Advanced Pathophyisology NRMS 5190/ NRMS5190: Exam 2 A+ Complete Study Guide ~ Latest Updated Fall 2025/26.

Advanced Pathophyisology NRMS 5190/ NRMS5190: Exam 2 A+ Complete Study Guide ~ Latest Updated Fall 2025/26. Chapter 30 Respiratory Disorder The movement of air between the atmosphere and the lungs follows the laws of physics as they relate to gases. The air in the alveoli contains a mixture of gases, including nitrogen, oxygen, carbon dioxide, and water vapor.. The pressure inside the airways and alveoli of the lungs is called intrapulmonary (or alveolar) pressure; the pressure in the pleural cavity is called pleural pressure; and the pressure in the thoracic cavity is called intrathoracic pressure. The diaphragm is the principal muscle of inspiration, assisted by the external intercostal muscles. Surfactant molecules, produced by type II alveolar cells, reduce the surface tension in the lungs and thereby increase lung compliance. ** Lung volumes and lung capacities = reflect the amount of air that is exchanged during normal and forced breathing. KNOW: The tidal volume (VT) is the amount of air that moves into and out of the lungs during normal breathing. The respirator system consists of air passages and lungs, where gas exchange takes place. The air passages can be divided into 2 parts, the conducting airways through which air moves as it passes into and out of the lungs, and the respiratory tissue where gas exchange actually takes place. • Respiration requires ventilation, or the movement of gases into and out of the lungs; perfusion , or movement of blood through the lungs; and diffusion of gases between the lungs and the blood. • Ventilation depends on the conducting airways, including the nasopharynx, oropharynx, larynx and tracheobronchial tree, which move air into and out of the lungs but do not participate in gas exchange, • Gas exchange takes place in the respiratory airways of the lungs where gases diffuse across the alveolar-capillary membrane as they are exchanged between the air in the lungs and the blood that flows through the pulmonary capillaries. • Conducting Zone: Upper respiratory tract • Respiratory Zone: Lower Airways • Conducting airways: nasal passages, mouth, pharynx, larynx, trachea, bronchi and bronchioles. Conducting airways act as a conduit for airflow but also warms, filters and humidifies air as it moves through these structures. KNOW *The conducting airways are lined with a mucociliary blanket – a protective layer with mucous and cilia (cells with hairlike projections that help sweep and trap particles such as bacteria, dust and other foreign substances – this is in an upward motion that brings back to the oropharynx where it is expectorated or swallowed. • ** Lung volumes and lung capacities reflect the amount of air that is exchanged during normal and forced breathing. The tidal volume (VT) is the amount of air that moves into and out of the lungs during normal breathing. • Common Cold- viral infection of the upper respiratory tract. Adults can have 3-4 per year, school age child may have 6-8 per year. • **Rhinovirus are most common cause for cold, others are parainfluenza virus, respiratory syncytial virus (RSV), human metapneumovirus (hMPV), coronaviruses, adenoviruses. • Pneumonia is the 8th leading cause of death in the US, especially in the elderly and those with compromised immune function. • TB affects 1/3 of the world’s population. • People who have compromised immune systems may be susceptible to a virus causing serious gas exchange or ventilation problems – in addition to other types of organisms such as bacteria and fungus which can cause lung infections. If patient has underlying history of asthma, this may be exacerbated by presence of a virus • Viral infections can damage bronchial epithelium, obstruct airways and lead to secondary bacterial infections. • Common cold is an acute and self limiting illness in otherwise healthy people – • **Rhinovirus are the most common cause of colds. The common cold spreads easily, handwashing is very important because fingers are the greatest source of spread and the nasal mucosa and conjunctival surface of eyes are most common portal of entry for virus. Symptoms begin with dryness and stuffiness in the nasopharynx, followed by excessive production of nasal secretions and tearing of the eyes. Secretions are usually clear and watery. Other symptoms – erythema and swelling of mucous membranes of upper respiratory tract , postnasal drip, sore throat, hoarseness, headaches and generalized malaise. Fevers chills and exhaustion can be seen in severe cases. Treatment is rest, OTCs (decongestants can cause systemic vasoconstriction and elevation of BP so should be avoided in people with HTN,, heart disease, diabetes, etc) • Rhinosinusitis is inflammation involving nasal sinuses. The most common conditions are those that obstruct the narrow ostia that drain the sinuses. Rhinosinusitis develops when a viral upper respiratory tract infection or allergic rhinitis causes mucosal swelling and obstructs the ostia and impairs the mucociliary clearance mechanism. • **The Mucociliary clearance mechanism helps keep the sinuses sterile by moving fluid and microorganisms out of the sinuses and into the nasal cavity. • A Mucociliary clearance mechanism helps keep the sinuses sterile by moving fluid and microorganisms out of the sinuses and into the nasal cavity. • Viral rhinosinusitis can be difficult to differentiate from common cold and allergic rhinitis. The S/S include facial pain, headache, purulent nasal discharge, diminished sense of smell and fever. **** Fever and facial pain are more commonly associated with rhinosinusitis rather than the common cold. Symptoms usually resolve in 5-7 days without medical treatment. • Bacterial rhinosinusitis – the symptoms that worsen after 5-7 days or persist beyond 10 days. People who are immunocompromised can present with fever of unknown origin, rhinorrhea or facial edema. • In chronic rhinosinusitis symptoms may consist of sinus pressure with nasal congestion. The patient may complain of headache that is dull and constant. Sinus headaches are exaggerated by bending forward, coughing or sneezing. The epithelial changes that occur during acute rhinosinusitis are usually reversible but the mucosal changes that occur with chronic rhinosinusitis are often irreversible. • Pt may need CT for cases of chronic rhinosinusitis to make sure there are no polyps or deformities that could be causing obstruction of drainage. • Treatments: 2/3rds of cases of acute bacterial rhinosinusitis improve without antibiotics. Most people with viral sinusitis improve within a week. Some people require antibiotics which can be 3-4 weeks, they may need nasal irrigation and intranasal, decongestants (should be limited 3-5 days to prevent rebound vasodilation) - Saline spray, mist humidification. • Mucosal changes are not permanent. • Influenza, combined with pneumonia, is the 8th leading cause of death in the US, and highest rates are in children and older adults. Transmission is not by contact but by inhalation of droplet nuclei. *The incubation period for influenza is 1-4 days with 2 days being the average. People become infectious starting 1 day before their symptoms begin and remain infectious for about 1 week after illness onset. • Influenza starts with abrupt onset of fevers and chills, rigors, malaise, muscle aches, headaches, profuse watery nasal discharge, nonproductive cough and sore throat. The rapid onset of profound malaise is a distinguishing feature of an influenza infection. Secondary complications are pneumonia, sinusitis, otitis media, bronchitis, bacterial pneumonia, croup in children. People with secondary bacterial pneumonia may say that they began to feel better but they experienced a return of fever, chills, pleuritic chest pain and productive cough • Influenza C is more like the common cold. • Viral pneumonia is a complication of the flu in older adults or people with cardiopulmonary disease but can be seen in pregnant women and health people as well. Viral pneumonia usually manifests within 1 day after onset of influenza and also has a rapid progression of symptoms, it progresses quickly and can cause hypoxemia and death within a few days of onset. Survivors can develop diffuse pulmonary fibrosis. • Amantadine and Rimantadine are only effective against influenza A. They inhibit the uncoating of viral RNA in the host cells and prevent its replication. Resistance to these drugs develop rapidly. Amantadine stimulates the release of catecholamine, which can produce central nervous system effects such as anxiety, depression and insomnia. • Zanamivir (Relenza) & Oseltamivir (Tamiflu) - effective against A & B viruses and have less resistance. Zanamivir is administered intranasally, and can cause bronchospasm so should be avoided with pts with asthma or COPD. Meds should be initiated within 48 hours of onset of symptoms. • All people 6 months of age and older are recommended to receive the influenza vaccine in the US. • CDC updates its recommendations yearly about the composition of the vaccine. On a good year – flu vaccine can prevent illness in 50-70% of healthy people younger than 65 years of age. Contraindicated in people with anaphylactic hypersentitivity to eggs, people with Hx of Guillain Barre syndrome, or people who have an acute febrile illness. • There is inflammation of parenchymal structures of the lung in the lower respiratory tract such as the alveoli and bronchioles. 8th leading cause of death in the US and most common cause of death from infectious disease. • PNEUMONIA • Streptococcus Pneuomoniae is a gram positive organism that possesses a capsule of polysaccharide. = makes it hard to The virulence of the pneumococcus is a function of its capsule, which prevents or delays digestion by phagocytes. • The pathogenesis of pneumococcal infection: Alveoli become filled with protein rich edema fluid. Marked capillary congestion follows, leading to massive outpouring of polymorphonuclear leukocytes and red blood cells. After 2 or more days, the next stage involves the arrival of macrophages that phagocytose the fragmented polymorphonuclear cells, red blood cells and other cellular debri. During this stage, the congestion has diminished. The alveolar exudate is then removed and the lung gradually returns to normal. • The bacterial attachment and colonization of the organism to the mucus and cells of the phasopharynx. This does not equate with sign of infection. Perfectly healthy people can be colonized and carry the organism, and spread the organism to others without being sick. • Acute bacterial pneumonia can be classified as lobar or bronchopneumonia based on their pattern of distribution. In general, lobar pneumonia refers to consolidation of a part or all of a lung, and bronchopneumonia signifies a patchy consolidation involving more than one lobe. • Typical pneumonia – result of infection by bacteria that multiply extracelluarly in the alveoli and cause inflammation and exudation of fluid into the air-filled spaces of the alveoli. *Streptococcus pneumoniae is most common cause of bacterial pneumonia. • Atypical pneumonia – caused by viral and mycoplasma infections that involve the alveolar septum and the interstitium of the lung. They produce less symptoms than typical pneumonia. • Community acquired – an infection that begins outside the hospital or is diagnosed within 48 hours of admission (as long as they don’t reside in a LTC facility for 14 days or more prior to admission)- • Hospital acquired – pneumonias that occur 48 hours or more after admission. Intubated patient’s or anyone requiring mechanical ventilation are at higher risk. These pneumonias are often resistant to antibiotics and are more difficult to treat. • TUBERCULOSIS • TB is the World’s foremost cause of death from a single infectious agent. M. Tuberculosis is a rod-shaped, aerobic bacterium that is resistant to destruction and can persist in necrotic and calcified lesions for prolonged periods and remain capable of reinstating growth. Macrophages are the primary cell infected. Inhaled droplets pass down the bronchial tree without settling on the epithelium and are deposited in the alveoli. Once in the lung, macrophages are unable to kill the organism, and they then initiate a cell mediated immune response that contains the infection. In people with intact cell-mediated immunity, the immune response develops into granulomatous lesions called a Ghon focus, which contains the tubercle bacilli. These Ghon complexes can undergo shrinkage, fibrous scarring and calcification (which can be seen on an xray), but small numbers of organisms remain viable for years. Later if immune mechanisms fail or decline, latent tuberculosis infection has the potential to develop into secondary tuberculosis. • Difficult to diagnose because people don’t always have classic symptoms. • Symptoms are nonspecific but include fever, weight loss, fatigue, and night sweats. They can also exhibit pleuritis(pain on inspiration) and lymphadenitis (swollen lymph nodes) . As disease spreads and the organism gains access to sputum, the infected person can infect others. • Early primary progressive TB can have a dry cough but later the cough becomes productive with purulent and sometimes blood tinged sputum. Dyspnea and orthopnea develop as the disease advances to late primary progressive TB. • BCG is a vaccine given outside of the US that will make a PPD come up positive. Quantiferon Gold is now the preferred test but its expensive. CXR needed if positive, pulmonary consult. • *Pt usually put on multiple medications such INH, rifampin etc for at least 6 months. • HISTOPLASMOSIS • Occurs mostly along major river valleys of the Midwest. The organism H. Capsulatum grows in soil and other areas where there is bird excrements and bat droppings. Histoplasmosis infection is acquired by inhaling the fungal spores that are released when dirt of dust from an infected area is disturbed. • Dissemination occurs during the first several weeks after infection. Incubation is 1-4 weeks after exposure. Depending on the host’s immune system, there may be no symptoms. Most people will remain asymptomatic or have mild respiratory illness. • Latent histoplasmosis is characterized by evidence of healed lesions in the lungs or hilar lymph nodes. • Chronic histoplasmosis can resemble TB. More common in middle-aged men who smoke and people with chronic lung condition. Can see productive cough, chest pain, fever, night sweats, weight loss. • In Disseminated histoplasmosis (which follows primary or chronic histoplasmosis), the macrophages of the reticuloendothelial system can remove the fungi from the bloodstream but are unable to destroy them. You may see high fever, generalized lymphadenopathy, hepatosplenomegaly, muscle wasting, anemia, leukopenia, ulcerations of tongue and mouth, N/V/D, and abdominal pain, and meningitis becomes a dominant feature of the disease. • LUNG CANCER • Most lung cancers arise from lung tissue, and lungs are often the site of metastasis from cancers in other parts of the body. Lung cancers can be aggressive, non aggressive, locally invasive, and widely metastatic tumors that arise from the epithelial lining of major bronchi. The tumors begin as small mucosal lesions that may follow one of several patterns of growth. They can form intraluminal masses that invade the bronchial mucosa and infiltrate the peribronchial connective tissue, or they may form large, bulky masses that extend into the adjacent lung tissue. Some large tumors undergo necrosis and acquire local areas of hemorrhage, and some invade the pleural cavity and chest wall and spread to adjacent intrathoracic structures. • All lung cancers, especially small cell lung carcinoma, have the capacity to synthesize bioactive products and produce paraneoplastic syndromes, These syndromes are a result of hormonal production of ectopic peptide by the tumor or from autoantibiodies released in response to the tumor. In general, the paraneoplastic syndromes are of endocrine, neurologic, and/or immunologic etiology. • Small cell carcinoma – these tumors can secrete polypeptide hormones. They are highly malignant and disseminate early in their course. They are rarely resectable. Brain metastases are common and may be the first evidence of the tumor. Small cell lung cancer is associated with several types of paraneoplastic syndrome, including SIADH, Cushing syndrome associated with ectopic production of adrenocorticotropic hormone, and Lambert-Eaton syndrome (neuromuscular disorder which leads to muscle weakness). • **Cushing Syndrome manifestations: Weight gain, moon face, buffalo hump, purple striae on abdomen. If there is swelling of face and neck, you should consider Superior Vena Cava Syndrome due to compression and impeding flow of superior vena cava by tumor mass. This is an emergency situation. • Non-small cell Lung cancers include Squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. • Squamous cell carcinomas – most common in men and closely correlated to smoking • Adenocarcinomas – most common type of lung cancer in women and nonsmokers • Large cells carcinoma – Difficult to categorize, they tend to occur in the periphery of the lung, invading subsegmental bronchi and larger airways, and have poor prognosis. • Most of the manifestations from lung cancer are from irritation and obstruction of the airways and invasion of the mediastinum and pleural space. Early symptoms are chronic cough, SOB, and wheezing due to airway irritation and obstruction. Hemoptysis happens when blood vessels are eroded by the lesion. Dull poorly localized retrosternal pain may be present in tumors that involve the mediastinum. Pain becomes more severe when the disease invades the pleura. • Diagnosis and treatment is based on the careful history and physical exam and other tests – CXR,, bronchoscopy, cytology of sputum, percutaneous needle biopsy of lung tissue, lymph node biopsy, CT Scan, MRI, sonogram, PET scan. All people with SCLC should have CT or MRI of the brain. • TNM staging (Tumor, Node, Metastasis) is not usually used for small cell lung cancers because it is assumed that there are already micrometastases at the time of diagnosis. • Embryonic period (weeks 4-6) • Pseudoglandular period (weeks 5-16) - conducting airways are formed • Canalicular period (weeks 17-27) – formation of primitive alveoli – By the 24th week, each bronchiole has given rise to two or more respiratory bronchioles and respiration is possible at this time because some primitive alveoli have developed at the ends of the bronchioles • Saccular period (weeks 27-35) development of the terminal alveolar sacs which facilitate gas exchange. The terminal sacs thin out and capillaries begin to bulge into the terminal sacs (type I alveolar cells). Type II alveolar cells begin to develop around 24 weeks. • By the 25th – 28th weeks, sufficient terminal sacs are present to permit survival. Before this time, premature lungs are incapable of adequate gas exchange. These cells produce surfactant, a substance capable of lowering the surface tension of the air-alveoli interace. By the 28th – 30th weeks, sufficient amounts of surfactant are available to prevent alveolar collapse when breathing begins. 30-36 weeks the saccular structures become alveoli. • Alveolar period (late fetal to early childhood) – marks the maturation and expansion of the alveoli. By late fetal period, the lungs are capable of respiration because the alveolar-capillary membrane is sufficiently thin to allow for gas exchange. • RDS is one of the most common causes of respiratory disease in premature infants. Pulmonary immaturity and surfactant deficiency leads to alveolar collapse. Premature infants are born with poorly functioning type II alveolar cells and have difficulty producing sufficient amounts of surfactant. Surfactant reduces the surface tension in the alveoli, thereby equalizing the retractive forces in the large and small alveoli and reducing the amount of pressure needed to inflate and hold the alveoli open. Without surfactant, the large alveoli remain open but the small alveoli become difficult to inflate. • At birth, the first breath requires high inspiratory pressures to expand the lungs. With normal surfactant the lungs retain up to 40% of residual volume after the first breath, and subsequent breaths require far lower inspiratory pressure. With surfactant deficiency, the lungs collapse between breaths, making the infant work hard with every breath. The airless portions of the lungs become stiff and noncompliant. *A fibrin-hyaline membrane forms inside the alveoli, and this is a barrier to gas exchange, causing hypoxemia and carbon dioxide retention. • Bronchopulmonary dysplasia – chronic disease that develops in preemies who were treated with long term mechanical ventilation (usually for RDS). The condition is considered to be present if the neonate is oxygen dependent at 36 weeks. Thought to be a result of early lung injury of the premature lung. High inspired oxygen concentration and injury from positive pressure ventilation are implicated. BPD is characterized by chronic respiratory distress, persistent hypoxemia on room air, reduced lung compliance, increased airway resistance and severe expiratory flow limitation. These infants can have barrel chest, tachycardia, rapid and shallow breathing, chest retractions, cough, and poor weight gain. Clubbing of fingers can occur in severe disease. Hepatomegaly and periorbital edema may develop in infants with right heart failure. • **Parainfluenza virus accounts for majority of cases of croup. Can also be caused by other viruses. Affects larynx, trachea and bronchi. It’s usually seen in ages 3months to 5 years. Symptoms are usually preceded by a URI that causes runny nose, hoarseness, low grade fever. Manifestation of croup – stridor and slight dyspnea. Symptoms usually subside when child is exposed to moist air (mist tent or running shower and bringing child into bathroom) – Cold air oken relieves severe symptoms. Viral coup doesn’t respond to antibiotics, bronchodilators, expectorants, etc. • If airway obstruction occurs you may see continuous stridor, nasal flaring, and chest retractions. Agitation and crying make symptoms worse, child may need ER for airway management. • Spasmodic croup – usually occurs at night – thought to have allergic origin. Again, high humidification, or cold air which can sometimes help. • Epiglottitis_ can be fatal. Child can be pale, lethargic, sitting up with mouth open and chin thrust forward, Has difficulty swallowing, muffled voice, drooling, fever and extreme anxiety. Stridor, flaring of nares, and inspiratory retractions, within hours, this can be fatal if it progresses to complete obstruction of the airway • Bronchiolitis: RSV most common virus. Usually occurs during 1st 2 years of life, peak incidence between 3-6 months of age. Can see wheezy cough, dyspnea and irritability. There is obstruction of the small airways and necrosis of the cells lining of the lower airways. Child can take in sufficient air but has trouble exhaling. Air becomes trapped in the lung distal to the site of obstruction and interferes with gas exchange. This can progress to hypoxemia and hypercapnia. Breathlessness with rapid respirations, a distressing cough, retraction of lower ribs and sternum. In severe obstruction, wheezing decreases as airflow diminishes. • Treatment is supportive and includes administration of supplemental oxygen if O2 sat falls consistently below 90%. Elevation of the head facilitates respiratory movements and avoids airway compression. • Severe increase in respiratory effort, severe retractions, grunting, HR 150, Tachypnea 60 breaths per minute in newborn to 5 months, or 30 breaths per minute in 6months – 2 years **** OR VERY DEPRESSED BREATHING ***** • Children have an increased risk for respiratory distress because of narrow airways and immature chemoreceptors that respond to oxygen and carbon dioxide levels in the blood.7 • Hypoxia, a decreased oxygen concentration in arterial blood, results from an increased need for oxygen.7 • Barrel chest is often present in infants and toddlers.7 • A decreased lung capacity and immature intercostal muscles result in less pulmonary reserve, placing children at risk for hypoxemia.7 • Chest retraction associated with respiratory distress is due to a compliant and flexible bony chest of a child.7 • Normal newborns have lower normal oxygen saturation taking at least an hour to reach the desired normal saturation levels of 88%.8 Chapter 31 Disorders of Ventilation and Gas Exchange Hypoxemia refers to the reduction in arterial blood oxygen levels, which is considered a PaO2 95mmHg. Can result from inadequate amount of O2 in the air, respiratory disorder, dysfunction of the neurologic system (ie head injury) , or alterations in circulatory function. Respiratory disorders that can cause hypoxemia are hypoventilation, impaired diffusion of gases, inadequate circulation of blood through pulmonary capillaries, and mismatching of ventilation and perfusion. Can have more that one mechanism causing hypoxemia. Mild hypoxemia produces few manifestations. Compensatory mechanisms – increase HR, peripheral vasoconstriction, diaphoresis and mild increase in blood pressure. Pt may have slight impairment of mental performance. With more pronounced hypoxemia, there may be confusion, personality changes, restlessness, agitation, combativeness, uncoordinated muscle movements, impaired judgement, delirium, eventually stupor and coma. Sometimes hypoxemia may be corrected by oxygen therapy Hypercapnia – increase in carbon dioxide of the arterial blood, this can occur in disorders that cause hypoventilation or mismatching of ventilation and perfusion. The diffusing capacity of carbon dioxide is 20 times that of oxygen, therefore hypercapnia without hypoxemia is usually observed only in hypoventilation. Can result from inadequate amount of O2 in the air, respiratory disorder, dysfunction of the neurologic system (head injury), or alterations in circulatory function. Respiratory disorders that can cause hypoxemia are hypoventilation, impaired diffusion of gases, inadequate circulation of blood through pulmonary capillaries, and mismatching of ventilation and perfusion. Can have more that one mechanism causing hypoxemia. Hypoxemia – decrease in arterial blood oxygen levels that results in a decrease in tissue oxygenation. Can be the result of hypoventilation, diffusion impairment, shunt, and ventilation-perfusion impairment. Acid based balance - The body normally compensates for increased in PCO2 (partial pressure of carbon dioxide) by increasing renal bicarbonate retention, which results in an increase in serum bicarb and pH levels. As long as the pH is within normal range, the main complications of hypercapnia are those resulting from the hypoxia. Hemothorax – blood in the pleural cavity, may be the result of chest injury or complication of surgery, or rupture of a great vessel such as aortic aneurysm. Manifests as alterations in oxygenation, respiratory effort and breath sounds. Pleuritis – (pleurisy) inflammation of the pleura – can be due to irritatition of the central part of the diaphragm. It’s common in infectious processes such as respiratory infections that involve the pleura. Unilateral Chest Pain is a frequent symptom. Pain is made worse with coughing and deep breath. Chylothorax – effusion of lymph in the thoracic cavity. This is a result of trauma, inflammation, surgical procedures, using great veins for TPN or hemodynamic monitoring, or malignant infiltration obstructing chyle transport from the thoracic duct into the central circulation. Atelectasis - incomplete expansion of a lung or a portion a lung Empyema – infection in the pleural cavity that results in an exudate – usually caused by adjacent pneumonia, rupture of a lung abscess, or other infections Pneumothorax refers to the presence of air in the pleural space which can cause partial or complete collapse of the affected lung. Spontaneous pneumothorax – usually occurs in tall males between 10-30 years. Smoking and family history are factors. Doesn’t usually occur in a short stature nonsmoker. Traumatic pneumothorax can also be result of medical procedures such as transthoracic needle aspirations, central lines, intubation,and CPR. Tension pneumothorax – a life threatening condition where injury to the chest or respiratory structure permits air to enter but not leave the pleural space. This results in a rapid increase in pressure within the chest that causes compression atelectasis of the unaffected lung, a shift in the mediastinum to the opposite side of the chest, and compression of the vena cava which results in a decrease in venous return to the heart and reduced cardiac output. Normally fluid enters the pleural space from capillaries in the parietal pleura and is removed by the lymphatic situated in the parietal pleura. When the fluid accumulates this is a pleural effusion. Fluid can also enter from interstitial spaces of the lung through the visceral pleura or from small holes in the diaphragm. Atelectasis – incomplete expansion of a lung or a portion a lung, it can be caused by airway obstruction, lung compression such as occurs in pneumothorax. A mucus plug in the airway or external compression by fluid, tumor mass, exudate or other matter in the area surrounding the airway can cause obstruction. Atelectasis is common in people with pleural effusion from congestive heart failure or cancer. Manifestations can be tachypnea, tachycardia, cyanosis, hypoxemia, etc. Some people have cold-air induced asthma .........Continued..........