Fibrotic Tissue Homeostasis

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

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.

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.

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.

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.

Lung function tests have revealed normal spirometry, gas transfer and static lung volumes. There appears to be a fall in pre-bronchodilator FEV1, but not so FVC and TLCO comparing back to 2007??. Maximal respiratory pressures are reduced indicative of respiratory muscle/diaphragm weakness. This is consistent with what has previously been observed and the previous diagnosis of mild left hemidiaphragm weakness. I note from Tony Dortimer’s most recent letter that the coronary angiogram

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

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,

Anatomical dead space and functional residual capacity (FRC) play a very important role to ensure the constancy of alveolar gas tensions. Firstly it is important to understand what the anatomical dead space and FRC actually are. The anatomical dead space refers to the gas in the conducting areas of the respiratory system where air does not come into contact with alveoli. Examples of places in the respiratory system where anatomical dead space is present are the mouth and trachea. The functional residual capacity is the amount of air that remains in the lungs after a normal and passive expiration. It is usually measured at approximately 2.5 litres of air.

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

Pulmonary fibrosis is a lung disease that occurs when the tissue deep in your lungs become thick and stiff. Over time, the damaged tissue forms scar tissue. The term for the scar tissue is fibrosis. When the scarred tissue becomes too thick, breathing becomes difficult and symptoms arise.

The alveoli in the lungs become inflamed and damaged and lose their elasticity as they become swollen and thick

The bronchi and bronchiole tubes are loosely wrapped with muscle. During regular breathing, the muscles around these airways are relaxed (5). This allows air to flow freely through these passageways to the alveoli. However, during an asthma attack, air has trouble reaching the alveoli, which prevents the body from receiving oxygen. This is because the airways become smaller. Firstly, the muscles around the airways spasm and contract. This then causes inflammation of the bronchioles and bronchi themselves, which causes a mucus to be produced.

Emphysema Emphysema is a condition in which there is over-inflation of structures in the lungs known as alveoli or air sacs. This over-inflation results from a breakdown of the walls of the alveoli, which causes a decrease in respiratory function (the way the lungs work) and often, breathlessness. Early symptoms of emphysema include shortness of breath and cough. Emphysema and chronic bronchitis together comprise chronic obstructive pulmonary disease (COPD).