Health Worlds

First, the lack of O2 and CO2 retention mechanism of
(A) lack of ventilation breathing air at rest, the total alveolar ventilation is about 4L/min, in order to maintain normal alveolar partial pressure of oxygen and carbon dioxide. Decreased alveolar ventilation, alveolar oxygen partial pressure decreased, carbon dioxide partial pressure increased. Breathing air condition (20.93% inspired oxygen concentration, carbon dioxide close to zero).
(B) of the ventilation / perfusion imbalance of ventilation and perfusion of alveolar capillary blood flow around the ratio must be coordinated to ensure effective gas exchange. Normal alveolar ventilation per minute (VA) 4L, pulmonary capillary blood flow (Q) 5L, the ratio between the 0.8. If alveolar ventilation is greater than the rate on blood flow (> 0.8). Increase in physiological dead space is formed, that is, dead space effect; alveolar ventilation in the ratio of less than the blood flow (<0.8), mixed venous blood to the pulmonary artery into the pulmonary vein without adequate oxygenation, the formation of arteriovenous-like shunt. Ventilation / perfusion imbalance, resulting in lack of O2, but no CO2 retention. This is due to mixed venous and arterial blood oxygen difference is much greater than the CO2 partial pressure, the former 7.98kPa, while the latter only 0.79kPa, a difference of 10 times. It may, by a healthy alveolar hyperventilation, and expel more CO2, the compensatory alveolar hypoventilation retention of C


O2, or even release more CO2, respiratory alkalosis. The hemoglobin oxygen dissociation curve characteristics, the normal alveolar capillary oxygen saturation has been in the flat segment, the increase in ventilation, breathing air, the alveolar oxygen partial pressure despite the increase, but little increase in oxygen saturation, so by improve alveolar ventilation can not be compensated over the alveolar hypoventilation due to lack of oxygen uptake, which occurred missing O (C) of the pulmonary artery - vein-like lung disease, such as split as alveolar collapse, atelectasis, pulmonary edema and pneumonia-like consolidation may lead to pulmonary artery shunt to increase, so that no with alveolar gas blood gas exchange opportunities. Therefore, raising the oxygen concentration does not improve arterial oxygen tension. Fractional flow the greater the oxygen partial pressure of oxygen after the effect of increased arterial blood worse, as more than 30% of sub-flow, oxygen on the partial pressure of oxygen is limited.
(D) diffusion barriers to oxygen diffusing capacity of carbon dioxide is only 1 / 20, so in the diffusion barrier, the resulting hypoxia.
(E) the increase in oxygen consumption increased oxygen consumption O2 missing one of the reasons, fever, chills, breathing difficulties and seizures are to increase oxygen consumption. Chills oxygen consumption up to 500ml/min, severe asthma, with increased work of breathing, oxygen consumption can be ten times as normal. Increased oxygen consumption, alveolar oxygen partial pressure decreased to normal with increased ventilation to prevent hypoxia. Figure 2-6-3 that breath the air, the change of oxygen consumption and alveolar ventilation, alveolar oxygen partial pressure relations. The figure the dashed curve and the point of intersection for different oxygen consumption, the maintenance of normal alveolar oxygen partial pressure required for alveolar ventilation, with the increase in oxygen consumption, was a corresponding increase in oxygen consumption per minute, respectively, 200ml, 400ml, 800ml, the alveolar ventilation respectively 3L, 6L, 12l. From the figure, each curve is steep front, features a flat rear section also shows that the increase in oxygen consumption in patients with ventilatory dysfunction, alveolar partial pressure of oxygen does not improve, hypoxia hardly eased.
Second, the lack of O2, CO2 retention effects on the body
(A) the impact on the central nervous about the whole body oxygen consumption of brain tissue consumption of 1/5-1/4. Central cortical neuron cells are most sensitive to hypoxia, lack of O2 Jihuan the extent and occurrence of central nervous system produce different effects on students meeting high prices. Such as a sudden break for O2, 20 seconds to change the nitrogen absorption can occur deep coma and convulsions. Decreasing the concentration of O2 absorption, the slow onset of symptoms, mild lack of O2 can cause lack of concentration, mental deterioration, disorientation; with the lack of increased O2, arterial oxygen pressure (PaO2) less than 6.66kPa can cause irritability, trance, delirium; below 3.99kPa, makes the loss of consciousness and even coma; below 2.66kPa is irreversible brain cell damage.
CO2 retention to increase the hydrogen ion concentration in cerebrospinal fluid and affect brain cell metabolism, reducing brain cell excitability, inhibition of cortical activity; as CO2 increases, the lower stimulation of the cortex to strengthen, causing cortical excitability; if CO2 continues to rise, subcortical suppression so nervous in the anesthetized state. Appeared before anesthesia in patients often have insomnia, excitement, restlessness, a harbinger of excitement symptoms.
Lack of O2 and CO2 retention are cause cerebral vasodilation, vascular resistance decreases, blood flow to compensate it. O2 serious shortage of brain cells occurs within the edema, increased vascular permeability, interstitial edema caused by the brain, leading to increased intracranial pressure, brain tissue extrusion, pressure vessels, thus increasing shortage of brain tissue O2, a vicious circle.
(B) of the heart, circulation of lack of O2 can stimulate the heart, the heart rate and stroke volume increased, increased blood pressure. O2 in the absence of coronary artery blood flow is significantly increased blood flow to the heart far more than the brain and other organs. Very sensitive to the lack of myocardial O2, early mild lack of O2 that is displayed on the ECG appearance of acute severe shortage of O2 can cause ventricular fibrillation or cardiac arrest. Lack of O2 and CO2 retention can lead to increased pulmonary vasoconstriction of small pulmonary vascular resistance, resulting in increased pulmonary hypertension and right heart burden.
CO2 concentration in the inhaled air, can heart rate, stroke volume increased, the brain, coronary vasodilation, superficial skin capillaries and veins expand, leaving the spleen and muscle vasoconstriction, coupled with increased stroke volume, so blood pressure remains elevated.
(C) lack of respiratory effects of O2 on the respiratory effects than CO2 retention is small. O2, mainly through lack of carotid sinus and aortic body chemoreceptor reflexes stimulated ventilation, such as the lack of O2 levels increased slowly, this reflex slow.
CO2 is a strong respiratory stimulants, inhalation of CO2 concentration, ventilation doubled, acute CO2 retention occurs deep rapid breathing; when inhaled 12% CO2 concentration, did not increase ventilation, the respiratory center in the be restrained. And chronic hypercapnia, there is no corresponding increase in ventilation, but declined, this slow reaction with the respiratory center, through the kidney bicarbonate reabsorption and H + excretion, so that no significant decrease of blood pH values, but also with patients Air resistance increases, a serious lung damage, chest movement dysfunction related to ventilation.
(D) of the liver, kidney and hematopoietic system of lack of O2 can be made directly or indirectly damage the liver alanine aminotransferase increased, but with the lack of O2 correction, liver function gradually returned to normal.
Arterial oxygen is reduced, renal blood flow, glomerular filtration volume, urinary excretion of sodium excretion and an increase in volume; when PaO2 <5.3kPa, the renal blood flow decreased and renal function was inhibited.
Low oxygen tension increases the organization to promote red blood cell proliferation of erythropoietin. Kidney and liver produces an enzyme activity of the blood-Africa erythropoietin activation of the precursor material into the EPO, to stimulate the bone marrow caused by secondary polycythemia. Help to increase blood oxygen carrying capacity, but also increased blood viscosity, increased pulmonary circulation and right heart burden.
CO2 retention would expand mild renal vessels and increase renal blood flow, urine volume increased; when PaCO2 than 8.64kPa, blood pH decreased, the renal vascular spasm, decreased blood flow, HCO3-and Na + resorption increased, decreased urine output.
(V) the impact of acid-base balance and electrolytes can inhibit the cell a serious shortage of energy on behalf of O2 in the middle of the process of shooting, such as the citric acid cycle, oxidative phosphorylation and related enzymatic activities. This not only reduces the efficiency of energy production, but also because of lactic acid and inorganic phosphorus induced metabolic acidosis. Because energy is insufficient, the body of the sodium pump was damaged ion transport, intracellular potassium ion to the bloodstream, while Na + and H + into the cell, causing intracellular acidosis and hyperkalemia. Metabolic acidosis resulting in a fixed acid and bicarbonate buffer system works, producing carbonic acid, carbon dioxide partial pressure increased an organization.
PH value depends on the ratio of bicarbonate and carbonate, the former regulation by the kidney (1-3 days), and regulation by lung carbonic acid (several hours). Discharged from the lung health of people every day as much carbonate of 15000mmol, so retention of acute respiratory failure on the pH of CO2 very quickly, often with metabolic acidosis exist, due to severe acidosis caused by decreased blood pressure, arrhythmia and even cardiac arrest . And chronic respiratory failure due to the slow development of CO2 retention, reduced renal bicarbonate excretion, does not result in significantly lower pH. Because the main anion in blood HCO3-and CI-of and is a constant, when HCO3-increases, the CI-be reduced, resulting in low chlorine hyperlipidemia.



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