How to treat high heart disease
summary
The incidence rate of heart disease in different people may be a little different. High altitude heart disease often occurs in the plains moving to the plateau or from the moderate altitude to the higher altitude. Many people in this life have this symptom, and the incidence rate increases with the elevation of altitude. In addition to individual differences in hypoxia, fatigue, cold and respiratory tract infection are often the inducing factors. How to treat high heart disease.
How to treat high heart disease
First, the right heart function is damaged by chronic hypoxia. It is not clear whether or to what extent the left ventricle is also involved. Hypobaric hypoxia is the root of the occurrence of hypercardiosis, and hypoxic pulmonary hypertension and pulmonary arteriole wall thickening or remodeling are the central link or basic characteristics of the pathogenesis.
Second: pulmonary hypertension through clinical and animal model research, chronic high altitude disease, especially high heart disease, pulmonary artery pressure has abnormal increase. Hultgren in Peru (4206m) reported 16 cases of Monge disease hemodynamic changes, the average pulmonary artery pressure was 44.47mmhg, the average pulmonary vascular resistance was 531sce-cm2; Yang et al. Reported in Qinghai (3950m), the average pulmonary artery pressure of mixed type of chronic high altitude disease was 30.7mmhg. Long term and persistent hypoxic pulmonary vasoconstriction and pulmonary hypertension aggravate the right ventricular afterload and cause compensatory hypertrophy of the right ventricle. When the course of disease continues to develop, the cardiac reserve will further decline. At the same time, hypoxia can damage myocardial cells, weaken the myocardial contractility and reduce the cardiac output, and eventually lead to right heart failure. Although many studies have been carried out on the mechanism of hypoxic pulmonary vasoconstriction, the exact mechanism remains unclear.
Third: the role of ion channels in the cell membrane: the change of ion permeability in the cell membrane and the ion transmembrane potential caused by it are known to play an important role in the relaxation and contraction of pulmonary vessels. The changes of ion channel have different effects on pulmonary blood vessels, such as the increase of intracellular K + concentration can relax blood vessels, while the increase of Ca2 concentration can contract blood vessels. The results showed that extracellular K + and Ca2 had competitive inhibition on the smooth muscle cell membrane; hypoxia could inhibit the K + influx of the smooth muscle cell membrane of pulmonary artery, depolarize the resting potential of the cell membrane and accelerate the Ca2 flow, resulting in the increase of intracellular free Ca2 concentration, thus promoting the contraction of the smooth muscle of pulmonary artery and increasing the pulmonary artery pressure. Verapamil, a calcium antagonist, can effectively treat pulmonary hypertension, which indicates that there is a certain relationship between calcium and pulmonary hypertension.
matters needing attention
In addition to the proliferation of smooth muscle cells in the middle layer, the intima and outer fibrous tissue also proliferated in the thickened vascular wall, and the endothelial cells of some arterioles swelled and protruded to the lumen, resulting in narrowing or even obstruction of the vascular lumen.
