Respiratory Function CHAPTER Whenyouseethisicon,Usethecodeatfrontofbooktoaccessonlinestudentresources

9781284042245_CH05.indd 115 community-acquired cilium chronic obstructivepulmonary chronic bronchitis bronchus bronchopneumonia bronchiolitis bronchiole blue bloaters bacterial pneumonia atelectasis asthma aspiration pneumonia alveolus acute respiratoryfailure(arF) acute respiratorydistress acute lunginjury(aLI) acute bronchitis active infection • • pneumonia disease (COpD) syndrome (arDS) respiratory system. Describe andcompareinfectiousdisordersofthe Discuss normalrespiratoryanatomyandphysiology. Respiratory Function CHAPTER Whenyouseethisicon,usethecodeatfrontofbooktoaccessonlinestudentresources.

KEY TERMS LEARNING OBJECTIVES © larynx laryngotracheobronchitis laryngitis intrinsic asthma interstitial pneumonia inspiratory reservevolume inspiration infl uenza infectious rhinitis forced vitalcapacity forced expiratoryvolumein extrinsic asthma expiratory reservevolume expiration exercise-induced asthma epiglottitis epiglottis emphysema drug-induced asthma diaphragm ficystic brosis Jones 1 second & Bartlett 5 Learning, LLC. NOT primary TBinfection pneumothorax pneumonia Pneumocystis jiroveci pleurisy pleural effusion pink puffers pharynx perfusion occupational asthma nosocomial pneumonia non-small-cell carcinoma nocturnal asthma Mycoplasma pneumoniae mucus minute respiratoryvolume Middle eastrespiratory lung cancer lobar pneumonia Legionnaires’ disease • • FOR pneumonia syndrome respiratory system. Describe andcomparerestrictivediseasesofthe respiratory system. Describe andcompareobstructivediseasesofthe SALE OR DISTRIBUTION vital capacity viral pneumonia ventilation/perfusion ratio ventilation type Cinfl uenza type Binfl uenza type ainfl uenza tuberculosis (TB) traumatic pneumothorax trachea tidal volume tension pneumothorax surfactant status asthmaticus spontaneous pneumothorax small-cell carcinoma sinusitis severe acuterespiratory secondary TBinfection residual volume (VQ ratio) syndrome (SarS) 115 2/13/2014 4:32:15 PM

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he respiratory system includes the act of breathing. The respiratory tract allows a organs and structures associated with person to breathe in and out approximately Tbreathing and gas exchange. The struc- 23,000 times each day. In fact, if you had a dollar tures of the respiratory system are grouped into for each breath, you would be a millionaire in a two branches—the upper respiratory tract month and a half. The act of breathing allows (mouth, nasal cavity, pharynx, and larynx) for gas exchange of oxygen and carbon dioxide. (Figure 5-1) and the lower respiratory tract (tra- Oxygen is necessary for cells to produce energy chea, bronchi, bronchioles, and alveoli). This through cellular metabolism; carbon dioxide is chapter focuses on normal and abnormal states the waste product of this process. Through these of the lungs. The respiratory tract functions functions, the respiratory system plays a pivotal automatically to provide cells with oxygen and role in maintaining homeostasis. to remove carbon dioxide waste. Disorders of The respiratory system consists of two basic the respiratory tract can become serious quickly functional divisions—an air-conducting portion because of the body’s critical need for oxygen. and a gas-exchanging portion (Table 5-1). The Patients with these disorders will need astute air-conducting portion delivers air to the lungs, nurses who respond quickly yet thoughtfully. while the gas-exchanging portion allows gas exchange to occur between the air and the blood (Figure 5-1). The gas-exchanging portion Anatomy and Physiology of the respiratory tract includes the lungs with The respiratory system provides vital oxygen their millions of alveoli and capillaries and removes toxic carbon dioxide through the (Figure 5-2).

Nasal cavity

Hard palate

Tongue Tonsils

Epiglottis

Larynx Trachea Esophagus

Vocal cords Figure 5-1 The upper respiratory tract. Chiras, D. (2011). Human biology (7th ed.). Burlington, MA: Jones & Bartlett Learning.

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Table 5-1 Summary of the Respiratory System

Organ Function

Air Conducting

Nasal cavity Filters, warms, and moistens air; also transports air to pharynx

Oral cavity Transports air to pharynx; warms and moistens air; helps produce sounds

pharynx Transports air to larynx

epiglottis Covers the opening to the trachea during swallowing

Larynx produces sounds; transports air to trachea; helps fi lter incoming air; warms and moistens incoming air

Trachea and bronchi Warm and moisten air; transport air to lungs; fi lter incoming air

Bronchioles Control air fl ow in the lungs; transport air to alveoli

Gas Exchange

alveoli provide area for exchange of oxygen and carbon dioxide

Chiras, D. (2011). Human biology (7th ed.). Burlington, Ma: Jones & Bartlett Learning.

Nasal Artery Alveolus cavity Bronchiole

Mouth Vein (oral cavity)

Pharynx

Larynx Capillary Trachea network

Terminal bronchiole Right Left A bronchus bronchus B Alveoli Capillaries Figure 5-2 The respiratory system. (a) This illustration shows the air-conducting portion and the gas-exchange portion of the human respiratory system. The insert shows a higher magnifi cation of the alveoli where oxygen and carbon dioxide exchange occurs. (b) a scanning electron micrograph of the alveoli, showing the rich capillary network surrounding them. © Jones & Bartlett Learning

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Epiglottis © CMSP/Custom Medical Stock Photo, Inc.

Thyroid Ventricular fold cartilage (false vocal cord) True vocal cord Tracheal cartilages

A BCVocal cords Figure 5-3 The vocal cords. (a) Uppermost portion of the respiratory system, showing the location of the vocal cords. (b) Longitudinal section of the larynx showing the location of the vocal cords. Note the presence of the false vocal cord, so named because it does not function in phonation. (c) View into the larynx of a patient showing the true vocal cords from above.

Air enters the respiratory system through the nose and mouth, traveling to the pharynx. The pharynx joins the larynx, or voice box (Figure 5-3). The larynx is made of cartilage and plays a central role in swallowing and talking. When food is swallowed, the larynx rises so that it is closed by the epiglottis. This process pre- vents food and liquids from entering the lungs, MD/Science Source Martin, © David M. where they would cause severe irritation. Food occasionally enters the lungs, often triggering the cough reflex (a primitive protective reflex). The larynx works much like the strings of a gui- tar or violin to produce sound—tightening and loosening to change pitch. It opens up into the trachea, or windpipe. From the trachea, the air travels to the mainstem bronchi, where it branches into the right and left bronchi, one for each lung (Figure 5-4). The left bronchus is nar- Figure 5-4 The bifurcation of the trachea at the carina into row and positioned more horizontally than the the right and left mainstem bronchi. right bronchus; the right bronchus is shorter and wider than the left bronchus and extends downward more vertically. Because of the dif- enter the lungs. In times of normal or de- ference in size between the two, objects are creased oxygen needs (e.g., during sleep), the more easily inhaled (aspirated) into the right airways may narrow (constrict) slightly. Dis- bronchus. ease processes may cause constriction to the Inside the lungs, the bronchi branch ex- point of impeding air flow—a dangerous tensively into smaller and smaller tubes, or development. bronchioles, until they reach the alveoli. The air entering the respiratory tract often This branching from larger to smaller mimics contains particles that can be harmful. These the vessels in the cardiovascular system. The particles may include infectious organisms walls of the bronchioles are also like the ves- (e.g., bacteria, viruses, and fungi) and environ- sel walls in that they mostly consist of smooth mental agents (e.g., dust, pollen, and pollut- muscle. The smooth muscle allows for con- ants). The respiratory system is equipped to striction and dilation of the bronchioles to filter out some of these particles as well as to control air flow. When oxygen needs are protect against the body those that gain entry. higher (e.g., during exercise or stress), the air- The air-conducting portion of the respiratory ways open more (dilate) to allow more air to tract filters many particles by trapping them in

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Cilia

Mucous cell B Mucous cell Cilia Dust particle Mucus

A To lungs Figure 5-5 Mucous trap. (a) Drawing of the lining of the trachea. Mucus produced by the mucous cells of the lining of much of the respiratory system traps bacteria, viruses, and other particulates in the air. The cilia transport the mucus toward the mouth. (b) Higher magnification of the lining showing a mucous cell and ciliated epithelial cells.

the mucous layer (Figure 5-5). Mucus is a incoming air, humidifying it to prevent drying thick, sticky substance produced by the goblet of the respiratory tract. The warm blood circu- cells in the epithelial lining of the nose, tra- lating through the capillaries warms this air prior chea, and bronchi. This epithelial lining also to entering the lungs, protecting the lungs from contains many cilia, or hair-like projections, cold temperatures. As the air leaves the respira- that move in a wavelike motion to propel the tory tract, much of the water that has been added mucus and trapped particles upward to the to the air condenses on the slightly cooler lining mouth, where they can be expectorated (spit of the nasal passages. The condensation is recy- out). Cigarette smoking and air pollution can cled for the next inhalation to conserve water, decrease mucus production and destroy cilia, and contributes to runny noses on cold days. increasing the risk of respiratory infections. Al- Alveoli are the site for gas exchange with cohol consumption can paralyze cilia, also in- the bloodstream (Figure 5-7). Oxygen is deliv- creasing infection risk. ered to the alveoli by the air-conducting portion Additionally, the immune system is outfit- of the respiratory system, and carbon dioxide is ted with IgA cells that prevent the attachment brought to the lungs by the circulatory system. and invasion of bacteria and viruses on mucous Each human lung contains approximately membranes (see the Body Defenses chapter). Mac- 150 million alveoli that create a surface area ap- rophages are also present around the alveoli in proximately the size of a tennis court for gas ex- the lungs; they keep the lungs clean by phago- change. The alveoli and capillaries are often a cytizing particles that gain access to this area single cell layer thick, which further facilitates (Figure 5-6). Once the macrophages fill with par- gas exchange. The amount of gas exchanged de- ticulates, they move into the surrounding con- pends on the total surface area available and the nective tissue. When an unusually large number thickness of the alveoli and capillary walls. The of particulates are present (e.g., with cigarette more surface area and the thinner the layers, and marijuana smoking and when breathing in the more rapidly gas diffuses. heavy pollution), the lungs become blackened Gas exchange in the alveoli requires ade- by the accumulation of the particles. quate ventilation of air and perfusion of blood The air-conducting portion of the respira- flow. Theventilation/perfusion ratio, or VQ tory system also moistens and warms incoming ratio, is a measurement of the efficacy and ad- air. An extensive network of capillaries lies be- equacy of these two processes. In the ideal lung, neath the epithelium of the respiratory tract. inspired air reaches all the alveoli and all the al- These capillaries release moisture into the veoli have the same blood supply. Actually,

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Alveolar macrophage Removes particles that reach the lung

Alveolus Alveolus

Pulmonary capillary Type II alveolar cell Produces surfactant

O2 CO2 RBCs Alveolus

Capillary endothelium O2 CO2 Type I alveolar cell Permits gases to Connective move into and out tissue cell of the alveoli Alveolus Connective Interstitial tissue fibers fluid Nucleus

Surfactant reduces surface Oxygen and carbon dioxide tension created by water and are exchanged here between keeps alveoli from collapsing the blood and the air in the lung

Figure 5-6 The alveolar macrophages. Chiras, D. (2011). Human biology (7th ed.). Burlington, MA: Jones & Bartlett Learning.

neither alveolar ventilation nor capillary blood system (Figure 5-8). Hemoglobin carries oxygen flow is uniform. The supply of air and blood to the cells, then releases it there. The rate at never match perfectly, even in healthy persons. which hemoglobin binds and releases oxygen is Because of gravity, the lower parts of the lungs affected by several factors, including temperature­ have greater blood flow than the upper parts. and pH, among other (Figure 5-9). Distribution of alveolar ventilation from the top The surface of the alveoli contains a sub- to the bottom of the lungs is also uneven. Nor- stance called surfactant. Surfactant is a li- mal ventilation is 4 liters of air per minute, and poprotein produced by alveoli cells that has a normal perfusion is 5 liters of blood per minute. detergent-like quality. This watery substance This makes the expected VQ ratio 4/5, or 0.8. A produces surface tension on the alveoli, which VQ ratio higher than 0.8 indicates that ventila- enhances pulmonary compliance (elasticity) tion exceeds perfusion, and a VQ ratio less than and prevents the alveoli from collapsing. Be- 0.8 indicates poor ventilation. Some respiratory cause the pressure in the lungs is negative com- disorders involve ventilation problems, whereas pared with the atmospheric pressure, the walls others result from perfusion issues. In any event, of the alveoli tend to draw inward, making the result is impaired gas exchange. them collapse. This pressure is much like that When air is inhaled, gases are exchanged seen with a vacuum-sealed pack of coffee. The between the alveoli and the capillaries; carbon pressure and, therefore, the risk of collapse fur- dioxide is removed through expiration, and ox- ther increase at the end of expiration. Surfac- ygen is delivered to cells by the cardiovascular tant promotes reinflation of the alveoli during

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Bronchiole Smooth muscle Artery 1 Deoxygenated blood is carried from the heart Vein (to the lungs) by the Capillary pulmonary arteries and arterioles. 2 Gas exchange takes place at the capillaries covering the alveoli. CO2 CO 2 CO2 Alveolar wall CO2 Capillary wall CO2 O2 O2 3 Alveoli O Oxygenated blood is 2 O2 carried from the lungs (to the heart) by the CO Carbon dioxide and oxygen 2 are exchanged across two pulmonary veins layers of epithelial cells. and venules. O2 One layer makes up the wall O of the capillary, and one 2 layer makes up the wall of the alveolus.

Figure 5-7 Gas exchange in the lungs. AAOS. (2004). Paramedic: Anatomy and physiology. Sudbury, MA: Jones & Bartlett.

Inhaled air inspiration. Disease states and other conditions can decrease surfactant, leading to the collapse of the alveoli (called atelectasis). For example,

Alveoli O2 premature infants lack surfactant, and smoking alters surfactant production. Synthetic surfac- tant may be administered to overcome any in- Plasma Dissolved O In lung adequacies in production. 2 capillaries The process of breathing is largely involun- tary and controlled by the medulla oblongata in the brain. This center is located in the brain O bound RBCs 2 to hemoglobin stem, which controls many vital functions in the body (e.g., heart rate, blood pressure, and tem- perature). Breathing includes two phases: in- In tissue spiration (inhalation—moving air in) and Plasma Dissolved O2 capillaries expiration (exhalation—moving air out). In- spiration is an active neural process that begins with nerve impulses traveling from the brain to Interstitial Dissolved O fluid 2 the diaphragm, a dome-shaped muscle that separates the thoracic and abdominal cavities (Figure 5-10). These impulses cause the dia- Dissolved O2 phragm to contract, lower, and flatten, which Cells draws air into the lungs. Inspiration also in- O2 consumption volves the intercostal muscles between the ribs. Figure 5-8 Oxygen diffusion. Oxygen travels from the Nerve impulses cause the intercostal muscles to alveoli into the blood plasma, then into the RBCs, where contract, lifting the ribs up and out. Contraction much of it binds to hemoglobin. When the oxygenated blood of the diaphragm and intercostal muscles reaches the tissues, oxygen is released from the RBCs and diffuses into the plasma, then into the interstitial fluid and changes the intrapulmonary pressure, causing body cells. air to naturally flow into the lungs. In contrast, Chiras, D. (2011). Human biology (7th ed.). Burlington, MA: Jones & Bartlett Learning. expiration is passive—it does not require

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100 INCREASED AFFINITY Acute alkalosis (↑ pH) Decreased PCO2 80 Decreased temperature Low levels of 2,3-DPG )

2 Carboxyhemoglobin Methemoglobin 60 Abnormal hemoglobin (left shift)

Normal

40 DECREASED AFFINITY Acute acidosis (↓ pH) rcent saturation (SO High PCO2 Pe Increased temperature 20 High levels of 2,3-DPG Abnormal hemoglobin (right shift)

0 20 40 60 80 100 Oxygen pressure (mm Hg)

Figure 5-9 Oxyhemoglobin dissociation curve.

­muscle contraction. As the lungs fill with air, the normal passive exhalation. The average expira- diaphragm and intercostal muscles relax, re- tory reserve volume is 1–1.5 liters. The vital ca- turning to their previous position. Returning to pacity is the sum of the tidal volume and their natural position decreases thoracic volume reserves. Some air is always present in the lungs, and increases intrapulmonary pressure. This which is called residual volume. Even after greater pressure forces air out of the lungs. Elas- the most forceful exhalation, 1–1.5 liters of air tic fibers in the lungs aid in passive expiration remains in the lungs, which ensures efficient by causing the lungs to recoil. Expiration can and consistent gas exchange. The forced expi- also be active—that is, created by contracting ratory volume in 1 second is compared to the the chest and abdominal muscles. Air flow, both forced vital capacity to diagnose pulmonary inspiratory and expiratory, can be measured to disease. aid in diagnosis of respiratory disorders The medulla controls breathing through (Figure 5-11). nerve cells that generate nerve impulses to the The pulmonary function test evaluates lung respiratory muscles. When the lungs are full, volumes and capacities. Tidal volume is the these impulses cease, allowing the muscles to amount of air involved in one normal inhala- relax. Chemoreceptors inside the brain and ar- tion and exhalation. The average tidal volume teries also regulate breathing. These receptors is 500 mL, but is smaller in shallow breathing. detect carbon dioxide levels and send messages The minute respiratory volume is the to the medulla. Carbon dioxide levels normally amount inhaled and exhaled in 1 minute. This drive breathing (Figure 5-12). When these levels volume is calculated by multiplying the tidal go up, respiration depth and rate increase to ex- volume by the number of respirations per min- crete the excess carbon dioxide, and vice versa. ute; the average is 6 liters per minute. The in- In some disease states, this drive becomes al- spiratory reserve volume is the amount of air tered, and oxygen levels drive breathing. Addi- beyond the tidal volume that can be taken in tionally, stretch receptors in the lungs aid in with the deepest inhalation. Inspiratory reserve breathing by detecting when the lungs are full. volume averages 2–3 liters. The expiratory re- In such a case, the stretch receptors in the lungs serve volume is the amount of air beyond tidal send a message to the medulla to cease firing. volume that can be forcibly exhaled beyond the This effect, which is called Hering-Breuer reflex,

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Neck muscles Breastbone moves up and Chest outward muscles

Intercostal muscles

Diaphragm Diaphragm at rest lowers © SIU/Visuals Unlimited, Inc. © SIU/Visuals Unlimited, Inc. © SIU/Visuals Unlimited, Heart Heart

ABExhalation Inspiration Figure 5-10 Breathing. The rising and falling of the chest wall through the contraction of the intercostal muscles (muscles between the ribs) is shown in the diagram, illustrating the bellows effect. Inspiration is assisted by the diaphragm, which lowers. Like pulling a plunger out on a syringe, the rising of the chest wall and the lowering of the diaphragm draw air into the lungs. Illustrations and X-rays showing the lungs in full exhalation (a) and full inspiration (b).

prevents overinfl ation of the lungs. The body (also see the Fluid, Electrolyte, and Acid–Base Ho- also has oxygen receptors, but they are not very meostasis chapter). sensitive. These receptors do not generate im- pulses until oxygen levels fall to a critical point. LEARNING POINTS In addition to regulating oxygen and carbon dioxide levels, the lungs aid in regulating pH by arbon dioxide is the normal driving force for breath- altering breathing rate and depth. Carbon diox- Cing. This means that breathing is controlled by carbon ide is a source of acid in the body. Increasing the dioxide levels. How does this translate into action? As carbon dioxide levels rise, the lungs will exhale to expel the excess respiratory rate and depth will lead to excretion carbon dioxide. To understand how strong this drive is, of more carbon dioxide, making the blood less consider holding your breath. If you take a deep breath and acidic. Conversely, decreasing the respiratory try to hold it, eventually you have to let the air out. No matter rate and depth will cause retention of more car- how hard you try, you cannot hold your breath forever. The bon dioxide, making the blood more acidic. This body can be trained to hold a breath longer and longer (as swimmers and divers do), but no matter the training, you will compensatory mechanism allows for a quick fi x eventually have to let it out. of pH imbalances to reestablish homeostasis

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A

Deep inhalation 6,000

Inspiratory 5,000 reserve volume 2,000 to 4,000 3,000 mL

3,000 − Tidal volume 500 mL Milliliters

2,000 Expiratory reserve volume 1,200 mL

1,000 Residual volume Forced 1,200 mL exhalation 0 B

Figure 5-11 Measuring air flow. (a) This machine allows healthcare workers to determine tidal volume, inspiratory reserve volume, and other lung-capacity measurements to determine the health of an individual’s lung. (b) This graph shows several common measurements.

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Normal cycle

Increased PCO in blood Retain more CO 2 2 and CSF

Slow respirations Stimulates central chemoreceptors in medulla

Decreased chemoreceptor Stimulates inspiratory stimulation muscles

Increases respiratory rate

Removes more CO2 Decreased PCO2 A from body

Hypoxic drive with chronic elevated PCO2 levels (e.g., emphysema)

Medullary chemoreceptors Respirations slow become insensitive to high PCO2

PCO2 decreased, No increase in respiration PO2 increases

Remove CO2 and take in Marked decrease in more O2 O2 levels

Very low PO2 stimulates peripheral chemoreceptors

Increased respirations Inspiratory muscles B stimulated Figure 5-12 Normal respiratory control and hypotoxic drive.

UNDERSTANDING CONDITIONS THAT AFFECT THE RESPIRATORY SYSTEM

hen considering alterations in the pathophysiological concepts include those con- respiratory system, organize them ditions that are infectious in nature, problems Wbased on their basic underlying patho- with ventilation, and issues with perfusion. physiology to increase understanding. Those Infectious conditions trigger the infl ammatory

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response, explaining many of the symptoms When considering these conditions, also associated with these conditions. The respiratory determine which respiratory-related nursing system requires both ventilation and perfusion diagnosis is in play—altered gas exchange or to function properly. Problems in either area will ineffective airway clearance. Altered gas ex- impair the respiratory system’s ability to meet change includes conditions that decrease gas the body’s needs. Ventilation conditions result exchange in the lungs (e.g., asthma, emphy- from problems with moving air in or out of the sema, and chronic bronchitis). Impaired airway lungs. Perfusion conditions result from problems clearance includes conditions in which secre- that prevent gas exchange; these conditions are tions are stagnant (e.g., pneumonia and cystic generally cardiovascular in nature (e.g., pulmo- fibrosis). nary embolism).

I n f e c t i o u s D i s o r d e r s

◾◾ Upper Respiratory Tract Infections are virally contaminated 60% of the time. The Infectious Rhinitis apparent increase in occurrence of the infectious rhinitis during rainy and cold weather is due to Infectious rhinitis, or the common cold, is a increased congregation in confined spaces. Those viral upper respiratory infection. The most fre- persons in closer contact with other people will quent culprit is the rhinovirus, but many viruses be at higher risk for developing the infection (e.g., adenovirus, coronavirus, and influenza) (e.g., children in daycare centers, healthcare can cause this illness. In fact, there are more providers, and teachers). The virus is highly con- than 100 causative organisms, making it difficult tagious because it is shed in large numbers from to develop immunity. the nasal mucosa, and the virus can survive for The infectious organism invades the epithe- several hours outside the body. lial lining of the nasal mucosa. Mild cellular in- An individual who contracts infectious rhi- flammation leads to nasal discharge, mucus nitis usually experiences an incubation period production, and shedding of the epithelial cells. between the invasion of the virus and the onset This break in the first line of defense increases of symptoms that usually lasts about 2–3 days, vulnerability to bacterial invasions. As a conse- but can be as long as 7 days. Clinical manifesta- quence, secondary bacterial infections (e.g., oti- tions include the following signs and tis media, sinusitis, bronchitis, and pneumonia) symptoms: are common with viral infections (Figure 5-13). The risk for secondary bacterial infections is fur- • Sneezing ther increased in individuals who smoke because • Nasal congestion or stuffiness of the chronic damage done by smoke to the mu- • Clear nasal discharge cosa and cilia. Despite popular misconceptions, • Sore throat wet and cold conditions do not cause or increase • Lacrimation (eye tearing) occurrences of infectious rhinitis. Close physical • Nonproductive cough contact with the virus transmits the infection • Malaise through exchanges with other humans (e.g., • Myalgia shaking hands) and surfaces (e.g., doorknobs • Low-grade fever and telephones). Transmission may occur • Hoarseness through both inhalation and contact (e.g., hand • Headache to hand or hand to mucous membrane). Hands • Chills

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MYTH BUSTERS

A common misconception is that you get colds closed spaces is responsible for the spread of from being cold or wet. The fuel for this myth the cold. The infectious rhinitis virus is viru- is the increased occurrence of colds during lent and highly contagious through close cold and wet weather. In fact, the weather contact. conditions themselves do not make you sick— Misconceptions are hard to change; it usu- but the weather does increase congregation of ally takes multiple efforts. So do your part to people indoors to avoid those weather condi- educate the public about the truth of cold trans- tions. The congregation of people in close, mission and prevention!

Primary viral infection (e.g., influenza or common cold virus)

Virus attaches firmly to respiratory mucosa Congestion and invades the tissue, causing necrosis, Obstructed airways inflammation, and swelling

Virus Inflammation

Healthy mucosa Necrosis Good air flow Poor air flow

Virus spreads along continuous Bacteria, sometimes resistant flora, mucosa invading ears (otitis media), penetrate the damaged mucous sinuses (sinusitis), bronchi and membranes, causing secondary lungs (pneumonia) BACTERIAL INFECTION

Frontal sinus Inflamed Ear tissue

Trachea Nasal cavity (wind pipe) Oral cavity

Lung Purulent exudate

Bacteria invade necrotic area

Figure 5-13 Complications of viral respiratory infections. © Jones & Bartlett Learning

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Diagnosis of infectious rhinitis is primarily Sinusitis made based on the presence of symptoms. Sinusitis is an inflammation of the sinus cavi- Treatment is symptomatic. Most over-the-coun- ties most often caused by a viral infection (e.g., ter cold preparations are ineffective in shorten- rhinovirus, influenza, or adenovirus). Other ing the course of the infection, and they should causative agents include bacteria (e.g., Strepto- be avoided in children younger than 4 years. coccus pneumoniae or Haemophilus influenzae) and Pharmacologic therapies that may be used in- fungi (e.g., Aspergillus or mucormycosis). Envi- clude antipyretics (for fever), analgesics (for dis- ronmental irritants (e.g., smoke exposure and comfort), decongestants (for nasal symptoms), air pollutants), being immunocompromised cough suppressants or expectorants, and anti- (e.g., HIV), conditions that increase mucus pro- biotics (only if a bacterial infection is present). duction (e.g., cystic fibrosis or asthma), and Humidifiers can liquefy secretions to aid in ex- nasal structural abnormalities (e.g., nasal pol- pectoration. Maintaining adequate hydration yps) can further increase risk. Sinusitis can be can also liquefy secretions and help manage fe- a result of a secondary bacterial infection asso- vers. Nasal saline can ease nasal discomfort. The ciated with infectious rhinitis or allergic rhinitis benefit of vitamin C in prevention and treat- in which the drainage from the sinus cavity has ment remains controversial. Proper hand wash- become blocked (Figure 5-14). The drainage ing remains the long-standing cornerstone of accumulation provides a supportive medium prevention because the hands are a significant for bacterial growth. Streptococcus pneumoniae source of transmission. Other measures will and Haemophilus influenzae are commonly found limit the spread of active infections to others: in the upper airways of healthy people. • Covering one’s mouth when coughing and Sinusitis can present in several different sneezing, using tissue or the upper sleeve of types: one’s shirt • Acute, which last up to 4 weeks • Disposing of tissue immediately after use • Subacute, which lasts 4–12 weeks

Blocked sinus Maxillary sinus

Figure 5-14 Blocked sinus.

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• Chronic, which lasts more than 12 weeks Epiglottitis and can continue for months or even Epiglottitis is a life-threatening condition of the years epiglottis, the protective cartilage lid covering the • Recurrent, with several attacks occurring trachea opening. In the past, Haemophilus influ- within a year enzae type B (Hib) was the most common cause As exudate accumulates, pressure builds in in the United States, but widespread use of the the sinus cavity, which causes facial bone pain Hib vaccine has dramatically decreased the rate and headache. The location of pain can indi- of H. influenzae infections in recent years. With cate which sinus is affected. Other clinical the Hib vaccine, epiglottitis is now very uncom- manifestations of sinusitis may already be pres- mon. Common culprits now include Group A ent, such as nasal congestion, purulent nasal beta-hemolytic Streptococcus, Streptococcus pneu- discharge, halitosis, mouth breathing, fever, moniae, and Staphylococcus aureus. Other causes sore throat, and malaise. Complications can in- include throat trauma from events such as drink- clude orbital cellulitis, meningitis, osteomyeli- ing hot liquids, swallowing a foreign object, a tis, and abscess. direct blow to the throat, or smoking crack or Diagnostic procedures for sinusitis include heroin. The inflammatory response is triggered a history, physical examination, nasal cultures, by these events, causing the epiglottis to quickly sinus X-ray, sinus computerized tomography swell and block the air entering the trachea, (CT), and sinus transillumination (Figure 5-15). leading to respiratory failure. The bacteria can Treatment usually includes decongestants (to also travel to the bloodstream, leading to sepsis, shrink swollen nasal membranes), analgesics, which is also life threatening because it activates and nasal corticosteroid spray (to shrink swol- a massive immune response. Epiglottitis was len nasal membranes) until the sinuses begin once most often seen in children ages 2–6, but draining. Bacterial infections require antibiotic rarely seen in adults. This trend may change with therapy to resolve. Other measures may include the impact of the Hib vaccine. humidifiers (to liquefy secretions and aid in The onset of clinical manifestations is typi- drainage) and avoidance of irritants (e.g., smoke, cally rapid and includes the following signs and chemicals, and other allergens). In children with symptoms: recurrent sinusitis and other upper respiratory • High fever infections, removing the adenoids may resolve • Chills and shaking the issue. • Sore throat and hoarseness

Transilluminator

Maxillary sinus

Hard palate

Figure 5-15 Transillumination of the sinuses.

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• Dysphagia (difficulty swallowing) LEARNING POINTS • Drooling with the mouth open • Mild inspiratory stridor (a harsh, high- piglottitis is often misdiagnosed as croup. One distinct pitched sound made as a result of air turbu- Edifference in manifestations can assist in moving to lence) appropriate life-saving treatment more quickly. With epiglot- titis, patients “look worse than they sound.” With croup, they • Respiratory distress “sound worse than they look” due to the seal-like barking • Central cyanosis (blue discoloration of the cough. Additionally, cough is not generally seen with epiglot- mouth and lips) titis. Although severe croup can cause complete airway • Anxiety, irritability, or restlessness (a result obstruction, it is rarely life threatening. Picking up on this of hypoxia) signifi cant manifestation can save the patient’s life! • Pallor • Assuming a sitting tripod position, often leaning slightly forward (a subconscious at- Clinical manifestations of laryngitis usually tempt to facilitate breathing) last less than a week and include the following If epiglottitis is suspected, maintaining the air- signs and symptoms: way and stabilizing respiratory status is a priority • Hoarseness before diagnostic procedures are performed. Ef- • Weak voice or voice loss forts to preserve respiratory function include hu- • Tickling sensation and raw feeling in the midifi ed oxygen therapy (likely delivered via throat mask), endotracheal intubation with mechanical • Sore, dry throat ventilation, and tracheotomy. Additional efforts to • Dry cough minimize oxygen consumption should include • Swollen nodes of the neck keeping the patient calm and controlling fever • Leukocytosis (if bacterial) (e.g., with antipyretics and hydration). Aerosol- • Difficulty breathing (in children) ized epinephrine and systemic steroids (often Diagnostic procedures for laryngitis include treatments for croup) should be avoided because a history, physical examination, CBC, and laryn- they may worsen the condition. Additionally, a goscopy. A biopsy may be conducted if symp- tongue depressor should not be used to examine toms persist, because throat cancer can mimic the patient. Once the patient is stabilized, diagnos- acute laryngitis. Treatment depends on the tic procedures include visualization of the epiglot- cause, and many times the laryngitis will im- tis through a fi ber-optic camera, X-rays (throat and prove without treatment. Treatment strategies chest), cultures (throat and blood), arterial blood aim to increase comfort or decrease the duration gases (ABGs), and a complete blood count (CBC). of the infl ammation: Intravenous antibiotics will be used to treat infections quickly. Hib vaccinations should be • Warm humidity encouraged for children, the elderly, and immu- • Resting the voice nocompromised persons so that transmission • Increasing fluid intake rates will continue to be low. Other prevention • Treating the underlying cause (e.g., infec- strategies include proper hand washing, avoid- tion or gastric reflux) ing crowds, cleaning objects (e.g., toys), and not • Analgesics sharing objects (e.g., pacifi ers and bottles). • Throat lozenges • Gargling with salt water Laryngitis • Avoidance of decongestants (they dry out Laryngitis is an infl ammation of the larynx that the mucous membranes) is usually a result of an infection, increased upper respiratory exudate, irritants (e.g., stom- Laryngotracheobronchitis ach acid, inhaled smoke, or chemicals), or over- Laryngotracheobronchitis, or croup, is a use. Viral infections (e.g., infl uenza, rhinovirous, common viral infection in children 3 months to and adenovirus) are the most common cause. 3 years of age. Other children and adults may With laryngitis, the vocal cords become irritated also contract it. Routine causative agents include and edematous because of the infl ammatory parainfl uenza viruses, adenoviruses, and respi- process. This infl ammation distorts sounds, lead- ratory syncytial virus. Additional causes include ing to hoarseness and in some cases making the bacterial infections, allergens, and irritants (e.g., voice undetectable. Occasionally, the airway can stomach acid, inhaled smoke, or chemicals). become blocked. Laryngitis can also be associ- Outbreaks and epidemics occur in autumn to ated with croup and epiglottitis. early winter, but cases can occur sporadically

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year-round. Croup was once a deadly disease inflammation is most commonly caused by a caused by diphtheria bacteria, but the introduc- wide range of viruses (e.g., influenza, rhinovi- tion of antibiotics and immunizations have rus, respiratory syncytial virus, and adenovirus). improved its prevention and treatment. Today, Bacterial invasions (e.g., Streptococcus pneumoniae most cases of croup are mild. Nevertheless, this and Haemophilus influenzae), irritant inhalation disease can still be dangerous. (e.g., smoke, marijuana, pollution, and ammo- Croup usually begins as an upper respira- nia), and allergic reactions are less frequent tory infection with nasal congestion and cough. causes. Young children, the elderly, and smokers The larynx and surrounding area swell, leading are at the highest risk for developing acute to airway narrowing and obstruction. This swell- bronchitis. ing can lead to respiratory failure. Clinical mani- In this condition, the airways become irri- festations worsen at night and usually resolve tated and narrowed due to the results of the in- in about a week. These manifestations include flammatory process (e.g., capillary dilation, the following signs and symptoms: edema, and exudate). Clinical manifestations of • Low-grade fever acute bronchitis are usually mild and resolve in • Nasal congestion 7–10 days, but coughing may linger for several • Seal-like barking cough (because of laryn- weeks after the infection is resolved. These man- geal swelling) ifestations include the following: • Hoarseness • Productive or nonproductive cough • Inspiratory stridor • Dyspnea • Mild expiratory wheezing • Wheezing • Dyspnea • Abnormal lung sounds (usually rales or • Anxiety rhonchi) • Cyanosis • Low-grade fever Diagnostic procedures for croup consist of a • Pharyngitis history, physical examination, X-rays (throat), throat cultures, ABGs, and CBC. A throat X-ray will reveal a narrowing of the trachea (often re- Courtesy of Hugh Dainer, MD, PhD ferred to as the steeple sign) in 50% of cases (Figure 5-16). Croup is usually self-limiting but can be life threatening without supportive therapy. Treat- ment strategies include cool humidity, cortico- steroids (to decrease edema), humidified oxygen (e.g., an oxygen tent over an infant’s crib), bron- chodilators (to open the airway), hydration (to combat fever, moisten the airway, and liquefy secretions), and aerosolized epinephrine (in se- vere respiratory distress). Cool humidity may decrease edema, but no studies have supported this treatment. This intervention should be avoided in patients with asthma because it may trigger bronchial constriction. Cool humidity can be accomplished with a cool-mist humidi- fier, exposure to cool outside air especially at night, and exposure to cold shower mist in a closed bathroom. Strategies to decrease oxygen consumption include keeping the patient calm and avoiding unnecessary procedures. Addition- ally, educating the public regarding diphtheria vaccination compliance is critical to manage this once life-threatening condition. Acute Bronchitis Acute bronchitis is an inflammation of the tracheobronchial tree or large bronchi. This Figure 5-16 Steeple sign.

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• Malaise types may exchange genes. This “reassorted” flu • Myalgia can sometimes spread from pigs to humans and • Chest discomfort may cause a more or less severe strain. In 1997, Diagnosis of acute bronchitis is usually for the first time, scientists found that a form of based on symptoms. Additionally, a CBC and avian H5N1 flu skipped the pig step and infected chest X-ray may be performed for differential humans directly. Alarmed health officials feared diagnosis purposes. a worldwide epidemic (a pandemic). Fortu- Acute bronchitis is generally self-limiting; nately, the virus could not pass from person to therefore, treatment is often supportive. Phar- person, so it did not spark an epidemic. As of macologic treatment may include antipyretics, August 2012, there had been 608 confirmed analgesics, antihistamines, decongestants, cases of this avian flu virus, which resulted in cough suppressants, bronchodilators, and anti- 359 deaths. biotics (if bacterial). Use cough suppressants Millions of Americans contract the flu each cautiously. Coughing mobilizes secretions and year. The flu season in the United States, when prevent pneumonia. Other strategies include in- the incidence is the highest, is typically between creasing fluid intake, avoiding smoke, and hu- November and March. The virus is transmitted midifying air. through the inhalation or contact with respira- tory droplets. Children are two to three times Influenza more likely than adults to contract the flu, and Influenza, or flu, is a viral infection that may children frequently spread the virus to others. affect the upper and lower respiratory tract. The 2012–2013 U.S. flu season saw mostly in- Three types are distinguished—A, B, and C. fluenza type A (H3N2), but influenza type B and These influenza viruses are highly adaptive and influenza type A (H1N1) were also reported constantly mutate, preventing the development (Centers for Disease Control and Prevention of any long-term immune defense. [CDC], 2013b). This flu season was moderately severe, when compared to the mild 2011–2012 • Type A influenza, which includes several season, but did not reach the pandemic levels of subtypes, is the most common type of influ- the 2009–2010 season. The 2012–2013 flu sea- enza virus. This type is usually responsible son saw a higher percentage of outpatient visits for the most serious epidemics and global for influenza-like illness, higher rates of hospi- pandemics, such as those that occurred in the talization, and more reported deaths attributed United States in 1918, 1957, 1968, and 2009. to pneumonia and influenza (mortality ex- A subgroup of type A is H1N1, colloquially ceeded the epidemic threshold at times) com- referred to as the swine flu, which was re- pared with recent years. Persons at greater risk sponsible for a serious pandemic that started for having negative outcomes because of the flu in the United States and Mexico in 2009. include children, elderly, individuals who are • Type B influenza outbreaks can also cause immunocompromised, pregnant women, and regional epidemics, but the disease is gener- individuals with preexisting chronic diseases. ally milder than that caused by type A. Often deaths associated with the flu are a result • Type C influenza causes sporadic cases and of secondary bacterial pneumonia. minor, local outbreaks. Type C has never The influenza virus has an incubation pe- been connected with a large epidemic. riod of 1–4 days, with peak transmission risk Type A influenza viruses are found in hu- starting at approximately 1 day before onset of mans and many animals (e.g., ducks, chickens, symptoms and lasting 4–7 days afterward in pigs, and whales). Type B is isolated primarily in adults. Children can be infectious for more than humans, whereas Type C is found in humans, 10 days, and young children can spread the virus pigs, and dogs. for 6 days before the onset of symptoms occurs. Type A influenza has been found in aquatic Severely immunocompromised persons can birds for years without causing harm to them, spread the virus for weeks or months. Flu differs but recently this frequently mutating flu virus from the common cold in that the flu usually has shown that it can jump the species barrier has a sudden onset of symptoms (Table 5-2). from wild birds to domesticated poultry and Clinical manifestations of the flu include the fol- swine. Pigs can be infected by avian and human lowing signs and symptoms: flu, especially in areas where human contact is frequent. If a pig becomes infected with the • Fever avian and human flu simultaneously, the two • Headache

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Table 5-2 Comparison of Infectious Rhinitis and Infl uenza Manifestations

Symptoms Infectious Rhinitis Influenza

Fever rarely Usual; high (100°F to 102°F, but occasionally higher, especially in young children); lasts 3–4 days

headache rare Common

Myalgia Slight Usual; often severe

Malaise Sometimes Usual; can last up to 2–3 weeks

exhaustion Never Usual; at the beginning of the illness

Stuffy nose Common Sometimes

Sneezing Usual Sometimes

Sore throat Common Sometimes

Chest discomfort, Mild to moderate; Common; can be severe cough nonproductive cough

adapted from National Institutes of allergy and Infectious Disease. (2008). Is it the cold or the fl u? retrieved from http://www.niaid.nih.gov/topics/Flu/Documents/sick.pdf

• Chills commonly administered to people 6 months • Dry cough and older), high-dose vaccine (for people aged • Body aches 65 and older), intradermal vaccine (for people • Nasal congestion aged 18–64), and intranasal fl u vaccine (pro- • Sore throat duced from a live, weakened virus, unlike the • Sweating other vaccines that are produced from a killed • Malaise virus; approved for healthy, nonpregnant peo- • Vomiting and diarrhea (more common in ple aged 2–49). Prior to each fl u season (usually children than in adults) before the previous season is over), the CDC develops a seasonal fl u vaccine based on predic- Typically, fever and body aches last 3–5 tions of the likely strain to be encountered. In days, while cough and fatigue may last for 2 or the United States, the seasonal fl u vaccine more weeks. should be administered each year in October Diagnostic procedures for infl uenza consist and is recommended to everyone age 6 months of a history, physical examinations, rapid fl u and older, especially those in high-risk groups screen, and fl u culture (a nasal culture that tests (e.g., persons with a chronic medical condition, for the presence of the virus). Treatment is age 65 or older, pregnant, living in a commu- symptomatic and supportive unless a secondary nity setting, healthcare providers, and house- bacterial infection is present. Antiviral medica- hold contacts). When outbreaks of other types tions can reduce the severity and the duration of the fl u occur, as with the H1N1 infl uenza in of the symptoms. These antivirals can also be 2009, the CDC develops vaccinations specifi c given on a postexposure basis to decrease the for those strains. likelihood of developing the fl u. Other strategies Vaccine development can be a lengthy pro- include increasing fl uids, rest, antipyretics, and cess. In many cases, the vaccines are grown in analgesics. Prevention strategies are similar to fertilized chicken eggs for approximately those used to prevent the common cold (e.g., 10 months. Therefore, fl u vaccines should not hand washing and avoiding crowds), but also be administered to persons with egg allergies. include vaccinations. Additionally, children younger than 6 months Currently, vaccinations exist for the sea- and people with a history of Guillain-Barré syn- sonal fl u and H1N1 fl u (if warranted). Four drome should not be vaccinated. People with an types of seasonal fl u vaccinations are produced— active febrile illness should wait to be vaccinated regular seasonal fl u vaccine (the form most until after the illness resolves.

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MYTH BUSTERS

A common misconception is that you can get the possibility that people may still have the fl u the fl u from the fl u vaccine. What fuels this even after receiving the vaccination. This infec- myth is that some people may experience very tion is not caused by the fl u vaccine; rather, it mild fl ulike symptoms (e.g., low-grade fever, occurs because the person encountered a strain aches, malaise) after receiving the vaccination. of the fl u that was not covered by the vaccina- These symptoms are not because the individual tion. Remember, the vaccination is based on has a mild case of the fl u; it is due to the im- predictions. Negative outcomes from the fl u mune system developing antibodies against the vaccine are rare and minimal. So get vaccinated virus. An additional factor fueling this myth is and encourage others to do the same!

◾ Lower Respiratory Tract Infections Diagnostic procedures include a history, physical examination, chest X-ray, mucus swab, Bronchiolitis CBC, and ABGs. Bronchiolitis can progress to Bronchiolitis is a common viral infection of the atelectasis (collapse of the alveoli) and respira- bronchioles, which is most frequently caused by tory failure without aggressive and early treat- the respiratory syncytial virus (RSV). The infec- ment; therefore, airway management and tion most often occurs in children younger than respiratory stability are the treatment foci. Hos- 1 year of age, and incidence increases in the fall pitalization is often required, and intubation and winter months. According to the CDC may be necessary if the child decompensates or (2010b), 2.1 million children younger than the respiratory failure occurs. Other treatment strat- age of 5 years seek medical attention annually egies include oxygen therapy, cool humidity, for RSV, and nearly all children will have an RSV suctioning secretions, increased fl uids (either by infection by the time they are 2 years old. Bron- mouth or intravenously), keeping the child chiolitis can also be caused by parainfl uenza, calm, bronchodilators, and corticosteroids (not infl uenza, adenoviruses, and metapneumovi- recommended for children). No specifi c treat- ruses (an emerging paramyxovirus). ment for RSV infection is available. Prevention When the virus infects the bronchioles, these strategies are the same as those previously dis- small airways become infl amed and swollen. As cussed for other infectious respiratory condi- a result of the infl ammatory process, mucus col- tions (e.g., hand washing and avoiding crowds). lects in these airways. The combination of edema Palivizumab (Synagis) can be given to at-risk and mucus prevents air fl ow into the alveoli. infants during RSV season to prevent and mini- Transmission of RSV occurs through contact with mize infection. A vaccine for RSV is in develop- or inhalation of infected respiratory droplets. ment but is not yet commercially available. Factors contributing to the development of bron- chiolitis include neonatal prematurity, asthma Pneumonia family history, and cigarette smoke exposure. Pneumonia is an infl ammatory process caused Clinical manifestations of bronchiolitis vary by numerous infectious agents (e.g., bacteria, in severity but include the following signs and viruses, and fungi) and injurious agents or symptoms: events (e.g., aspiration and smoke). According • Nasal drainage to the CDC (2010a), pneumonia accounts for • Nasal congestion 1.1 million hospitalizations and nearly 50,000 • Cough deaths annually. Streptococcus pneumoniae is • Wheezing responsible for 75% of all cases of pneumonia, • Abnormal lung sounds (e.g., rhonchi or and the most common viral causes are infl uenza, rales) parainfl uenza, and RSV.Viral pneumonia and • Rapid, shallow respirations bacterial pneumonia have some notable dif- • Labored breathing (e.g., chest retractions, ferences (Table 5-3). Viral pneumonia is usually nasal flaring, and grunting) mild and heals without intervention, but it can • Dyspnea or tachypnea lead to virulent bacterial pneumonia. • Fever Irritating agents or events can also lead to • Tachycardia pneumonia—for example, aspiration of gastric • Malaise contents, endotracheal intubation, respiratory

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Table 5-3 Comparison of Viral and Bacterial Pneumonia

Viral Bacterial

Cough Nonproductive productive

Fever Low grade higher

WBC Normal (low) elevated

X-ray Minimal change Infi ltrates

Severity Less More

antibiotics No Yes

suctioning, and inhalation of smoke or chemi- secretions moving, and adequate hydrations cals. Aspiration pneumonia frequently occurs keep secretions thin. When these secretions be- when the gag refl ex is impaired because of a come thick and stagnate, ciliary action cannot brain injury or anesthesia. Aspiration can also remove the bacteria-laden mucus, leading to occur because of impaired lower esophageal pneumonia. sphincter closure secondary to nasogastric tube Pneumonia is classifi ed based on the caus- placement or disease (e.g., gastroesophageal re- ative agents or events previously discussed and fl ux disease). Additionally, inappropriate tube- its location in the lung (Table 5-4). Lobar feeding placement can lead to tube-feeding pneumonia is confi ned to a single lobe and is formulas entering the lungs rather than the described based on the affected lobe (e.g., right stomach. Gastric contents and tube-feeding for- upper lobe). Bronchopneumonia is the most mulas irritate the lung tissue, triggering the in- frequent type and is a patchy pneumonia spread flammatory response. The inflammatory throughout several lobes. Interstitial pneu- response increases mucus production, which monia, or atypical pneumonia, occurs in the can in turn lead to atelectasis and pneumonia. areas between the alveoli. Interstitial pneumo- Tube-feeding formulas also contain sugar and nia is routinely caused by viruses (e.g., infl uenza protein, creating a superior medium in which type A and B) or by uncommon bacteria (e.g., bacteria can grow and fl ourish. Finally, pneu- Legionella pneumophilia and Mycoplasma monia can develop from stasis of pulmonary se- pneumoniae). cretions. Activities such as movement, talking, Legionnaires’ disease is a specifi c type of and coughing normally keep pulmonary pneumonia that is caused by Legionella

Table 5-4 Types of Pneumonia

Lobar Pneumonia Bronchopneumonia Interstitial Pneumonia

Distribution all of one or two lobes Scattered small patches Scattered small patches

Cause Streptococcus pneumoniae Multiple bacteria Infl uenza virus;Mycoplasma

pathophysiology Infl ammation of the alveolar Infl ammation and purulent Interstitial infl ammation wall and leakage of cells, fi brin, exudates in alveoli, often around alveoli and fl uid into alveoli, causing developing from pooled Necrosis of bronchial consolidation secretions or irritation epithelium

Onset Sudden and acute Insidious Variable

Signs high fever Mild fever Variable fever Chills productive cough of Nonproductive hacking cough productive cough of rusty sputum yellow-green sputum headache rales progressing to absent Dyspnea Myalgia breath sounds in affected lobes

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pneumophilia. These bacteria thrive in warm, ventilation support may be required as moist environments (e.g., air-conditioning sys- hypoxia worsens. tems, standing freshwater, respiratory therapy An emerging illness in the same coronavirus equipment, and whirlpools). Legionnaires’ dis- family is Middle East respiratory syndrome ease is not contagious. Instead, most people ac- (MERS-CoV). Since its discovery in April 2012 quire this type of pneumonia from inhaling the through July 2013, 77 cases and 42 deaths from bacteria as they are spread by an air-conditioning this disease had been reported. The virus is cur- system or spa. Persons with a weakened immune rently isolated to four countries in the Arabian system are at highest risk for developing Legion- Peninsula. It seems to spread through close con- naires’ disease. Although most people with this tact, but the CDC is still working on better un- type of pneumonia recover without incident, the derstanding the virus (CDC, 2013c). disease can be fatal if untreated. Symptoms are Pneumonia is also classified according to similar to other types of pneumonia and usually where it is acquired. Nosocomial pneumonia appear 10–14 days post exposure. Additional refers to pneumonia that develops more than symptoms may include nausea, vomiting, and 48 hours after a hospital admission. Ventilator- diarrhea. In addition to the usual pneumonia di- associated pneumonia (VAP) is an example of agnostic procedures, a urine test can be per- nosocomial pneumonia. With this disease, the formed to identify the presence of Legionella endotracheal tube breaks the body’s first line of antigens. Treatment of Legionnaires’ disease fol- defense and provides a portal of entry for lows the usual pneumonia treatment protocol. ­bacteria. In contrast, community-acquired Mycoplasma pneumoniae is a common ­pneumonia is acquired outside the hospital or type of pneumonia that usually affects people healthcare setting. younger than 40 years of age. People who live Most healthy people do not develop pneu- or work in crowded places such as schools, monia from fungal exposure. Many of these ill- homeless, and prisons are at higher risk of de- nesses occur instead as opportunistic infections, veloping this type of pneumonia. Mycoplasma which can be fatal in immunocompromised infection is usually mild and responds well to ­individuals (e.g., children and persons antibiotics, but it can be serious. Skin rash, ar- with AIDS or cancer). Pneumocystis jiroveci thralgia, and hemolysis may also be present. ­pneumonia, formerly known as ­Pneumocystis Severe acute respiratory syndrome carinii pneumonia, is a specific type of pneumo- (SARS) is a rapidly spreading respiratory illness nia that is caused by yeastlike fungus. Its diag- that presents similarly to atypical pneumonia. nosis is accomplished through identification of First identified in China, its prevalence rates re- the fungus through a sputum culture. Aggres- main higher in Asian countries. SARS is caused sive and early treatment will improve outcomes by a coronavirus, SARS-CoV. Transmission oc- in these vulnerable patients. Other fungal-­ curs through inhalation of respiratory droplets related pneumonias include histoplasmosis, or close contact, although oral–fecal contact coccidiomycosis, and cryptococcal pneumonia. may also be a mechanism of transmission. SARS In addition to previously discussed risk factors, has high mortality and morbidity rates. The in- persons at risk for developing pneumonia and cubation period for this disease is 2–7 days. The having serious complications include children, first stage presents as a flulike syndrome (e.g., the elderly, immunocompromised individuals, fever, chills, headache, myalgia, anorexia, and those with existing chronic disease conditions, diarrhea) that lasts 3–7 days. Several days later, smokers, and alcoholics. Otherwise-healthy pa- a dry cough and dyspnea develop as the lungs tients usually recover completely from pneu- become damaged and the patient moves into monia when treated properly. Those high-risk the second stage of the disease. Interstitial con- persons are more likely to develop complica- gestion and hypoxia progress rapidly. Addition- tions including septicemia, pulmonary edema, ally, liver damage can occur. If the patient lung abscess, pleural effusion, and acute respi- continues to the third stage, severe and some- ratory distress syndrome. times fatal respiratory distress can develop. Di- Clinical manifestations of pneumonia in- agnostic procedures for SARS consist of a clude the following signs and symptoms: history, physical examination, and chest X-ray. Treatment focuses on maintaining oxygenation • Productive or nonproductive cough and respiratory status. Strategies include oxygen • Fatigue therapy, bronchodilators, and antiviral drugs. • Pleuritic pain Endotracheal intubation with mechanical­ • Dyspnea

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• Fever disease because of an intact, healthy immune • Chills system or early treatment. A growing number • Abnormal lung sounds (e.g., crackles or of multidrug-resistant TB strains are emerging, rales) however, increasing treatment concerns and • Pleural rub prevalence rates. Fifteen percent of persons in- • Tachypnea fected with TB in the United States have a mul- • Mental status changes (especially in the el- tidrug-resistant strain. derly) Although TB most frequently involves the • Leukocytosis lungs, it can also affect other organs and tissues (e.g., liver, brain, and bone marrow). TB is often Early diagnosis and treatment of pneumo- considered an opportunistic infection because it nia are paramount to have positive outcomes. is more likely to become active in someone with Diagnostic procedures may include a history, a weakened immune system. Therefore, at-risk physical examination, chest X-ray, sputum cul- persons include those with immune deficiency tures, CBC, ABGs, and bronchoscopy. Endotra- (e.g., AIDS and cancer), malnutrition, diabetes cheal intubation may be necessary to provide mellitus, and alcoholism. Poverty, overcrowd- ventilation support and maintain oxygenation. ing, homelessness, and drug abuse also increase Additional treatment strategies include antibi- the risk for acquiring TB. otics (if bacterial infection is present), broncho- There are two stages of TB pathogenesis— dilators, corticosteroids, antipyretics, analgesics, primary and secondary infection. Primary TB humidified oxygen therapy, chest physiother- infection occurs when the bacillus first enters apy, increased fluids (either by mouth or intra- the body. In this phase, macrophages engulf the venously), and rest. If aspiration is the cause of microbe, causing a local inflammatory response. the pneumonia, additional treatment includes Some bacilli travel to the lymph nodes, activat- eliminating the causes and not giving the pa- ing the type IV hypersensitivity reaction (see the tient anything by mouth until swallowing stud- Body Defenses chapter). Lymphocytes and mac- ies can be performed. Pneumonia prevention rophages congregate to form a granuloma (an strategies include hand washing, avoiding epithelial nodule). The granuloma contains crowds, vaccinations (e.g., for pneumococcus, some live bacilli, forming a tubercle. Caseous influenza, and Hib), mobilizing secretions (e.g., necrosis, a cottage cheese–like material, devel- turning, coughing, deep breathing), and smok- ops in the center of the tubercle (see the Cellular ing cessation. Function chapter). An intact immune system can resist this development, so the lesions— referred Tuberculosis to as Ghon complexes (Figure 5-18)—remain Tuberculosis (TB), an ancient disease, is one small, become walled off by fibrous tissue, and of the world’s deadliest conditions. Although on calcify. The bacilli can remain dormant and vi- the decline, TB remains a major cause of illness, able in the tubercle for years as long as the im- with one-third of the world’s population being mune system is intact. In this phase, the infected. According to the World Health Orga- individual has been infected by the bacilli and nization (WHO), TB was responsible for approx- remains asymptomatic. When the primary in- imately 1.4 million deaths worldwide in 2011, fection can no longer be controlled, the infection and it is the leading cause of death for persons progresses to the secondary, or active, infected with HIV (CDC, 2012). In the United ­infection phase. During this phase, TB can States, TB rates are higher among Asians, Native spread throughout the lungs and to other Hawaiians, and other Pacific Islanders. organs. TB is caused by Mycobacterium tuberculosis, a Clinical manifestations begin to appear in slow-growing aerobic (requires oxygen) bacillus the secondary infection phase: that is somewhat resistant to the body’s immune • Productive cough efforts. Person-to-person transmission occurs • Hemoptysis (coughing up blood or bloody through the inhalation of tiny infected aerosol sputum) droplets (Figure 5-17). Only people with active • Night sweats TB can spread the disease to others. The bacillus is capable of surviving in dried sputum for • Fever weeks. Ultraviolet light, heat, alcohol, glutaral- • Chills dehyde, and formaldehyde destroy the bacillus. • Fatigue Many people contract TB but do not develop the • Unexplained weight loss

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Tuberculosis

Risk factors: Weak immune system Overcrowded living conditions Malnutrition Substance abuse

Exposure to airborne droplets

Droplet enters alveoli Inflammatory process begins Bacilli isolated and phagocytized

Some bacilli Some bacilli enter killed a dormant stage

PPD positive PPD positive Formation of tubercles

Tubercles calcified

Immune system weakens Breakdown of tubercle

Reactivation of disease Person becomes infectious

Symptoms develop Positive chest X-ray Positive sputum culture

Treatment: Antimycobacterial therapy with multiple medications to prevent mutation/resistance Prophylactic drug therapy after exposure Bacille Calmette-Guérin vaccine after exposure when medications are not available

Figure 5-17 Tuberculosis. Madara, M., & Pomarico-Denino, V. (2008). Quick look nursing: Pathophysiology (2nd ed.). Sudbury, MA: Jones & Bartlett.

LEARNING POINTS • Anorexia • Miscellaneous symptoms depending on B skin testing is only useful as a screening tool to other organ involvement Tidentify new TB exposure cases. Once a person’s immune system has developed antibodies against TB, the person Diagnostic procedures for TB are multifac- tests positive. This immunity reaction happens after the fi rst eted, beginning with a TB skin test (Mantoux exposure and vaccination administration. A person can be test). For the TB skin test, a small amount of a treated for TB, and he or she will continue to test positive purifi ed protein derivative tuberculin is injected because the antibodies are still present. Chest X-rays and just below the dermis. If the person has been in- sputum cultures are better diagnostic procedures once someone has tested positive. So remember . . . once positive, fected by the bacilli, a local reaction (e.g., red- always positive! ness and induration) will occur (Figure 5-19). Persons will test positive once the bacilli trigger

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creates, chest X-rays and sputum cultures (most definitive) are used after a positive TB skin test is noted (either to confirm an original case or to assess reinfection). A computerized tomography (CT) scan can also be used to visualize TB lesions

Courtesy of Benjamin M. Marais Courtesy of Benjamin M. because this imaging modality is more sensitive than an X-ray. Nucleic acid amplification may be performed on the sputum to detect the pres- ence of resistant strains. TB is often successfully treated in the home setting; however, treatment requires diligence to eradicate the disease. Treatment requires an average of 6–9 months of antimicrobial therapy. Combination therapy (consisting of two or more drugs) is recommended to prevent the Figure 5-18 Ghon complexes. emergence of resistant strains. The slow-­ growing bacilli have a high mutation rate, with those mutations often appearing when the pathogen is exposed to monotherapy. Because TB is a public health risk, antituberculin medi- cations are provided free of charge by the U.S.

© Phototake, Inc./Alamy © Phototake, Public Health Service. In some states, therapy noncompliance is unlawful, and imprisonment may be used to ensure adherence when other measures fail (e.g., direct observed therapy). Compliance is a common problem in treating TB because of the length of therapy and the medication side effects (e.g., nausea, paresthe- sias, and discolored bodily secretions). Patient Figure 5-19 Positive TB skin test. education, including an emphasis on taking the entire regimen of drugs as ordered, is crucial to maximize therapy success and prevent resis- the inflammatory response (Figure5- 18). A his- tance. Strategies to prevent the transmission of tory of bacillus Calmette-Guérin (BCG) vaccina- TB include respiratory precautions (e.g., TB- tion will produce a false-positive reaction. approved masks, covering one’s mouth when Additionally, previously treated TB will generate coughing, and disposing of tissues), adequate a false-positive reaction. Conversely, persons ventilation (if the patient is at home), placing with immature (e.g., children) or compromised the patient in a negative-pressure isolation (e.g., AIDS or cancer) immune systems may not room (if he or she is hospitalized), and the ba- generate enough of a response to test positive. cillus Calmette-Guérin vaccination (primarily Because of the uncertainty that the TB skin test used in children and in developing countries).

A l t e r a t i o n s i n V e n t i l a t i o n

◾◾ Asthma Diagnosis, hospitalizations, and death rates asso- Asthma is a chronic pulmonary disease that ciated with asthma all increased from 1996 to produces intermittent, reversible airway obstruc- 2006 (CDC, 2009). These rate increases may be tion. It is characterized by acute airway inflam- a result of surging urbanization and pollution. mation, bronchoconstriction, bronchospasm, Another theory, referred to as the hygiene bronchiole edema, and mucus production hypothesis, is that the modern Western lifestyle’s (Figure 5-20). Asthma is one of the most common focus on hygiene and sanitation limits early chronic illness in children in the United States. childhood allergen and infection exposure,

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Figure 5-20 Asthma. (a) Location of the lungs and airways in the body. (b) Cross section of a normal airway. (c) Cross section of an airway during asthma symptoms. National Heart, Lung, and Blood Institute (www.nhlbi.nih.gov)

thereby rendering individuals more vulnerable usually presents after age 35 years. Intrinsic trig- when they do finally encounter allergens and gers include upper respiratory infections, air pol- infectious agents. Women are more likely to lution, emotional stress, smoke, exercise, and have asthma than men, but in children, boys are cold exposure. more likely to have asthma than girls. Mixed- Nocturnal asthma usually occurs between race and African American adults and children 3:00 and 7:00 a.m. and is thought to be related are more likely to have asthma than Caucasian to circadian rhythms. At night, cortisol and epi- adults and children. Other risk factors include nephrine levels decrease, while histamine levels lower socioeconomic status, obesity, smoke increase. Changes in these naturally occurring exposure, and family history. substances lead to bronchoconstriction. Asthma is usually classified according to Exercise-induced asthma is common cause (extrinsic, intrinsic, nocturnal, exercise-­ and usually occurs 10–15 minutes after physi- induced, occupational, or drug-induced) and by cal activity ends. Symptoms can linger for an severity (mild intermittent, mild persistent, hour with this type of asthma. The airways moderate persistent, and severe persistent) can become cool and dry during exercise, and (Table 5-5). Extrinsic­ asthma is a result of in- asthmatic symptoms may be a compensatory creased IgE synthesis and airway inflammation, mechanism to warm and moisten the airways. which leads to mast cell destruction and inflam- Following each episode of exercise-induced matory mediator release. Extrinsic triggers in- asthma, a refractory (symptom-free) period clude allergens such as food, pollen, dust, and begins within 30 minutes and can last 90 min- medications. The release of the inflammatory utes. During this time, little or no broncho- mediators in response to these triggers causes spasm can be induced even if the person is bronchoconstriction, increased capillary perme- rechallenged with vigorous exercise. Athletes ability, and mucus production. Extrinsic asthma often take advantage of this fact by warming up generally presents in childhood or adolescence. vigorously to induce a refractory period prior Intrinsic asthma is not an allergic reaction and to competition.

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Table 5-5 Classifi cation of Asthma Severity

Step/Classification* Daytime Symptoms Nighttime Symptoms PEF or FEV1† PEF Variability

Step 1: Mild intermittent ≤ 2/wk ≤ 2/wk ≥ 80% < 20%

Step 2: Mild persistent > 2/wk, but < daily > 2 nights/mo > 80% 20–30%

Step 3: Moderate persistent Daily > 1 night/wk 60–80% > 30%

Step 4: Severe persistent Continual Frequent ≤ 60% > 30%

*Classifi cation is based on symptoms and lung function before treatment. patients should be assigned to the most severe step in which any feature occurs. †percentage of predicted function. peF = peak expiratory fl ow (rate); FeV1 = forced expiratory volume in 1 second. National heart, Lung, and Blood Institute (www.nhlbi.nih.gov).

Occupational asthma is caused by a reac- • Tachypnea tion to substances encountered at work (e.g., • Anxiety plastic or formaldehyde). Symptoms develop Status asthmaticus is a life-threatening, over time, worsening with each exposure and prolonged asthma attack that does not respond improving when away from work (e.g., on to usual treatment. Maintaining a patent airway weekends or during vacations). is critical in such cases, and endotracheal intuba- Drug-induced asthma is frequently tion with ventilation support may be necessary. caused by aspirin and can be fatal. Reactions can In addition, acid–base imbalances—specifi cally be delayed up to 12 hours after drug ingestion. respiratory alkalosis (from expelling too much Aspirin and other drugs (e.g., nonsteroidal anti- carbon dioxide because of tachypnea)—can de- infl ammatory drugs) prevent the conversion of velop. Treatment of these conditions will be cru- prostaglandins, which stimulate leukotriene cial to improve outcomes. release—a powerful bronchoconstrictor. Diagnostic procedures can be used to iden- Regardless of the classifi cation system used, tify those persons with asthma as well as to track asthma attacks are the body’s response to bron- progression of the disease. These diagnostic pro- chial infl ammation. Stage 1 of an acute asthma cedures include a history, physical examination, attack is primarily related to bronchospasm, and pulmonary function tests (Figure 5-11), chest is usually signaled by coughing. Peaking within X-ray, ABGs, CBC, challenge testing, and aller- 15 to 30 minutes, the infl ammatory mediators gen testing. responsible for this stage include leukotrienes, Asthma cannot be cured, but its symptoms histamine, and some interleukins. Stage 2 of an can be controlled. Unless treated promptly, asthma attack peaks within 6 hours of symptom asthma attacks can lead to impaired gas exchange onset. This stage is a result of airway edema and and death. Left untreated, long-term asthma can mucus production. The alveolar hyperinfl ation result in bronchial damage and scarring. The causes air trapping. Bronchospasm, smooth goals of treatment are to minimize the occurrence muscle contraction, infl ammation, and mucus and severity of asthma attacks. Pharmacologic production combine to narrow the airways. treatment includes inhaled and systemic cortico- Clinical manifestations of asthma include steroids, bronchodilators, beta agonists, nebulizer the following: treatments, leukotriene mediators, mast cell sta- • Wheezing bilizers, and anticholinergics. Additional strate- • Shortness of breath gies include the following measures: • Dyspnea • Develop an asthma plan (Figure 5-21) and • Chest tightness teach it to all caregivers • Cough • Avoid triggers

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Figure 5-21 Example of asthma action plan. National Heart, Lung, and Blood Institute (www.nhlbi.nih.gov).

• Keep the environment clean risk of developing COPD also include Caucasians, • Limit environmental fabrics women, individuals of lower socioeconomic sta- • Filter indoor air tus, and persons with a history of asthma. • Maintain a healthy immune system (e.g., Prevalence rates are likely underestimated exercise, get adequate nutrition) because COPD is often asymptomatic in its early stages or is masked by smoking symptoms. Ac- ◾◾ Chronic Obstructive Pulmonary Disease cording to the CDC (2013b), COPD was the third leading cause of death in the United States in Chronic obstructive pulmonary disease 2011. Twelve million Americans are currently (COPD) describes a group of chronic respiratory disorders characterized by irreversible, progres- diagnosed with COPD, and an additional 12 mil- sive tissue degeneration and airway obstruction. lion Americans may have this disease and not These debilitating conditions can impair an indi- know it. Symptoms usually present around vidual’s ability to work and function indepen- 60 years of age. A rare familial type of COPD dently. Severe hypoxia and hypercapnia can (emphysema only), alpha-1 antitrypsin defi- lead to respiratory failure. The chronic hyper- ciency, presents much earlier—in the 30s or 40s. capnia shifts the normal breathing drive from COPD is often one of or a mixture of two the need to expel excess carbon dioxide to the diseases—chronic bronchitis and emphysema Figure 5-22). These two diseases are discussed need to raise oxygen levels (Figure 5-12). Addi- ( next. tionally, COPD can lead to cor pulmonale, right- sided heart failure due to lung disease (see the Cardiovascular Function chapter). ◾◾ Chronic Bronchitis The most significant contributing factor to Chronic bronchitis is an obstructive respiratory developing COPD is cigarette smoking. Other disorder characterized by inflammation of the contributing factors include the inhalation of bronchi, a productive cough, and excessive pollution and chemical irritants. Groups at higher mucus production. This disorder differs from

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Normal bronchiole Bronchiole

Trachea Alveoli (wind pipe)

Bronchiole

Lung Chronic bronchitis

Excess mucus

Emphysema Collapsed bronchiole Inflamed bronchiole

Enlarged alveoli

Figure 5-22 Chronic obstructive pulmonary disease (COPD) is often one disease or a mixture of two diseases—chronic bronchitis and emphysema. © Jones & Bartlett Learning

acute bronchitis in that the chronic type is not activity) result in frequent respiratory infections necessarily caused by an infection and symptoms and, in some cases, respiratory failure. persist longer. As previously mentioned, cigarette Airway resistance results in hypoventila- smoking is the greatest contributing factor for tion, hypoxemia, cyanosis, hypercapnia, poly- chronic bronchitis. The inflammatory response cythemia, clubbing of fingers, and dyspnea at results in mucous gland hyperplasia, edema, rest. Additional clinical manifestations include excessive mucus production, bronchoconstric- the following signs and symptoms: tion, and cough in defense against inhaled irri- • Abnormal lung sounds (e.g., wheezing and tants. Airway resistance affects inspiratory and rhonchi) expiratory air flow. Impaired pulmonary defenses • Edema (e.g., cilia damage and decreased phagocytic • Weight gain

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LEARNING POINTS • Chest tightness • Tachypnea atients with chronic bronchitis are unable to increase • Hypoxia Pventilatory effort to maintain adequate gas exchange; • Hypercapnia therefore, they eventually develop cyanosis. This cyanosis • Activity intolerance coupled with the edema that develops gives these patients the nickname “blue bloaters.” Additionally, chronic • Anorexia bronchitis pathogenesis can be remembered by these three • Malaise S’s—Sputum, Swelling, and Spasm. Diagnosis and progress monitoring are ac- complished through the same procedures thatare used for chronic bronchitis. Treatment strategies • Malaise include those identifi ed for chronic bronchitis, • Chest pain plus pursed-lip breathing and lung reduction • Fever surgery. Pursed-lip breathing increases expira- tory resistance and produces airway backpres- Diagnostic procedures for chronic bronchitis sure, preventing collapse of the alveoli. consist of a history (persistent, productive cough for at least 3 months in a year for 2 consecutive ◾ Cystic Fibrosis years), physical examination, chest X-ray, pul- Cystic fi brosis is a common inherited respira- monary function tests (Figure 5-11), ABGs, and tory disorder (about 1,000 patients diagnosed CBC. The goal of treatment is to maintain air- per year in the United States) that presents at way patency. Treatment strategies include oxy- birth (Cystic Fibrosis Foundation, n.d.). Cauca- gen therapy (in limited amounts, because too sians are more likely to develop cystic fi brosis much will knock out the newly oxygen- centered than other ethnic groups, followed by Latinos drive for breathing), bronchodilators, cortico- and American Indians. This life-threatening con- steroids, antibiotics (if bacterial infection is pres- dition causes severe lung damage and nutrition ent), postural drainage, chest physiotherapy, defi cits. Cystic fi brosis changes the cells that pro- and increased hydration. duce mucus, sweat, saliva, and digestive secre- ◾ Emphysema tions. As a result, these normally thin secretions become thick and tenacious. Instead of lubricat- Emphysema is an obstructive respiratory dis- ing the respiratory tract, the secretions occlude order that results in the destruction of the alveo- airways, ducts, and passageways. The genetic lar walls, leading to large, permanently infl ated defect that leads to cystic fi brosis has been iso- alveoli. Lung tissue normally remodels during lated to chromosome 7, and transmission fol- periods of growth and repair related to infections lows an autosomal recessive pattern (see the and infl ammation. Enzymes are involved in this Cellular Function chapter). More than 10 million process to prevent excessive tissue damage. Americans are carriers of this faulty gene, and Enzyme defi ciency, however, may result from many do not know they are carriers. The genetic genetic predisposition (less than 2% of cases) defi cit is related to a protein involved in sodium, and smoking. Smoking initiates infl ammation, chloride, and water cellular transport. The lungs causing changes in these enzyme levels and and pancreas are primarily affected, but other leading to structural changes. Emphysema grad- organs can also be involved (e.g., liver, intes- ually turns the alveoli into large, irregular pock- tines, sinuses, and reproductive organs). ets with gaping holes, which in turn limits the Atelectasis develops as airways are ob- amount of oxygen entering the bloodstream. structed, leading to permanent damage The elastic fi bers and surfactant that normally (Figure 5-23). Mucus stagnates, becoming a prime keep the alveoli open are slowly destroyed, so medium for bacterial growth. Infections are re- the alveoli collapse during expiration, trapping current and contribute to the progressive lung air in the lungs. The loss of elastic recoil and hyperinfl ation of the alveoli narrow the termi- nal bronchioles, but inspiration is not affected. LEARNING POINTS Coughing is usually not a symptom. Instead, atients with emphysema often hyperventilate, creating a emphysema is characterized by the following Ppink appearance to their skin. This panting-like breath- clinical manifestations: ing pattern coupled with the pink skin has earned emphy- • Dyspnea upon exertion sema patients the nickname “pink puffers.” Additionally, the pathogenesis of emphysema can described as “lung dry • Diminished breath sounds rot.” • Wheezing

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Cystic fibrosis—an autosomal recessive disorder

Exocrine Gland Dysfunction

Excessive amounts of thick, sticky mucus obstruct ducts of exocrine glands

Lungs Digestive tract Reproductive Sweat glands tract

Obstruction of Meconium Obstruction of Cervical mucus Excess Na+ and airways and ileus vas deferens blocks sperm Cl– content frequent infections (intestinal blocks sperm entry obstruction flow in newborn) Fibrosis

Obstruction Obstruction Infertility Electrolyte Cor pulmonale of pancreatic of bile ducts imbalance and ducts in liver dehydration

Fibrosis Biliary cirrhosis

Diabetes mellitus

Malabsorption Malnutrition

Figure 5-23 Cystic fibrosis.

destruction. Bronchiectasis and emphysema-like Sweat glands produce sweat high in sodium chlo- changes are common as fibrosis and obstructions ride, which can cause electrolyte imbalances in advance. Respiratory failure is the most common times of excessive loss (e.g., during exercise or cause of death in people who have cystic fibrosis. hot weather). Obstructions in the reproductive Ultimately, cor pulmonale (right-sided heart fail- system can lead to sterility and infertility. ure) or respiratory failure occurs. In the digestive Clinical manifestations of cystic fibrosis may tract, the mucus blocks the intestines, producing appear at birth and progressively worsen a meconium ileus in the newborn. It also blocks throughout the life span. Lung function often pancreas ducts, leading to a pancreatic enzyme starts declining in early childhood. These mani- excretion deficit. Without these digestive en- festations, which vary in severity, include the zymes, malabsorption and malnutrition develop. following signs and symptoms: The trapped digestive enzymes damage pancre- • Meconium ileus atic tissue, contributing to the development of • Salty skin (parents may notice that their ba- diabetes mellitus and osteoporosis. Blocked bile by’s skin tastes salty when they kiss the child) ducts add to the malabsorption issues and in- • Steatorrhea (fatty, foul-smelling stools) crease risk for developing cirrhosis. Salivary • Fat-soluble vitamin deficiency (vitamins A, glands are only mildly affected by blockages. D, E, and K)

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• Voracious appetite • Regular, moderate exercise • Chronic cough with tenacious sputum (may • Early, aggressive treatment of infections include hemoptysis) with antibiotics • Frequent respiratory infections • Oxygen therapy • Hypoxia • Avoidance of respiratory irritants (e.g., • Audible rhonchi and wheezing smoke, pollution, dust, and allergens) • Dyspnea • Heart–lung transplant • Fatigue • Activity intolerance ◾◾ Lung Cancer • Digital clubbing Lung cancer is the second most often diagnosed • Delayed growth and development cancer in men and women and the leading cause • Complication development (e.g., chronic of cancer in the United States (U.S. Cancer Sta- bronchitis, failure to thrive, cardiomegaly, tistics Working Group, 2012). After increasing diabetes mellitus, pancreatitis, rectal pro- for decades, lung cancer incidence and mortality lapse, liver disease, cholelithiasis, osteopo- rates are now decreasing in parallel with rosis, hyponatremia, metabolic alkalosis, decreases in rates of cigarette smoking in this and infertility) country. Frequently, other cancers—such as Diagnosis of cystic fibrosis can be accom- breast and liver, to name a few—metastasize plished prenatally when family history warrants (spread) to the lung tissue. Smoking contributes testing. Sweat analysis can be conducted at to the majority (80–90%) of lung cancer cases. about 2–3 weeks of age to detect electrolyte ab- The more than 4,000 chemicals in cigarette normalities. Some states include cystic fibrosis smoke include carcinogens and chemicals that testing as a part of their newborn screening. The paralyze cilia. The risk for developing lung can- Delta F508 test can identify the chromosome cer is directly related to the length of time a per- 7 mutation, and it is often used if a false-negative son smokes and the number of cigarettes smoked. sweat test is suspected or to identify carrier sta- Secondhand smoke can also be a significant con- tus of siblings. In addition, stool can be evaluated tributing factor, and in fact, some research has for the presence of pancreatic content. Other indicated that it may be worse than firsthand tests that assess lung function include chest smoking. Smoking cessation or removing the X-rays, pulmonary function tests, and ABGs. smoke exposure will gradually decrease risk. Cystic fibrosis treatment requires diligent Inhalation of other chemicals (e.g., asbestos, family involvement and an interdisciplinary ap- radon gas, tar, and pollution) and chronic lung proach because of the progressive, multisystem disease can also increase risk (Figure 5-24). nature of the disease. Improved treatment regi- The lungs provide an optimal environment mens have improved the life expectancy for pa- for tumor development and growth. Carcino- tients who have cystic fibrosis, with some people gens can seek refuge in the many nooks and living into their 40s or 50s. Treatment often re- crannies of the air passages, having an opportu- quires a multidisciplinary approach involving nity to cause cellular changes (usually metapla- cystic fibrosis specialists, respiratory therapists, sia) there. The scores of blood vessels supplying dieticians, and psychological counselors. Strate- the lungs serve as entrance points for distant gies include the following measures: cancer cells to gain access, and those vessels fur- • Pancreatic enzyme replacement nish the cancer with a rich blood source to fa- • Bile salt replacement cilitate its growth. • A well-balanced, high-protein, low-fat, Lung cancers are divided into two types— high-sodium diet small cell and non–small cell. Small-cell carci- • Fat-soluble vitamin replacement noma, often referred to as oat-cell carcinoma, • Increased fluid intake occurs almost exclusively in heavy smokers and • Intensive chest physiotherapy (includes is less frequent than non-small-cell cancers. chest clapping or percussion, which can be Non-small-cell carcinoma, often referred to done by hand or with a mechanical percus- as bronchogenic carcinoma, is the most common sor) type of malignant lung cancer, accounting for • Postural drainage 75% of all cases of lung cancer. This very aggres- • Coughing exercises sive lung cancer is classified into several • Humidified air ­subgroups—squamous cell carcinoma, adeno- • Bronchodilators carcinoma, and bronchioalveolar carcinoma.

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Lung Cancer

Smoking Secondhand smoke Air pollution Chronic lung injury

Initial phase: Epithelial cell damage Deoxyribonucleic acid (DNA) mutation p53 gene mutation Courtesy of National Cancer Institute If exposure is If exposure stopped, the effects continues: are reversed

Phase 2: Cancer develops Metastasis

Treatment: Smoking cessation Chemotherapy Radiation therapy Surgical resection Scan for and treat metastasis

Figure 5-24 Lung cancer. Madara, M., & Pomarico-Denino, V. (2008). Quick look nursing: Pathophysiology (2nd ed.). Sudbury, MA: Jones & Bartlett.

Upon exposure to the carcinogen, irrevers- ible oncogene DNA mutations and inactivation of tumor suppressor genes occur. If carcinogen ex­ - posure continues, cancer develops (Figure 5-25). Tumors in the lungs lead to several issues, including the following: • Airway obstruction • Inflammation of lung tissue, eliciting cough- Figure 5-25 The normal (top) and cancerous (bottom) lung. ing and contributing to infections © University of Alabama at Birmingham Department of Pathology PEIR Digital Library (http://peir.net) • Fluid accumulation in the pleural space (e.g., pleural effusion, hemothorax, and pneumothorax) • Chest pain • Paraneoplastic syndrome (endocrine dys- • Hoarseness function associated with hormone secretion • Weight loss from the tumor) • Anorexia Clinical manifestations of lung cancer are • Anemia insidious because they mimic signs of • Fatigue smoking: • Other symptoms specific to the site(s) of • Persistent cough or a change in usual cough ­metastasis • Dyspnea Diagnostic procedures for lung cancer in- • Hemoptysis clude a history, physical examination, chest • Frequent respiratory infections X-ray, CT, MRI, bronchoscopy, sputum studies,

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Table 5-6 Staging and Treatment of Non-Small-Cell Lung Cancer

Stage Description Usual Treatment Plan

Stage I Cancer has invaded the underlying lung tissue Surgery but has not spread to the lymph nodes.

Stage II Cancer has spread to neighboring lymph nodes Surgery, radiation, and chemotherapy or invaded the chest wall.

Stage IIIA Cancer has spread from the lung to lymph nodes Combined chemotherapy and radiation, in the center of the chest. sometimes surgery based on results of treatment

Stage IIIB Cancer has spread locally to areas such as the Chemotherapy, sometimes radiation heart, blood vessels, trachea, and esophagus— all within the chest—or to lymph nodes in the area of the collarbone or to the tissue that surrounds the lungs within the rib cage (pleura).

Stage IV Cancer has spread to other parts of the body, Chemotherapy, targeted drug therapy, clinical such as the liver, bones, or brain. trials, supportive care

Table 5-7 Staging and Treatment of Small-Cell Lung Cancer

Stage Description Usual Treatment Plan

Limited Cancer is confi ned to one lung and to its Combined chemotherapy and radiation, neighboring lymph nodes. sometimes surgery

Extensive Cancer has spread beyond one lung and nearby Chemotherapy, clinical trials, supportive care lymph nodes, and may have invaded both lungs, more remote lymph nodes, or other organs.

biopsy, positron emission tomography, bone effusion includes exudates (due to infl amma- scans, and pulmonary function tests. Treatment tion), transudate (due to increased hydrostatic is based on staging and follows usual cancer pressure), blood (due to trauma), and pus (due treatment—chemotherapy, surgery, and radia- to infection). The consequence of this effusion tion (Table 5-6; Table 5-7). The treatment is depends on its type, location, amount, and fl uid generally palliative because the tumor does not accumulation rate. Large amounts of fl uids can usually respond favorably to treatment. Early cause the pleural membranes to separate, pre- diagnosis and treatment will improve this prog- venting their cohesion during inhalation nosis. Other strategies include those to maintain (Figure 5-26; Figure 5-27). This lack of cohesion optimal respiratory function—oxygen therapy, impedes full expansion, leading to atelectasis bronchodilators, and antibiotics (if bacterial in- and a pneumothorax. Large effusions can also fections are present). impair venous return in the inferior vena cava and cardiac fi lling by putting pressure on those ◾ Pleural Effusion structures. A pleural effusion is the accumulation of Pleurisy, or pleuritis, can precede or follow excess fl uid in the pleural cavity. Normally, a the effusion, or it may occur independently. very small amount of fl uid drained from the Pleurisy refers to infl ammation of the pleural lymphatic system is present in this space to membranes, which leads to swollen and irregu- lubricate the constantly moving lungs. Excessive lar tissue. This infl ammation is often associated fl uid in the pleural cavity can compress the lung with pneumonia and creates friction in the pleu- and limit expansion during inhalation. Effusions ral membranes. vary in nature and may affect both lungs or one Clinical manifestations of pleural effusion lung. Fluid that can accumulate to create the include the following signs and symptoms:

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Diagnostic procedures for pleural effusion include a history, physical examination, chest X-ray, CT, ABGs, CBC, and thoracentesis (needle aspiration of fluid) with subsequent examina- Trachea tion of fluid. Treatment focuses on addressing the underlying cause. Nevertheless, regardless Pleura Lung (lung lining) of etiology, removal of the fluid is necessary to promote full expansion of the lungs. Strategies to do so may include thoracentesis, placement of a chest drainage tube, and antibiotics.

◾◾ Pneumothorax Pneumothorax refers to air in the pleural cav- ity. The presence of atmospheric air in the pleu- ral cavity and the separation of pleural membranes can lead to atelectasis. The resulting Pleura effusion pressure can cause a partial or complete collapse (fluid between pleural space) of a lung (Figure 5-28; Figure 5-29). A small pneumothorax causes mild symptoms and may Figure 5-26 Pleural effusion is a buildup of fluid in the heal on its own. A larger pneumothorax gener- lining of the lungs. © Jones & Bartlett Learning ally requires aggressive treatment to remove the air and reestablish pulmonary negative pressure. Risk factors for developing pneumothorax include smoking, tall stature, and history of lung Courtesy of Michael-Joseph F. Agbayani disease or previous pneumothorax. Several types of pneumothorax are distin- guished, based on their cause. A spontaneous pneumothorax develops when air enters the pleural cavity from an opening in the internal airways. Primary spontaneous pneumothorax occurs when a small air blister (bleb) on the top of the lung ruptures. Blebs are caused by a weak- ness in the lung tissue and can rupture from changes in air pressure, such as occurs in scuba diving, flying, mountain climbing, or listening to extremely loud music. Additionally, a primary spontaneous pneumothorax may happen while smoking marijuana—a deep inhalation, fol- lowed by slow breathing out against partially closed lips, forces the smoke deeper into the lungs. Most commonly, these blebs rupture for no obvious reason, although genetic factors may Figure 5-27 X-ray of pleural effusion. play a role. A primary spontaneous pneumotho- rax is usually mild because pressure from the collapsed portion of the lung may, in turn, col- lapse the bleb. A secondary spontaneous pneu- • Dyspnea mothorax develops in people with preexisting • Chest pain (usually sharp and worsening lung disease (e.g., emphysema, pneumonia, cys- with inhalation) tic fibrosis, or lung cancer). In these cases, the • Tachypnea pneumothorax occurs because the diseased lung • Tracheal deviation (toward the unaffected tissue is weakened. Secondary spontaneous side) pneumothorax can be more severe and even life • Diminished or absent lung sounds over the threatening because diseased tissue can create a affected area larger opening, allowing more air to enter the • Dullness to percussion over affected area pleural space. Additionally, pulmonary disease • Tachycardia reduces lung reserves, making any further re- • Pleural friction rub (pleurisy) duction in lung function more serious.

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Parietal pleura

Air in the pleural space Lung

Heart

Wound site

Collapsed lung

Air in the pleural space

Diaphragm

Figure 5-28 A pneumothorax occurs when air leaks into the pleural space between the parietal and visceral pleura. The lung collapses as air fills the pleural space and the two pleural membranes are no longer in contact with each other. © Jones & Bartlett Learning

Figure 5-29 X-ray of pneumothorax. Courtesy of Leonard V. Crowley, MD, Century College.

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A traumatic pneumothorax stems from • Decreased breath sounds over the affected any blunt trauma (e.g., vehicle air bag deploy- area ment) or penetrating injury (e.g., knife or gun- • Asymmetrical chest movement shot wounds) to the chest. These injuries can • Trachea and mediastinum deviation toward inadvertently occur during certain medical pro- the unaffected side cedures, such as chest tube insertion, cardiopul- • Anxiety monary resuscitation, and lung or liver • Tachycardia biopsies. • Pallor A tension pneumothorax is the most se- • Hypotension rious type of pneumothorax; it occurs when the Diagnostic procedures for pneumothorax pressure in the pleural space is greater than the consist of a history, physical examination, chest atmospheric pressure. This increased pressure X-ray, CT, and ABGs. Treatment usually involves arises due to trapped air in the pleural space or removal of the air and reestablishment of nega- entering air from a positive-pressure mechanical tive pressure, allowing for full expansion of the ventilator. The force of the air can cause the af- lungs. Such strategies may include a thoracen- fected lung to collapse completely and shift the tesis and placement of a chest drainage tube heart toward the uncollapsed lung (called a me- with suction (which removes fluid and reestab- diastinal shift), compressing the unaffected lung lishes negative pressure). Surgery may be re- and the heart (Figure 5-30). Tension pneumo- quired in some cases to correct and prevent thorax progresses rapidly and is fatal if not future episodes. During surgery, the leak is re- treated quickly. paired and a chemical may be used to scar the Clinical manifestations vary in severity area (pleurodesis). ­depending on the type of pneumothorax. These manifestations include the following signs and ◾◾ Acute Respiratory Distress Syndrome symptoms: Acute respiratory distress syndrome • Sudden chest pain over the affected lung (ARDS) is a sudden failure of the respiratory • Chest tightness system, often as a result of fluid accumulation • Dyspnea in the alveoli. ARDS has many other names, • Tachypnea such as shock lung, wet lung, and stiff lung.

Inspiration Expiration

One-way Valve valve (open) closed

Figure 5-30 Tension pneumothorax. A one-way valve allows air into the pleural space during inspiration, but not out during expiration. © Jones & Bartlett Learning

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Acute lung injury (ALI) refers to a slightly less septicemia, acute pancreatitis, drug overdose, severe form of ARDS. Multiple conditions can cardiopulmonary bypass, or transfusion reac- precipitate ARDS, including prolonged shock, tion) or pulmonary event (e.g., illicit drug and burns, aspiration, and smoke inhalation. This toxic gas inhalation, pneumonia, RSV, gastric condition involves an acute hypoxemia result- acid aspiration, near drowning, and fat embo- ing from a systemic event (e.g., trauma, lism) that is not cardiac in origin. ARDS develops

Acute Respiratory Distress Syndrome (ARDS)

Systemic inflammatory Lung injury response

Phase 1: Injury to pulmonary capillary endothelium

Phase 2: Injury to the basement membrane, interstitial space, and alveolar epithelium

Fluid, blood cells, protein, and fibrin fill the interstitial space Gas exchange is decreased The lung becomes noncompliant

Phase 3: Type II alveolar cell damage– surfactant production decreases

Atelectasis and hypoxemia develop– reactive pulmonary vasoconstriction

Phase 4: Fibrin and byproducts of cell damage line the alveoli

Hyaline membrane formation Respiratory acidosis Irreversible lung damage Cardiac failure Multisystem organ failure

Treatment: ARDS Pulmonary emboli (PE) Mechanical ventilation Thrombolytic therapy Intravenous steroids Embolectomy Medical support Oral anticoagulants Greenfield filter (vena cava)

Figure 5-31 Acute respiratory distress syndrome (ARDS). Madara, M., & Pomarico-Denino, V. (2008). Quick look nursing: Pathophysiology (2nd ed.). Sudbury, MA: Jones & Bartlett.

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rapidly, often within 90 minutes of a systemic pathogenesis to disseminated intravascular co- inflammatory response or within 48 hours of a agulation (DIC) (see the Hematopoietic Function lung injury. Other risk factors include the pres- chapter). ence of a chronic lung disease (e.g., emphysema, ARDS is a serious condition that can lead to chronic bronchitis, and asthma), alcoholism, age several complications: greater than 65 years, and mechanical ventila- • Respiratory failure tion. ARDS is fatal in one-third of cases. Indi- • Respiratory and metabolic acidosis viduals who survive will fully recover, but it may • Pulmonary fibrosis take as long as a year for them to regain com- • Pneumothorax plete lung function. • Bacterial lung infections (e.g., stasis pneu- In ARDS, injury to the alveoli and the capil- monia and VAP) lary membranes leads to the release of chemical • Decreased lung function inflammatory mediators (Figure 5-31; Figure 5-32). • Renal failure These mediators increase capillary permeability, • Stress ulcer promote fluid and protein accumulation in the • Thromboembolism alveoli, and damage surfactant-producing cells. • Muscle wasting These events result in decreased gas exchange, • Memory, cognitive, and emotional issues reduced pulmonary blood flow, and limited lung (due to brain damage as a result of the hy- expansion. Diffuse atelectasis and reduced lung poxia) capacity ensue. Lung damage progresses as neu- trophils migrate to the site, releasing proteases Clinical manifestations of ARDS can de- and other mediators once there. A hyaline mem- velop suddenly and include the following: brane, or a thin layer of tissue, forms in the al- • Dyspnea veoli and causes them to become stiff. • Labored (requiring the use of accessory Additionally, increased platelet aggregation pro- muscles), shallow respirations motes microemboli development. If the patient • Abnormal lung sounds (e.g., rales and survives, scattered necrosis and fibrosis are ap- rhonchi) parent throughout the lungs. ARDS is similar in • Productive cough with frothy sputum

Edema and exudate Type II pneumocyte Hyaline membrane Acute respiratory distress syndrome:

In ARDS, type I cells die as a result of diffuse alveolar damage.

Intra-alveolar edema follows, after which there is formation of hyaline membrane composed of proteinaceous axudate and cell debris. Alveolus

Neutrophil In the acute phase, the lungs are Capillary markedly congested and heavy.

Type II cells multiply to line the alveolar surface.

Interstitial inflammation is characteristic.

The lesion may heal completely or progress to interstitial fibrosis.

Figure 5-32 Acute respiratory distress syndrome.

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• Hypoxia is to maintain adequate oxygenation and respi- • Cyanosis ratory status. Such strategies include endotra- • Fever cheal intubation with a mechanical ventilator • Hypotension (including positive end-expiratory pressure • Tachycardia [PEEP]), high-dose oxygen therapy, corticoste- • Restlessness roids, inhaled beta agonists, and antibiotics (if • Confusion bacterial infections are present), as well as pre- • Lethargy vention and treatment of emboli (e.g., embolec- • Anxiety tomy, anticoagulants, and antiplatelet agents). Diagnostic procedures for ARDS consist of Other strategies include nutritional support a history, physical examination, ABGs, chest (e.g., enteral feedings), conservative fluid ther- X-ray, CT, and CBC. The main goal of treatment apy, sedation, and stress ulcer prophylaxis.

A l t e r a t i o n s i n V e n t i l a t i o n a n d P e r f u s i o n

◾◾ Atelectasis The clinical manifestations of atelectasis are Atelectasis refers to incomplete alveolar expan- due to impaired ventilation and perfusion: sion or collapse of the alveoli. It occurs when the • Diminished breath sounds walls of the alveoli stick together. Atelectasis may • Dyspnea be caused by the following conditions: • Tachypnea • Asymmetrical lung movement • Surfactant deficiencies (surfactant is the li- • Anxiety poprotein that coats the inside of the alveoli, • Restlessness allowing them to remain open at the end of • Tracheal deviation expiration) • Tachycardia • Bronchus obstruction (e.g., foreign objects, mucus plugs, and tumors) Diagnostic procedures for atelectasis include • Lung tissue compression (e.g., tumor, pneu- a history, physical examination, chest X-ray mothorax, and pleural effusion) (Figure 5-33), CT, bronchoscopy, ABGs, and CBC. Treatment of atelectasis focuses on treating the • Increased surface tension (e.g., pulmonary underlying causes (e.g., antibiotics, thoracentesis) edema) and reinflating the alveoli. Incentive spirometry • Lung fibrosis (e.g., emphysema) (a device to promote ventilation) is effective in When alveoli are not filled with air, they reinflating the alveoli. For more severe cases, con- shrivel much like a raisin. This ventilation issue tinuous positive airway pressure or endotracheal can, in turn, impair blood flow through the lung. intubation may be necessary for ventilation sup- Ineffective ventilation and perfusion impair gas port. Prevention strategies include increasing mo- exchange. Surgery and immobility increase the bility (e.g., turning and ambulating), coughing, risk for developing atelectasis for this reason. and deep breathing exercises (e.g., incentive spi- Atelectasis can occur in smaller or larger rometry) every 1–2 hours. Effective pain manage- areas. If only a small area is affected, the respi- ment and postoperative incisional splinting ratory rate will increase to control carbon diox- increase the likelihood that these interventions ide levels (increasing the respiratory rate will will be performed adequately. increase the excretion of carbon dioxide). The larger the area affected, the more severe the ◾◾ Acute Respiratory Failure symptoms experienced. Necrosis, infection (e.g., Acute respiratory failure (ARF) is a serious, pneumonia), and permanent lung damage can life-threatening condition that can be the result occur if the alveoli are not reinflated quickly. of many disorders (e.g., COPD, asthma, ARDS,

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A B

Figure 5-33 X-ray of atelectasis (a) Normal; (b) Atelectasis. Courtesy of Leonard V. Crowley, MD, Century College.

amyotrophic lateral sclerosis, alcohol or drug Clinical manifestations are usually evident overdose, and spinal cord injury). In ARF, the and result from the impaired gas exchange: oxygen levels become dangerously low (less • Shallow respirations than 50 mm Hg) or carbon dioxide levels • Headache become dangerously high (greater than 50 mm • Tachycardia Hg). Normally, oxygen levels are in the range of • Dysrhythmias 80–100 mm Hg and carbon dioxide levels are in • Lethargy the range of 35–45 mm Hg. The low oxygen • Confusion levels observed in ARF are not sufficient to meet the body’s metabolic needs, and the nervous Diagnostic procedures for ARF consist of a system quickly becomes affected by the short- history, physical examination, ABGs, chest age of oxygen. This gas level becomes progres- X-ray, electrocardiogram (EKG), and CBC. sively worse as the patient’s condition worsens. Treatment focuses on resolving the cause and Respiratory acidosis develops as the carbon maintaining adequate respiratory status. Strate- dioxide levels rise (see the Fluid, Electrolyte, and gies include oxygen therapy, endotracheal intu- Acid–Base Homeostasis chapter). The hypoxia and bation with ventilation support (may require a acidosis trigger a reflex pulmonary vasocon- tracheostomy), bronchodilators, antibiotics (if striction, further impairing gas exchange and bacterial infection is present), corticosteroids, increasing cardiac workload. The heart decom- and treatment of emboli (e.g., embolectomy and pensates from the lack of oxygen, which could anticoagulants). Cardiac support is usually in- lead to cardiac arrest. Respiratory arrest may evitable as the heart arrests under the strain occur as the respiratory system ceases all activity (e.g., cardiopulmonary resuscitation, sympatho- from the strain. mimetic medications, and inotropic agents).

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application to practice

© Bruce Rolff/Shutterstock, Inc.

Now that we have learned what can Once again, you go through the this patient is in any respiratory dis- go wrong in the respiratory system, usual thought process—who would die tress. The 40-year-old likely has the fl u. let’s put that knowledge into practice. fi rst, acute versus chronic conditions, Although extremely uncomfortable, While working in the emergency de- Maslow’s hierarchy of needs, and pa- the fl u is not usually life threatening in partment, the following patients tient safety. Starting with the 6-month- otherwise healthy adults. Also, this pa- need to be triaged. Which patient old, the combination of manifestations tient is not displaying any respiratory would have the highest priority? refl ects the possibility of epiglottitis or distress. Finally, consider the 59-year- • 6-month-old female with fever, some other acute infectious respiratory old with lung cancer. Lung cancer is audible inspiratory stridor, and process. Inspiratory stridor indicates often life threatening, but this patient restlessness that the child may have limited air en- was admitted with pain and nausea. • 25-year-old male with nasal tering the lungs due to an obstruction. Although nausea and pain are uncom- drainage and hoarseness The restlessness could be an indication fortable, they are not life-threatening • 40-year-old female with fever, of hypoxia. Additionally, the patient’s conditions. Furthermore, this patient severe body aches, and nasal young age increases the likelihood of is not exhibiting any manifestations in- congestion her decompensating quickly. This pa- dicating respiratory distress. After con- • 59-year-old male with stage III tient defi nitely needs to stay on your sidering all the patients to be triaged, it bronchiogenic carcinoma com- radar. The 25-year-old is exhibiting becomes clear that the 6-month-old plaining of nausea and pain manifestations likely due to laryngitis, should take priority and be seen fi rst that measures a 6 on a 0–10 which is not usually life threatening. because she is exhibiting signs of respi- scale Additionally, there is no indication that ratory distress.

application to practice

© Bruce Rolff/Shutterstock, Inc.

Emma is a 7-year-old girl who has suddenly worsened. They reported • ABG: pH 7.32, PaO2 72 mm Hg, been admitted to the intensive care that over the course of a few hours, PaCO2 48 mm Hg, HCO3 23 mm Hg unit with severe respiratory distress. her breathing became more and • CBC: WBC 16,000 mm3, neutro- Her parents report that 3 days ago she more labored, her fever spiked, and phils 8,000 mm3 developed a fever, aches, and nasal coughing started. The emergency de- 1. What are the priority nursing in- discharge, at which time she was partment healthcare provider diag- terventions for Emma? taken to her pediatrician. Her pedia- nosed her with a secondary bacterial 2. Describe the progression of this trician diagnosed her with the H1N1 pneumonia that had quickly pro- patient’s condition from the sim- strain of infl uenza. Emma was pre- gressed to acute respiratory distress ple flu to the life-threatening scribed antiviral drugs, and her par- syndrome. ARDS. ents were given instructions on fever In the emergency department, 3. What is the significance of her and hydration management. Twenty- Emma was intubated, placed on ven- lab findings? four hours ago, her parents said she tilator support, given bronchodila- 4. What do you think this patient’s was improving—her fever was mini- tors, and started on intravenous prognosis is? Give your mal, she was drinking more, and she antibiotics. Upon admission to the in- rationale. was beginning to play. Emma’s par- tensive care unit, she was stable but 5. What do you expect the treat- ents brought her into the emergency fragile. The following are her latest ment plan to include? department because her symptoms laboratory fi ndings:

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CHAPTER SUMMARY

The respiratory system plays a crucial role in supplying these diseases are preventable; therefore, identifying oxygen essential for cellular metabolism as well as those persons at increased risk and implementing pre- excreting the carbon dioxide waste product of that vention strategies can limit the severity or halt the metabolism. Because of this vital function, respiratory development of these debilitating conditions. Preven- disorders can cause extensive and devastating prob- tion, early detection, and prompt treatment will lems throughout the body. Often the healthcare team improve outcomes of persons suffering from these con- has a limited amount of time to identify and respond ditions, and nurses are uniquely positioned to have a to some of these respiratory disorders so as to control positive infl uence on their health. their negative consequences. Additionally, many of

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