Respiratory failure
| Respiratory failure | |
|---|---|
| A classification and outside reference information | |
| ICD-10 | J96 |
| ICD-9 | 518.81 |
| DiseasesDB | 6623 |
| eMedicine | med/2011 |
| MeSH | D012131 |
I am defined as "the state that arterial blood gas shows an abnormal value, and the living body runs a normal function to save it, and it does not get", and, with the respiratory failure (こきゅうふぜん, respiratory failure), an arterial blood oxygen tension (PaO2) at the time of the room mind inhalation points to the abnormality state equivalent to respiratory functional disorder becoming less than 60Torr or it and diagnoses this with respiratory failure (Ministry of Health and Welfare specific disease "respiratory failure" investigation study group 1981 report).
A respiratory obstacle exists and, at time when medullary cyanosis is recognized even if arterial blood gas under the indoor mind inhalation cannot measure it, I diagnose it with respiratory failure from a value of the arterial blood oxygen saturation (SaO2) and do not interfere. PaO2 60Torr is almost equivalent to SaO290%.
The respiratory failure is classified as follows more by the degree of the arterial blood carbon dioxide partial pressure (PaCO2).
Type I respiratory failure………PaCO2s are less than 45Torr
Type II respiratory failure…… A PaCO2 is beyond 45Torr
In addition, a PaO2 is beyond 60Torr, and the associate respiratory failure says less than 70Torr.
Table of contents
Being PaO2 <= 60Torr which is why or
When a PaO2 becomes steep from a point of 60Torr, I am listed in many textbooks, but the lurch of the oxygen estrangement curve of the hemoglobin is a mistake. It shows the form of the estrangement curve at a glance like that. However, when an estrangement curve demands the value of the PaO2 becoming steep by a calculation, the value is 30 - 40Torr and is not 60Torr.
Then I show the reason from the oxygen supply to the organization why it is 60Torr. When hypoxemia is caused, and a PaO2 decreases when the entrance to the organization is a PaO2, and an exit assumes it a venous blood oxygen tension (PvO2), and PvO2 which is the exit of the organization decreases together, the oxygen consumption that is used in the organization if the bloodstream to the organization is the same is the same as in front of where the hypoxemia is angry at. However, the neighboring organizations fall into lack of oxygen when PvO2 of the exit of the organization decreases. A far-off cell falls into lack of oxygen from blood vessel. Therefore PvO2 does not fall to a certain value even if a PaO2 decreases in the living bodies. The value is PaO2 = 60Torr.
This study is a thing for COPD patients, but it is said that PvO2 decreases for the pulmonary artery-related pulmonary hypertension (primary pulmonary hypertension) from PaO2 80Torr (for an application disease of the at-home oxygen therapy with "having hypoxemia or not pulmonary hypertension").
Mechanism of the hypoxemia
Case without the rise in PaCO2
1) Ventilation/perfusion ratio disproportion (VA/Q mismatch)
Ventilation and the ratio of the bloodstream are concerned with gas exchange when they assume an alveolus and bloodstream to perform gas exchange there one gas exchange unit. In other words, there is too much ventilation, and the PaO2 of the part approaches the alveolus mind oxygen tension in the place with a little bloodstream. However, the ventilation becomes extra. Dead space effect means this. On the other hand, on the contrary, there is little ventilation, and the PaO2 becomes near PvO2 even if there is too much bloodstream. This is called physiologic シャント effect. If there are many balanced alveoluses of VA/Q, the PaO2 is improved. It is around 0.8 in the physically unimpaired people. Relations with a PaO2 and the PaCO2 by different VA/Q are usually shown by O2-CO2 die gram. In other words, the PaO2 is normal in the alveolus of high VA/Q, but the PaO2 decreases in the alveolus of low VA/Q. The PaCO2 decreases in high VA/Q to be affected by the alveolus ventilation. VA/Q decreases a base of lung with the standing position for influence of the circulation of the blood in the lungs by the gravity in the normal lungs. On the other hand, maldistribution of VA/Q is caused by the disease lungs by various kinds of factors. Maldistribution abnormality of VA/Q is an important factor of the hypoxemia with alveolus low ventilation in the chronic obstructive pulmonary disease patients. Because dissolution speed is approximately 25 times of oxygen, as for the CO2, the PaCO2 does not change very much even if VA/Q becomes smaller than 0.8. On the other hand, the PaCO2 decreases if it becomes bigger than 0.8.
2) Right → left シャント (anatomical シャント and physiologic シャント)
Anatomical シャント says that venous blood gets mixed with arterial blood for 肺動静脈瘻, congenital interventricular septum deficiency and atrial septal defect. On the other hand, physiologic シャント shows the bloodstream that VA/Q flows through 0 alveoluses. 100% of measurement of the シャント rate measures a PaO2 in the state that let you inhale oxygen for 20 minutes and are demanded than a principle of Fick. If a シャント rate is high, the PaO2 does not rise even if I make oxygen inhalation.
3) A diffusion disorder
Oxygen of the alveolus mind passes an alveolus epithelium cell, a stroma, a capillary endothelium, plasma with the hemoglobin in the red blood cell in the capillary from an alveolus cavity. This phenomenon is called diffusion. The disorder of this process causes the hypoxemia. In addition, the ability for diffusion of the CO2 is approximately 20 times of oxygen, and there is not the diffusion disorder with a problem.
This diffusive process is measured as ability for pulmonary diffusion. I let this inhale low-concentrated CO (0.1-0.3%) and find pulmonary diffusing capacity (DLCO) in quantity of CO (ml/min)/ average alveolus mind CO partial pressure (Torr) spreading through pulmonary capillary for one minute. Because this calculation supposes the lungs to be a single model to the last, the DLCO is affected by the VA/Q mismatch.
When it is accompanied by the rise in PaCO2, I it
It is explained by a following alveolus type. In other words, it is PaCO2 = 0.863 x VCO2/VA-------(1)
In VCO2, CO2-producing quantity, VA (V dot A) show an alveolus amount of ventilation here.
PAO2 = 150 - PaCO2/0.8------------(2)
The PAO2 shows an alveolus mind oxygen tension here, and the alveolus mind CO2 partial pressure is equal to a PaCO2.
In other words, when alveolus low ventilation exists, the PaCO2 rises than a (1) type and the PAO2 decreases, as a result, (2)-type, to be shown and is connected for the drop of the PaO2.
Acute respiratory failure and chronic respiratory failure
Acute respiratory failure
I am understood to be angry respiratory failure in acute progress, but there is not the definition of the clear period. Not only I merely mean time progress, but also the condition of a patient changes every moment, and quick correspondence must understand the acute respiratory failure with a required abnormality state.
Chronic respiratory failure
I say the thing that a state of the respiratory failure lasts more than at least one month.
Condition of a patient of the chronic respiratory failure
1) Respiratory muscle fatigue
Respiratory muscle fatigue is decided on the energy supply for the respiratory muscle with the balance of the breathing work load and is caused a drop (heart failure, hypoxemia) of the bloodstream for the (1) respiratory muscle, a (2) hypoalimentation state, a drop of the diaphragm line ventilation efficiency for diaphragm low degree by the (3) lung capacity increase by the increase of the respiratory muscle work load by the elasticity of the lungs and the viscosity resistance increase (4). For respiratory muscle fatigue with respiratory illness, it becomes the tachypnoea, and the amounts of ventilation decrease once. In addition, the strange breathing that the abdomen recesses at the time of intake by diaphragm muscle fatigue appears. It is ventilated an alveolus low when it progresses, and the hypoxemia with the high carbon dioxide blood symptom is caused, and CO2 null Coe cis に falls into it. Because not only the intake muscle fatigue but also the expiration muscle fatigue exists in the COPD patients at the same time, I can wave the rectus abdominis muscle which is an expiration line firmly.
2) A circulation of the blood in the lungs disorder
The chronic respiratory failure patient is complicated with pulmonary hypertension to a high rate. I am associated with degree of the hypoxemia, and, as for approximately 90% of COPD patients who fell into chronic respiratory failure, mean pulmonary arterial pressure is beyond 20Torr. The merger of the pulmonary hypertension is one of the poor-prognosis genes. The architectural destruction of the pulmonary blood vessel by disease in itself and hypoxia-related pulmonary vasoconstrictive participation are big as a cause of the pulmonary hypertension. When pulmonary hypertension lasts; called the cor pulmonale with right heart enlargement and right heart failure is in a condition. The clinical evidence accepts tachycardia, arrhythmia, jugular vein overswelling, hepatomegaly, abdominal dropsy. When pulmonary artery expansion particularly right pulmonary artery descending branch diameter is more than 15mm, I doubt a merger of the pulmonary hypertension with a chest x-ray film. When the electrocardiography was accompanied by right ventricle enlargement, it presents an expensive R wave and right leg block of V1. I often accept pneumonic p (pointed p wave more than II, III, 0.25mV of aVF), but, in the case of COPD, it is for the axis shift of the p wave by the turn of the right atrium by diaphragm low degree and a drop-formed heart and is poor for diagnosis grounds of the pulmonary hypertension. It varies according to an underlying disease, but, about the left heart function, it is reported that left heart failure is complicated with 10-46% of the COPD patient.
3) A central nerve disorder
It often presents a depressed mental state and an uneasy state in the chronic respiratory failure patients. However, as for immediate correspondence being required by clinical practice, a chronic respiratory failure patient is an acute central nerve obstacle to take place when I aggravate it with infection. Brain fever pneumonic for disturbance of consciousness caused as a result of high hypoxemia and high carbon dioxide blood symptom and the case due to the good high carbon dioxide blood symptom are CO2 null Coe cis という. Not the direct action to brain of the CO2 null Coe cis は carbon dioxide, it depends on a drop of pH in the brain tissue. Therefore, a PaCO2 is a high price, but does not have CO2 null Coe cis は when the compensation of the kidney is done for chronic type II respiratory failure enough, and pH is kept approximately normally.
When it is accompanied by a high carbon dioxide blood symptom for hypoxemia by a headache, shaking, convulsions, deep sleep, there are many symptoms. A headache, the shaking are important as an early symptom. In addition, I am careful about mind, nerve abnormality as the side effect of use drug.
4) GI tract disturbance
The merger of the gastric ulcer is common in respiratory failure patients. I am seen in approximately 30% of COPD patients. A gastric mucosa disorder is caused by sthenia of the gastric acid secretion due to the hypoxemia, a drop of the gastric mucosa bloodstream, a rise in histamine density.
5) A liver function disorder
There are rather few liver damages by hypoxemia alone and is easy to appear when I am complicated with a cor pulmonale. The oxygen supply to liver is carried out through a hepatic artery and pro-low pressure portal vein. When central venous pressure rises by right heart failure, the perfusion pressure on liver through the portal vein decreases. Therefore the oxygen supply to liver falls, and the hypoxemia increases, too, and hepatocytes disorder is caused. A sinusoid (sinusoid) is magnified by an upswing in central venous pressure, and it becomes the factor to exacerbate a liver damage that neighboring hepatocytes are pressed physically.
6) A renal damage
The kidney relatively has resistance for hypoxia, but oliguria, high urea azotemia, a rise of the serum creatinine are seen in approximately 15% of respiratory failure.
7) Blood abnormality
It presents vicarious plethora as a result of chronic hypoxemia in the highlands inhabitants. However, there is little plethora for the chronic respiratory failure based on respiratory illness, and there is rather more anemia.
Treatment of the chronic respiratory failure
I continue the treatment for the underlying disease and provide the following treatment.
1) Oxygen therapy
The purpose of the oxygen therapy improves hypoxemia and not only I improve the oxygen supply to the organization, but also reduce the work load that increased of the lungs and heart by returning an amount of ventilation and the heart rate that I aggravated for a compensation to hypoxemia to the cause. In addition, I prevent hypoxia-related pulmonary angiospasm in the circulation of the blood in the lungs and prevent pulmonary hypertension.
(1) a PaO2 to start oxygen inhalation
When PaO2s became less than 60Torr, I start oxygen inhalation. However, for the patient complicated with anemia and a heart trouble for acute hypoxemia and hypoxemia, I start oxygen inhalation even if PaO2s are more than 60 Torr.
There are a patient appealing for dyspnea without hypoxemia and the patient who does not notice dyspnea even if there is hypoxemia adversely.
I perform oxygen inhalation even if I appeal for dyspnea after confirming hypoxemia by arterial blood gas analysis or the SpO2 measurement.
Dyspnea ≠ hypoxemia ≠ oxygen inhalation should note it.
※Dyspnea "4 is reference for dyspnea"
(2)PaO2 after the oxygen inhalation
As for the target value, the PaO2 of the chronic respiratory failure patient aims at more than at least 60Torr.
There are a few rises in SaO2 even if I do a PaO2 than 60Torr to be clear from an oxygen dissociation curve of the oxygenicity hemoglobin. In other words, there is a little increase of the arterial blood oxygen content. In addition, as for the time to arterial blood drawing blood from oxygen inhalation, it is necessary for 15-30 minutes, and a check of the presence of the rise in PaCO2 is important as well as a PaO2.
For a patient of the type II respiratory failure, ventilation restraint happens when I let you inhale highly-concentrated oxygen from the beginning, and a PaCO2 rises, and CO2 null Coe cis に is in danger of falling into it. Therefore I let you inhale the beginning from low-concentrated oxygen. Even if a PaCO2 is high, pH does not have to return a PaCO2 to the normalcy area in respirators when it is kept relatively well by the compensation of the kidney. However, I attach a respirator for the high type II respiratory failure that was suddenly caused. In addition, noninvasive artificial respiration (non-invasive positive pressure ventilation;NPPV) spreads recently, and the effectiveness is reported.
(3) a pulmonary obstacle (oxygen poisoning) by the highly-concentrated oxygen inhalation
A fatal pulmonary disorder is caused when exposed to 100% of oxygen by the animal experiment for a few days. In the person, a drop of the pulmonary compliance, an open size of alveolus mind, the arterial blood oxygen tension range (A-aDO2), pulmonary blood vessel hyperpermeability appear for the inhalation for 100% oxygen 24 hours. There is individual difference in the degree of the obstacle, but the degree of the pulmonary obstacle reinforces it in proportion to inhalational oxygen density (oxygen tension of the inhalational mind) and inhalational time. Therefore, I treat the inhalational oxygen density to do it in less than 60% (if it is possible, less than 50%) as much as possible.
2) At-home oxygen therapy
As for the at-home oxygen therapy, an insurance application was accepted for the first time in 1985. The revision of the application standard is carried out and reaches it afterwards at the present. An oxygen concentrator and liquefaction oxygen are used for the oxygen supply device. I choose it in consideration of age, the physical strength of the patient, activities of daily living range, a home environment.
3) Breathing rehabilitation
The breathing rehabilitation reduces dyspnea with the body movement and improves exercise tolerance. Furthermore, as well as improvement of the QOL, it is reported that uneasiness and dejection states improve a psychosocial symptom. However, it is important for the effect to continue when it stops rehabilitation to return to the cause. The basics perform exercise more than quantity of load decided by kinesitherapy per day more than three times a week.
4) Nourishment management
It is often accompanied by hypoalimentation in the chronic respiratory failure patients. Because hypoalimentation is one of the poor-prognosis genes, I perform the measures.
5) The infection prevention
Most of chronic respiratory failure patients aggravate it with infection, and hospitalization medical treatment is necessary. Particularly, I do not return to a state before the infection even if infection heals the breathing function worsened by infection. I let you refrain from going out of the time when an enforcement, influenza of hand-washing and the gargle after the return are prevalent. I recommend the influenza vaccine inoculation every year. When the Streptococcus pneumoniae vaccine is effective and passes from the first inoculation more than five years, I can inoculate it again.
Convalescence of the chronic respiratory failure patient
Naturally, according to the collaborative investigation of the Ministry of Health and Welfare specific disease "respiratory failure" investigation study group, as for the convalescence according to the underlying disease of the patient receiving at-home oxygen therapy for chronic respiratory failure, a lung cancer patient has a poor prognosis (6.6% of five years survival rates). Then, it is stroma-related pneumonia (21.2%), chronic pulmonary emphysema (41.7%), chronic bronchitis (45.5%), the order of pulmonary tuberculosis aftereffects (52.4%).
Dyspnea
Definition
It is an unpleasant sense with the breathing and is seen in not only respiratory illness but also a circulatory organ disease (heart failure due to various kinds of diseases), a neuromuscular disease (muscular dystrophy, Guillain-Barre syndrome), the mind nerve disease (neurosis, hyperventilation syndrome) and is a complaint to sit astride the plural clinical departments. In addition, it is different by by the patient including the feeling to do the wheeze that breath sucks in the way of feeling (suit), and insufficient breath is clogged up or a cause disease.
Outbreak mechanism
There are some opinions, but is still unknown. Above all, the output information from a respiratory center to a respiratory movement nerve is projected on a higher sense center at the same time and motor command theory saying that they recognize dyspnea in a cerebral cortex sensory area is convincing, but cannot explain all by this mechanism.
Receptor about the feeling of dyspnea outbreak
- Chemical receptor in response to hypoxemia and a high carbon dioxide blood symptom, acidosis,
- イリタント receptor and C-fiber distributed over the respiratory tract and the lungs,
- The mechanical receptor that there is to a line and a tendon, the joint of the fort,
- Excitement of the emotion of the limbic system and the optional respiratory movement center.
Rating system
Fletcher, Hugh-Jones classification were used as a rating system of the shortness of breath with the daily living activity in Japan, but modified MRC (Medical Research Council) classification is common now.
Because Visual analogue scale and Borg scale or modified Borg scale can digitize degree of the shortness of breath, it is useful for an evaluation of dyspnea before and after the treatment. However, it is difficult to compare dyspnea at that time if quantity of load is different. The values that divided dyspnea score by walk distance and an oxygen consumption for the purpose of being standardized are used.
Borg scale (6-20) is a respiratory field, and modified Borg scale (0-10) is used in the field of the circulatory organ.
Dyspnea measures: There are oxygen therapy, breathing rehabilitation, an inhalational therapy, art of pulmonary capacity reduction (for pulmonary emphysema).
Footnote
References
![[icon]](https://upload.wikimedia.org/wikipedia/commons/thumb/1/1c/Wiki_letter_w_cropped.svg/20px-Wiki_letter_w_cropped.svg.png){kind=small} | The correction of this knob is expected. |
- Ciba guest symposium. Terminology, definitions, and classification of chronic pulmonary emphysema and related condition. It is 286-299, 1959 Thorax 14.
- Kawakami Y et al. Criteria for pulmonary and respiratory failure in COPD patients - a theoretical study based on clinical data. Respiration 43:436-443,1982.
- Ministry of Health and Welfare specific disease "respiratory failure" investigation study group, 1981 study achievements, p1, 1982.
- Yoshikazu Kawakami, others. An effect on blood of the oxygen inhalation in the respiratory failure and organization oxygenicity. It is 680-686, 1977 日胸疾会誌 15.
- Ministry of Health and Welfare specific disease "respiratory failure" investigation study group "guidelines for a respiratory failure diagnosis and treatment." p10-13, medical review company, Tokyo, 1996.
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