pulmonary anatomy and physiology and the effects of...

Pulmonary Anatomy and Physiology and the Effects of COPD

Chronic obstructive pulmonary disease(COPD) refers to a group of chronic andprogressive respiratory diseases, includ-

ing both chronic bronchitis and emphysema(American Lung Association [ALA], 2003;O’Brien & Saiers, 2003; U.S. Department ofHealth and Human Services [USDHHS], 2003).As a progressive respiratory disease, COPD ischaracterized by irreversible airflow obstruc-tion resulting from chronic bronchitis and/oremphysema (Honig & Ingram, 2002; O’Brien &Saiers). These diseases often exist in combina-tion, complicating their recognition, assess-ment, and management.

EpidemiologyIncidence and PrevalenceCurrently claiming the lives of more than 117,000Americans annually, COPD is the fourth leadingcause of death in the United States (ALA, 2003;USDHHS, 2003). Of the 10 leading causes of deathin the United States, COPD is the only diseasewhose mortality rate is increasing (Honig & In-gram, 2002; O’Brien & Saiers, 2003).

vol. 23 • no. 3 • March 2005 © 2005 Lippincott Williams & Wilkins, Inc. Home Healthcare Nurse 167

Chronic obstructive pulmonary disease (COPD) is thefourth leading cause of death in the United States, yetit has received relatively little attention in the litera-ture compared with other leading killers such as can-

Stephanie Lacerda Farquhar, RN, MS, CNS,and Lesley Fantasia, RN, MSN, CCRN

cer and heart disease. To identify, assess, intervene, and care for patients with COPD in thehome, a comprehensive understanding of this disease and its effects is imperative. This ar-ticle discusses the epidemiology of COPD, reviews normal pulmonary anatomy and phys-iology, and explains the physiological changes to the pulmonary system caused by COPD.

By the year 2020, COPD is projected to be thethird leading cause of death in the United Statesfor both men and women (USDHHS, 2003). Al-though more than 16 million Americans currentlyhave COPD, estimates indicate roughly 24 millionadults have impaired lung function, suggestingthat COPD is significantly underdiagnosed (USD-HHS, 2003).

Overall, COPD affects men more than women,and whites are more frequently affected than areAfrican Americans. Although mortality is increas-ing in both sexes, the mortality rate in females isincreasing far more rapidly than in men, with fe-male mortality rates more than doubling betweenthe years 1980 (20.1 deaths/100,000 women) and2000 (56.7 deaths/100,000 women) (Mannino et al.,2002; O’Brien & Saiers, 2003; USDHHS, 2003).

The cause for the rapid increase in mortalityfor females remains suppositional but may be a re-flection of the increase in smoking by women inthe United States compared with men (Mannino et

al., 2002). Overall, the COPD death rate was 46%higher in males than females and 63% higher inwhites than African Americans (USDHHS, 2003).

Risk FactorsCigarette smoking is the single most importantrisk factor for COPD, accounting for 80% to 90% ofCOPD diagnoses (ALA, 2003; UDHHS, 2003). Ap-proximately 15% to 20% of smokers developCOPD, suggesting that host factors (most likelygenetic) may also contribute to the pathogenesisof the disease (Snider, 2003). Occupational expo-sure to dusts, chemicals, and passive exposure tocigarette smoke are the other main causes (USD-HHS). Smoking cessation and overall avoidanceare the salient actions one can take to preventCOPD or stop its progression (USDHHS).

Chronic bronchitis (CB) accounts for as manyas 11 million of the 16 million patients with COPD(ALA, 2003). The ALA (2003) defines CB as an “in-flammation and eventual scarring of the lining ofthe bronchial tubes.” Females of both races hadhigher rates of chronic bronchitis than did theirmale counterparts across all age groups (USDHHS,2003). CB is most prevalent in the 65� age group(Honig & Ingram, 2002; USDDHS). In 2001, 3.7 mil-lion males, in contrast with 7.5 million females,had a diagnosis of CB (ALA).

Emphysema affects as many as 3 million Amer-icans (ALA, 2003; USDHHS, 2003). Defined byHonig & Ingram (2002) as a “permanent and de-structive enlargement of airspaces distal to theterminal bronchioles without obvious fibrosis andwith loss of normal architecture,” emphysema isseen more commonly in men than women (p. 1).Fifty-seven percent of those with the condition aremale (ALA). Gender is the only demographic onemphysema that is dissimilar to those seen with

CB. As in CB, whites are af-fected by emphysema more fre-quently than their African-American counterparts, andthose older than 65 years havethe highest prevalence of thisdisease (USDHHS).

COPD’s Impact In addition to the human toll,COPD exacts an enormous eco-nomic toll on the healthcaresystem and society. The USD-HHS (2003) and the ALA (2003)report that the annual cost to

the nation for COPD in 2002 was a staggering $32.1billion. Direct healthcare expenditures accountedfor $18 billion of this total. The remaining $14.1 bil-lion was in indirect expenses related to morbidity,disability, and premature mortality (USDHHS).

Equally stunning are the reported Medicare ex-penses for beneficiaries with COPD, which were2.5 times that of the expenditures for all other pa-tients (USDHHS, 2003). Seventy percent of COPD-related costs are accounted for by the 10% of pa-tients with the most severe symptoms of thedisease (O’Brien & Saiers, 2003).

In 2000 alone, COPD was responsible for 8 mil-lion physician office and outpatient office visits(Mannino et al., 2002). Emergency departments(ED) and hospitals also feel the effects of this dis-ease because many patients require emergent

168 Home Healthcare Nurse www.homehealthcarenurseonline.com

Of the 10 leading causes of death in the UnitedStates, COPD is the only disease for which themortality rate is increasing. By the year 2020,COPD is projected to move from the fourthleading cause of death in the United States tothe third for both men and women.

treatment and hospitalization during exacerba-tions. COPD was responsible for 1.5 million ED vis-its and 726,000 hospitalizations in the year 2000(Mannino et al.).

With COPD on the rise, nurses have a pivotalrole in caring for these patients in a variety ofpractice settings. Proper assessment, early recog-nition, and treatment of COPD may change thecourse of this disease for patients. A fundamentalunderstanding of pulmonary anatomy and physi-ology is the foundation nurses must have to as-sess and intervene on behalf of patients withCOPD.

Pulmonary AnatomyThis article focuses on the structure and functionof the lower respiratory tract, which consists ofthe trachea, the left and right mainstem bronchi,the lungs, bronchioles, and alveoli. The pul-monary system’s main purpose is to exchangegases between the air and the blood. This is ac-complished through three processes: ventilation,diffusion, and perfusion. The pulmonary system isresponsible for ventilation and diffusion, whereas

the cardiovascular system is responsible for per-fusion.

Ventilation is defined simply as “the movementof air into and out of the lungs” (McCance &Huether, 2002, p. 1082).

Diffusion is “the movement of gases between airspaces in the lungs and bloodstream” (McCance &Huether, 2002, p. 1082).

The trachea, which connects the larynx to thebronchi, is part of the conducting airways of thepulmonary system (Figure 1). The conducting air-ways are a set of “tubes” that carry air to all theareas of the lungs. The trachea divides into theleft and right mainstem bronchi (McCance &Huether, 2002). The right and left mainstembronchi enter each respective lung. Both lungsare divided into lobes: three in the right lung, andtwo in the left. Each lobe divides into segmentsand lobules.

The right and left mainstem bronchi branch offseveral times into smaller conducting airways,ending at the terminal bronchioles. Air is deliv-ered to each section of the lungs through theseairways. This division results in very small air-

vol. 23 • no. 3 • March 2005 Home Healthcare Nurse 169

Figure 1. Pulmonary anatomy. From K. L. Moore & A. F. Dalley II, 1999. Clinical Oriented Anatomy,

(4th ed.). Baltimore: Lippincott Williams & Wilkins. Copyright 1999 by Lippincott Williams & Wilkins.

Reprinted with permission.

ways in the gas exchange portions of the lungsthat have decreased airflow compared with theirlarger counterparts. The end effect is optimal dif-fusion (McCance & Huether, 2002).

The gas exchange airways, consisting of therespiratory bronchioles, alveolar ducts, and alve-oli, start where the conducting airways end. Inthese airways “oxygen (O2) enters the blood andcarbon dioxide (CO2) is removed from it” (Mc-Cance & Huether, 2002, p. 1084). The alveoli arethe main gas exchange components of the pul-monary system.

Pulmonary CirculationBlood enters the pulmonary circulation from theright ventricle of the heart. The unoxygenatedblood pumped from this chamber enters the pul-monary artery, which splits into the right and leftpulmonary arteries (Figure 2). These two arteriestransport the unoxygenated blood from the right

side of the heart to each respective lung. The pul-monary arteries, much like the conducting air-ways, divide multiple times so that each bronchusand bronchiole has an accompanying artery or ar-teriole.

Arterioles divide at the terminal bronchiole tomake a network of pulmonary capillaries that sur-round the gas exchange airways. Capillary wallsoften fuse with the alveolus membrane, creatingthe alveolocapillary membrane. Gas exchange inthe blood occurs across this membrane. Any dis-ease that thickens the alveolocapillary membraneimpairs gas exchange (McCance & Huether, 2002).

Four pulmonary veins, two from each lung, carryoxygenated blood from the lungs to the left side ofthe heart. Each vein drains several pulmonary cap-illaries, and unlike the pulmonary arteries, theveins are dispersed randomly throughout the lung.The oxygenated blood is deposited into the leftatrium, then the left ventricle (LV). The LV then


Figure 2. Pulmonary vasculature. From K. L. Moore & A. F. Dalley II, 1999. Clinical Oriented Anatomy,

(4th ed.). Baltimore: Lippincott Williams & Wilkins. Copyright 1999 by Lippincott Williams & Wilkins.

Reprinted with permission.

pumps the oxygenated blood out into the aorta,which delivers it into systemic circulation.

Ventilation and Gas Exchange“Ventilation is the mechanical movement of gas orair into and out of the lungs” (McCance & Huether,2002, p. 1088). A patient’s respiratory rate is his orher ventilatory rate. With each breath in, oxygenis inhaled, and upon exhalation CO2 is eliminated.This process is essential to maintain a normalacid base balance. The only definitive way to as-sess adequacy of ventilation is through obtainingan arterial blood gas to measure the arterial CO2(PaCO2) level. Normal is 40 mm Hg.

Gas exchange has four basic steps:

■ Ventilation, ■ Diffusion of O2 across the

alveolocapillary membrane,■ Perfusion of the systemic

capillaries with oxygenatedblood, and

■ Diffusion of O2 from the cap-illaries to the cells (Mc-Cance & Huether, 2002).

■ When referring to CO2 re-moval, the steps are re-versed:

• Diffusion of CO2 from thecells into the systemic capillaries,

• Pulmonary capillary perfusion by unoxy-genated venous blood,

• Diffusion of CO2 into the alveoli, and• Removal of CO2 by the exhalation phase of

ventilation (McCance & Huether, 2002).

CO2 must be eliminated on a continual basis tomaintain the body’s acid base balance. Acid basebalance is monitored within the body by chemore-ceptors. Chemoreceptors located near the body’srespiratory center are sensitive to changes in thepH of cerebrospinal fluid (CSF) (McCance &Huether, 2002). When there is inadequate ventila-tion, the pH drops and PaCO2 rises. This stimu-lates the respiratory center to increase the size ofeach breath and the respiratory rate to removethe CO2. These receptors are sensitive to smallchanges in pH.

If hypoventilation is chronic, as may be thecase in patients with COPD, chemoreceptorsloose their sensitivity and control PaCO2 inade-quately. In addition, prolonged hypoventilation

can result in compensation by the renal system,with the kidneys retaining bicarbonate to normal-ize the body’s pH. This deletes the effect a low pH,as a result of a high PaCO2, has on the respiratorydrive (McCance & Huether, 2002).

When central chemoreceptors fail, peripheralchemoreceptors step in to regulate pulmonaryfunction and acid base balance. Peripheralchemoreceptors are sensitive to the amount ofoxygen in arterial blood (PaO2). Therefore, the pa-tient’s stimulus to breathe is originated from a lowPaO2 sensed by the peripheral receptors.

If the PaO2 is increased too significantly by in-stituting supplemental O2, the peripheralchemoreceptors will not stimulate breathing. Thiscreates a rise in PaCO2, ultimately resulting inapnea (McCance & Huether, 2002). A PaO2 of 60 is

optimal. If adequate oxygenation, as reflected byarterial blood gases (ABG) monitoring, cannot beachieved without loss of respiratory drive, me-chanical ventilation must be instituted.

COPDCOPD is characterized by airflow limitation that isnot fully reversible (Snider, 2003). The mecha-nisms of airflow limitation are different in both CBand emphysema.

In CB, airflow is limited because of inflamma-tion and thickening of bronchial walls. This in-flammation is caused by exposure to inhaled irri-tants, such as cigarette smoke (McCance &Huether, 2002). The inflammation causes in-creased sputum production, which often becomesa source of infection (McCance & Huether).

Airflow limitation in emphysema is caused byactual structural remodeling in lung tissue in com-parison to the solely inflammatory changes seenin CB. In emphysema, gas exchange airways arepermanently enlarged, which results in the de-struction of the alveolar walls without fibrosis


Careful assessment and monitoring of the patientwith COPD is essential when supplemental O2 isused because of the risk of respiratory depression.It is imperative to remember that COPD itself is absolutely irreversible.

being present (McCance & Huether, 2002). Em-physema has two main causes: an inherited en-zyme deficiency (1%–2% of cases) or injury to thelung from inhaled toxins (McCance & Huether).

The diagnosis of COPD may be difficult in theearly stages of the illness and may be misdiag-nosed as chronic bronchitis, emphysema, orasthma. Accurate diagnosis of COPD is based onpatient history, signs and symptoms, physical ex-amination, chest radiography, ABG, and pul-monary function tests (PFTs).

Signs and Symptoms of COPDEarly COPDIn the early phase of COPD, patients may begin toexperience wheezing, chronic productive cough,and minimal shortness of breath. Patients may notbe aware of these subtle symptoms (Snider, 2003).However, the patient’s quality of life diminishes asthe disease progresses. Symptoms include wors-ening dypsnea, progressive exercise intolerance,intermittent chest illness (occurring with greaterfrequency), increased cough, purulent sputum,with subsequent increased intervals and severityof acute exacerbations (Table 1) (Kleinschmidt,2004; Snider).

Acute Phase of COPDIn the acute phases of the illness, exacerbationscause hypoxemia and hypercapnia. Hypoxemiain patients with COPD is most commonly causedby hypoventilation (McCance & Huether, 2002).Hypercapnia, defined as “increased carbon diox-

ide in the arterial blood” (McCance & Huether,2002, p. 1108) is caused by hypoventilation of thealveoli.

Patients notice a significant decline in theirquality of life during exacerbation. Supplementaloxygen or mechanical ventilatory support may berequired during these phases (ALA, 2003). Carefulassessment of the patient is essential when sup-plemental O2 is used because of the risk of respi-ratory depression discussed earlier.

Physical Examination The physical examination of a patient with COPDalso changes with disease progression. In theearly phase of the disease, the patient maydemonstrate:

• Prolonged expiration,• Wheezing on forced exhalation (Snider, 2003),• Chronic cough, which may be present with

varying degrees of sputum production, and• “Barrel chest.”

As airflow obstruction progresses because ofinflammation (in CB) or structural damage to air-way walls (emphysema), air gets trapped in thelungs, making them hyperinflated (McCance &Huether, 2002; Snider, 2003). The prolonged,forced expiration seen in patients with COPD isa result of the body trying to fully exhale thetrapped gases. Hyperinflation eventually causeschest wall deformity, described as “barrelchest.”


Chronic Bronchitis Emphysema COPD

Airflow obstruction Yes Yes Yes (as a result of inflamma-tion and destruction)

Wheezing Occasional Minimal Occasional

Dyspnea Late in disease course Yes Yes (worsening later incourse)

Productive cough Yes (classic sign) Occasional (later indisease course) Yes (chronic)

Exercise intolerance Yes Yes Yes

Prolonged expiration Yes Yes Yes

Barrel chest Occasional Yes (classic sign) Occasional

Table 1. Signs and Symptoms of Chronic Bronchitis, Emphysema, and COPD

Note. COPD = chronic obstructive pulmonary disease.

Late in the disease:

• Accessory muscles will be used to breathe,• Purse-lip breathing may be evident,• Breath sounds become decreased,• Patient will sit in tripod position to relieve

dyspnea,• Coarse crackles and wheezing often can be

auscultated, • Heart sounds are distant, • Evidence of right-sided heart failure devel-

ops, including: • Edema• An enlarged, tender liver (Kleinschmidt,

2004; Snider, 2003).

Right-sided heart failure de-velops because of increased re-sistance to flow in the lungscaused by the narrowing and/orobstruction of the pulmonaryarteries caused by COPD (Klein-schmidt, 2004; Snider, 2003).Pulmonary hypertension mayalso occur in the late phase ofCOPD secondary to severe hy-poxemia and hypercapnia. It isassociated with right-sidedheart failure and indicative of apoor prognosis (National Heart, Lung and BloodInstitute, National Institutes of Health & the WorldHealth Organization, 1998).

DiagnosisChest radiography is a helpful tool in diagnosingCOPD. Flattening of the diaphragm and overdis-tention of the lungs can be seen (Snider, 2003).ABG analysis provides information regarding theseverity and progression of the disease. ABG re-sults show mild to moderate hypoxemia in theearly stages of the disease. Hypoxemia graduallybecomes more severe. Eventually, hypoxemia andhypercapnia are seen together (Snider, 2003).Blood gas abnormalities worsen with disease pro-gression and acute exacerbation and may worsenduring exercise and sleep (Snider). A pH of 7.3 orless is indicative of acute respiratory compromise(Kleinschmidt, 2004).

Lastly, PFTs provide important informationthat is necessary in diagnosing and monitoringthe progression of COPD (Snider, 2003). PFTs pro-vide information about the functional quality ofthe lung. The values most important in diagnosing

COPD are the forced expiratory volume in 1 sec-ond (FEV1), the forced vital capacity (FVC), thetotal lung capacity (TLC), and the residual volume(RV). Patients with COPD have an increased ornormal TLC and FVC, with an increase in RV(Kleinschmidt, 2004). This is a result of the pro-gressive airflow obstruction.

The FEV1 and the FEV1/FVC ratio decrease pro-gressively as the disease worsens, further demon-strating lung damage (Snider, 2003). The FEV1 isconsidered to be the gold standard in diagnosingairflow obstruction because of its accuracy inmeasuring airway dynamics (Snider). Patientswith COPD demonstrate poor or absent re-versibility with bronchodilator therapy duringPFT (Kleinschmidt, 2004).

It is imperative to remember that COPD itself isabsolutely irreversible. The focus of treatment andmanagement of this disease must be placed onstopping its progression through eliminating ex-posure to causative agents and limiting acute “ex-acerbations” of the disease by careful monitoringfor, and treatment of, infection. Pharmacologicmaintenance with bronchodilators will help main-tain the patient’s functional status and ultimatelyreduce the number of acute episodes they experi-ence.

ConclusionCOPD is a formidable health threat for manyAmericans, with the numbers affected anticipatedto rise. A clear understanding of the pulmonarysystem, COPD, and its progression and treatmentare essential for home health nurses, who will beproviding care for more of these patients in theirhomes. This is a disease that greatly affects a pa-tient’s quality of life. Helping to maintain the pa-tient’s health and limit acute exacerbations willhelp preserve the patient’s functional abilities andsubsequently quality of life.


The focus of treatment and management of this disease must be placed on stopping its progres-sion through eliminating exposure to causativeagents and limiting acute “exacerbations” of thedisease by careful monitoring for, and treatmentof, infection.

Stephanie Lacerda Farquhar, RN, MS, CNS, is aStaff Nurse on the Medical Intensive Care Unit atRhode Island Hospital in Providence, RI. Address forcorrespondence: 358 Dwelly Street, Fall River, MA02724 ([email protected]).

Lesley Fantasia, RN, MSN, CCRN, is a Clinical Su-pervisor at Saint Anne’s Hospital in Fall River, MA([email protected]).

The authors of this article have no significant ties, fi-nancial or otherwise, to any company that might havean interest in the publication of this educational activity.

REFERENCESAmerican Lung Association. (2003, October). Chronic ob-

structive pulmonary disease (COPD) fact sheet. Re-trieved May 9, 2004 from http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35020

Honig, E., & Ingram, R. H., Jr. (2002). Chronic bronchitis, em-physema, and airway obstruction (chap. 258). RetrievedApril 4, 2004, from http://harrisons.accessmedicine.com/server-java/Arknoid/amed/harrisons/co_chap-ters/ch258/ch258_p01.html

Kleinschmidt, P. (2004, April 8). Chronic obstructive pul-monary disease and emphysema. Retrieved fromhttp://www.emedicine.com/emerg/topic99.htm

Mannino, D. M., Homa, D. M., Akinbami, L. J., Ford, E. S.,& Redd, S. C. (2002). Chronic obstructive pulmonarydisease surveillance—United States, 1971–2000. Mor-bidity and Mortality Weekly Report, 51(SS06), 1–16. Re-trieved May 9, 2004 from http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5106a1.htm

McCance, K. L., & Huether, S. E. (2002). Pathophysiology:The biologic basis for disease in adults & children.Philadelphia: Mosby.

National Heart, Lung and Blood Institute, National Insti-tutes of Health & the World Health Organization.(1998). Global initiative for chronic obstructive pul-monary disease: IV. Pathogenesis, pathology andpathophysiology. Retrieved 2004 from http://uptoda-teonline.com

O’Brien, A., & Saiers, J. (2003). Update on epidemiol-ogy and pathogenesis of chronic obstructive pul-monary disease. Clinical Pulmonary Medicine,10(2), 63–66.

Snider, G. L. (2003, February 27). Diagnosis of chronic ob-structive pulmonary disease. Retrieved April 4, 2004,from http://uptodateonline.com

U.S. Department of Health and Human Services. (2003).Data fact sheet: Chronic obstructive pulmonary disease(NIH Publication No. 03-5229). Bethesda, MD: Na-tional Heart, Lung and Blood Institute.


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GENERAL PURPOSE

To present registered professional nurses withinformation on the epidemiology of chronicobstructive pulmonary disease (COPD) and toexplain how COPD changes the anatomy andphysiology of the pulmonary system.

LEARNING OBJECTIVES

After reading this article and taking this test,you will be able to:

1. List the epidemiology and manifestations ofchronic obstructive pulmonary disease(COPD).

2. Outline pulmonary physiology andpathophysiology as they pertain to thedevelopment and progression of COPD.

3. Discuss the effects of advancing COPD andimplications for nursing practice.

1. Of the ten leading causes of deathin the United States, COPD is theonly diseasea. that is completely preventable.b. whose overall incidence has decreased.c. that is totally irreversible.d. whose mortality rate is increasing.

2. The single most common risk factor for COPD isa. occupational exposure.b. cigarette smoking.c. genetic predisposition.d. impaired immunity.

3. Chronic bronchitis is especiallyprevalent amonga. older adults.b. males.c. African Americans.d. children.

4. A classic manifestation of emphysema isa. wheezing.b. productive cough.c. crackles.d. barrel chest.

5. A classic manifestation of chronicbronchitis isa. wheezing.b. productive cough.c. dyspnea.d. barrel chest.

6. The movement of gases betweenair spaces in the lungs and bloodstream is calleda. ventilation.b. aeration.c. diffusion.d. perfusion.

7. The main gas exchange components of the pulmonary system are thea. alveoli.b. respiratory bronchioles.c. bronchi.d. terminal bronchioles.

8. Unoxygenated blood is transportedfrom the right side of the heart toeach lung by thea. pulmonary veins.b. right ventricle.c. pulmonary arteries.d. aorta.

9. The first step of the removal of carbon dioxide (CO2) from theblood isa. pulmonary capillary perfusion by

unoxygenated venous blood.b. diffusion of CO2 into each

lung's alveoli.c. perfusion of the systemic capillaries with

oxygenated blood.d. diffusion of CO2 from the cells into the

systemic capillaries.

10. With inadequate ventilationa. pH drops and PaCO2 rises.b. pH and PaCO2 both rise.c. pH rises and PaCO2 drops.d. pH and PaCO2 both drop.

11. With emphysema, airflow is limited primarily bya. extensive fibrosis.b. persistent inflammation.c. structurally remodeled lung tissue.d. thickened bronchial walls.

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CE TestPulmonary Anatomy and Physiology and the Effects of COPD

CE TEST QUESTIONS


12. An early sign/symptom of COPD isa. exercise intolerance.b. prolonged expiration.c. intermittent chest illness.d. copious purulent sputum.

13. Hypoxemia in COPD patients ismost often caused bya. persistent cough.b. infection.c. hyperinflation.d. hypoventilation.

14. Patients who have advancedCOPD tend to assume which position to facilitate breathing?a. tripodb. semi-Fowler'sc. side-lyingd. supine

15. An especially poor prognosticsign in patients who have COPD isa. right-sided heart failure.b. pulmonary hypertension.c. wheezing on forced exhalation.d. moderate dyspnea.

16. As COPD worsens, which pulmonary function value decreases progressively?a. forced vital capacityb. total lung capacityc. forced expiratory volume in one secondd. residual volume

Test Answers: Darken one for your answer to each question.B

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