Alterations of Pulmonary Function Chapter 32 Deborah Williams

Clinical Manifestations of Pulmonary Alterations Pulmonary disease is often classified as acute or chronic, obstructive or restrictive, and infectious or noninfectious; it is caused by lung or heart failure.
S/S of Pulmonary Disease o Dyspnea the subjective sensation of uncomfortable breathing, the feeling of being unable to get enough air movement. Described as breathlessness, air hunger, shortness of breath, labored breathing & preoccupation with breathing. Usually caused by diffuse and extensive pulmonary disease but can be caused by focal pulmonary disorders. Disturbances of ventilation, gas exchange or ventilation-perfusion relationships can cause dyspnea as can increase WOB or diseases that damage lung tissue [lung parenchyma]. Orthopnea is dyspnea when the individual is lying down caused by horizontal position, which redistributes body water, causes the abdominal contents to exert pressure on the diaphragm & decreases the efficiency of the respiratory muscles. Paroxysmal nocturnal dyspnea [PND] positional dyspnea experienced by some individuals with left ventricular failure waking up at night gasping for air and must sit up or stand to relieve the dyspnea. This is cause from fluid in the lungs caused by the redistribution of body water while the individual is recumbent. o Abnormal Breathing patterns Eupnea [normal breathing patter] is rhythmic and effortless. Kussmaul Respiration [hyperpnea] is slightly increased ventilatory rate, very large tidal volume & no expiratory pause. Obstructed breathing [COPD] consists of slow ventilatory rate, large tidal volume, increased effort & prolonged inspiration or expiration, depending on site of obstruction. Audible wheezing or stridor sounds made during inspiration is often present. Restricted breathing occurs with disorders [pulmonary fibrosis] that stiffen the lungs or chest wall and decrease compliance & is characterized by small tidal volumes and rapid ventilatory rate. Panting occurs with exercise. Gasping respirations with shock & sever cerebral hypoxia consist of irregular, quick inspirations with an expiratory pause. Sighing respirations - irregular breathing characterized by frequent, deep sighing inspirations [anxiety induced].

Cheyne-Stokes respirations alternating periods of deep and shallow breathing with apneic periods lasting 15-60 secs that increase in volume until a peak is reached, after which ventilation [tidal volume] decreases again to apnea. Hypoventilation and Hyperventilation Hypoventilation inadequate alveolar ventilation in relation to metabolic demands. Caused by alterations in pulmonary mechanics or in the neurologic control of breathing. CO2 removal doesnt keep up with CO2 production and Paco2 increases causing hypercapnia [Paco2 >44mm Hg]. Hyperventilation alveolar ventilation that exceeds metabolic demands. Lungs remove CO2 @ a faster rate than it is produced by cellular metabolism, resulting in decreased Paco2 or hypocapnia [Paco2 less than 36 mm Hg}. Both are determined by blood gas analysis. Cough Acute cough resolves within 2-3 weeks of the onset of illness or resolves with treatment of the underlying condition. Chronic cough persists for more than 3 weeks, although some authors have suggested that 7-8 weeks is a more appropriate timeframe because acute cough & bronchial hyperactivity can be prolonged in some cases of viral infection. This is exacerbated in individuals taking angiotensin-converting enzyme inhibitors for cardiovascular disease. Hemoptysis Coughing up of blood or bloody sections.. Usually as a result of bronchiectasis, lung ca, bronchitis, TB and pneumonia. Cyanosis A bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin in the blood. Pain Caused by pulmonary disorders originates in the pleurae, airways or chest wall. Pleural pain is the most common pain caused by pulmonary disease and is usually sharp or stabbing in character. Is a central chest pain that is pronounced after coughing and occurs in individuals with infection and inflammation of the trachea or bronchi. Clubbing Selective bulbous enlargement of the end [distal segment] of a digit [finger or toe], whose severity can be graded from 1 5 based on the extent of nail bed hypertrophy and the amount of changes in the nails themselves. Abnormal Sputum

Color, consistency, odor & amt of sputum vary with different pulmonary disorders. Distinctive color or odor may indicate infection by a specific microorganism. Changes in amt and consistency of sputum provide information about progression of disease and effectiveness of therapy. Conditions Caused by Pulmonary Disease or Injury o Hypercapnia increased [Paco2] carbon dioxide in the arterial blood. Caused by hypoventilation of the alveoli. Causes include Depression of the repiratory center by drugs Diseases of the medulla including infections of the central nervous system or trauma Abnormalities of the spinal conducting pathways, as in spinal cord disruption or poliomyelitis Diseases of the neuromuscular junction or of the respiratory muscles themselves, as in myasthenia gravis or muscular dystrophy Thoracic cage abnormalities, as in chest injury or congenital deformity Large airway obstruction, as in tumors or sleep apnea and Increased WOB or physiologic dead space, as in emphysema o Hypoxemia or reduced oxygenation of arterial blood [reduced Pao2} is caused by repiratory alterations, whereas hypoxia, or reduced oxygenation of cells in tissues, may be caused by alterations of other systems as well. Causes include: Decreased o2 content of inspired gas Hypoventilation Effusion abnormalities Abnormal ventilation perfusion ratios & Pulmonary right to left shunt. [See table 32-1 pp.1109] o Acute Respiratory Failure Inadequate gas exchange, hypoxemia. o Pulmonary Edema Excess water in the lung. Common cause is heart disease [see Fig32-3 pp.1110]. o Aspiration Passage of fluid & solid particles into the lung. Tends to occur in individuals whose normal swallow mechanism and cough reflex are impaired by a decreased level of consciousness or central nervous system abnormalities. o Atelectasis Collapse of lung tissue. The two types of atelectasis are compression and absorption.

Compression atelectasis caused by the external pressure exerted by a tumor, fluid, or air in the pleural space or by an abdominal distention pressing on a portion of the lung, causing the alveoli to collapse. Absorption atelectasis results from removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated o2 or anesthetic agents. o Bronchiectasis persistent abnormal dilation of the bronchi Usually occurs in conjunction with other respiratory conditions and can be caused by obstruction of an airway with mucous plugs, atelectasis, aspiration of a foreign body, infection, cystic fibrosis, tuberculosis, congenital weakness of the bronchial wall or impaired defense mechanisms. Cylindrical with symmetrically dilated airways as is commonly seen after pneumonia and is reversible Saccular which the bronchi become large and balloon like Varicose which constrictions and dilations deform the bronchi. o Bronchiolitis an inflammatory obstruction of the small airways of bronchioles. Bronchiolitis obliterans late-stage fibrotic process that occludes the airways and causes permanent scarring of the lungs Pleural Abnormalities o Pneumothorax presence of air or gas in the pleural space caused by a rupture in the visceral pleura or the parietal pleura and chest wall. Open or communicating pneumothorax air pressure in the pleural space equals barometric pressure because air that is drawn into the pleural space during inspiration is forced back out during expiration Tension pneumothorax site of pleural rupture acts a s a one way valve, permitting air entry on inspiration but preventing its escape by closing up during expiration Spontaneous Pneumothorax occurs unexpectedly in healthy individuals age 20 40 & is caused by the spontaneous rupture of blebs on the visceral pleura. Secondary pneumothorax can be caused by chest trauma, such as rib fracture or stab and bullet wounds that tear the pleura; rupture of a bleb or bulla, as occurs in COPD; or mechanical ventilation, particularly if it includes PEEP. o Pleural Effusion presence of fluid in the pleural space. Transudative effusion the fluid or transudate is watery and diffuses out of the capillaries as a result of disorders that increase blood pressure or decrease capillary oncotic pressure. Exudative effusion less watery and contains high concentrations of WBCS & plasma proteins. Occurs in response to

inflammation, infection or malignancy and involves inflammatory processes that increase capillary permeability. o Empyema or presence of pus in the pleural space, is a complication of respiratory infection, usually pneumonia caused by Staph, E. coli, anaerobic bacteria or Klebsiella pneumonia. o Pleurisy inflammation of the pleura. o Abscess Formation and Cavitation Abscess is circumscribed area of suppuration and destruction of lung parenchyma, follows consolidation of lung tissue, in which inflammation causes alveoli to fill with fluid, pus, and microorganisms. Cavitation process of abscess emptying and cavity formation. o Pulmonary Fibrosis Excessive amount of fibrous or connective tissue in the lung. o Chest Wall Restriction if it is deformed immobilized or made heavy by fat, the work of breathing is increased and ventilation may be compromised due to a decrease in tidal volume. o Flail chest results from the fx of several consecutive ribs consecutive ribs in more than one place, or the fx of the sternum plus several consecutive ribs. Inhalation Disorders o Exposures to Toxic Gases- Inhalation of gaseous irritants can cause significant respiratory dysfunction. Commonly encountered toxic gases include smoke, ammonia, H2O2hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide. Inhalation of a toxic gas results o Results in severe inflammation of the airways, alveolar and capillary damage, and & pulmonary edema. o Oxygen toxicity prolonged exposure to high concentrations of supplemental oxygen resulting in a relatively rare iatrogenic condition that is associated with injury to cells of the lungs. Initial symptoms include burning of the eyes, nose and throat; coughing; chest tightness; and dyspnea. Hypoxemia is common. Treatment supplemental oxygen, mechanical ventilation with PEEP (aids in rerecruiting lung tissue), and support of the CV system. Sometimes steroids are used. o Pneumoconiosis represents any change in the lung caused by inhalation of inorganic dust particles, usually in the work place. The individuals hx of exposure is important in determining diagnosis from the workplace. The dusts of silica, asbestos and coal are most common. Others include talc, fiberglass, clays, mica, slate, cement, cadmium, beryllium, tungsten, cobalt, aluminum and iron. Irregardless the substance, the damage is permanent and treatment focus is on prevention of further exposure and improving working conditions.

Silicosis- a type of pneumoconiosis resulting from the inhalation of free silica & causes acute inflammation and chronic fibrosis of the lung tissue and has been shown to result in apoptosis of lung cells. Coal worker pneumoconiosis- [Black Lung] is caused by coal dust deposits in the lung. Its mild form is asymptomatic, except for possible chronic bronchitis. The advanced form consists of severe pulmonary fibrosis. Asbestosis Asbestos exposure can result in a type of pulmonary fibrosis or in tumor formation, depending on the amount of exposure. o Allergic Alveolitis Inhalation of organic dusts can result in an allergic inflammatory response [hypersensitivity pneumonitis]. This condition can be acute, subacute or chronic. Pulmonary Disorders o Adult Respiratory Distress Syndrome [ARDS] is a fulminant form of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury. [See fig 32-8 pp1118] Pathophysiology ARDS acutely injure the alveolocapillary membrane and cause severe pulmonary edema. The alveolocapillary damage can occur directly, as with the aspiration of highly acidic gastric contents or inhalation of toxic gases, or indirectly from chemical mediators released in response to systemic disorders, as with sepsis and trauma. Several cell types and inflammatory mediators play key roles in the [black lung injury. The most important of these are neutrophils, macrophages, complement, endotoxin, interleukin-1 (IL-1), & tumor necrosis factor (TNF). ] The initial injury to the lungs damages the pulmonary capillary endothelium, activating complement and stimulating platelet aggregation, and intravascular thrombus formation. Platelets release substances that attract and activate neutrophils. In ARDS caused by sepsis, endotoxin [lipopolysaccharide (LPS)] is recognized by the CD14 receptor on macrophages and results in chemotaxis of large numbers of netrophils to the lungs. A cascade of inflammatory mediators is released by the macrophages, including RNF, IL-1 alpha and beta chemokines and other interleukings. Activated neutrophils release a battery of inflammatory mediators, among them proteolytic enzymes, O2 free radicals, arachidonic acid metabolites, and platelet-activating factor. These mediators cause extensive damage of the alveolocapillary membrane and greatly increase capillary membrane permeability [hallmark of ARDS]. This allows fluids, proteins, and blood cells to leak from the capillary bed into the pulmonary interstitium and alveoli. Mediators released by neutrophils and to a certain extent by macrophages, also cause pulmonary vasoconstriction. Pulmonary

HTN occurs early in the course of the disease secondary to vasoconstriction and to vascular occlusion by aggregated neutrophils, macrophages and platelets. Initial lung injury damages the alveolar epithelium and vascular endothelium. Surfactant is inactivated, and its production by type II alveolar cells is impaired as alveoli and respiratory bronchioles fill with fluid or collapse. Compliance to lungs decreases, resulting in decreased ventilation of alveoli, right to left shunting of pulmonary blood flow, and increased WOB. 24 48hrs after the acute, hemorrahagic phase of ARDS, hyaline membranes form and after approx 7 days, fibrosis progressively obliterates the alveoli, respiratory bronchioles, and interstitium. This leads to a decrease in functional residual capacity [FRC] and even more sever right-to-left shunting. This result of this overwhelming inflammatory response by the lungs is acute respiratory failure. The chemical mediators responsible for the alveolocapillary damage of ARDS often cause widespread inflammation, endothelial damage, and capillary permeability throughout the body resulting in the systemic inflammatory response syndrome (SIRS), which then leads to multiple organ dysfunction syndrome (MODS) associated with ARDS. o Clinical Manifestations Classic s/s of ARDS are rapid, shallow breathing; respiratory alkalosis; marked dyspnea; decreased lung compliance; hypoxemia unresponsive to oxygen therapy [refractory hypoxemia]; and diffuse alveolar infiltrates seen on chest radiographs, without evidence of cardiac disease. Initially pts hyperventilate, causing resp alkalosis. As the work of breathing increases because of the decrease in compliance caused by alveolar filling and collapse, the pt experiences dyspnea and hypoxemia which worsens despite oxygen therapy and diffuse crackles can be heard on auscultation. Progressive clinical course of ARDS: hyperventilation > respiratory alkalosis >dyspnea and hypoxemia > metabolic acidosis > respiratory acidosis > further hypoxemia > hypotension, decreased cardiac output > death. o Evaluation and Treatment Initial physical examination may show fine crackles and the chest film may be clear or show a few scattered infiltrates, progressing to crackles throughout the lungs and radiographs showing extensive bilateral infiltrates. Treatment is based on early detection, supportive therapy and prevention of complications. Mechanical ventilation with PEEP & high oxygen concentrations are also used. Sedation may be used to

decrease oxygen consumption, drug may be used to increase cardiac output, and steroids may be used. o Postoperative Respiratory Failure Atelectasis, pneumonia, pulmonary edema and pulmonary emboli are most common complications. Prevention includes frequent turning, deep breathing and early ambulation to prevent atelectasis and accumulation of secretions. Humidification of inspired air can help loosen secretions. IS gives individuals immediate feedback about tidal volumes and encourages them to breathe deeply. Supplemental oxygen is given for hypoxemia and antibiotics are given as appropriate to treat infection. Obstructive Pulmonary Disease- characterized by airway obstruction that is worse with expiration. Unifying symptom is dyspnea; the unifying sign is wheezing. Individuals have an increased work of breathing, ventilation-perfusion mismatching and a decreased forced expiratory volume in one second. o The most common obstructive diseases are asthma, chronic bronchitis and emphysema. Asthma [See table 32-3 pp1122] Inflammation resulting in hyperresponsiveness of the airways. IgE & irritant mediated mast cell degranulation causes the release of a large number of inflammatory mediators, such as histamine, prostaglandins & leukotrienes. Additionally chemotactic factors are produced that result in bronchial infiltration by neutrophils, eosinophils & lymphocytes. The resulting inflammatory process produces bronchial smooth muscle spasm, vascular congestion, increased vascular permeability, edema formation, production of thick tenacious mucus, impaired mucociliary function, thickening of airway walls and increased contractile response of bronchial smooth muscle. Because of regional differences in airway resistance, theres an uneven distribution of inspired air with more reaching less resistant portions. Clinical manifestations o Asymptomatic with normal pulmonary function tests (PFTs) during remission. o Partial remission no clinical symptoms, abnormal PFTs. o During attacks individuals are dyspneic and respiratory effort is marked. Breath sounds are decreased except for considerable wheezing. C/os of chest constriction, inspiratory and expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia and tachypnea occur at the beginning of an attack. Accessory muscles are prominent in severe attacks. Eval & treatment

o Spirometry shows decreases in expiratory flow rate, ABG shows hypoxemia with early respiratory alkalosis or late respiratory acidosis. o Treatment eliminate causative agents. Treatment with drugs that are geared toward reversing bronchospasm and airway inflammation. o http://www.pulmonology.co.za/guidelines/asthma %20adult%20chart.htm Chronic Obstructive Pulmonary Disease defined as pathologic lung changes consistent with emphysema or chronic bronchitis. Characterized by abnormal tests of expiratory airflow that does not change markedly over time, and without a reversible response to pharmacological agents. Pathophysiology Inspired irritants increase mucus production, increase the size and number of mucous glands and goblet cells in airway epithelium. The mucus produced is thicker and more tenacious than normal, and more likely to have bacteria embedded where they reproduce rapidly. Ciliary function is impaired reducing clearance. With increased mucus production the bronchial walls become inflamed and thickened from edema and accumulation of inflammatory cells. The thick mucus and hypertrophied bronchial smooth muscle obstruct the airways and lead to closure, particularly during expiration when the airways are narrowed. Evaluation and Treatment the best treatment is prevention. Bronchodilators and expectorants are prescribed to increase airway caliber, improve secretion removal and maximize as exchange. Chest physical therapy, including deep breathing, postural drainage (when >30ml/day of sputum is produced), & percussion is used. Nutritional counseling, respiratory hygiene, recognition of early signs of infection and techniques to relieve dyspnea (pursed-lip breathing) Emphysema abnormal permanent enlargement of gas exchange airways (acini) accompanied by destruction of alveolar walls and without obvious fibrosis. Obstruction results from changes in lung tissues. http://www.handsonhealth-sc.org/page.php?id=1238 Evaluation and treatment the most definitive evidence for the presence of emphysema is from pulmonary function measurements. On radiographs the diaphragm appears flattened and the lung fields appear translucent. Marked and persistent overdistention of the lungs is suggestive of emphysema. The usual disease course is prolonged, with increasing dyspnea and intermittent bouts of infection that

culminate in failure of the right side of the heart (cor pulmonale) and death. Inhaled anticholinergic agents are now considered first-line therapy for emphysema. A stepwise approach to adding other bronchodilators is suggested. Last resort use of corticosteroids should be considered in the steroid responsive. Low flow oxygen can improve symptoms and prevent cor pulmonale. Relaxation exercises, reconditioning and breathing retraining can improve dyspnea. o Respiratory Tract Infections the common cold, pharyngitis (sore throat) and laryngitis involve upper airways. Infections of the lower respiratory tract occur most frequently in the young, the very old or individuals with impaired immunity or underlying disease. Pneumonia- caused by bacteria, viruses, fungi, protozoa or parasites. Aspiration of oropharyngeal secretions is the most common route although inhalation of microorganisms that have been released into the air when an infected individual coughs, sneezes or talks or from aerosolized water, such as that from contaminated respiratory therapy equipment. Diagnosis is confirmed by finding infiltrates on chest x-ray. WBC count is usually elevated and sputum gram stain is indicated in all patients with pneumonia. Treatment or management of pneumonia is establishing adequate ventilation and oxygenation, adequate hydration and good pulmonary hygiene. Antibiotics are used to treat bacterial infections and should be chosen based on the likely causative microorganism & pts underlying condition. Tuberculosis (TB) Mycobacterium tuberculosis, an acid fast bacillus that affects the lungs and can invade other body systems. TB is transmitted person to person in airborne droplets. Microorganisms lodge in the lung periphery, usually in the upper lobe. Once bacilli are inspired into the lung, they multiply and cause nonspecific pneumonitis. After neutrophils & macrophages seal off colonies of bacilli, infected tissues within the tubercle die and collagenous scar tissue then grows around the tubercle completing isolation of the bacilli in 10 days or so. Clinical manifestations: fatigue, wt loss, lethargy, anorexia and low-grade fever usually in the afternoon. Productive cough producing purulent sputum develops slowly and becomes more frequent over several weeks or months. Night sweats and general anxiety develop as does dyspnea, chest pain and Hemoptysis.

Diagnosed by a positive purified protein derivative skin test. When active pulmonary disease is present, the tubercle bacillus can be cultured from sputum. CXR show characteristic changes. Treatment consists of antibiotic therapy to control active or dormant tuberculosis and prevent transmission for a period of 6 -9 months. Acute Bronchitis acute infection or inflammation of airway or bronchi, self-limiting and commonly follows a viral illness. Clinical manifestations similar to pneumonia (fever, cough, chills, malaise) without signs of pulmonary consolidation and negative for infiltrates on CXR. Treatment consists of rest, aspirin, humidity and a cough suppressant. o Pulmonary Vascular Disease Pulmonary Embolism occlusion of a portion of the pulmonary vascular bed by an embolus: a thrombus {blood clot), a tissue fragment, lipids, or an air bubble. Massive occlusion causes profound shock, hypotension tachypnea, tachycardia, severe pulmonary hypertension and chest pain. Manifestations of emboli that cause infarction are pleural pain, dyspnea, pleural friction rub, pleural effusion, Hemoptysis, fever and leukocytosis. Pulmonary embolism without infarction is most common and difficult to evaluate. The patient has sudden onset of tachypnea, tachycardia, dyspnea and unexplained anxiety with occasional syncope or pleural pain. Ideally prevention through risk factor analysis and elimination of predisposing factors for individuals at risk. Anticoagulant therapy is primary treatment for pulmonary embolism. o Pulmonary Hypertension Rise in pulmonary artery pressure (normally 15-18 mm Hg) of 5-10 mm Hg. Vessel narrowing or obliteration increases resistance and causes the pulmonary hypertension. 4 causes of secondary pulmonary hypertension: Elevated left ventricular filling pressures [like with CAD & mitral valve disease} Left to right shunts, as occurs with a VSD or PDA. Obliteration or obstruction of pulmonary vascular bed by a pulmonary embolus or by chronic destruction of an alveolar wall Vasoconstriction of the vascular bed as occurs with hypoxemia, acidosis or their combination. May not clinically detectable until pulmonary artery pressure is equal to systemic blood pressure. Often the first indicator is an

abnormality seen on a chest X-ray or EKG that shows right ventricular hypertrophy. Manifestations of fatigue, chest discomfort, tachypnea, dyspnea especially with exercise are common. Diagnosis can only be made with right-sided heart catheterization There is no effective treatment for primary pulmonary hypertension except lung transplantation, but supplemental oxygen, digitalis and diuretics are used as palliative measures. Treatment for secondary pulmonary hypertension is treatment of primary disorder. o Cor Pulmonale, also called pulmonary heart disease consists of right ventricular enlargement secondary to pulmonary hypertension. Develops as pulmonary hypertension creates chronic pressure overload in the right ventricle similar to the created in the left by systemic hypertension. Clinical manifestations may be obscured by primary respiratory disease and appear only during exercise testing. Peripheral edema, hepatic congestion and jugular vein distention may be present. Diagnosis is based on physical examination, radiologic examination and electrocardiogram or echocardiogram. Goal of treatment is to decrease the workload of the right ventricle by lowering pulmonary artery pressure. Cancers o Lip Cancer Most common form termed exophytic, the lesion usually develops in the outer part of the lip along the vermilion border. The lesion becomes thickened evolving to an ulcerated center with raised border. Verrucous-type lesions are less common, have an irregular surface, follow cracks in the lip extending toward the inner surface. Squamous cell carcinoma is the most common type. Blister leads to malignant lesion after superficial ulceration. Biopsy confirms presence of malignant cells. Surgical removal and subsequent cosmetic surgeries for larger lesions proved effective with interstitial irradiation and radioactive implants. o Laryngeal Cancer risk increased by the amount of tobacco smoked & further heightened with the combination of smoking and alcohol consumption. Carcinoma of the true vocal cords (glottis). Squamous cell carcinoma is the most frequent cell type, although small cell carcinomas also occur. Metastasis develops by spread to draining lymph nodes. Patient presents with hoarseness, dyspnea and cough. Progressive hoarseness is most significant symptom. Laryngeal pain is likely to be present with supraglottic lesions. Indirect laryngoscopy with biopsy or direct laryngoscopy with can visualize tumor. CT identifies tumor boundaries and degree of extension to surrounding tissue. Radiation therapy has shown

good results for early carcinoma of the vocal cords. Chemo may be useful as an adjunct to surgery. Partial laryngectomies are the preferred treatment for small supraglottic and sublottic malignancies, total laryngectomies are required when lesions are extensive and involve the cartilage. o Lung Cancer- arises from the epithelium of the respiratory tract. [See Table 32-5 pp 1137]. http://www.mamashealth.com/lung.asp http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=38494

References: http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=38494 http://www.mamashealth.com/lung.asp http://www.handsonhealth-sc.org/page.php?id=1238 http://www.pulmonology.co.za/guidelines/asthma%20adult%20chart.htm Huther, S.E. & McCance, K.L. (2002). The Biologic Basis for Disease in Adults & Children. St. Louis, Missouri: Mosby, Inc.