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Eisenmenger syndrome or Eisenmenger's syndrome is defined as the process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect (typically by a ventricular septal defect, atrial septal defect, or less commonly, patent ductus arteriosus) causes pulmonary hypertension [1] [2] and eventual reversal of the shunt into a cyanotic right-to-left shunt.
Treatment of pulmonary hypertension is determined by whether the PH is arterial, venous, hypoxic, thromboembolic, or miscellaneous. If it is caused by left heart disease, the treatment is to optimize left ventricular function by the use of medication or to repair/replace the mitral valve or aortic valve. [68]
A pulmonary artery wedge pressure being less than 15 mmHg (also measured by right heart catheterization) excludes post-capillary bed (in the veins distal to the capillary bed) pulmonary hypertension. Pulmonary arterial hypertension is a subgroup of pulmonary hypertension and is categorized as World Health Organization as group 1. [3]
Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema; severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude. [9] [13]
A diagram explaining factors affecting arterial pressure. Pathophysiology is a study which explains the function of the body as it relates to diseases and conditions. The pathophysiology of hypertension is an area which attempts to explain mechanistically the causes of hypertension, which is a chronic disease characterized by elevation of blood pressure.
Chronic thromboembolic pulmonary hypertension (CTEPH) is a long-term disease caused by a blockage in the blood vessels that deliver blood from the heart to the lungs (the pulmonary arterial tree). These blockages cause increased resistance to flow in the pulmonary arterial tree which in turn leads to rise in pressure in these arteries ...
The pathophysiology of pulmonary heart disease (cor pulmonale) has always indicated that an increase in right ventricular afterload causes RV failure (pulmonary vasoconstriction, anatomic disruption/pulmonary vascular bed and increased blood viscosity are usually involved [1]), however most of the time, the right ventricle adjusts to an ...
Other signs provide evidence for specific causes of pressure overload. Hypertension is diagnosed by sphygmomanometry. A narrow pulse pressure is a sign of aortic stenosis. The chest x-ray may show pulmonary hyperaemia in the case of pulmonary hypertension, and pulmonary oligemia in pulmonary stenosis.
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