The Cause And Causes Of Pulmonary Hypertension

It results when one or both of these gas-exchanging functions are inadequate . It is not a disease but a symptom of an underlying pathology affecting lung tissue function, 02 delivery, cardiac output, or the baseline metabolic state. It is a condition that occurs because of one or more diseases involving the lungs or other body systems. Symptoms of this is hypoexia and hypercapnia.

Hypoxia is one of the major problems associated with this increase in altitude. This is due to the fact that the partial pressure of oxygen decreases proportionately with increases in altitude. Carbon dioxide that is continually excreted from the pulmonary blood to the alveoli along with water vaporizing in the inspired air from the respiratory surfaces dilute the oxygen in the alveoli which cause the oxygen concentration to decrease.

Hemothorax is a type of pleural effusion in which blood accumulates in the pleural space. The excess fluid can interfere with normal breathing by limiting expansion of the lungs.

Pulmonary hypertension is a lung disorder. The arteries that carry blood from the heart to the lungs become narrowed, making it very hard for the blood to get through the vessels, this then causes the pressure in the arteries to increase more than usual (high blood pressure). Scientists think that the procedure starts with injury to the layer of cells that line the small blood vessels of the lungs.

The increased resistance of blood flow through the pulmonary semilunar valve from the right ventricle backs up the pressure of blood

Heart failure is when the heart cannot keep up with the immense demands placed on it by the body, and it starts to compensate causing remodeling of the cardiac cells due to stronger cardiac contractions. The heart chambers expand so they can fill with more blood to pump to the rest of the body, and the heart rate will increase to meet these demands (American Heart Association, 2015). Heart failure is the inability of the heart to fill and pump effectively enough to meet the metabolic demands of the body resulting in pulmonary and venous congestion (Lam et al., 2007). Over time the body can no longer compensate, and the person becomes symptomatic and progresses into worsening heart failure. The pulmonary and venous congestion or “fluid overload” will manifest itself in the form of lower extremity edema, shortness of breath, fatigue and even chest pain, which interferes with quality of life (Colucci, 2015).

-Stage 2-Invlovment of chest area place places, mediastinum {structure at the middle of the heart}, pericardium or contralateral {opposite side} pleura

Recent results from genome wide association studies show that lung-relevant phenotype have emphasized how powerful the shortcomings are in their approach. Even though new genes and changes have been identified a large part has still been unidentified. As well as, in the disease development the function and mechanisms of how they develop the disease is still unknown. The National Heart, Lung, and Blood Institiute assembled a 2 day workshop to address the shortcomings and consider future directions for lung phenotypes.

There are a number of factors that lead to the etiology of a right-sided heart failure, including left-sided heart failure and chronic lung disorder. “High pulmonary pressure, or weak, or poorly contractile cardiac muscles, or both, can be responsible for decreased right ventricular emptying” (Rockwell, 1999). The left and right ventricles work together routinely in that, when the left ventricle fails to work properly; it puts the pressure on the right ventricles, weakening the right ventricle. Pulmonary hypertension is when the blood pressure in the lungs is too high, reducing the oxygen to the tissues (hypoxia), and causing the walls of the blood vessels to become inflamed and narrowed. While pulmonary hypertension continues, the right ventricle tries to compensate by expanding and thickening it walls, increasing the blood volume in the lungs and overtime weakening the right ventricle from the work overload, resulting in right-side heart failure.

It involves the tightening of blood vessels connected to and within the lugs. This makes it harder for the heart to pump blood thorough the lungs, much as it is harder to make water flow through a narrow pipe as opposed to a wide one. Over time, the affected blood vessels become both stiffer and thicker, further increasing the blood pressure within the lungs and impairing blood flow. In addition, the increase workload of the heart causes thickening and enlargement of the right ventricle, making the heart less able to pump blood through the lungs, causing right heart failure. As the blood flowing through the lungs decreases, the left side of the heart receives less blood. This blood may also carry less oxygen than normal. Therefore it becomes harder and harder for the left side of the heart to pump to supply sufficient oxygen to the rest of the body, especially during physical activity.

Pulmonary hypertension in this case likely resulted as a product of the initial pulmonary fibrosis. As the lungs stop working, the pulmonary blood pressure rises, which creates additional work for the right

Pulmonary embolism is described to be the "sudden blockage of a major blood vessel artery in the lung" (WebMD, 2014) which can usually be caused by a blood clot. The most common factor of pulmonary embolism is blood clots breaking loose from the leg and traveling to the lungs. Unfortunately, having pulmonary embolism can be fatal due to a large clot stopping blood flow going into the lung.

Pulmonary hypertension or (PH) is a rare disease that causes high arterial blood pressure in the lungs due to the blockage, narrowing, or destruction of arteries. High blood pressure in the pulmonary arteries can strain the right ventricle, causing it to overwork, and can eventually lead to right heart failure and even death. There are two types of pulmonary hypertension, primary and secondary. Primary pulmonary hypertension is known as idiopathic pulmonary arterial hypertension or (IPAH). IPAH currently has no known cause and mainly affects women in their childbearing years. Secondary pulmonary hypertension is typically caused by various diseases and commonly found in older individuals. For this experiment it was hypothesized that protein

arteriovenous malformation group 2: defined by direct arteriovenous shunts between a branch of the retinal artery and vein, without any capillary plexus interposition; medium caliber vessels are typically involved (Figure 8).

Eisenmenger syndrome was initially described in 1897 when German physician, Victor Eisenmenger, reported on a patient with symptoms of dyspnea and cyanosis from infancy that subsequently developed heart failure (Kopeć, 2014). The postmortem description was revealed and a ventricular septal defect was discovered (Dillar, 2006). With that being said, this had been the first time that the link between a large congenital cardiac shunt defect and the development of pulmonary hypertension had ever been noted (Dillar, 2006). In terms of the heart, a normal one has four chambers; the two upper chambers are separated from each other by the atrial septum (Krexi,