Respiratory System Pathophysiology PDF

PHYSIOLOGY OF RESPIRATORY SYSTEM (RS) BY DR LSK  Introduction Definition of Respiration and RS Stages of Respiration Definition of RS and Respiration Respiration is the process of supplying O2 to & removing CO2 from cells in the body. It involves the entire...

PHYSIOLOGY OF RESPIRATORY SYSTEM (RS) BY DR LSK  Introduction Definition of Respiration and RS Stages of Respiration Definition of RS and Respiration Respiration is the process of supplying O2 to & removing CO2 from cells in the body. It involves the entire process of exchanging gases between the atmosphere & body cells. (not just lungs) Why do we need O2??? Why do we need to remove CO2??? Any importance of CO2 to the body?? RS is a body system in  Stages of Respiration i. breathing or ventilation- rhythmical process, in which air is drawn into the alveoli of the lungs via inhalation & the air is subsequently expelled via exhalation. That is, the movement/transport of air into and out of the alveoli. A breath in & out (respiratory rate) occurs 12 to 15 times per minute and it brings in ~7 L of air per minute into the lungs at rest. If not rest??? ii. external respiration – Gas exchange (O2 & CO2) by simple diffusion between the blood & the air in the lungs, mainly in the alveoli. iii. gas transport in the blood between the lungs and body cells. iv. internal respiration – gas exchange (O2 & CO2) by simple diffusion between the blood & the tissue cells. v. cellular respiration – the process of O2 utilization, and CO2 and energy (ATP) production at the cellular level.  Anatomical division Structures/Organs of RS The RS organs can be divided into the respiratory tract & the lungs ( houses part of the tract called the bronchial tree). Respiratory tract is the air passages or airways (path) followed by the inhaled air from the nose to the pulmonary alveoli. It includes: Nose- The facial structure made of muscle, bone & cartilage, & covered with the skin. It has 2 openings (nostrils/external nares). Its internal hairs prevent entry of large particles with air. Nasal cavity - 2 hollow spaces behind the nose and within the skull. Paranasal sinuses, Pharynx - the muscular tube posterior to the nasal cavity, oral cavity & larynx. Larynx, trachea and bronchial tree. Respiratory tract is divided into upper and lower respiratory tracts. a. The upper respiratory tract (parts outside the chest cavity) b. The lower respiratory tract also called the respiratory tree or tracheobronchial tree. It is the parts within the chest cavity.  Upper Respiratory Tract (URT) The nose, nasal cavity, paranasal sinuses, pharynx, larynx & upper trachea. URT organs are lined by pseudostratified ciliated epithelium!! Pseudostratified Ciliated Epithelium URT organs are lined by mucosa (respiratory epithelium) called pseudostratified ciliated epithelium rich in goblet cells and an extensive network of blood vessels!! Function of cilia??  Paranasal Sinuses A group of 4 paired air-filled spaces that surround, developed or outgrew from & open/drain into the nasal cavity. They: keep the cavity from drying out reduce the weight of the head, humidify & heat inhaled air, increase the resonance of speech, serve as a crumple zone to protect vital structures in They are named case of facial trauma. according to the facial bone in which they are located!!! The Larynx It is an enlargement in the airway superior to the trachea consisting of muscles & cartilages bound by elastic tissue. The Vocal Cords of The Larynx (False True vocal cords & vocal the opening cords) between them formthe glottis. Sound Formation by Larynx Vocal sounds are created when air is forced between true vocal cords, vibrating them. The sound waves are converted into words by changing the shapes of the pharynx and oral cavity and by using the tongue and lips. Contraction of laryngeal muscles increases tension on the vocal cords thereby producing a higher pitch (musical tone) of voice. Relaxation of laryngeal muscles decreases tension on the vocal cords thereby producing a lower pitch (musical tone) of voice. The intensity (loudness) of a vocal sound depends upon the force of the air passing over the vocal cords. Stronger blasts of air result in greater vibration of the vocal cords and louder sound.  During speaking, the intrinsic muscles of the larynx pull the vocal cords across the glottis, exhaled air vibrates the vocal cords to produce sounds that can be turned into speech.  During normal breathing the vocal cords remain relaxed, and the glottis is a triangular. When food or liquid is swallowed, muscles in false vocal folds close the glottis. Along with closing of the epiglottis, this action prevents food or liquid from entering the trachea. Aspiration pneumonia in unconscious or anesthetized patients??? Incomplete glottic closure allows vomitus to enter The Bronchial Tree The branching and dividing structure of airways leading/originating from trachea to alveoli (microscopic air sacs). It includes: the bronchi (main bronchus, lobar bronchus, segmental bronchus), bronchioles (conducting bronchiole, terminal bronchiole, respiratory bronchiole), alveolar duct, alveolar sac and alveolus. When the associated blood vessels and tissues are removed, bronchial tree together with the trachea looks like a tree turned upside- down. The Bronchial Tree contd. Its branches begin with the right & left main (primary) bronchi, which arise from the trachea (bifurcation of trachea) at the carina. The bronchi enter the lungs at the hilum with arteries, veins, and lymphatics. Right bronchi is shorter, larger & more vertical. Foreign object invasion??? The main bronchi continue branching and dividing (3 in right, 2 in downwards to give an average of left) 23 generations (division points). Branches of Bronchial Tree Right and left primary (main or mainstem) bronchi Secondary or lobar bronchi- branch out of 1o bronchi. Each supplies a lung lobe Tertiary or segmental bronchi. Branch from lobar bronchi. Each supplies a bronchopulmonary segment Intralobular bronchioles. Small branches of the segmental bronchi that enter the basic units of the lung—the lobules. A lobule (respiratory unit) = respiratory bronchiole, alveolar ducts, arteries, and alveoli. Terminal bronchioles (TB)- Branches from an intralobular bronchiole within a lobule. ~50-80 in a lobule Respiratory bronchioles (RB)- Alveolar ducts - Alveolar ducts branch from each respiratory bronchiole Alveolar sacs – Thin-walled, closely packed outpouchings of the alveolar ducts. Alveoli – outpouchings from respiratory bronchioles, alveolar Functional Division of RS It is based on whether they transport gases or exchange them. The whole RS is divided into: Conducting zones- from nose to terminal bronchioles. Include URT and tracheobronchial tree up to terminal bronchioles (~1-16th generations). They carry out air conditioning function (filtration, warming & humidifying) mainly in URT & especially in the nose. Their epithelial cells secrete molecules that aid in lung defense. E.g. IgA, collectins (e.g. surfactant protein (SP) -A & SP-D), defensins & proteases, reactive oxygen species (ROS) & RNS. Respiratory zones- from respiratory bronchioles (transitional zone ~17- 19th generation) to alveoli. Participate Summarized Properties of the Airways Structures of the Lower Respiratory Tract The Alveoli- the main gas exchange structure They are pouch-like evaginations of the walls of the respiratory zones. ~300 million in each of human lungs & rimmed with elastic fibers. They responsible for ~90% of gas exchange (~10% in respiratory bronchioles & alveolar ducts). ~0.2 mm in diameter Lined by 2 types of epithelial cells: Type I cells (primary lining cells) - Flat cells (simple squamous epithelium) with large cytoplasmic extensions. It covers ~95% of the alveolar epithelial surface area (SA). Any effect of the SA on gaseous exchange??? Type II cells (granu­lar pneumocytes) - thicker & contain numerous lamel­- lar inclusion bodies (membrane-bound organelles containing phospholipids). Type II cells make up only 5% of the SA, but are 60% of the epithelial cells in the alveoli (in term of number) They are important in the regeneration of type I & type II pneumocytes (alveolar repair) and in the production of surfactants. Also contain main defense cells called pulmonary alveolar macrophages (PAMs, or AMs) that ingest dust & debris and then move to the bronchioles. Cilia action in alveoli?? PAMs CAN CAUSE INFLAMMATION!!! Mucociliary Escalator – mucus + cilia that move particles The direction of cilia “power stroke” is always downward or upward toward the pharynx. Ciliary motility can be defective due to smoking, other environmental conditions genetic deficiencies Difference between right and left lungs Functions of RS 1. Primary function- Transport of gases (mainly O 2 & CO2) in & out of the body. 2. Filtration – occurs mainly in the URT especially in the nose Internal hairs guard the nostrils preventing larger particles (30-50μm diameter) from being inhaled. Turbulent precipitation- (entrapping of particles within the air in the mucus as the air passes through nasal conchae (mainly) & septum) traps particles of diameter >6 μm. Gravitational filtration makes many 1-5 μm particles settle in bronchioles. Coal miners usually have bronchiolar disease. Some of during expiration bcos of ST?? Surfactant removal is slow Compliance of the lung (CL) In a healthy person Note: different shape Surfactant of the curves for production is slow expiration & inhalation = HYSTERESIS Surfactant, Surface Tension (ST) & Collapse of the Alveoli The net effect of ST in the liquid-interface of the alveoli is to cause an elastic contractile force of the entire lungs, which is called the surface tension elastic force. Pulmonary surfactant is a surface-active phospholipoprotein complex greatly reduces the surface tension at the air/liquid interface. In the alveoli, it is secreted by type II alveolar epithelial cells. Functions of Surfactant 1.it reduces the surface tension 2. It increases lung compliance, reducing the work of expanding the lungs during inspiration 3. Surfactant also helps prevent pulmonary oedema. Neonatal respiratory distress syndrome and surfactant?? In the fetus, surfactant synthesis begins at ~week 24. Infants born between weeks 24 and 35 will have uncertain surfactant status. Control of Respiration 1. NEURAL CONTROL It involves the respiratory center The respiratory center is composed of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem. It is divided into 3 major collections of neurons: (1) a dorsal respiratory group- Located in the dorsal portion of the medulla. Mainly causes inspiration (2) a ventral respiratory group- located in the ventrolateral part of the medulla in each side of medulla Mainly causes expiration (3) the pneumotaxic center- located dorsally in the superior portion of the pons mainly controls rate & depth of breathing. Chemical control of respiration This controls ventilation according to respiratory needs of the body. It maintains proper concentrations of O2, CO2, and hydrogen ions in the tissues. Controls respiration directly & indirectly through respiratory center. Excess CO2 or H in the blood mainly act directly on the respiratory center, causing greatly increased strength of both the inspiratory and the expiratory motor signals to the respiratory muscles. Oxygen mainly acts indirectly through peripheral chemoreceptors located in the carotid and aortic bodies, which then transmit signals to the respiratory center for control of respiration. Regulation of respiration during exercise Most of the increase in respiration/alveolar ventilation results from neurogenic signals transmitted directly into the brain stem respiratory center at the same time that signals go to the body muscles to cause muscle contraction. Most of total increase in ventilation begins immediately upon initiation of the exercise. the brain provides an “anticipatory” stimulation of respiration at the onset of exercise, causing extra alveolar ventilation even before it is necessary. Neurogenic response to control respiration is partly a learned response that may even involve cerebral cortex. Thus, increased ventilation might not largely due to change in chemicals This is because the arterial PO2, PCO2, and pH remain almost exactly normal in healthy athlete – the increased CO2 generated from exercising muscles is matched with increased ventilation Occasionally, however, the nervous respiratory control signals are either too strong or too weak. Chemical factors then play a significant role in bringing about the final adjustment of respiration required to keep the O2, CO2, and hydrogen ion concentrations of the body fluids as nearly normal as possible OBSTRUCTIVE & RESTRICTIVE LUNG DISORDERS.  Obstructive & Restrictive Lung Disorders Restrictive Lung Disorder There's a decrease in the total volume of air that the lungs are able to hold (hypoventilation). Can be: Intrinsic -:Caused by drug exposure, granulomas, pneumoconiosis, auto antibodies} –all lead to lung fibrosis Extrinsic -:Caused by chest wall deformities e.g. Kyphoscoliosis , and neuromuscular dysfunction. Intrinsic - Is any lung disease caused by the inhalation of organic or nonorganic airborne dust e. g Pneumoconiosis coal miners lung Extrinsic- Involve the chest wall, pleura & respiratory muscles. Diseases of these structures result in lung restriction. e.g. Kyphoscoliosis Restrictive Lung disorders Kyphoscoliosis- a condition characterized by an abnormal curvature of the spine. There is an anteroposterior angulation of the spine (kyphosis) and lateral displacement of or curvature of the spine (Scoliosis) The abnormal shape restricts lung compliance and capacity This may cause Difficulty breathing Increased respiratory rate Exercise intolerance Sleep apnea Restrictive Lung disorders Vagus Nerve compression can disrupt normal respiratory function by affecting the control of breathing. In severe cases, it can lead to symptoms like difficulty breathing, reduced respiratory rate, or even respiratory arrest. The vagus nerve plays a key role in regulating the muscles involved in breathing and the reflexes that protect the airway  Obstructive & Restrictive Lung Disorders Obstructive Lung Disorder There’s narrowing of the airways inside the lungs, the exhaled air comes out more slowly than it should, E.g. Asthma, Cystic Fibrosis, Chronic Obstructive Pulmonary Disease, emphysema Cystic fibrosis Cystic fibrosis (CF) is a genetic disease that causes sticky, thick mucus to build up in organs, blocking and damaging them. The mutations results in a buildup of thick mucus throughout the body, leading to respiratory insufficiency, along with many other systemic obstructions and abnormalities. It affects the lungs and airways, which can make it hard to breathe and cause frequent infections Cystic Fibrosis  Chronic Obstructive Pulmonary Disorder Progressive disorder of airway obstruction with little or no reversibility It includes: chronic bronchitis and emphysema Chronic bronchitis – inflammation of bronchi causing excessive mucous production and swelling of the bronchial wall Emphysema: Abnormal permanent enlargement of air spaces Chronic Obstructive Pulmonary Disorder Changes in the lung & airways in COPD include; Loss of elasticity in airways and alveoli Inflammation, scarring (fibrosis) and narrowing of airway Thick mucus production in the airway Destruction of the walls between alveoli Characteristics Of Restrictive And Obstructive Lung Disorder  FEV1: Volume that has been exhaled at the end of the first second of forced expiration  Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test  The FEV1 /FVC ratio below the lower limits of normal is consistent with airflow obstruction Characteristics Of Restrictive And Obstructive Lung Disorder Symptoms of Obstructive & Restrictive Lung disorders Causes of Obstructive & Restrictive Lung Disease  Diagnosis of Restrictive/Obstructive Lung disorders The diagnosis of obstructive /restrictive lung disease can be done through taking medical history and performing physical exam( e.g. Auscultation) The diagnosis can also include pulmonary function tests and imaging that helps to figure out what condition one may have. Pulmonary function tests Pulmonary function tests look at: Forced vital capacity (FVC) : measures the amount of air you can breathe out forcefully after taking a deep a breath as you can. Forced expiratory volume in one second (fev1): the test measures the total amount of air that can be forcibly exhaled in the first second of the FVC test. Healthy people generally expel around 75% to 85%. Fev1 is lower in obstructive lung diseases and normal to only a little lower in restrictive lung diseases.  Diagnosis of Restrictive/Obstructive Lung disorders Fev1/Fvc Ratio: the ratio of FEV1 to FVC measures the amount of air a person can forcefully exhale in one second relative to the total amount of air they can exhale. The ratio is lower in obstructive lung disorders and normal in restrictive lung disorders. In an adult, a normal FEV1/FVC ratio is 70% to 80% and in a child, a normal ratio is 85% or greater. Can be used to figure out the severity of obstructive lung disease. Total lung capacity (TLC): is calculated by adding the volume of air left in the lungs after breathing out (the residual volume) to the FVC. TLC is normal or higher in obstructive defects and lower in restrictive ones. In obstructive lung diseases, air is left in the lungs (air trapping or hyperinflation), causing a TLC increase.  Pulmonary Function Tests Spirometry Tests how your lungs are functioning. It measures how much air you inhale and how much and how quickly you exhale. It helps to determine whether a lung condition is obstructive (in which exhalation is impaired) or restrictive (in which inhalation is impaired). It can help to determine if a treatment is working or needs to be modified. Lung plethysmography: estimates how much air is left in the lungs after expiration. Diffusing capacity: measures how well oxygen and carbon dioxide can diffuse between alveoli and capillaries in the lungs  Pulmonary Function Tests IMAGING TESTS: Procedures like BRONCHOSCOPY:A flexible tube with a camera and tools on its tip to view inside the airways Chest X-rays Computed Tomography (CT scan) of the chest LAB TEST Oximetry: a measure of the oxygen content in the blood Arterial blood gases: Hb level  Pulmonary Function Tests Spirometry Illustration  Treatment of Obstructive/ Restrictive Lung Disorder The treatment options are significantly different for obstructive and restrictive lung diseases Obstructive Lung diseases: Medication that dilate the airways (bronchodilators) can be very helpful Inhaled or oral steroids are frequently used to reduce inflammation Restrictive Lung Disease: Treatment of the underlying causes may result in improvement Supportive Treatment Helpful for both Includes supplemental O2 , Non-invasive ventilation (cPAP) or mechanical ventilation When severe Lung transplant is option  Collapse of Alveoli Alveoli are microscopic balloon-shaped structures located at the end of the respiratory tree. They expand during inhalation and shrink during exhalation. This is where gaseous exchange takes place. Surfactant deficiency is a lung disorder that causes breathing problems, it results from abnormalities and dysfunction of surfactant. Without normal surfactant, the tissue surrounding the alveoli sticks together because of a force called surface tension after exhalation, causing the alveoli to collapse. As a result, filling the lungs with air on each breath becomes very difficult, and the delivery of oxygen is impaired. The disease first attributed to surfactant deficiency is infant respiratory distress syndrome. Other diseases that may be caused by or lead to abnormalities in surfactant production or function, including: Acute respiratory distress syndrome (ARDS), alveolar proteinosis, Asthma and COPD, Pulmonary fibrosis, hypersensitivity pneumonitis, infectious lung processes such as pneumonia, AIDS & patients who smoke. 57  Infant Respiratory Distress Syndrome Aka surfactant deficiency disorder. Is a syndrome, in premature infants caused by developmental insufficiency of pulmonary surfactant production and structural immaturity in the lungs. As such the alveoli and distal airways cannot remain open during expiration and cannot effectively exchange gases. Up to 50 per cent of infants born between 26 and 28 weeks and fewer than 30 per cent of infants born between 30 and 31 weeks develop IRDS. Premature infants can be administered artificial or man-made surfactants. There are two types of artificial surfactants i.e synthetic pulmonary surfactants ( e.g.Pumactant- a mixture of DPPC + PG) and animal-derived surfactants (e.g. survanta from minced cow lung with additional DPPC) 58 Nursing Management of Infant Respiratory Distress Syndrome SIGNS AND SYMPTOMS Management Arterial blood gas and monitor oxygen Nasal flaring with each concentration breath Control oxygen volumes Cyanosis Semi-fowlers position Use less invasive methods for Chest in-drawing administration of surfactant e.g. CPAP Low saturation machine Monitor Feeding; NG Tube or Parenteral Grunting feeding 59  Pulmonary Alveolar Proteinosis(pap) an uncommon lung condition where surfactant and lipoproteinaceous builds up in the alveoli as a result of reduced clearance as opposed to increased production(impaired clearance) surfactant buildup in alveoli can occur through three different pathways: autoimmune, secondary, and congenital. instead of increasing surfactant production, all three of these routes lead to a decrease in surfactant clearance, leading to impaired gas exchange and then respiratory distress Ninety per cent of cases with known pathophysiologic mechanisms are caused by autoimmune pap. Surfactant proteins a, b, c, and d are the four primary subtypes of surfactant. these compounds are all associated with the genes sfptd, sftpb, sftpc, and sftpa These genes are mutated to produce defective surfactant, which builds up inside type ii alveolar epithelial cells and results in inefficient surfactant removal from the alveoli and cell death. 60  Clinical Diagnosis Chest radiography which may show bilateral alveolar opacities, Bio markers-checking levels of surfactant protein A,B and D,they are usually increased in PAP Bronchoscopy-it’s the gold standard for diagnosis 61  Signs and Symptoms of pap Shortness of breath Cough Low grade fever Weight loss haemoptosis 62  Treatment of pap Whole lung lavage Lung transplantation Plasmapheresis Rituximab The last two are alternative therapies 63  Difference Between Upper and Lower Respiratory Tract Infections & Clinical Features The main difference between upper and lower respiratory illnesses is the location. The respiratory system is divided into two parts: the upper tract and the lower tract. Upper Respiratory Illnesses Upper respiratory infections (URIs) are typically caused by a virus. They are one of the most common infectious illnesses in the world, affecting billions of people every year. Common URIs include colds, sinusitis, tonsillitis, laryngitis, and flu (influenza).  Upper Respiratory Infections Clinical Features URIs present with a range of symptoms that affect the upper respiratory tract. These can differ from person to person, but frequently include: Sneezing Sore Throat Nasal Congestion or Disc Headaches Facial Pain Fatigue and/or Malaise Most URIs are mild and will resolve without treatment within 7-10 days. If symptoms persist for longer than two weeks or become severe, it’s best to visit your doctor for an accurate diagnosis and treatment plan. TONSILITIS Tonsillitis is Inflammation of the tonsils Caused by viral or bacterial pathogens as they bind to antigen presenting cells that relay message to T helper cells that relay message to macrophages, B cells and Killer cells. Symptoms include: sore throat, pain when swallowing ,general muscle aching ,malaise and fever. Pharynx and tonsils appear red and peritonsillar tissues become swollen. Sometimes exudates drain from crypts in the tonsils Not all pathogens penetrates mucosal membrane to cause infection, some are destroyed by antibodies eg. IgA while still on the surface NB!! It Can be acute or recurrent Components of Tonsils Tonsils are part of immune system They have 4 components: a) Epithelium: a layer of epithelium cells b) Tonsillar crypts: deep folds on the surface that trap and process pathogens c) Lymphoid tissue: contains lymphocytes and other immune cells that detect and respond to infections d) Connective tissue: supportive connective tissue framework that maintains the tonsil structure. Types of Tonsils Classification By Characteristics: a) Acute tonsillitis: sudden b) Chronic tonsillitis: persists for a long time c) Recurrent tonsillitis: frequent episodes of acute infection....…..continuation Classification By Cause: a) Viral Tonsillitis: Epstein-Barr Virus, adenoviruses, herpes simplex viruses, influenza viruses b) Bacterial Tonsillitis: Group A Streptococcus, Staphylococcus aureus c) Fungal Tonsillitis: Candida d) Allergic Tonsillitis: allergens or irritants Waldeyer’s Ring The Waldeyer’s ring is formed by Nasopharyngeal tonsils (Adenoids):located on the roof of the nasopharynx, under the sphenoid bone Palatine Tonsils (simly tonsils):located in the oropharynx Lingual tonsil: a collection of lymphatic tissue located on the back part of the tongue Tubal tonsils:on each side, where each auditory tube opens into the nasopharynx  Purpose of Weldeyers Ring Prevents the invasion of microorganisms from entering the air and food passages. Helps the defense mechanism of the respiratory and alimentary system For Formation of Lymphocytes and and Antibodies Clinical Significance: the inflammatory condition is due to viral or bacterial infection Treatment: Painkillers and antibiotics for immune- compromised , severe or painful cases They can be removed operation called Tonsillectomy  Complications a) Peritonsillar abscess: Pus accumulate near the tonsils b) Spread of infection: to parts of the throat ears, sinuses, skin, joints, Kidneys and the heart c) Breathing difficulties: swollen tonsils can obstruct airway Tonsils with exudates  Lower Respiratory Tract Infections Clinical Features They are typically more serious than upper respiratory infections, especially in vulnerable populations. Common LRIs include pneumonia, bronchitis, bronchiolitis, and the flu (influenza). Coughing is the primary symptom of lower respiratory infections. Other symptoms include: Increased mucus (phlegm) Fever Chest Pain Shortness of Breath Fatigue Body Aches Lower Respiratory Illnesses (LRIs) are caused by viruses or bacteria that infect lower respiratory tract. The Severe Acute Respiratory Syndrome (SARS) Coronavirus-2 The disease is caused the virus termed coronavirus disease 19 or simply COVID-19, Its an Upper airway infection Transmitted by respiratory droplets from infected persons Enters host via respiratory droplets Binds to receptors on cells and enters the cell through membrane fusion or endocytosis Anatomy Of Coronavirus Made of 4 structural proteins: a)Membrane b)Envelope c)Nucleocapsid: d)Spike: host attachment and penetration It has 6 accessory proteins: ORF (3a, 6,7a,7b,8,10) 16 non-structural Pathophysiology of respiratory infections When airways get irritated, they swell up and fill with mucus, causing cough. cough can last days to a couple of weeks. Whistling or rattling sounds may be heard when breathing (wheezing) due to an inflamed airway. LRI Risk factors Anyone can get LRI, but you’re at higher risk if you: Smoke or are around someone who does. Have asthma, COPD or other breathing conditions. Have GERD (chronic acid reflux). Have an autoimmune disorder or other illness that causes inflammation. Are around air pollutants (like smoke or chemicals). Airway epithelium Immune Response Bacteria infected lung Chest X-Ray film  Management Of Upper And Lower Respiratory Infections Goals Of Treatment Application of preventive measures to prevent cross infection during provision of care Symptoms relieve, e.g. headache, decongestion Treat infection fully Prevent disease progression (complications) Improve the quality of life Improve oxygenation  MEDICAL MANAGEMENT (NSAIDs), such as ibuprofen, paracemol, or aspirin can relieve pain and fever Antibiotics for bacterial infections, e.g. cephalosporins, penicillins, macrolides Antihistamines, e.g. allergex, promethazine Steroids e.g. hydrocortisone, dexamethasone Humidified Oxygen therapy Ventilator support, e.g. CPAP, BiPAP  NURSING MANAGEMENT Respiratory assessment, auscultation of lung sounds, Measurement of oxygen saturation (SP02), and assessment of respiratory rate and effort. Assessment of vital signs, including temperature, heart rate, and blood pressure. Evaluation of cough characteristics, sputum production, and any associated symptoms, such as chest pain or shortness of breath. Administration of oxygen therapy as prescribed e.g. oxgen at 15L/min per non re-breather mask, to SP02 ≥95% Administration of medications prescribed e.g. IV ceftriaxone, oral azithromycin. Monitor blood chemistry, ABGs IV fluid hydration, if unable to take oral fluids: NB clear off pulmonary effusion prior hydration