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TABLE 13-4. Causes of Respiratory Acidosis
Central
Opiates
Sedatives
Stroke
Trauma
Head injury
Status epilepticus
Perfusion abnormalities
Pulmonary embolism
Cardiac arrest
Airway abnormalities
Obstruction
Asthma
Chronic obstructive pulmonary disease
Pneumonia
Pulmonary edema
Acute respiratory distress syndrome
Neuromuscular
Brainstem or cervical cord injury
Guillain-Barré syndrome
Myastenia gravis
Parenteral nutrition
LEARNING POINTS
1. Can an acid–base disorder exist if a patient presents with
a normal pH?
ANSWER: Yes, an acid–base disorder can still exist even when
the pH is within the normal range. pH is determined by the ratio
of base to acid as opposed to the individual concentration of one
(ie, acid or base) independently. Therefore, an acidosis can be
present without an acidemia if a coexisting alkalosis is present.
Conversely, an alkalosis can be present without an alkalemia if a
coexisting acidosis is present. In these settings, evaluation of the
PaCO2 and HCO3 reveals abnormal values (hence a pathophysiologic process), but each offsets the other and the net effect on pH
is negligible. Careful evaluation of the patient’s history, clinical
presentation, physical exam, and laboratory values is necessary
to identify the acid–base disorders that are present.
2. What are the steps to follow to assess an ABG?
ANSWER: The rst step is to determine if an acidemia or alkale-
mia is present. This is done by evaluating the pH. Once the correct categorization is made, the second step is to determine if
the primary cause is metabolic or respiratory. This is performed
by assessing the PaCO2 and the HCO3 on the ABG. Once the
primary cause is determined, the opposing side should compensate. The third step is to assess if the degree of compensation
TABLE 13-5. Causes of Respiratory Alkalosis
CNS-Respiratory Stimulation
Anxiety
Pain
Fever
Sepsis
Pregnancy
Progesterone derivatives
Salicylates
Cerebrovascular accidents
Hypoxemia
Pneumonia
Congestive heart failure
High altitude
Pulmonary edema
Pulmonary embolism
is appropriate. If it is not, then a secondary disorder is present.
Finally, if the primary problem is metabolic acidosis, or metabolic
alkalosis, then the anion gap or urinary chloride, respectively,
should be assessed to assist with identication of the possible
cause.
3.
How can the anion gap be used to assess acid–base
disorders?
ANSWER: The anion gap is an estimate of the relative abun-
dance of unmeasured anions. It can suggest the possible causes
of metabolic acidosis, particularly if the disorder is secondary to
an accumulation of nonvolatile acids or a net loss of bicarbonate. When the anion gap is normal, the acidosis is usually caused
by a loss of bicarbonate ions; common causes include diarrhea,
early renal insufciency, and infusion of large amounts of isotonic
saline. When the anion gap is elevated, causes may include lactic acidosis, ketoacidosis, end- stage renal failure, or certain toxic
ingestions. Correction of the anion gap for hypoalbuminemia can
improve the accuracy of this approach. The anion gap represents
one factor that can help determine the etiologic cause of metabolic acidosis and should not be interpreted as absolute, especially in a complex intensive care unit (ICU) patient.
REFERENCES
1. Berend K, de Vries AP, Gans RO. Physiological approach to assessment of
acid- base disturbances. N Engl J Med. 2014;371(15):1434-1445.PubMed
2. Marino PL. Marino’s e ICU Book. 4th ed. Philadelphia, PA: Wolters
Kluwer Health/Lippincott Williams & Wilkins; 2014.
3. Adrogué HJ, Madias NE. Management of life- threatening acid- base
disorders. Second of two parts. N Engl J Med. 1998;338(2):107-111.
PubMed
4. Narins RG, Emmett M. Simple and mixed acid- base disorders: a practical
approach. Medicine (Baltimore). 1980;59(3):161-187.PubMed
5. Weil MH, Rackow EC, Trevino R, et al. Dierence in acid- base state
between venous and arterial blood during cardiopulmonary resuscitation.
N Engl J Med. 1986;315(3):153-156.PubMed

CHAPTER 13 • ARTERiAl Blood GAsEs And ACid–BAsEBAlAnCE 297
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6. Faridi AB, Weisberg LS. Acid-Base, Electrolyte and Metabolic
Abnormalities. Parrillo JE, and Dellinger RP, eds. Critical Care Medicine:
Principles of Diagnosis and Management in the Adult. 3rd ed. Philadelphia,
PA: Mosby Elsevier; 2008:1203-1243.
7. Ranieri VM, Rubenfeld GD, ompson BT, et al. Acute respiratory
distress syndrome: the Berlin Denition. JAMA. 2012;307(23):2526-2533.
PubMed
8. Wilson RF. Critical Care Manual: Applied Physiology and Principles of
erapy. 2nd ed. Philadelphia, PA: F.A. Davis Company; 1992.
9. Figge J, Jabor A, Kazda A, et al. Anion gap and hypoalbuminemia. Crit
Care Med. 1998;26(11):1807-1810.PubMed
10. Al-Jaghbeer M, Kellum JA. Acid- base disturbances in intensive care
patients: etiology, pathophysiology and treatment. Nephrol Dial
Transplant. 2015;30(7):1104-1111.PubMed
11. Gilx BM, Bique M, Magder S. A physical chemical approach to
the analysis of acid- base balance in the clinical setting. J Crit Care.
1993;8(4):187-197.PubMed
12. Kellum JA. Disorders of acid- base balance. Crit Care Med. 2007;35(11):2630-
2636.PubMed
13. Salem MM, Mujais SK. Gaps in the anion gap. Arch Intern Med. 1992;152(8):
1625-1629.PubMed
14. Singer M, Deutschman CS, Seymour CW, et al. e ird International
Consensus denitions for sepsis and septic shock (sepsis-3). JAMA.
2016;315(8):801-810.
15. Aduen J, Bernstein WK, Khastgir T, et al. e use and clinical importance
of a substrate- specic electrode for rapid determination of blood lactate
concentrations. JAMA. 1994;272(21):1678-1685.PubMed
16. Levy MM, Evans LE, Rhodes A. e Surviving Sepsis Campaign Bundle:
2018 Update. Crit Care Med. 2018;46(6):997-1000.PubMed
17. Jansen TC, van Bommel J, Schoonderbeek FJ, et al. Early lactate- guided
therapy in intensive care unit patients: a multicenter, open- label,
randomized controlled trial. Am J Respir Crit Care Med. 2010;182(6):752-
761.PubMed
PubMed
18. Vincent JL, Dufaye P, Berré J, et al. Serial lactate determinations during
circulatory shock. Crit Care Med. 1983;11(6):449-451.PubMed
19. Vincent JL, De Backer D. Circulatory shock. N Engl J Med.
2013;369(18):1726-1734.PubMed
20. Marik PE. Early management of severe sepsis: concepts and controversies.
Chest. 2014;145(6):1407-1418.PubMed
21. Reinhart K, Kuhn HJ, Hartog C, et al. Continuous central venous and
pulmonary artery oxygen saturation monitoring in the critically ill.
Intensive Care Med. 2004;30(8):1572-1578.PubMed
22. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign:
International Guidelines for Management of Sepsis and Septic Shock:
2016. Crit Care Med. 2017;45(3):486-552.PubMed
23. Pope JV, Jones AE, Gaieski DF, et al. Multicenter study of central venous
oxygen saturation (ScvO2) as a predictor of mortality in patients with
sepsis. Ann Emerg Med. 2010;55(1):40-46.e1.PubMed
24. Stewart PA. Modern quantitative acid- base chemistry. Can J Physiol
Pharmacol. 1983;61(12):1444-1461.PubMed
25. Kellum JA. Determinants of blood pH in health and disease. Crit Care.
2000;4(1):6-14.PubMed
26. Morgan TJ. e meaning of acid- base abnormalities in the intensive care
unit: part III. Eects of uid administration. Crit Care. 2005;9(2):204-211.
PubMed
27. Rose DB, Post TW. Clinical Physiology of Acid-Base and Electrolyte
Disorders. 5th ed. New York, NY: McGraw-Hill; 2001.
28. Dzierba AL, Abraham P. A practical approach to understanding
acid- base abnormalities in critical illness. J Pharm Pract. 2011;24(1):17-
26.PubMed
29. Kaplan LJ, Frangos S. Clinical review: acid- base abnormalities in the
intensive care unit. Part II. Crit Care. 2005;9(2):198-203.PubMed
30. Mehta AN, Emmett JB, Emmett M. GOLD MARK: an anion gap
mnemonic for the 21st century. Lancet. 2008;372(9642):892.PubMed

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QUICKVIEW | Venous Total Carbon Dioxide Content (Venous Serum Bicarbonate)
PARAMETER DESCRIPTION COMMENTS
Common reference range
Adults 22–30 mEq/L Venous bicarbonate can be 1.5–3 mEq/L
higher than arterial measure of
bicarbonate
Critical value <10 mEq/L or >40 mEq/L Reference range and critical values may
vary based on local laboratory standards
Inherent activity Yes Primary substance responsible for
buffering acids
Location
Production Byproduct of typical cell metabolism
Storage Exchanged via circulation
Secretion/excretion Renal excretion (reabsorption occurs at
proximal tubule)
Causes of abnormal values
−
High Metabolic alkalosis and respiratory
acidosis
Change in HCO
of metabolic acid–base disorders. In
contrast, change in HCO
method of compensation for respiratory
disorders.
is the primary cause
3
−
is the primary
3
Low Metabolic acidosis and respiratory
alkalosis
Signs and symptoms
High level Related to primary process
Low level Related to primary process
After event, time to….
Initial elevation 6–12 hr to initiate compensation Assumes acute insult
Peak values None (will rise until pH balanced) Assumes insult not yet removed
Normalization 3–5 days to complete compensation Assumes insult removed and
nonpermanent damage
Causes of spurious results Inadvertent venous sampling, delayed
time to analysis

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QUICKVIEW | Arterial Partial Pressure of Carbon Dioxide
PARAMETER DESCRIPTION COMMENTS
Common reference range
Adults 35–45 mm Hg
Critical value >70 mm Hg (may require mechanical
ventilation)
Inherent activity Yes Primary volatile acid in the body
Location
Production Generated intracellularly from carbon
dioxide and water
Storage N/A
Secretion/excretion Excreted by the lungs during expiration
Causes of abnormal values
High Respiratory acidosis and metabolic
alkalosis
Change is PaCO
respiratory acid–base disorders. In contrast,
is the primary cause of
2
change in PaCO2 is the primary method of
compensation for metabolic disorders.
Low Respiratory alkalosis and metabolic
acidosis
Signs and symptoms
High level Respiratory failure
Low level Related to primary process
After event, time to….
Initial elevation Minutes to hours Assumes acute insult
Peak values None Assumes insult not yet removed
Normalization Hours to days Assumes insult removed and nonpermanent
damage
Causes of spurious results Inadvertent venous sampling, delayed
Higher carbon dioxide content
time to analysis
N/A = not applicable.

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Pulmonary Function and
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RelatedTests
14
OBJECTIVES
After completing this chapter, the
reader should be able to
•
Identify common pulmonary
function tests and list their purpose
and limitations
•
Describe how pulmonary function
tests are performed and discuss
factors affecting the validity of the
results
•
Interpret commonly used pulmonary
function tests, given clinical
information
•
Discuss how pulmonary function
tests provide objective measurement
to aid in the diagnosis of pulmonary
diseases
•
Discuss how pulmonary function
tests assist with monitoring efcacy
and toxicity of various drug therapies
DOI 10.37573/9781585286423.014
Lori A. Wilken and Min J. Joo
Pulmonary function tests (PFTs) provide objective and quantiable measures of lung
function and are useful in diagnosing, evaluating, and monitoring respiratory disease. Diagnosing and monitoring many pulmonary diseases, including diseases of gas
exchange, oen require measuring the ow or volume of air inhaled and exhaled by
the patient. Spirometry, a test that measures the movement of air into and out of the
lungs during various breathing maneuvers, is the most frequently used PFT. Clinicians use spirometry to aid in the diagnosis of respiratory diseases such as asthma and
chronic obstructive pulmonary disease (COPD). Other tests of lung function include
lung volume assessment, carbon monoxide diusion capacity (DLCO), exercise testing, and bronchial provocation tests. Arterial blood gases (ABGs) can be measured
with PFTs and are useful for assessing lung function. (Interpretation of arterial blood
gases is discussed in Chapter13.) is chapter discusses the mechanics and interpretation of PFTs.
ANATOMY AND PHYSIOLOGY OF LUNGS
e purpose of the lungs is to take oxygen from the atmosphere and exchange it for
carbon dioxide in the blood. e movement of air in and out of the lungs is called
ventilation; the movement of blood through the lungs is termed perfusion.
Air enters the body through the mouth and nose and travels through the pharynx
to the trachea. e trachea splits into the le and right main stem bronchi, which
deliver inspired air to the respective lungs. e le and right lungs are in the pleural
cavity of the thorax. ese two spongy, conical structures are the primary organs of
respiration. e right lung has three lobes, whereas the le lung has only two lobes,
thus leaving space for the heart. Within the lungs, the main bronchi continue to split
successively into smaller bronchi, bronchioles, terminal bronchioles, and nally alveoli. In the alveoli, carbon dioxide is exchanged for oxygen across a thin membrane
separating capillary blood from inspired air.
e thoracic cavity is separated from the abdominal cavity by the diaphragm. e
diaphragm, a thin sheet of dome- shaped muscle, contracts and relaxes during breathing. e lungs are contained within the rib cage but rest on the diaphragm. Between
the ribs are two sets of intercostal muscles, which attach to each upper and lower
rib. During inhalation, the intercostal muscles and the diaphragm contract, which
enlarges the thoracic cavity. is action generates a negative intrathoracic pressure,
allowing air to rush in through the nose and mouth down into the pharynx, trachea,
and lungs. During exhalation, these muscles relax, and a positive intrathoracic pressure causes air to be pushed out of the lungs. Normal expiration is a passive process
that results from the natural recoil of the expanded lungs. However, in people with
rapid or labored breathing or airow limitation, the accessory muscles and abdominal muscles oen must contract to help force air out of the lungs more quickly or
completely.
e ability of the lungs to expand and contract to inhale and exhale air is aected
by the compliance of the lungs, which is a measure of the ease of expansion of the
lungs and thorax. Processes that result in scarring of lung tissue (eg, pulmonary
brosis) can decrease compliance, thus decreasing the ow and volume of air moved
by the lungs, and increase the work to breathe. e degree of ease in which air travels through the airways is known as resistance. e length and radius of the airways
1
301

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as well as the viscosity of the gas inhaled determine resistance.
Apatient with a high degree of airway resistance may not be
able to take a full breath in or exhale fully (some air may become
trapped in the lungs).
To have an adequate exchange of the gases, there must be a
matching of ventilation (V) and perfusion (Q) at the alveolar
level. An average V:Q ratio, determined by dividing total alveolar
ventilation (4 L/min) by cardiac output (5 L/min), is 0.8. A mismatch of ventilation and perfusion may result from a shunt or
dead space. A shunt occurs when there is ow of blood adjacent
to alveoli that are not ventilated. is could be physiologic (eg, at
rest, some alveoli are collapsed or partially opened but perfused)
or pathologic when alveoli are lled with uid (eg, heart failure)
or cellular debris (eg, pneumonia) or are collapsed (eg, atelec
tasis). A shunt can also occur when airways are obstructed by
mucus or collapse on exhalation (eg, COPD). In a shunt, blood
moves from the venous circulation to the arterial circulation
without being oxygenated.
Dead space occurs when there is ventilation of functional
lung tissue without adjacent blood ow for gas exchange. Dead
space can be physiologic (eg, the trachea) or pathologic because
of airow limitation of blood ow (eg, pulmonary embolism).
e body uses a few mechanisms to normalize the V:Q ratio,
such as hypoxic vasoconstriction and bronchoconstriction.
When the V:Q ratio is low, hypoxic vasoconstriction leads to
decreased perfusion to the hypoxic regions of the lungs, thus
redirecting perfusion to functional areas of the lungs, which
leads to an increase in the V:Q ratio. When the V:Q ratio is high,
the bronchi constrict in areas that are not well perfused, which
leads to a decrease in the amount of ventilation to areas that are
not well perfused, a decrease in the amount of alveolar dead
space, and a decrease in the V:Q ratio.
For the respiration process to be complete, gas diffusion
must occur between the alveoli and the pulmonary capillaries. By the diffusion mechanism, gases equilibrate from
areas of high concentration to areas of low concentration.
Hemoglobin (Hgb) releases carbon dioxide and adsorbs oxygen as it diffuses through the alveolar walls. If these walls
thicken, diffusion is hampered, potentially causing carbon
dioxide retention, hypoxia, or both. Membrane formation
with secondary thickening of the alveolar wall may result
from an acute or chronic inflammatory process such as interstitial pneumonia and pulmonary fibrosis. The pulmonary
diffusing capacity is also reduced in the presence of a V:Q
mismatch, loss of lung surface areas (eg, emphysema, lung
resection), or decrease in oxygen- carrying capacity (eg, anemia). The various PFTs can measure airflow in or out of the
lungs, indicate how much air is in the lungs, and provide
information on gas diffusion or specific changes in airway
tone or reactivity.
CLINICAL USE OF PULMONARY
FUNCTION TESTING
Pulmonary function tests are useful in many clinical situations.2
ey aid in the diagnostic dierentiation of various pulmonary
diseases. PFT results are divided into two types of pulmonary
abnormalities: obstructive and restrictive lung diseases. Obstruc-
tive diseases (eg, asthma and COPD) decrease the ow rate of
air (liters/minute) out of the lungs but have less impact on the
total volume of air per breath. In restrictive diseases (eg, kyphosis or sarcoidosis), the lungs are limited in the amount of air
they can contain. Restrictive diseases usually decrease the total
volume of air per breath in a similar ratio to the ow rate of air.
Table14-1 summarizes common pulmonary disease states with
PFT results.
In addition, serial PFTs allow tracking of the progression
of pulmonary diseases and the need for or response to various
treatments. ey also help to establish a baseline of respiratory function before surgical, medical, or radiation therapy.
Subsequent serial measurements then aid in the detection
and tracking of changes in lung function caused by these
therapies. Similarly, serial PFTs can be used to evaluate the
risk of lung damage from exposure to environmental or occupational hazards. Table14-2 summarizes the selected uses
of PFTs.
PULMONARY FUNCTION TESTS AND
MEASUREMENTS
Pulmonary function tests use equations based on an individual’s age, height, sex, and race (when available) to calculate reference values from the population. e reference values
most commonly used for spirometry is the National Health
and Nutrition Examination Survey III and, more recently, the
Global Lung Function Initiative (GLI)-2012.3 e individual’s
measurement is then compared with the calculated reference
values and the lower limit of normal (LLN). e LLN value is
set at the h percentile, indicating that if the measured value
is less than the lower h percentile of a normal population,
then it is considered reduced and may be associated with disease. Using both the reference measurement and the LLN helps
decrease overdiagnosing by removing bias from age seen in
xed value cutos.
3
Spirometry
Spirometry is a PFT that helps detect airow limitation that can
be manifested in asthma or COPD. Spirometry measures the
ow of air in volume per time. e physical forces of the airow
and the total amount of air inhaled and exhaled are converted
by transducers to electrical signals, which are displayed on a
computer screen.
During this maneuver, a volume- time curve— a plot of the
volume exhaled against time— and a ow- volume curve or ow-
volume loop— a diagram with ow (liters/second) on the vertical
axis and volume on the horizontal axis (liters)— are generated
as the report (Figure14-1). Aer the data are generated, the
patient’s spirometry results are compared with the reference
values. e ow- volume curve is visually useful for diagnosing
airow limitation. e Global Initiative for Chronic Obstructive Lung Disease (GOLD) strategy suggests suspecting COPD
in patients >40 years old with symptoms and/or risk factors
and recommends spirometry to denitively diagnose COPD.5
Once diagnosed with COPD, spirometry, in conjunction with

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TABLE 14-1. Pulmonary Disease States and Common PFT Results
PULMONARY
ABNORMALITY PATHOPHYSIOLOGY
Obstructive
Fixed airow limitation Asthma with
lung disease,
chronic
Obstructive
lung disease,
Reversible (eg,
bronchoconstriction)
reversible and
stable
Restrictive lung
disease
Parenchymal
inltration or brosis
Extrathoracic
compression
DISEASE STATE
COMMON PFT RESULTS
EXAMPLES
xed airow
/FVC FEV
1
1
Decreased Decreased Normal or
FVC RV TLC
decreased
Normal or
increased
Normal or
increased
FEV
limitation, COPD,
cystic brosis,
bronchiectasis
Asthma Normal Normal Normal Normal Normal
Idiopathic
pulmonary
Normal or
increased
Decreased Decreased Decreased Decreased
brosis and other
idiopathic interstitial
pneumonias, drug
induced, secondary
to autoimmune
diseases, sarcoidosis
Kyphosis, morbid
obesity, ascites, chest
Normal or
increased
Decreased Decreased Decreased Decreased
wall deformities,
pregnancy
Neuromuscular causes Guillain-Barré
syndrome,
Normal or
increased
Decreased Decreased Decreased Decreased
myasthenia gravis,
muscular dystrophy,
amyotrophic lateral
sclerosis
Mixed
obstructive and
restrictive
FEV1 = forced expiratory volume in 1 second; FVC = forced vital capacity; RV= residual volume; TLC = total lung capacity
symptoms and history of exacerbations, can be used to monitor
disease state severity.5 When asthma is suspected, spirometry
can be used to assess for airow variation and is recommended
at the time of diagnosis, 3 to 6 months aer starting treatment,
at least every 1 to 2 years, and as needed to assess ongoing risk
of exacerbations.
Combinations of
restrictive and
obstructive processes
6
Both restrictive and
obstructive diseases
Decreased Decreased Decreased Increased,
normal, or
decreased
when there is less than a 0.025L change in volume for at least
1second, or the forced expiratory time has reached 15 seconds,
or the FVC is within 0.150L of another FVC measurement if
the patient is older than 6 years of age. When the full inhalationexhalation procedure is repeated slowly— instead of forcefully
and rapidly— it is called the slow vital capacity (SVC). is value
is the maximum amount of air exhaled aer a full and com-
Spirometry Measurements
Spirometry routinely assesses forced vital capacity (FVC), forced
expiratory volume in 1 second (FEV1), and FEV1/FVC.
plete inhalation. In patients with normal airway function, FVC
and SVC are usually similar and constitute the vital capacity.
In patients with diseases such as COPD, the FVC may be lower
than the SVC due to collapse of narrowed or oppy airways dur-
Forced Vital Capacity
e FVC is the total volume of air, measured in liters, forcefully
and rapidly exhaled in one breath (from maximum inhalation to
end of forced expiration). End of forced expiration is achieved
ing forced expiration. Because of this, some interpretive strategies recommend using the FEV1/SVC ratio to determine the
presence of airow limitation, especially for pronounced airow limitation.
5
Decreased

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Forced Expiratory Volume in One Second
e full, forced inhalation- exhalation procedure was already
described as the FVC. During this maneuver, the computer can
discern the amount of air exhaled at specic time intervals of
the FVC. By convention, FEV
, FEV
0.5
, FEV1, FEV3, and FEV6
0.75
are the amounts of air exhaled aer one- half, three- fourths, 1, 3,
and 6 seconds, respectively. Usually, a patient’s value is described
in liters and as a percentage of a predicted value based on reference values adjusted for age, height, sex, and race. Of these
TABLE 14-2. Selected Uses of PFTs
Diagnosis
Evaluate signs and symptoms of respiratory disease
Screen at-
Evaluation
Assess the health status before initiating physical activity
or rehabilitation
Determine preoperative risk of having pulmonaryissues during surgery
Monitoring
Describe the course of lung function from a respiratory
disease
Monitor respiratory changes for occupational or
environmental exposure to toxins
Assess therapeutic drug effectiveness (eg, inhaled
corticosteroids or bronchodilators for asthma)
Monitor adverse drug effects on pulmonary function
(eg,
risk individuals for pulmonary disease
related
amiodarone)
measurements, FEV1 has the most clinical relevance, primarily
as an indicator of airway function. A value ≥80% of the predicted normal value or greater than the LLN is considered normal. Normal values can be seen in patients with asthma when
the disease is mild or well controlled. FEV1 is an important value
for predicting clinical outcomes, such as mortality, hospitalizations, and lung transplantation.5 For children aged 6 years and
younger, FEV
expired by time is less than 1 second.
is used instead of FEV1 if the maximal volume
0.75
4
Forced Expiratory Volume in One Second/Forced
Vital Capacity
e ratio of FEV1 to the FVC is used to estimate the presence
and amount of airow limitation in the airways. is ratio indicates the amount of air mobilized in 1 second as a percentage
of the total amount of movable air. Normal, healthy individuals
can exhale approximately 50% of their FVC in the rst one- half
second, about 80% in 1 second, and about 98% in 3 seconds.
Patients with obstructive disease usually show a decreased ratio,
and the actual percentage reduction varies with the severity of
airow limitation. In COPD, the GOLD strategy denes persis
tent airow limitation as a postbronchodilator FEV1/FVC ratio
<0.70.5 Table14-3 summarizes the denition of airow limita-
tion severity for COPD. Minicase 1 discusses how spirometry
is used to diagnose COPD.
Spirometry can also show airow variability necessary for the
diagnosis of asthma. However, frequency of asthma symptoms,
quick- relief medication use, and level of medications required to
control symptoms are also necessary to assess asthma severity.
Generally, the FEV1/FVC is normal (or high) in patients
with restrictive diseases. In mild restriction, the FVC alone
may be decreased, resulting in a high ratio. Oen in restrictive
-
FIGURE 14-1. The ow- volume curve and volume- time curve from an effort meeting American Thoracic Society
(ATS) acceptability criteria. The ow- volume curve has a deep inspiratory effort with a sharp complete expiratory
ow. The volume-time curve demonstrates a plateau without complete attening signifying the end of expiration or
very-low ow.

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lung disease, both the FVC and FEV1 are similarly reduced
compared with predicted values resulting in a normal ratio.
It is important to note that this pattern is consistent with a
restrictive pattern on spirometry, but lung volumes are needed
to conrm restriction.
Flow-Volume Curves
Figure 14-2 shows several flow- volume curves in which
the expiratory ow is plotted against the exhaled volume.
TABLE 14-3. Severity of Airow Limitation for
COPD with the Postbronchodilator FEV
GOLD
GRADE SEVERITY
1 Mild ≥80
2 Moderate 50–79
3 Severe 30–49
4 Very severe <30
Refer to the Global Initiative for Chronic Obstructive Lung Disease
(GOLDCOPD) 2022 Report
POSTBRONCHODILATOR
FEV1 (% PREDICTED)
4
for more information.
/FVC <0.7
1
Asexplained earlier, these curves are graphic representations
of inspiration and expiration. e shape of the curve can indicate both the type of disease and the severity of airow limitation. Obstructive changes result in decreased airow, revealing
a characteristic concave appearance. Restrictive changes result
in a shape similar to that of a healthy individual, but the size is
considerably smaller. e ow- volume loop also reveals mixed
obstructive and restrictive disease by a combination of the two
patterns.
Standardization of Spirometry Measurements
Spirometry is performed by having a person breathe into a tube
(mouthpiece) connected to a machine (spirometer) that measures the amount and ow of inhaled and exhaled air. Prior to
performing spirometry, relative contraindications such as recent
brain, eye, or sinus surgery are assessed.4 Spirometry results
depend greatly on the completeness and speed of the patient’s
inhalation and exhalation, so the importance of completely lling and emptying the lungs of air during the test is emphasized.
During spirometry, nose clips are worn to minimize air loss
through the nose. e patient is seated comfortably without
leaning or slumping, and any restrictive clothing (such as ties
or tight belts) is loosened or removed. e patient is coached to
take a full deep breath in and then blast the air out as quickly
and forcefully as possible and to keep blowing the air out, while
MINICASE 1
Using Spirometry to Diagnose Asthma and COPD
Debra T. is a 56- year- old woman who reports chronic cough and
shortness of breath when walking up a few stairs. She has been
admitted several times each year for COPD exacerbations and
pneumonia. She has a 40 pack- year- history of tobacco use. She
is allergic to dust mites and dogs and has had a history of asthma
since childhood. Today, on exam, she is wheezing and has nasal
congestion.
QUESTION: How do the results from this patient’s spirometry test
support the diagnosis of asthma and COPD?
DISCUSSION: A postbronchodilator measurement for FEV1/FVC
<0.70 is consistent with COPD using the GOLD criteria
clinical setting. She has a postbronchodilator FEV1/FVC of <0.70 at
PREBRONCHODILATOR POSTBRONCHODILATOR
PFT LLN MEASURED % PREDICTED MEASURED % PREDICTED % CHANGE
FVC (L) 2.07 1.70 66 2.13 82.48 +24.97
(L) 1.59 1.15 55.18 1.37 65.69 19.04
FEV
1
FEV
/FVC 0.696 0.676 0.643
1
4
in the right
0.643 consistent with a diagnosis of COPD. A postbronchodilator
FEV1 of 65.69% of her predicted is considered moderate airflow
limitation or GOLD Grade 2 COPD.
Her FEV1 increased by more than 12% and 200 mL, which are the
criteria for a positive bronchodilator test. Patients with asthma and
COPD can have a positive bronchodilator test, but patients with
asthma usually have a more extreme response. In addition, her
clinical picture substantiates a diagnosis of both asthma and COPD:
significant smoking history and shortness of breath on exertion are
common with COPD, whereas allergies are associated more with
asthma. Many patients, like Debra T., have both asthma and COPD
that can be detected with PFTs and need to be treated appropriately.
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