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Lung tissue, pulm


onary vascular and pathological changes of the heart caused by pulmonary heart disease is the basis of pathophysiology. The respiratory and circulatory systems have a strong compensatory ability, chronic respiratory disease from the beginning to right heart failure, often have a very long process. In this process, the pathophysiological changes occur, a certain degree of reversibility. Therefore, to improve the pathophysiological changes of pulmonary heart disease understanding, prevention and treatment for pulmonary heart disease is important.
1. Changes in respiratory function
(1) ventilatory defect: different pathological changes induced ventilatory dysfunction are also different. In pulmonary heart disease, the most common disease for COPD, and these diseases can cause airway obstruction, resistance increases, excessive expansion of alveolar rupture, so that reduced lung capacity, residual volume and total lung capacity increases. Increase in the residual gas, reducing the concentration of O2 in the inhaled gas, the alveolar oxygen partial pressure decline, causing hypoxemia. Another one for the restrictive ventilatory dysfunction, these diseases so that thoracic limited mobility, can cause lung capacity, residual volume and total lung capacity decreased, resulting in alveolar hypoventilation, can lead to hypoxemia.
(2) ventilatory disorders: ventilation dysfunction can be caused by the following two aspects:
gas diffusion impairment: between alveolar and pulmonary capillary gas exchange is achieved through the dispersion, the size of the gas diffusing capacity, and alveolar - capillary partial pressure difference between the gas, gas solubility, the total area of the alveolar membrane and the alveolar - capillary membrane thickness are closely related. Under normal conditions, alveolar capillary blood oxygen and carbon dioxide exchange in the balance of time is less than O.3s, and normal pulmonary blood flow through pulmonary capillaries when the time is 0.75s, so there is plenty of time by diffusion process to be exchanged. When patients with chronic obstructive pulmonary disease, pulmonary inflammation, pulmonary fibrosis, pulmonary vascular wall thickening and some blood clots, etc., can reduce the total area of the alveoli, alveolar - capillary membrane thickness and the amount of gas diffusion. When the alveolar capillary membrane thickness to the diffusion process than 0.75s, or alveolar area decreased to 50% below normal, can cause breathing dysfunction, caused by hypoxia.
As in the resting state of the solubility of CO2 in body fluids and diffusing capacity 20 times larger than the O2. Therefore, the main gas diffusion dysfunction disease, blood pressure decreased compared with C02 partial pressure increased for the first, or even due to hyperventilation, and anti-so PaC02 lower than normal.
ventilation - perfusion ratio imbalance: Under normal circumstances, alveolar ventilation is 4L/min, pulmonary blood flow 5L/min, ventilation / perfusion ratio of 0.8, alveolar ventilation and pulmonary blood flow distribution must be uniform to be coordinated to ensure effective gas exchange, ventilation and blood flow, regardless of any party to increase or decrease, can cause ventilation - perfusion ratio imbalance. The pathological changes, due to involvement of the adjacent bronchial inflammation around small pulmonary arteries, causing part of the inflammatory changes in vessel wall thickening, lumen, or fibrosis and completely closed, resulting in a total area of pulmonary capillaries significantly reduced or in some pulmonary embolism, physiological dead space increases with the amount. In this case, alveolar ventilation may be normal and part of the pulmonary blood flow reduction, the ratio of the two increases, the lesions were not adequately exchange gas, can cause severe hypoxemia. In addition, pulmonary heart disease due to severe emphysema, the bronchial obstruction, or lobular atelectasis, alveolar ventilation can reduce some or complete loss of ventilation, pulmonary blood flow at this time if the lesion is still normal, due to alveolar ventilation reduce the ventilation - perfusion ratio decreased blood oxygenation will be without adequate access to the systemic circulation, resulting in increased pulmonary circulation right to left shunt, partial pressure of oxygen is correspondingly reduced, thus causing hypoxemia.
2. Hemodynamic changes: pulmonary heart disease such as hypoxia and acidosis caused by spasmodic contraction of pulmonary artery, pulmonary capillary blanket damage, vascular area reduction, and long-term hypoxia secondary to increased red blood cells, blood viscosity increases, etc., can cause increased pulmonary resistance, resulting in pulmonary hypertension and other changes.
(1) the production of pulmonary hypertension: the above reasons can cause contraction of pulmonary artery, pulmonary vascular resistance increased and pulmonary hypertension. Hypoxic contraction of small pulmonary arteries caused by the mechanism, though aly a large number of studies, but has not yet been fully elucidated. Together the following points; Youzhu were attenuated by blockers induced by the hypoxic pulmonary vasoconstriction, indicating that this reaction exists in the sympathetic role, but retained from pulmonary vasoconstrictor response to hypoxia, that neural reflexes may not be the main mechanism. Many reports in hypoxia, blood histamine, prostaglandins, such as angiotensin and cyclic nucleotide content increased. So that the alveolar lung mast cells by hypoxia and vascular endothelial cells and release of vasoactive substances lead to pulmonary vasoconstriction. A lot of research in this area, the results are inconsistent conclusions difficult. In addition Youzhu reported an oxygen content of pulmonary artery wall to reduce the potassium, sodium content increases, vascular smooth muscle membrane potential and increased excitability, muscle cells, calcium ions also increased, so that muscle contraction increased, causing increased pulmonary vascular resistance and pulmonary hypertension. This may be due directly to changes in oxygen permeability of vascular smooth muscle due to the ion, it remains to be studied further.
Caused by hypoxia in pulmonary arteries, often with the increased presence of acidosis, hydrogen ion concentration, can the sensitivity of pulmonary vessels to hypoxia increases, so in the presence of acidosis is mild hypoxia also can significantly increase pulmonary artery pressure, in addition, hypoxia can cause polycythemia, increased blood viscosity and blood flow, but also easy to form blood clots, for the cause of pulmonary hypertension also have a role.
Severe obstructive pulmonary emphysema, lung swell, so a lot of fusion of alveolar septal rupture and the formation of bullae, pulmonary vascular bed to reduce pulmonary artery pressure increased despite a certain role, but less than 50%, pulmonary artery pressure was significantly rise.
Pulmonary hypertension caused by the above can be reversed at an early stage, through early treatment, to improve hypoxia, pulmonary hypertension can be decreased, so early detection of pulmonary heart disease and early treatment can get good results.
But the long-term sustained pulmonary vasoconstriction and pulmonary hypertension, can make the middle hyperplasia hypertrophy of pulmonary arterioles, intimal fibrous hyperplasia, stenosis, or fibrosis, thus greatly reducing the lung capillary bed, pulmonary vascular resistance increases, causing a vicious cycle , then it will show a continued increase in pulmonary artery pressure, becoming irreversible, a treatment difficult.
(2) Cor changes in cardiac output: cardiac output in patients with pulmonary heart disease is decreased or normal majority, Burrow, etc. hemodynamics in pulmonary heart disease patients found that cardiac index at rest was 2.5L/min/m2 , and after exercise up to 3.5L/min/m2. 90 cases of FORCES and other hemodynamic pulmonary heart disease patients also found that cardiac index was observed 2.960.99L/min/m2, which is less than 2.5L/min/m2 29 cases, while only 6 cases more than 4L/min/m2 . In short Cor reduced cardiac output increased by more than those in the rescue work in pulmonary heart disease cardiac output is estimated to be correct.
(3) changes in heart function with pulmonary heart disease: the normal case for the thin-walled right ventricle, easy expansion of the muscle pump, although there is a greater change in venous blood Rhodobryum; right heart filling pressure do not change significantly, when the pulmonary artery pressure continued to increase, right ventricular load increase, gradually thickened right ventricle. As soon as acute right ventricular afterload increase, the right room to expand, Mahler measure the systolic and diastolic volume estimated right ventricular volume, right heart afterload can increase right ventricular enlargement.
In addition, the time when the pulmonary hypertension and right ventricular oxygen demand increased and decreased oxygen supply, resulting in lack of oxygen supply and demand, further deterioration of myocardial blood supply. When the respiratory tract infection, hypoxia increased pulmonary arterial pressure or other reasons rather than to further increase the affordability of the right ventricle, the right ventricular blood is not completely discharged, the residual lifetime systolic blood too, so that increase in right ventricular end diastolic pressure and right ventricular dilation increased, leading to heart failure. At this point increase in plasma volume, venous stasis in the systemic circulation, pulmonary interstitial water content also increased.
(4) the problem of left heart function: heart failure, pulmonary heart disease may occur, but damage to the lung problems of left ventricular heart disease is still a controversial issue, pulmonary heart disease patients with acute attack, often cough and respiratory difficulties increase, and even orthopnea. Whether these symptoms appear or the Department of Respiratory dysfunction due to left ventricular dysfunction, both in clinical practice is sometimes not easy to distinguish. In recent years, due to some non-invasive techniques such as radionuclide, echocardiographic determination of right ventricular function such as greater progress, on the left and right pulmonary heart disease were a lot of heart function. Pathological left ventricular hypertrophy in patients with pulmonary heart disease found the incidence rate of 25% to 93%. The standard measurement of left ventricular hypertrophy, and some by weight, and some to visual, and most of the visual for the determination of left ventricular wall thickness. Determination of hypertrophy because different standards, leading to the incidence of the poor.


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