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The respiratory system is situated in the thorax, and is responsible for gaseous exchange between the circulatory system

and the outside world. Air is taken in via the upper airways (the nasal cavity, pharynx and larynx) through the lower airways (trachea, primary bronchi and bronchial tree) and into the small bronchioles and alveoli within the lung tissue. Move the pointer over the coloured regions of the diagram; the names will appear at the bottom of the screen) The lungs are divided into lobes; The left lung is composed of the upper lobe, the lower lobe and the lingula (a small remnant next to the apex of the heart), the right lung is composed of the upper, the middle and the lower lobes. Mechanics of Breathing To take a breath in, the external intercostal muscles contract, moving the ribcage up and out. The diaphragm moves down at the same time, creating negative pressure within the thorax. The lungs are held to the thoracic wall by the pleural membranes, and so expand outwards as well. This creates negative pressure within the lungs, and so air rushes in through the upper and lower airways. Expiration is mainly due to the natural elasticity of the lungs, which tend to collapse if they are not held against the thoracic wall. This is the mechanism behind lung collapse if there is air in the pleural space (pneumothorax).

Physiology of Gas Exchange Each branch of the bronchial tree eventually sub-divides to form very narrow terminal bronchioles, which terminate in the alveoli. There are many millions of alveloi in each lung, and these are the areas responsible for gaseous exchange, presenting a massive surface area for exchange to occur over. Each alveolus is very closely associated with a network of capillaries containing deoxygenated blood from the pulmonary artery. The capillary and alveolar walls are very thin, allowing rapid exchange of gases by passive diffusion along concentration gradients. CO2 moves into the alveolus as the concentration is much lower in the alveolus than in the blood, and O2 moves out of the alveolus as the continuous flow of blood through the capillaries prevents saturation of the blood with O2 and allows maximal transfer across the membrane.

Precipitating factors: >lifestyle >bacteria: staphylococcus pneumoniae Predisposing factors: >age >sex staphylococcus pneumoniae enters the respiratory system through inhalation/aspiration Activation of defense mechanism Penetration in the sterile lower respiratory tract Proliferation in the Alveoli Colonization of lungs by the bacteria Exudates that come from the bateria erode from the lung infection vasodilation Increase blood flow Accumulation of edematous fluids Pleural effusion Inflamed and fluid filled alveolar sac Decrease CO2 Lung consolidation hypoxia Impaired CO2 and O2 exchange >increased RR Occluded airway Increase mucus production Irritation of airways Increase goblet cells >cough >crackles Hyperventilation Airway constriction DOB .

and timing of presentation for medical treatment Parapneumonic effusion It is a common complication of bacterial pneumonia (about 40%). This loculation makes complete pleural space drainage difficult. bacteria. 2. These untreated effusions may also drain spontaneously through the chest wall (empyema necessitans) or into the lung to produce a bronchopleural fistula. and retroperitoneal spaces may spread to the pleura resulting in the development of effusion. The pleural fluid is an exudate with primarily PMNs. and a normal pH level. Most parapneumonic effusions are small and resolve with appropriate antibiotic therapy. Fibrin membrane partitions result in loculated effusion.Parapneumonic effusion is defined as pleural effusion associated with lung infection (ie. . The initial sterile free flowing exudative parapneumonic effusions may rapidly progress (within a day) to the second stage. and cellular debris. The exudative stage which results from a focus of parenchymal infection leading to increased pulmonary interstitial fluid. The fibropurulent stage characterized by infection of sterile pleural fluid. Fibroblasts grow into the exudate from both the visceral and parietal pleural surface to produce an inelastic membrane called the pleural peel. and bacterial organisms or frank pus may be present. 3. During this stage. Fibrin deposits cover both the visceral and parietal pleura. Some of this fluid crosses the visceral pleura and accumulates as a small sterile pleural effusion. the pleura becomes inflamed. Pleural fluid further accumulates and contains many PMNs. vertebral. These effusions result from the spread of inflammation and infection to the pleura. although they are not sharply defined and represent a point on a continuous spectrum. Thoracentesis should be done if the effusion layers out to a thickness equal to or greater than 10 mm on the lateral decubitus chest radiograph to determine as early as possible if a chest tube should be placed. bacteria invade the fluid. subsequent leakage of proteins. resulting in empyema. such as the retropharyngeal. the pleural fluid pH and glucose levels become low. LDH levels increase. With time. fluid. the pleural effusion is usually sterile with a low leukocyte count. The organization stage. Antibiotics begun in this stage will affect resolution of both the pneumonic and pleural process. abdominal. Pathophysiology: The spectrum of parapneumonic effusions has been divided into three stages. 1. which is defined as the presence of grossly purulent fluid in the pleural cavity. infections in other adjacent areas. a normal glucose level. pneumonia). bacterial virulence. Much less commonly. The development of pleural empyema is determined by a balance between host resistance. and leukocytes into the pleural space forms the effusion. At the time of formation. Early in the course of parapneumonic effusion.