Pulmonary hypertension. From vasomotor molecules to treatment

Pulmonary Hypertension is characterized by the increase of the pulmonary systolic pressure above 30 mm Hg or 25 of mean pressure. Different diseases generate changes in the physiology of the vessel wall. The balance between vasoconstrictor and vasodilator molecules, mainly released by the endothelium, is lost in favor of vasoconstrictors, which in addition to generating an inadequate vasoconstrictor response, induce proliferative changes of different cell lines that modify the structure of the vessel wall, from the hypertrophy of the media until progressive occlusion of the arteriolar beds, formation of angiomatous lesions, micro aneurysms, plexiform lesions, thrombotic occlusions and necrotizing arteritis corresponding to the different degrees of pulmonary hypertension. The symptoms of right ventricular failure, the radiographic and electrocardiographic data of right ventricular growth or dilatation, allow us to suspect the diagnosis that can be confirmed by echocardiography, measuring the peak velocity of the tricuspid regurgitation that corresponds to the systolic pressure of the pulmonary artery. The progressive severity of the lesions allows the treatment to be staggered, including measures to compensate for heart failure with loop diuretics, permanent anticoagulation, and vasodilators such as Calcium Channel Blockers and to greater severity, endothelin antagonists, phosphodiesterase 5 inhibitors, prostacyclin and derivatives and combinations of several of these drugs. The creation of a right to left shunt decompresses the lung bed, reducing pressure, with desaturation and an increase in systemic output, but improving exercise tolerance and survival.