Editing Haemodynamic response (section)

===Pulmonary arterial hypertension===
Pulmonary hypertension (PAH) is disease of small pulmonary arteries that is usually caused by more than one mechanism. This includes [[pneumonia]], parasitic infections, street drugs, such as [[cocaine]] and [[methamphetamines]] that cause constriction of blood vessels, and many more. Vasoactive mediators, such as nitric oxide and [[prostacyclin]], along with overexpression of vasoconstrictors not only affect vascular tone but also promote vascular remodeling. PAH deals with increase blood pressure in pulmonary arteries, which leads to shortness of breath, dizziness, fainting, rarely [[hemoptysis]], and many other symptoms. PAH can be a severe disease, which may lead to decreased exercise tolerance, and ultimately heart failure. It involves vasoconstrictions of blood vessels connected to and within the lungs. As a result, the heart has a hard time pumping blood through the lungs, and the blood vessels eventually undergoes [[fibrosis]]. The increased workload on the heart causes [[hypertrophy]] of the right ventricle, which leads less blood being pump through the lungs and decreased blood to the left side of the heart. As a result of all of this, the left side of the heart has a hard time pumping a sufficient supply of oxygen to the rest of the body, which deteriorates the effect of the haemodynamic response. Impaired haemodynamic responses in turn diminish exercise capacity in patients with PAH. The severity of haemodynamic dysfunction during progressive exercise in PAH can be recorded using cardiopulmonary exercise testing (CPET), and/or [[impedance cardiography]] (ICG). Furthermore, there are no current cures for pulmonary arterial hypertension, but there are treatment options for patients with the disease to help prolong their survival and quality of life. A few of these treatments include basic therapy, calcium-channel blockers, and prostacyclin therapy. Basic therapy can lead to dramatic clinical improvements in patients with right heart failure by instituting diuretic therapy. This reduces the right ventricular preload. Moreover, high-dose calcium-channel blockers among patients who have a response to this treatment can prolong survival and improve pulmonary haemodynamics. Calcium channel blocking drugs results in regression of right ventricular hypertrophy. On the other hand, prostacyclin therapy prolongs survival by inducing relaxation of vascular smooth muscles. This stimulates the production of [[cyclic AMP]] (cAMP), which inhibits the growth of smooth-muscle cells.<ref>{{cite journal | author = Humbert Marc | year = 2004| title = Treatment of Pulmonary Arterial Hypertension | journal = The New England Journal of Medicine | volume = 351 | issue = 14| pages = 1425–1436| doi = 10.1056/NEJMra040291 | pmid = 15459304}}</ref>

Overall, pulmonary arterial tension and acute coronary syndromes are few of the many diseases that lead to hypoxia of neuronal tissue, which in turns deteriorates the haemodynamic response and leads to neuronal death. Prolonged hypoxia induces neuronal death via apoptosis. With a dysfunctional haemodynamic response, active neuronal tissue due to membrane depolarization lacks the necessary energy to propagate signals, as a result of blood flow hindrance. This affects many functions in the body, and may lead to severe symptoms.