In medicine, pulmonary hypertension (PH) is an increase in blood pressure in the pulmonary artery or lung vasculature. Depending on the cause, it can be a severe disease with a markedly decreased exercise tolerance and right-sided heart failure. It was first identified by Dr Ernst von Romberg in 1891[1]. It can be one of five different types, arterial, venous, hypoxic, thromboembolic, or miscellaneous. A history usually reveals gradual onset of shortness of breath, fatigue, non-productive cough, angina pectoris, syncope (fainting), peripheral edema, and rarely hemoptysis. Pulmonary arterial hypertension (PAH) typically does not present with orthopnea or paroxysmal nocturnal dyspnea, while pulmonary venous hypertension typically does. In order to establish the cause, the physician will generally conduct a thorough medical history. A detailed family history is taken to determine whether the disease might be familial. Physical examination is performed to look for typical signs of pulmonary hyertension including a loud P2 (pulmonic valve closure sound), (para)sternal heave, jugular venous distension, pedal edema, ascites, hepatojugular reflux, etc Causes The most common cause of pulmonary hypertension is left heart failure leading to pulmonary venous hypertension. This may be due to systolic or diastolic malfunction of the left ventricle or due to valvular dysfunction such as mitral regurgitation or mitral stenosis. It usually manifests as pulmonary edema. Common causes of pulmonary arterial hypertension (PAH) include HIV, scleroderma and other autoimmune disorders, cirrhosis and portal hypertension, sickle cell disease[2], congenital heart disease, thyroid diseases[3], and others. Use of weight loss pills such as Fen-Phen, Aminorex, fenfluramine (Pondimin), and phentermine led to the development of PAH in the past[4]. Other causes include sarcoidosis, histiocytosis X, and fibrosing mediastinitis. Pulmonary embolism also leads to pulmonary hypertension, acutely as well as chronically. When none of these causes can be found, the disease is termed idiopathic pulmonary arterial hypertension (IPAH). Lung diseases that lower oxygen in the blood (hypoxia) are well known causes of pulmonary hypertension, including COPD, interstitial lung disease, Pickwickian syndrome or obesity-hypoventilation syndrome, and possibly sleep apnea. Human herpesvirus 8, also associated with Kaposi s sarcoma, has been demonstrated in patients with PAH, suggesting that this virus may play a role in its development[5]. When a family history exists, the disease is termed familial pulmonary arterial hypertension (FPAH). IPAH and FPAH are now considered to be genetic disorders linked to mutations in the BMPR2 gene, which encodes a receptor for bone morphogenic proteins[6], as well as the 5-HT(2B) gene, which codes for a serotonin receptor Diagnosis Normal pulmonary arterial pressure in a person living at sea level has a mean value of 12–16 mm Hg (1600–2100 Pa). Definite pulmonary hypertension is present when mean pressures at rest exceed 25 mm Hg (3300 Pa). If mean pulmonary artery pressure rises above 30 mm Hg (4000 Pa) with exercise, that is also considered pulmonary hypertension. Diagnosis of PAH requires the presence of pulmonary hypertension with two other conditions. Pulmonary artery occlusion pressure (PAOP or PCWP) must be less than 15 mm Hg (2000 Pa) and pulmonary vascular resistance (PVR) must be greater than 3 Wood units (240 dyn?s?cm-5 or 2.4 mN?s?cm-5). Although pulmonary arterial pressure can be estimated on the basis of echocardiography, pressure sampling with a Swan-Ganz catheter provides the most definite measurement. PAOP and PVR can not be measured directly with echocardiography. Therefore diagnosis of PAH requires a cardiac catheterization. Swan-Ganz catheter can also measure the cardiac output, which is far more important in measuring disease severity than the pulmonary arterial pressure. Other diagnostic tests generally include pulmonary function tests, blood tests, electrocardiography (ECG), arterial blood gas measurements, X-rays of the chest (followed by high-resolution CT scanning if interstitial lung disease is suspected), and ventilation-perfusion or V/Q scanning to exclude chronic thromboembolic pulmonary hypertension. Biopsy of the lung is usually not indicated unless the pulmonary hypertension is thought to be secondary to an underlying interstitial lung disease but is fraught with risks of bleeding because of high pressure. Clinical improvement is often measured by a quot;six-minute walk testquot;, i.e. the distance a patient can walk in six minutes. Stability and improvement in this measurement correlate with reduced mortality. I think I answered your question.
If you need treatment info., etc., go to the website. Also, if this isn t enough info., try Google; there s a ton of info. out there. Pulmonary Hypertension What It Is High blood pressure in the arteries that supply the lungs is called pulmonary hypertension (PHT). The blood pressure measured by cuff on your arm isn t directly related to the pressure in your lungs. The blood vessels that supply the lungs constrict and their walls thicken, so they can t carry as much blood. As in a kinked garden hose, pressure builds up and backs up. The heart works harder, trying to force the blood through. If the pressure is high enough, eventually the heart can t keep up, and less blood can circulate through the lungs to pick up oxygen. Patients then become tired, dizzy and short of breath. If a pre-existing disease triggered the PHT, doctors call it secondary PHT. That s because it s secondary to another problem, such as a heart or lung disorder. Congenital heart disease can cause PHT. It s important to repair congenital heart problems (when possible) before permanent pulmonary hypertensive changes develop. Intracardiac left-to-right shunts (such as a ventricular or atrial septal defect, a hole in the wall between the two ventricles or atria) can cause too much blood flow through the lungs. This situation is sometimes called Eisenmenger complex. Heart valve conditions, such as mitral stenosis (a narrowing of the mitral valve), can also cause PHT. Fixing the valve usually reverses the PHT.
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