Fibrotic Tissue Homeostasis

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.

The presence of fluid in the alveolar space could potentially cause the lung capacity to be effected as well.

Choking gases irritate the lower branches of the lungs. The gases can destroy the sensitive lung tissue leading

Cystic fibrosis causes the alveoli to be filled with secretions that the patient cannot cough up or eliminate. The diffusion from the lungs to the blood is decreased because of the secretion filled alveoli. When the PaO2 is less than 60 mm Hg, the carotid bodies are triggered and send an afferent signal from the body to the brain and producing the feeling of dyspnea.

Both rapid, shallow breathing patterns and hypoventilation effect gas exchange. Arterial blood gases will be monitored and changes discussed with provider. Alteration in PaCO2 and PaO2 levels are signs of respiratory failure. Patient’s body position will be properly aligned for optimum respiratory excursion, this promotes lung expansion and improved air exchange. Patient will be suctioned as needed to clear secretions and maintain patent airways. The expected outcome is that the patient’s airway and gas exchange will be maintained as evidence by normal arterial blood gases (Herdman,

No information is given to determine previous medical history, so all possible causes can be taken into consideration related to F.T’s shortness of breath. A history of Chronic Obstructive Pulmonary Disease could contribute to this acute episode of shortness of breath, and warrants further assessment due to the risk of Cor Pulmonale associated with COPD. The indication of his increased use of an albuterol inhaler also leads me to believe that he has a previous pulmonary complication, which could be likely be COPD, or possibly Asthma as the medication is

He also had a history of shortness of breath for several months (2014). He was evaluated by the cardiologist; the test results indicated that the heart was not causing the shortness of breath. Later he was referred to a lung specialist for further evaluation.

Chronic inflammation leads to structural changes, narrowing of the small airways, and destruction of lung tissue, which diminishes the ability of the airways to remain open during expiration

Small air sacks called alveoli are at the tips of the bronchioles. When air reaches them, the oxygen concentration is high, which causes diffusion into red blood cells travelling through pulmonary capillaries (7). The red blood cells then distribute the new oxygen to the rest of the body. When they reach the alveoli again, they exchange carbon dioxide (a form of cell waste) for new oxygen, and repeat the process. The carbon dioxide is moved through the bronchioles, bronchi, and trachea in the form of exhalation.

It causes a decrease in lung functions, and very often, shows signs of breathlessness. It is indeed a destructive disease of the lung in which the alveoli (small sacs) that promote oxygen exchange between the air and the bloodstream are destroyed. Emphysema is a progressive, degenerative kind of disease that destroys many alveolar walls. As a result, clusters of small air sacs merge into larger chambers, which decrease the total surface area of the alveolar walls. At the same time, the alveolar walls lose their elasticity and the capillary networks associated with the alveoli diminish (Shier et al; 2010). It is in this sense that a person with emphysema finds it very difficult and increasingly hard to breath, has to force air out of the lungs because the tissue elasticity of the lungs and for that matter, the alveolar sacs have reduced or completely destroyed. Furthermore, abnormal muscular efforts are required to compensate for the lack of elastic recoil that normally contributes to

alveoli toward the end of the bronchioles get to be irritated in midst of the breakdown

Ineffective breathing pattern related to decreased oxygen saturation, poor tissue perfusion, obesity, decreased air entry to bases of both lungs, gout and arthritic pain, decreased cardiac output, disease process of COPD, and stress as evidenced by shortness of breath, BMI > 30 abnormal breathing patterns (rapid, shallow breathing), abnormal skin colour (slightly purplish), excessive diaphoresis, nasal flaring and use of accessory muscles, statement of joint pain, oxygen saturations of 85-95% 2L NP, immobility 95% of the day, and adventitious sounds throughout lungs (crackles) secondary to CHF, hypertension, pain caused by gout and arthritis, and obesity

Progress inside the bronchi generally makes this affected individual experience less than breathing. They should find them selves breathing problems along with breathing problems, experiencing ache in stomach place or, using some circumstances, breathing problems along with paying blood. Others will present signs along with signs

The lung function tests showed a moderate degree of airflow obstruction with normal gas transfer factor which would be consistent with moderate degree COPD.

This "dead space" of air needs to stay in your lungs constantly; otherwise the lung will completely deflate. If the lung has every bit of air sucked out of it, it will collapse and need to be re-inflated.