Chronic respiratory failure

Etiopathologic etiology and pathogenesis of chronic respiratory failure often bronchial-pulmonary diseases are caused by chronic obstructive pulmonary disease, severe tuberculosis, pulmonary interstitial fibrosis, such as pneumoconiosis. Thoracic diseases and thoracic surgery, trauma, extensive pleural thickening, thoracic deformity can lead to chronic respiratory failure. Pathogenesis and pathophysiology one, na O2 and CO2 retention mechanism for the occurrence of (a) lack of ventilation in the resting breathing air, alveolar ventilation total about 4 L / min, in order to maintain the normal alveolar oxygen and carbon dioxide partial pressure. Decreased alveolar ventilation, alveolar oxygen partial pressure decreased partial pressure of carbon dioxide increased. Breathing air conditions (concentration of inhaled oxygen 20.93%, carbon dioxide is close to zero), alveolar oxygen partial pressure of carbon dioxide and alveolar ventilation volume and the relationship Chart 2 -6-1. Figure 2-6-1 alveolar oxygen and carbon dioxide partial pressure and the amount of alveolar ventilation (2) ventilation / blood ratio of pulmonary disorders ventilation and perfusion of peripheral capillary blood flow ratio must be coordinated in order to ensure the effective gas exchange. Every minute of normal alveolar ventilation (VA) 4L, pulmonary capillary blood flow (Q) 5L, whichever is the ratio of 0.8. If alveolar ventilation volume ratio of greater than in blood flow ( "0.8). Was formed physiological dead space, it is null and void cavity effect; Alveolar ventilation volume is less than the ratio of blood flow ( "0.8). Mixed pulmonary arterial blood oxygenation without full access to the pulmonary veins, it forms kind arteriovenous shunt (Figure 2 -6-2). Ventilation / blood disorder, which have na O2, CO2 without retention. Because of this mixed venous and arterial blood oxygen partial pressure of CO2 worse than the much more pressure for the former 7.98 kPa. and the latter only 0.79 kPa, a difference of 10 times. It may sound excessive alveolar ventilation, higher emissions of CO2 to compensate alveolar ventilation inadequate retention of CO2, emit even more CO2, respiratory alkalosis. As hemoglobin oxygen dissociation curve characteristics, and normal pulmonary capillary blood oxygen saturation at a flat, Even if ventilation and air suction, the alveolar oxygen partial pressure has been increased, but the oxygen saturation increased little, So by the sound of alveolar ventilation can not be over-compensate the shortage of alveolar ventilation caused by oxygen shortage the resulting lack of O2. Ventilation "normal blood flow" ventilation (dead space effect) (effective ventilation) (EIAB static effect) Figure 2-6 - 2 ventilation / blood ratio of gas exchange in (3) pulmonary arterio - venous shunt-like lung lesions as if alveolar collapse. atelectasis, pulmonary edema and pneumonia, it can cause pulmonary changes like triage, make any contact with blood gas alveolar gas exchange opportunities. Therefore, raising the oxygen concentration and would not improve arterial blood oxygen. - Flow is, after improving arterial oxygen partial pressure of the worse effects, such as flow-over 30%, Oxygen partial pressure of a limited impact. (4) diffusion barriers oxygen diffusing capacity of carbon dioxide is only 1 / 20, the dispersion of the obstacles, produced a simple lack of oxygen. (5) oxygen consumption increased oxygen consumption is increased hypoxia one of the reasons, fever, chills, breathing difficulties and convulsion were to increase oxygen consumption. Shivering oxygen consumption up to 500 ml / min, severe asthma, with the increased work of breathing. oxygen consumption to 10 times normal. Oxygen consumption increased alveolar oxygen pressure drop through normal volume increased ventilation to prevent hypoxia. Figure 2 -6-3 said breathing air, oxygen consumption changes and the right pulmonary alveolar ventilation volume relationship. Map of the curve and the dotted line to the point of intersection of different oxygen consumption, maintain normal pulmonary alveolar ventilation in the amount of Along with the increase in oxygen consumption and the corresponding increased significantly, oxygen consumption per minute to 200 ml, 400 ml, 800 ml, alveolar ventilation volume reached 3L, 6L, 12L. Each map from the preceding steep curve, the back of the flat features can see, oxygen consumption increased ventilation in patients with dysfunction of pulmonary not improve, would not alleviate hypoxia. Figure 2 -6-3 different oxygen consumption alveolar ventilation volume and the alveolar oxygen partial pressure (curve adjacent oxygen consumption figures ml / min) 2, and none O2, CO2 retention effects on the body (1) the effects on the central nervous brain tissue oxygen consumption volume of about a systemic / 5-1 / 4. Central cortex cells most sensitive to hypoxia, na O2 and the extent of alternates from one extreme to the middle of the central nervous meeting the highest hygiene different effects. If suddenly interrupted for O2, switch to the active 20 seconds, there will be deep coma and body convulsion. Gradually reduce the concentration of O2, and the symptoms appeared slow, mild hypoxia can lead to inattention, mental decline, disorientation; With the increasing shortage of O2, arterial partial pressure of oxygen (PaO2) to be lower than 6.66kPa irritability, a trance-like state of mind. delirium; less than 3.99 kPa, would lose consciousness, and even coma; 2.66 kPa below will be irreversible brain cell injury. CO2 retention enable CSF increase in the concentration of hydrogen ions, the effects of brain cell metabolism, reducing brain cell excitability, cortical inhibition; With the increase of CO2, the lower cortical stimulation to strengthen caused cortical excitability; If CO2 continues to rise, subcortical restrained, the central nervous at the anesthesia. In the event of pre-anesthesia patients often suffer from insomnia, nervous excitement, irritability indication excited symptoms. Na O2 and CO2 retention-will cerebral vasodilator, vascular resistance decreased blood flow to compensate's. Serious shortage of oxygen will occur within brain cells edema, increased vascular permeability and cerebral interstitial edema, resulting in increased intracranial pressure, Squeeze brain tissue, vascular compression, thus compounding the brain tissue hypoxia, creating a vicious cycle. (2) of the heart, the effects of hypoxia can stimulate the heart, heart rate and stroke volume increase, a rise in blood pressure. Coronary blood flow in the absence of O2 at significantly increased cardiac blood flow far exceeds the brain and other organs. Lack of myocardial oxygen sensitive, early or mild hypoxia on the electrocardiogram showed there, Acute serious shortage of oxygen can lead to ventricular fibrillation or cardiac arrest. Na O2 and CO2 retention can cause pulmonary vasoconstriction and the small increase in pulmonary vascular resistance. lead to pulmonary hypertension and right heart additional burden. Inhaling gas CO2 concentration increased, enable rapid heart rate, stroke volume increased, brain, the coronary vasodilation. subcutaneous superficial capillaries and veins expansion, so the spleen and muscle vasoconstriction, coupled with increased stroke volume, Therefore, the blood pressure is still elevated. (3) lack of respiratory effects of breathing oxygen than the impact of CO2 retention of small. O2 mainly through lack of carotid sinus and aortic body chemoreceptor stimulation of the reflex ventilation, If na extent O2 slow increase, which reflected slow. CO2 is a powerful respiratory center stimulants, inhalants increase in the concentration of CO2, ventilation volume increased exponentially, Acute CO2 retention appeared deep rapid breathing; However, when the child inhales smoke of more than 12% CO2 concentration, ventilation volume will not increase, the respiratory center in the inhibited state. And chronic hypercapnia, there is no corresponding increase in ventilation capacity, but has declined, and the respiratory center reactive retardation. right kidney through bicarbonate absorption and re-emission of H +, blood pH no significant decrease in patients with increased air resistance, Serious damage to lung tissue, the thorax movement of the hypofunction. (4) the liver, kidney and hematopoietic system, the lack of O2 directly or indirectly damage the liver so that GPT rise But with the lack of redress O2, liver function returned to normal gradually. Oxyhemoglobin reduced, renal blood flow, volume of glomerular filtration and urinary excretion of sodium and emissions of both increased; But PaO2 "5.3kPa, renal blood flow, renal function was inhibited. Organization low oxygen pressure increased erythropoietin prompted RBC hyperplasia. Kidney and liver produce an enzyme, the activity of the blood Africa erythropoietin, the predecessor of material generated by stimulating factors, stimulate the bone marrow caused secondary erythrocytosis. Helps increase the oxygen-carrying capacity of blood, but also increased blood viscosity, increased pulmonary circulation and right heart burden. CO2 retention mildly dilated renal vascular will increase renal blood flow, increased urine output; When PaCO2 more than 8.64 kPa, decreased blood pH, renal vascular spasm, reduced blood flow, HCO3-and Na + reabsorption, decreased urine output. (5) electrolyte and acid-base balance of a serious shortage of oxygen can inhibit cell energy generation process launched in the middle, If herbs cycle, oxidative phosphorylation and the role of the enzyme activities. This will not only reduce energy efficiency have also produced by the lactic acid and inorganic phosphorus cause metabolic acidosis. As the energy shortage in vivo ion transport the sodium pump was damaged, potassium ion cells transferred to the blood, and Na + and H + into cells, causing intracellular acidosis and hyperkalemia. Metabolic acidosis the fixed buffer acid and bicarbonate system works, produced carbonate, enable organizations increased partial pressure of carbon dioxide. PH value depends on the bicarbonate and carbonate ratio, the former regulation on the kidney (1-3 days). Carbonate and regulation on lung (a few hours). Healthy daily discharges from lung mmol carbonate reach as many as 15,000. Therefore, acute respiratory failure CO2 retention pH of the impact is very rapid, often with metabolic acidosis existing at the same time, due to severe acidosis caused decreased blood pressure, arrhythmia, and even cardiac arrest. And chronic respiratory failure due to CO2 retention, the slow renal bicarbonate to reduce emissions, and the result is not significantly lower pH. Mainly due to blood anion HCO3-and CI - was taken as a constant, HCO3-, then CI-reduced accordingly, have low Hyperchloremia.