The incidence of respiratory failure mechanisms and pathophysiology

The incidence of respiratory failure mechanisms and pathophysiology

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. Figure 2-6-3 that 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. From the map in each of the earlier steep, after the characteristics of the flat can see that the increase in oxygen consumption dysfunction in patients with ventilation, alveolar oxygen can not be raised, hypoxia hardly eased.

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

(A) the impact of 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, 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.