmonary circulatory resistance and pulmonary artery pressure, enhance myocardial contractility, thus improving patients’ activity endurance and prolonging survival time.
Increase ventilation and reduce CO2 retention
The efficacy of mechanical ventilation in the treatment of respiratory failure has been confirmed; however, the application of respiratory stimulants is still debated because of their varying efficacy. The following is a brief introduction.
(a) Rational application of respiratory stimulants: Respiratory stimulants stimulate the respiratory center or peripheral chemoreceptors, and increase respiratory rate and tidal volume to improve ventilation by enhancing the excitability of the respiratory center. At the same time, the patient’s oxygen consumption and CO2 production also increase accordingly, and are positively correlated with the ventilation volume. Because of its simplicity, economy and efficacy, it is still widely used in clinical practice, but its clinical indications should be mastered. If the patient’s hypoventilation is mainly due to central inhibition, respiratory stimulants are more effective; in chronic obstructive pulmonary disease (COPD) expiratory failure, hypoventilation is caused by bronchopulmonary pathology, central hyporesponsiveness or respiratory muscle fatigue, the advantages and disadvantages of applying respiratory stimulants should be determined according to the priority of the above three factors. In cases of neurotransmission system and respiratory muscle pathology, as well as pneumonia, pulmonary edema and extensive interstitial fibrosis of the lung with ventilatory dysfunction, respiratory stimulants have disadvantages rather than advantages and should not be used.
While applying respiratory stimulants, attention should be paid to reducing the mechanical load on the chest, lungs and airways, such as drainage of secretions, application of bronchial antispasmodics, elimination of interstitial pulmonary edema and other factors that affect the compliance of the chest and lungs. Otherwise, the ventilatory drive will aggravate shortness of breath and increase respiratory work, while the concentration of inhaled oxygen needs to be increased. In addition, it is necessary to make full use of some respiratory stimulants for neurological resuscitation, and the patient should be encouraged to cough and expel sputum to keep the airway open. If necessary, nasal or nasal mask mechanical ventilation support can be used.
Niclosamide is a commonly used central respiratory stimulant that increases ventilation and also has some soporific effect. Patients who are drowsy can be given 0.375g-0.75g intravenously by slow push, followed by 3-3.75g in 500ml of liquid and dosed quietly at 25-30 drops/min. Closely observe the patient’s lash reaction, mental changes, and respiratory frequency, amplitude and rhythm, and follow up the arterial blood gas in order to adjust the dose. If side effects such as skin pruritus and irritability occur, the drip rate must be slowed down. If the dose is not effective after 4h-12h, or if there is a serious reaction to muscle twitching, it should be stopped and replaced by mechanical ventilation support if necessary.
(B) Rational application of mechanical ventilation: With the development of respiratory physiology and pathophysiology, the continuous improvement of nasal and oral-nasal masks, artificial airway, respiratory monitoring and ventilator performance, mechanical ventilation can bring patients with respiratory failure back to life. Practice has shown that the success or failure of mechanical ventilation in the treatment of respiratory failure is not only related to the performance of the ventilator, but more importantly, the medical staff can always grasp the pathophysiological changes of patients with respiratory failure and apply mechanical ventilation reasonably. By increasing the ventilation volume and providing appropriate oxygen concentration, the ventilation function can be improved and the consumption of respiratory work can be reduced to a certain extent, so that the O2 deficiency, CO2 retention and acid-base imbalance in patients with respiratory failure can be improved and corrected to varying degrees, and generally do not lead to death from respiratory failure. Attention should also be paid to the prevention and treatment of complications such as airway infection, airway obstruction by secretions, and high-pressure lung trauma that may be fatal. Even in some patients with severe respiratory failure combined with multiple organ failure, after mechanical ventilation treatment, the patient’s heart, brain, kidney, liver and other organs improve the oxygen supply and the intrinsic environment of the body, and then given nasal feeding or intravenous nutritional support to create conditions for patient recovery, saving the lives of many dying patients.
For patients with mild to moderate mental clarity and cooperative respiratory failure, they can be mechanically ventilated by nasal or oral-nasal mask; for patients with serious conditions, clear mental clarity but uncooperative, coma or large amount of respiratory secretions, an artificial airway should be established in time, such as mechanical ventilation by nasal (or oral) tracheal intubation, using a PVC or silicone catheter with a high-capacity low-pressure balloon (<3.3kPa) with good histocompatibility, which can be retained for more than half a month. Avoid using rubber catheters with latex low-capacity high-pressure balloons, which can cause significant congestion, edema, erosion, and even ulceration of the airway mucosa due to the large reaction. In patients with very poor lung function, recurrent respiratory failure, secretions, extreme weakness, malnutrition, and need for long-term mechanical ventilation support, tracheotomy can be performed and long-term mechanical ventilation treatment with an indwelling tracheal tube.
Before using the ventilator, medical personnel must understand the pathophysiology of the patient’s breathing and give various parameters such as tidal volume, respiratory rate and respiratory ratio, such as obstructive ventilation requires a large tidal volume and slow expiratory breathing with a slightly longer frequency, while the opposite is true for patients with restrictive ventilation. The patient’s clinical performance, such as changes in thoracic mobility, airway pressure and oxygen saturation, can be monitored, and the ventilator parameters can be further adjusted after 20 min of follow-up arterial blood gas. In different periods of mechanical ventilation, different forms of ventilation should be selected, such as control equivalent to hand-controlled respiratory bag assisted ventilation or called assisted intermittent positive pressure ventilation (IPPV), end-expiratory positive pressure ventilation (PEEP), synchronized intermittent mandatory ventilation (SIMV), and pressure support ventilation (PSV). Different forms of ventilation can also be combined, such as PEEP + PSV as bi-level positive pressure ventilation (BiPAP.) PEEP improves ventilation, and SIMV and PSV facilitate disengagement from the ventilator in order to avoid hyperventilation or hypoventilation. Reduce the impact on cardiac circulation. To enhance airway and ventilator management during mechanical ventilation. For example, good wetting of the airway and suctioning of secretions to keep the airway open; cleaning and disinfection of the ventilator and maintenance to avoid cross infection. Special emphasis should be placed on the need to strengthen respiratory and cardiovascular monitoring, early detection of problems, analysis of problems, and appropriate solutions, so as to give full play to the positive role of mechanical ventilation in the treatment of respiratory failure, to achieve a reasonable and effective application of mechanical ventilation, improve its efficacy, and reduce the occurrence of complications.
Correct acid-base imbalance and electrolyte disturbance
In the diagnosis and treatment of respiratory failure, the following types of acid-base balance disorders are common.
(a) Respiratory acidosis: Due to insufficient alveolar ventilation, CO2 retention in the body produces hypercapnia, which changes the normal ratio of BHCO3/H2CO3 1/20 and produces acute respiratory acidosis. In patients with chronic respiratory failure, the pH is brought close to normal by the action of the blood buffering system and regulation by the kidneys (secretion of H+ and absorption of Na+ combined with HCO3- to form NaHCO3). Exhalation failure loss of generation acidosis can be temporarily corrected by alkali (5% NaHCO3) but it will reduce ventilation and further aggravate CO2 retention, so the underlying cause of acidosis is not removed. Only increasing alveolar ventilation can correct respiratory acidosis.
(b) Respiratory acidosis combined with metabolic acidosis: Due to hypo-O2emia, hypovolemia, reduced cardiac output and peripheral circulation disorders, fixed acids such as lactic acid increase in the body and renal impairment affects the excretion of acidic metabolites. Therefore, metabolic acidosis can be complicated on the basis of exhaled acid. There is an increase in fixed acid in the anion, a corresponding decrease in HCO3-, and a decrease in pH. Acidosis causes a shift of potassium ions from intracellular to extracellular, an increase in blood K+, a decrease in HCO3-, an expansive rise in blood CI-, and a movement of Na+ into the cells. When treating acidosis, supplementation with alkaline agents should be done only when the blood pressure is severely affected by acidosis or when the pH is <7.25, because NaHCO3 increases the risk of CO2 retention (NaHCO3 + HAC → NaAC + H2O + CO2). In this case, ventilation should be increased to correct CO2 retention and to treat the cause of metabolic acidosis.
(iii) Respiratory acidosis combined with metabolic alkalosis: During the treatment of chronic respiratory acidosis, it is often due to the application of mechanical ventilation, which makes CO2 excretion too fast; excessive supplementation of alkaline drugs; application of glucocorticoids and diuretics, which increases potassium excretion; or because of the correction of acidosis, potassium ions are transferred to the cells, producing hypokalemia. Vomiting or diuretics that lower blood chloride may also produce metabolic alkalosis with high pH and positive BE. Treatment should prevent the above medical factors of alkalosis from occurring and avoid too fast CO2 excretion, and give appropriate amount of Cushion chloride to relieve alkalosis, once it occurs, it should be treated promptly.
(iv) Respiratory alkalosis: This is respiratory alkalosis caused by excessive CO2 excretion due to hyperventilation in patients without respiratory system diseases who are mechanically ventilated in the event of cardiac arrest.
(E) Respiratory alkalosis combined with metabolic alkalosis: This is caused by mechanical ventilation in patients with chronic respiratory failure, which excretes too much CO2 in a short period of time and is lower than the normal value; and due to renal compensation, the absolute amount of bicarbonate in the body increases.
It can also be due to improper treatment, the patient in respiratory and metabolic acidosis, on top of low potassium, low chlorine caused by the triple acid-base balance disorder of alkali substitution.
V. Rational use of diuretics
In respiratory failure, the alveolar atrophy and pulmonary atelectasis caused by interstitial lung, alveolar, and fine bronchial bronchial mucous membrane edema affect the ventilatory function, and the water and sodium retention caused by the increase of aldosterone in the body and the increase of antidiuretic hormone due to the use of mechanical ventilation in respiratory failure. Therefore, in the case of heart failure in expiration, a trial of furosemide (10-20 mg) followed by a rise in oxygen saturation confirms the indication for diuretics. However, it must be used in the absence of electrolyte disturbances, and supplemental potassium chloride and sodium chloride (administered mainly by the digestive tract) must be given promptly to prevent alkalosis.
In summary, in the management of expiration, as long as mechanical ventilation, oxygen administration, diuretics and alkali agents are reasonably applied, nasal and intravenous supplementation of nutrition and electrolytes, especially in patients with chronic obstructive pulmonary heart disease who rarely eat and take diuretics for a longer period of time. Therefore, the acid-base balance imbalance and electrolyte disorder of respiratory failure can be investigated and prevented.
Sixth, anti-infection treatment
Respiratory tract infections often trigger respiratory failure, and the accumulation of secretions aggravate the infection, especially in patients with artificial airway mechanical ventilation and immunocompromised patients can repeatedly occur infection, and it is not easy to control the infection. Therefore, patients with respiratory failure must choose effective drugs to control respiratory tract infection under the condition of keeping the airway drainage unobstructed and according to the sputum culture and its drug sensitivity test. It must also be pointed out that patients with chronic obstructive pulmonary heart disease have repeated infections and often do not have fever, blood leukocytes are not high toxic symptoms, only feeling shortness of breath aggravated, decreased appetite, if not timely treatment, mild infection can also lead to decompensated respiratory failure.
VII. Prevention and control of gastrointestinal bleeding
For patients with severe O2 deficiency and CO2 retention, cimetidine or ranitidine should be routinely given orally to prevent gastrointestinal bleeding. In case of massive vomiting of blood or tarry stools, fresh blood should be transfused or norepinephrine ice water should be instilled into the stomach. H2 receptor antagonist or omeprazole must be given intravenously. The key to preventing and treating gastrointestinal bleeding is to correct O2 deficiency and CO2 retention.
VIII. Shock
There are many causes of shock, such as acidosis and electrolyte disorders, serious infection, gastrointestinal bleeding, hypovolemia, heart failure, and high airway pressure with mechanical ventilation, so appropriate measures should be taken for the cause. If no improvement is seen after treatment, vasoactive drugs such as dopamine and alamine should be given to maintain blood pressure.
IX. Nutritional support
Patients with respiratory failure are in negative metabolism due to insufficient caloric intake and increased respiratory work and fever, resulting in increased energy consumption. For a long time, it will reduce the immune function of the body, infection is not easy to control, respiratory fatigue, so that respiratory pump failure occurs, so that the failure of resuscitation or prolong the course of the disease. Therefore, during resuscitation, nasal feeding with high protein, high fat and low carbohydrate, as well as multivitamins and trace elements is routinely given, and intravenous high nutrition therapy is given if necessary, generally up to 14.6k/kg of daily calories.