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296 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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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 identication 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 insufciency, 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. Dierence 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–BAsEBAlAnCE 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 Denition. 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. Gilx 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 denitions 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- specic 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. Eects 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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RelatedTests
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 efcacy
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 quantiable 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, oen 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 diusion 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 Chapter13.) 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 airow limitation, the accessory muscles and abdomi­nal muscles oen 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 aected 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. Apatient 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 airow 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 dierentiation 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.
Table14-1 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. Table14-2 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 cutos.
3
Spirometry
Spirometry is a PFT that helps detect airow limitation that can be manifested in asthma or COPD. Spirometry measures the ow of air in volume per time. e physical forces of the airow 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 (Figure14-1). Aer the data are generated, the patient’s spirometry results are compared with the reference values. e ow- volume curve is visually useful for diagnosing airow 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 denitively 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 airow limitation Asthma with lung disease, chronic
Obstructive lung disease,
Reversible (eg,
bronchoconstriction) reversible and stable
Restrictive lung disease
Parenchymal
inltration or brosis
Extrathoracic
compression
DISEASE STATE
COMMON PFT RESULTS
EXAMPLES
xed airow
/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 airow variation and is recommended at the time of diagnosis, 3 to 6 months aer 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 0.025L change in volume for at least 1second, or the forced expiratory time has reached 15 seconds, or the FVC is within 0.150L 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 aer 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 airow limitation, especially for pronounced air­ow 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 specic time intervals of the FVC. By convention, FEV
, FEV
0.5
, FEV1, FEV3, and FEV6
0.75
are the amounts of air exhaled aer 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 airow 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 airow limitation. In COPD, the GOLD strategy denes persis tent airow limitation as a postbronchodilator FEV1/FVC ratio <0.70.5 Table14-3 summarizes the denition of airow limita- tion severity for COPD. Minicase 1 discusses how spirometry is used to diagnose COPD.
Spirometry can also show airow 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. Oen 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 conrm 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 Airow 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
Asexplained 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 airow limita­tion. Obstructive changes result in decreased airow, 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.