eMedicine - Pulmonary Function Testing : Article by Kevin McCarthy

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Pulmonary Function Testing

Article Last Updated: Nov 6, 2006

Spirometry (Current Procedural Terminology [CPT] code 94010 [spirometry], 94060 [spirometry before and after bronchodilators]) measures the mechanical function of the lung, chest wall, and respiratory muscles by assessing the total volume of air exhaled from a full lung (total lung capacity [TLC]) to an empty lung (residual volume). This volume, the forced vital capacity (FVC) and the forced expiratory volume in the first second of the forceful exhalation (FEV₁), should be reproducible to within 0.15 L upon repeat efforts unless the largest value for either parameter is less than 1 L. In this case, the expected reproducibility is to within 0.1 L of the largest value. The patient is instructed to inhale as much as possible and then exhale rapidly and forcefully for as long as flow can be maintained.

Reduction in the amount of air exhaled forcefully in the first second of the forced exhalation (FEV₁) may reflect reduction in the maximum inflation of the lungs (TLC), obstruction of the airways, loss of lung elastic recoil, or respiratory muscle weakness. Airway obstruction is the most common cause of reduction in FEV₁. Response of FEV₁ to inhaled bronchodilators is used to assess the reversibility of airway obstruction.

Spirometry is used to establish baseline lung function, evaluate dyspnea, detect pulmonary disease, monitor effects of therapies used to treat respiratory disease, evaluate respiratory impairment, evaluate operative risk, and perform surveillance for occupational-related lung disease.

Relative contraindications for spirometry include hemoptysis of unknown origin, pneumothorax, unstable angina pectoris, recent myocardial infarction, thoracic aneurysms, abdominal aneurysms, cerebral aneurysms, recent eye surgery (increased intraocular pressure during forced expiration), recent abdominal or thoracic surgical procedures, and patients with a history of syncope associated with forced exhalation.

Two choices are available with respect to bronchodilator and medication use prior to testing. Patients may withhold oral and inhaled bronchodilators to establish baseline lung function and evaluate maximum bronchodilator response, or they may continue taking medication as prescribed. If medications are withheld, a risk of exacerbation of bronchial spasm exists.

Interpretation of spirometry results should begin with an assessment of test quality. Failure to meet performance standards can result in unreliable test results (see Image 1). The American Thoracic Society (ATS) defines acceptable spirometry as an expiratory effort that shows (1) minimal hesitation at the start of the forced expiration (extrapolated volume (EV) £5% of the FVC or 0.15 L, whichever is larger), (2) no cough in the first second of forced exhalation, and (3) meets 1 of 3 criteria that define a valid end-of-test: (a) smooth curvilinear rise of the volume-time tracing to a plateau of at least 1-second duration; (b) if a test fails to exhibit an expiratory plateau, a forced expiratory time (FET) of 15 seconds; or (c) when the patient cannot or should not continue forced exhalation for valid medical reasons.

Additionally, the 2 largest values for FVC and the 2 largest values for FEV₁ should vary by no more than 0.15 L (0.1 L if the largest value is <1 L). A recent study has shown start-of-test problems (affecting FEV₁ measurements) to be relatively uncommon (2% prevalence in one series) and end-of-test problems (affecting FVC quality) being very common (61-84% prevalence). Allowing the patient to relax and push gently after 3-4 seconds of forced exhalation has been shown to greatly enhance the ability of patients with airflow obstruction to satisfy end-of-test criteria.

Inspection of the volume-time tracing aids in identification of early termination of expiration by evaluating the presence of an expiratory plateau. In the absence of an expiratory plateau, a 12- to 15-second expiratory time ensures the quality of the FVC. Inspection of the start of the volume-time tracing can identify a hesitant start, which can result in a falsely low FEV₁. Reproducibility of the FVC and the FEV₁ helps ensure that the results truly represent the patient's lung function. Attention should be focused on 3 key parameters: FVC, FEV₁, and the FEV₁-to-FVC ratio.

In the United States, normal values and lower limits of normal defined by Hankinson et al (the National Health and Nutrition Examination Survey [NHANES] III predicted set) should be used. These provide specific equations for whites, African Americans and Mexican Americans. If the patient belongs to another ethnic group, the predicted values and lower limits of normal provided for Caucasians by Hankinson et al should be reduced by 12% by multiplying by 0.88 before comparison with the patient's results.

Disproportionate reduction in the FEV₁ as compared to the FVC (and therefore the FEV₁-to-FVC ratio, also called FEV₁%) is the hallmark of obstructive lung diseases. This physiologic category of lung diseases includes but is not limited to asthma, acute and chronic bronchitis, emphysema, bronchiectasis, cystic fibrosis, pneumonia, alpha1-antitrypsin deficiency, and bronchiolitis. The expiratory flow at any given expiratory volume is reduced. The mechanism responsible for the reduction in airflow can be bronchial spasm, airway inflammation, increased intraluminal secretions, and/or reduction in parenchymal support of the airways due to loss of lung elastic recoil.

When airway obstruction is identified on spirometry, assessing response to inhaled bronchodilators is useful. The ATS has recommended that the threshold for significant response be demonstration of an increase of at least 12% and 0.2 L in either FVC or FEV₁ on a spirogram performed 10-15 minutes after inhalation of a therapeutic dose of a bronchodilating agent. New standards recommend the use of 4 inhalations (100 mcg each, 400 mcg total dose) of albuterol administered through a valved spacer device. When concern about tremor or heart rate exists, lower doses may be used. Response to an anticholinergic drug may be assessed 30 minutes after 4 inhalations (40 mcg each, 160 mcg total dose) of ipratropium bromide. Failure to respond to bronchodilator challenge does not preclude clinical benefit from bronchodilators. A positive response to the bronchodilators may correlate with response to steroid therapy.

Reduction in the FVC with a normal or elevated FEV₁-to-FVC ratio defines the classification of restrictive lung diseases as assessed by spirometry. Because the FEV₁ is a fraction of the FVC, it also is reduced, but the FEV₁-to-FVC ratio is preserved at a normal or elevated level. Measuring the TLC and residual volume (RV) can confirm restriction suggested by spirometry (see Image 2).

In normal spirometry, FVC, FEV₁, and FEV₁-to-FVC ratio are above the lower limit of normal. The lower limit of normal is defined as the result of the mean predicted value (based on the patient's sex, age, and height) minus 1.64 times the standard error of the estimate from the population study on which the reference equation is based. If the lower limit of normal is not available, the FVC and FEV₁ should be greater than or equal to 80% of predicted, and the FEV₁-to-FVC ratio should be no more than 8-9 absolute percentage points below the predicted ratio. The ATS has recommended the use of lower limits of normal instead of the 80% of predicted for setting the threshold that defines abnormal test results.

A reduced FVC on spirometry in the absence of a reduced FEV₁-to-FVC ratio suggests a restrictive ventilatory problem. An inappropriately shortened exhalation during spirometry can (and often does) result in a reduced FVC. Causes of restriction on spirometry include obesity, cardiomegaly, ascites, pregnancy, pleural effusion, pleural tumors, kyphoscoliosis, pulmonary fibrosis, neuromuscular disease, diaphragm weakness or paralysis, space-occupying lesions, lung resection, congestive heart failure, inadequate inspiration or expiration secondary to pain, and severe obstructive lung disease. The severity of reductions in the FVC and/or the FEV₁ can be characterized by the following scheme:

Note that small airway obstruction may be present even when the FEV₁/FVC% is above the lower limit of normal. The mid-flow rate or forced expiratory flow occurring in the middle 50% of the patient's exhaled volume (FEF_25-75%) may fall below its lower limit of normal even when the FVC, FEV₁, and FEV₁/FVC% are all normal.

The lower limit of normal for the FEF_25-75% can be less than 50% of the mean predicted value, making it important to use the lower limit of normal defined by the 95% confidence limit of the mean predicted value rather than a threshold defined by a fixed percentage of the predicted value. The FEF_25-75% is also very dependent on expiratory time. If expiratory times of spirometry efforts vary by more than 10%, comparisons before and after bronchodilator challenge are difficult. Early termination of expiration shifts the middle 50% of the exhaled volume toward the start of the exhalation, artifactually raising the FEF_25-75%.

Sitting versus supine vital capacity: Evaluation of diaphragm strength can be accomplished by measuring the vital capacity in an upright or sitting position followed by a measurement made in the supine position. A reduction in the vital capacity to less than 90% of the upright vital capacity suggests diaphragm weakness or paralysis. Interpreting an increased reduction in vital capacity in the supine position as diaphragm dysfunction should be made cautiously if the patient is obese. Studies reporting the normal reduction of the vital capacity of less than 10% from upright to supine were conducted with individuals who were not obese. Slightly greater reductions in obese individuals in a supine position may not indicate diaphragm dysfunction, but rather an increase in the resistance to diaphragm descent.

Upper airway obstructions: The configuration of the flow-volume curve of a properly performed spirometry test can be used to demonstrate various abnormalities of the larger central airways (larynx, trachea, right and left mainstem bronchi). Three patterns of flow-volume abnormalities can be detected: (1) variable intrathoracic obstructions, (2) variable extrathoracic obstructions, and (3) fixed upper airway obstructions. Reproducing these findings on every effort is important because spurious nonreproducible reductions in inspiratory flow are not uncommon after completion of forced expirations in subjects without upper airway obstruction. Examples of variable intrathoracic obstruction include localized tumors of the lower trachea or mainstem bronchus, tracheomalacia, and airway changes associated with polychondritis (see Image 3).

Variable upper airway obstructions demonstrate flow reductions that vary with the phase of forced respirations. Variable intrathoracic obstructions demonstrate reduction of airflow during forced expirations with preservation of a normal inspiratory flow configuration. This is observed as a plateau across a broad volume range on the expired flow limb of the flow-volume curve. The reduction in airflow results from a narrowing of the airway inside the thorax, in part because of a narrowing or collapse of the airway secondary to extraluminal pressures exceeding intraluminal pressures during expiration.

Variable extrathoracic obstructions demonstrate reduction of inspired flows during forced inspirations with preservation of expiratory flows. Again, the major cause of the reduced flow during inspiration is airway narrowing secondary to extraluminal pressures exceeding intraluminal pressures during inspiration. Causes of this type of upper airway obstruction include unilateral and bilateral vocal cord paralysis, vocal cord adhesions, vocal cord constriction, laryngeal edema, and upper airway narrowing associated with obstructive sleep apnea.

Fixed upper airway obstructions demonstrate plateaus of flow during both forced inspiration and forced expiration. Causes of fixed upper airway obstruction include goiters, endotracheal neoplasms, stenosis of both main bronchi, postintubation stenosis, and performance of the test through a tracheostomy tube or other fixed orifice device.

While no single test can effectively predict intraoperative and postoperative morbidity and mortality from pulmonary complications, the FEV₁ obtained from good quality spirometry is a useful tool. When the FEV₁ is greater than 2 L or 50% of predicted, major complications are rare.

Operative risk is heavily dependent on the surgical site, with chest surgery having the highest risk for postoperative complications, followed by upper and lower abdominal sites. Patient-related factors associated with increased operative risk for pulmonary complications include preexisting pulmonary disease, cardiovascular disease, pulmonary hypertension, dyspnea upon exertion, heavy smoking history, respiratory infection, cough (particularly productive cough), advanced age (>70 y), malnutrition, general debilitation, obesity, and prolonged surgery.

Assessment for lung surgery typically involves prediction of a postoperative FEV₁ by using the preoperative FEV₁. In a borderline case, consideration of the contribution of the remaining portions can be assessed by a perfusion scan. The relative percentage of perfusion (Q) of the remaining lung or lung segments usually is proportional to its contribution to ventilation and can be used to estimate postoperative function as shown in the following equation:

For example, if the preoperative FEV₁ is 1.6 L and the lung to be resected demonstrates 40% perfusion, the postoperative FEV₁ would be 1.6 x 0.6 = 0.96 L. An estimated postoperative FEV₁ of less than 0.8 L often is associated with chronic respiratory failure and may indicate an unacceptable degree of operative risk. Arterial blood gases (ABGs) and cardiopulmonary exercise testing may help evaluate operative risk in patients who have a preoperative FEV₁ below 2 L or 50% of predicted.

The algorithm for clearance of candidates for lung resection proposed by Bolinger and Perruchoud has been successfully evaluated in 137 consecutive patients who were referred for resection by Wyser et al with an overall mortality rate of 1.5% and is detailed in Cardiopulmonary Stress Testing. Patients with a negative cardiac history and ECG that demonstrate an FEV₁ and a diffusing capacity of lung for carbon monoxide (DLCO) that are greater than 80% of predicted are judged to be able to undergo pneumonectomy safely.

The ATS has published guidelines for a standardized technique that includes spirometer performance standards. A reasonable end-point for the maneuver in the absence of true flow cessation (ie, airway obstruction is present) is 15 seconds. Patients often discontinue the forced exhalation prematurely because of the discomfort of prolonged forced exhalation. A modified technique in which the patient exhales with maximum force for 3 seconds followed by continued relaxed exhalation has been shown to enhance the patient's ability to sustain expiration, thereby yielding a larger FVC in patients with airflow obstruction.

Recently, the National Lung Health and Education Program (NLHEP) has proposed an initiative to identify approximately 13 million Americans with undiagnosed chronic obstructive pulmonary disease (COPD) by performing spirometry on 2 groups of patients, ie, (1) those aged 45 years or older who are actively smoking or who have quit within the last year and (2) those aged 25 years or older who have respiratory symptoms (eg, cough, dyspnea, wheezing), regardless of smoking history. Based on the last NHANES survey, approximately 50-60 million Americans fall into one of these groups.

The proposal suggests that every primary care practitioner, internist and general practitioner should have the capability of administering a form of spirometry test that would presumably be easier to administer than the standard spirometry test. This test, called "office spirometry" would differ from standard spirometry in both instrumentation and procedure. Office spirometry exhalations would automatically terminate at 6 seconds rather than continuing to an expiratory plateau. The forced expiratory volume at 6 seconds (FEV₆) would act as a surrogate for the FVC. Likewise, the FEV₁/FEV₆% would act as a surrogate for the FEV₁/FVC%. Normal values for both the FEV₆ and the FEV₁/FEV₆% are provided by Hankinson et al (NHANES III predicted set).

A recent study suggests that the sensitivity for detecting obstruction using the FEV₁/FEV₆% is greater than 95%. The NLHEP recommends that abnormalities detected by office spirometry be confirmed by diagnostic spirometry (using the FVC and the FEV₁/FVC%) and lung volumes, if necessary.

Functional reserve capacity (FRC), helium dilution lung volumes, nitrogen washout lung volumes, static lung volumes, lung subdivisions

Lung volumes determinations (CPT code 94240 [FRC or RV], 94260 [thoracic gas volume by body plethysmography]) are used in the evaluation of suspected restrictive lung disease and the evaluation of hyperinflation.

Inability to follow instructions is a contraindication. Patients with claustrophobia may not tolerate being closed into a confined space (body plethysmograph).

Use of supplemental oxygen just prior to a nitrogen washout test may cause underestimation of FRC unless the initial exhaled nitrogen is considered in the calculations. Duplicate measurements of FRC by either gas dilution technique should be delayed until a post-test interval is equivalent to 1.5 times the equilibration time to eliminate the effects of residual oxygen or helium.

Lung volumes provide useful information that confirms the presence of restrictive lung disease suggested by a low vital capacity on a spirometry test. Hyperinflation, elevation of the RV and TLC can be demonstrated by this test. The test is dependent first on an accurate measurement of the volume of gas in the lungs at a resting end-expiration, known as the FRC, which represents the balance of the elastic recoil properties of the lung and the chest wall.

FRC can be measured by 1 of 3 techniques, inert gas dilution, nitrogen washout, or whole-body plethysmography. Both gas dilution techniques are subject to error by leak at the mouthpiece or nose clip or, occasionally, even small leaks from the eardrum. When measured by whole-body plethysmography, resting end-expiratory volume is known as the intrathoracic gas volume (ITGV) and will include the volume of gas contained in noncommunicating spaces such as blebs or bullae that the FRC measured by gas dilution techniques will not measure. In addition to this advantage, body plethysmography allows multiple determinations of lung volumes to be made rapidly.

When measured by inert gas dilution or nitrogen washout, premature termination of the procedure before adequate demonstration of equilibrium or washout results in underestimation of FRC, RV, and TLC. Repeat measurements should allow a recovery period of 1.5-times the wash-in or wash-out time to prevent residual helium or oxygen from affecting the new measurement. Body plethysmography is performed rapidly, allowing multiple determinations in minutes. Ideally, each measurement of lung subdivisions should be linked to each FRC or ITGV measurement (patient should remain on the mouthpiece).

FRC or ITGV is expressed in liters. This is the volume of gas in the lungs at the end of an average resting expiration. It is comprised of the expiratory reserve volume (ERV), the volume of gas that can be voluntarily exhaled beyond the FRC or ITGV, and the RV. The TLC then can be calculated by adding the RV to the vital capacity (VC). RV also is expressed as a fraction of the TLC, the RV-to-TLC ratio (see Image 2).

Obstructive lung diseases, particularly emphysema, result in an increase in the RV and RV-to-TLC ratio. In severe emphysema, particularly bullous emphysema, the TLC can show a marked increase. Bronchial spasm, airway inflammation, excessive secretions in the airway, and loss of elastic recoil increase the airway's resistance and result in an insidious progressive increase in the end-expiratory lung volume that results in chronic hyperinflation (elevated RV, TLC, and RV-to-TLC ratio). Other pulmonary causes of increased RV include pulmonary vascular congestion and mitral stenosis. Extrapulmonic causes of increased RV include expiratory muscle weakness as observed in spinal cord injuries and myopathies.

A reduced TLC is the hallmark of restrictive lung disease. An isolated reduction of the residual volume may be an early sign of restrictive lung disease. Pulmonary processes that can reduce the TLC include interstitial lung disease, atelectasis, pneumothorax, pneumonectomy, consolidation, edema, and fibrosis. Extrapulmonary causes of restriction include obesity, respiratory muscle weakness, thoracic deformities, and disease of the pleura.

Transfer factor (TL, mmol/min/kilopascal, Europe); DLCO; diffusing capacity of lung (DL, mL/min/mmHg); diffusing capacity of lung/alveolar volume (DL/VA); rate of carbon monoxide (CO) uptake (KCO), which is equivalent to the DL/VA; and alveolar volume (VA, L), which is the single-breath estimate of the TLC determined by the dilution of the helium concentration

Inability to follow instructions is a contraindication to a DLCO test (CPT code 94070). Patients should be alert, oriented, able to exhale completely and inhale to total lung capacity, able to maintain an airtight seal on a mouthpiece, and able to hold a large breath for 10 seconds.

Refrain from smoking for several hours before the test. Alcohol vapors can affect the accuracy of some fuel cell types of CO analyzers, and alcoholic beverages should be withheld for 8 hours.

DLCO, also known as the transfer factor of the lung for CO (TLCO), is a measurement of the ease of transfer for CO molecules from alveolar gas to the hemoglobin of the red blood cells in the pulmonary circulation. It often is helpful for evaluating the presence of possible parenchymal lung disease when spirometry and/or lung volume determinations suggest a reduced vital capacity, RV, and/or TLC.

Most pulmonary laboratories in the United States perform this test by the single-breath technique (DLCO SB) because it is quicker to perform and more reproducible than other techniques. Other techniques, such as the rebreathing technique, are not commonly available and are not described here. In the single-breath technique, the subject exhales to RV and then inspires the test gas (10% helium, 0.3% CO, 21% oxygen, and balance nitrogen) briskly to TLC. This vital capacity size breath is held for 10 seconds and then exhaled into a sample bag after an initial discard of 0.5-0.75 L to account for dead space.

The grab sample (0.5-1 L) then is analyzed for helium and CO. The helium dilution of the vital capacity breath of test gas by the patient's RV provides both a means to estimate the initial alveolar concentration of CO and to estimate the patient's TLC. The rate of diffusion of the CO can be estimated by the change from this initial alveolar level to that of the expired grab sample. This change in the CO concentration is then multiplied by the single-breath estimate of TLC to calculate the diffusing capacity. Abnormal hemoglobin (Hb) levels can affect the diffusing capacity and, if known, should be used to mathematically correct the measured diffusing capacity to normal Hb.

The measured DLCO also can be adjusted for elevated levels of carboxyhemoglobin, as follows:

The diffusing capacity is a measure of the conductance of the CO molecule from the alveolar gas to Hb in the pulmonary capillary blood. The transfer of the CO molecule is limited by both perfusion and diffusion. CO (and oxygen) must pass through the alveolar epithelium, tissue interstitium, capillary endothelium, blood plasma, and red cell membrane and cytoplasm before attaching to the Hb molecule.

Reported parameters typically include the DLCO (mL/min/mm Hg) and the DL/VA, the average inspiratory vital capacity (IVC) of 2 reproducible measurements and the average calculated alveolar volume (VA), and Hb-corrected and carboxyhemoglobin-corrected values.

Because the DLCO is directly proportional to VA (the single-breath dilutional estimate of TLC), nonpulmonary processes that reduce the TLC cause reductions in the DLCO. If VA can be assessed accurately, these reductions produce a normal or elevated DL-to-VA ratio. Examples of this include lung resection, thoracic cage abnormalities (eg, kyphoscoliosis), and small lungs. DLCO is reduced in pulmonary emphysema; however, because of the poor distribution of the inspired test gas, the VA may grossly underestimate the TLC, and the resultant DL/VA may be normal. A reduced DLCO and a reduced DL-to-VA ratio suggest a true interstitial disease such as pulmonary fibrosis or pulmonary vascular disease. Recent work has shown that, in normal patients, the DL/VA is increased to above normal levels when the DLCO test is performed at volumes less than the TLC. This suggests that a low DLCO and a normal DL/VA may be a function of an inappropriately low predicted value for DL/VA when TLC is reduced.

The pattern of a low DLCO and a normal DL/VA may not be sufficient to rule out the presence of parenchymal disease. The recent works of Johnson and Chinn et al advocate the volume correction of the predicted value for DLCO by using the measured VA to "correct" the predicted DLCO for low or high lung volumes. Further work is warranted, but studies demonstrating the nonlinearity of the relationship between lung volume and DLCO are sufficiently convincing that the practice of interpreting a low DLCO and a normal DL/VA as normal should not be performed. The degree of severity of reduction in the diffusing capacity can be assigned according to the following scheme: less than the lower limit of normal (LLN) but greater than 60% of predicted is mild, between 40 and 60% of predicted is moderate, and less than 40% is severe.

Nonperfusion of ventilated alveoli, such as in pulmonary vascular disease, produces reduction of both the DLCO and the DL/VA. Anemia produces a virtual reduction in pulmonary capillary blood volume that causes a reduction in DLCO that can be adjusted mathematically for the reduced Hb. The DLCO may be reduced temporarily in a variety of disorders such as pneumonia, interstitial infiltrative disorders, and alveolar proteinosis. The importance of obtaining an inspiratory vital capacity (IVC) greater than 90% of the best measured VC from the day of the test cannot be overemphasized. Inability to achieve an IVC of greater than or equal to 90% of the largest VC measured that day must be noted on the report.

Maximum inspiratory pressures (MIP), maximum expiratory pressures (MEP), negative inspiratory force (NIF), respiratory pressures, maximum respiratory pressures

Assessing respiratory muscle strength allows for assessment ventilatory failure, restrictive lung disease, and respiratory muscle strength.

Determinations of respiratory muscle pressures are a quick and noninvasive means of assessing respiratory muscle strength.

MIP: Patients breathe through a flanged mouthpiece with nose clips in place. Patients are instructed to exhale to RV. At RV, a valve or shutter is closed and the patient is coached to inhale as forcefully as possible. Maximum pull should be maintained for 1-2 seconds. A standardized leak must be present in the measurement system to eliminate significant overstatement of MIP by allowing the cheek muscles to contribute to the measured pressures. Initial maximum negative pressures that cannot be maintained for 1 full second are ignored.

MEP: Patients breathe through a flanged mouthpiece with nose clips in place. Patients are instructed to inhale to TLC. At TLC, a valve or shutter is closed and the patient is coached to exhale as forcefully as possible. Maximum push should be maintained for 1-2 seconds. Initial maximum positive pressures that cannot be maintained for 1 full second are ignored.

A new procedure, measurement of sniff nasal-inspiratory force (SNIF) has recently been shown to have promising utility in predicting mortality in patients with amyotrophic lateral sclerosis (ALS). A standardized device is not commercially available. A polyethylene catheter ending in a plug is attached to a pressure transducer, and the plug end is inserted into a nostril. The contralateral nostril is occluded, and the patient is instructed to exhale to FRC, then close the mouth and take a deep sniff or a maximal inspiratory effort. Both nostrils are tested, and the highest of 6 recorded pressures sustained for at least 1 second is reported.

Maximal inspiratory mouth pressure (PImax), maximal expiratory mouth pressure (PEmax), and SNIF are reported in centimeters of water pressure.

As many as 10 efforts are needed before consistency (2 measurements within 10% of the highest measured pressure) is achieved in some patients. When respiratory muscle fatigue or neuromuscular disease is present, fatigue may set in before consistency is achieved. Adequate rest between efforts is important.

The range of normal values is broad, suggesting wide variations in respiratory muscle strength among normal values. This makes interpretation of low values difficult. Initial values should be compared to the lower limit of normal values for the patient's age.

In general, a PImax of less than -80 cm water pressure and a PEmax of greater than +80 cm water pressure excludes important weakness of the respiratory muscles. Patients with a PEmax less than 50 cm water pressure may have difficulty generating sufficient cough to clear respiratory secretions.

In patients with ALS, a SNIF pressure less than 40 cmH₂O was associated with a hazard risk for death of 9.1 (confidence interval [CI], 4-20.8) and the median mortality was 6 ± 0.3 months (95% CI, 2.5-8.5 mo).

All tests are dependent on effort and technique. Good instruction, vigorous coaching, and adequate rest between efforts are essential. Maximum values should be reproducible within the greater of 10% or 5 cm water pressure. A controlled leak (1 mm diameter, 15 mm length) must be part of the system to prevent erroneously high MIP readings resulting from the use of cheek muscles. This leak is not needed for MEP or SNIF pressure measurements.

Oximetry, oxygen saturation check, oxygen sat check, exercise oximetry, oxygen titration by oximetry, oxygen saturation measured using pulse oxymetry (SpO₂), oxygen desaturation test

Standard pulse oximeter probes may be placed on fingers or earlobes of ambulatory patients. Some oximeters offer reflectance probes that can be placed on the forehead. Fingernail polish should be removed, and peripheral circulation should be maximized by warming or by applying vasodilating cream, if necessary.

Although widely used, the practice of assessing oxygen desaturation by pulse oximetry is poorly standardized. The principle of oximetry measurement by spectrophotometry, although improving, is not as reliable as many practitioners believe. One side of the oximeter probe acts as a light-emitting source, and the other side acts as a photodetector. The probe is placed on a finger or earlobe. A forehead reflectance probe may also be used. The relative absorption of red (absorbed by oxygenated blood) and infrared (absorbed by deoxygenated blood) light of the pulsatile (systolic) component of the absorption waveform correlates to arterial blood oxygen saturation.

Resting readings should be for at least 5 minutes, and the stability of the reading should be characterized by the report. If a finger probe is used, the hand should be placed on the chest at the level of the heart to minimize venous pulsation, which can falsely lower the reading. Correlation of the heart rate displayed on the oximeter with an ECG rate or a manually palpated pulse can help characterize the quality of the signal. Agreement within 5 or more beats per minute generally rules out significant motion artifact. Ideally, correlation of pulse oximetry saturation should be made with a measured oxygen saturation by multiple wavelength spectrophotometry on a simultaneously obtained arterial blood gas sample.

Documentation of the type of pulse oximeter used, probe type, and probe site should be included on each report. The heart rate and SpO₂ readings at rest should be reported.

When obtaining pulse oximetry readings during exercise, the type and intensity of exercise (eg, walking speed, duration of activity) along with the heart rate and SpO₂ at the end of the activity should be reported. When desaturation is detected, the activity should be repeated with supplemental oxygen in place to demonstrate improvement in SpO₂ values.

Pulse oximetry is often performed (though optional) in the setting of the 6-minute walk test, a standardized measure of functional exercise capacity. This test is a measure of the maximum distance the patient is able to walk in a hallway with a minimum of 100 feet marked in 5-foot increments. The patient is permitted to slow down or even stop, if required; however, the elapsed time counter continues during rest periods. This test should be performed while exercise oxygen needs are being adequately met with portable oxygen delivery. Borg dyspnea and fatigue scores are collected immediately after completion of the walk.

Interpretation of oximetry studies, while seemingly simple, generally is not possible without characterizing oximeter accuracy by correlating SpO₂ with at least one simultaneously obtained arterial oxygen saturation (SaO₂). Laboratories should characterize the average oximeter bias (SpO₂ - SaO₂) through pooled data to better understand the limitations of using the oximeter, but this does not eliminate the possibility that oximeter readings on individual patients may exhibit larger biases. While SpO₂ readings greater than 95% make the probability of clinically significant hypoxemia unlikely, clinical suspicion of hypoxemia should initiate the examination of ABGs. The goal of titration of supplemental oxygen should be a stable SpO₂ reading of 93% or higher. Arterial desaturation can be considered present when the pulse oximeter saturation falls more than 4% below the baseline reading.

The role of pulse oximetry in the Medicare guidelines for reimbursement for continuous supplemental oxygen therapy are demonstration of one of the following while at rest and breathing room air: PaO₂ less than or equal to 55 mm Hg, SaO₂ less than or equal to 88%, or SpO₂ less than or equal to 88%.

If supplemental oxygen is prescribed at a flow rate of greater than 4 liters per minute (LPM), the results of a PaO₂ or oxygen saturation (SaO₂ or SpO₂) taken on 4 LPM supplemental oxygen must be provided.

Patients may qualify for supplemental oxygen therapy reimbursement even if the PaO₂ is greater than 55 mm Hg and the SaO₂ or SpO₂ is greater than 88% if one of the following conditions is met: (1) dependent edema due to congestive heart failure; (2) cor pulmonale documented by P pulmonale on an ECG or by an echocardiogram, gated blood pool scan, or direct pulmonary artery pressure measurement, and (3) hematocrit greater than 56%.

Carboxyhemoglobin (CoHb) and methemoglobin (metHb) absorb light at the same wavelength as deoxyhemoglobin, causing a very significant overestimation of SaO₂ when these are elevated. Pulse oximetry has other shortcomings. It does not provide information about the oxygen content of the arterial blood. Tissue hypoxia can exist when SpO₂ is normal when anemia is present. Elevated levels of dysfunctional hemoglobins (CoHb, metHb) can cause significant overestimation of the actual SaO₂.

Additionally, pulse oximetry does not address the adequacy of ventilation, which can be assessed only by evaluation of the partial pressure of carbon dioxide in arterial gas (PaCO₂). Motion of the finger within the probe can cause a motion artifact secondary to equal rhythmic absorption of red and infrared light that most oximeters interpret as an SpO₂ reading of 85%. Disposable finger probes fixed to the probe site with adhesive and fixed positioning of the probe site during walking can minimize this.

Pulse oximetry tends to overestimate SaO₂. One reason for this is the fact that pulse oximetry expresses the percentage of oxyhemoglobin without consideration for CoHb or metHb.

In contrast, spectrophotometrically determined oxygen saturation from an ABG sample expresses oxygen saturation as the percentage of the sum of reduced hemoglobin, oxyhemoglobin, CoHb, and MetHb.

This significant difference generally results in pulse oximeters reporting an oxyhemoglobin value that is 2-3% higher than the spectrophotometrically determined oxygen saturation, even when the pulse oximeter is functioning perfectly.

While the accuracy of pulse oximetry generally is good in population studies (SaO₂ - SpO₂ <2%), SpO₂ values in individual patients may show a much greater bias, even when dysfunctional Hb levels are normal. Anemia and polycythemia can cause greater oximeter overestimation. SaO₂ from simultaneously obtained ABG determinations should be used to characterize oximeter bias in individual patients, although this is not commonly performed.

ABG determinations should be considered whenever the clinical suspicion of hypoxemia exists, even when the oximeter displays a value over the threshold of 88%. Finally, the shape of the oxygen dissociation curve causes the pulse oximeter to be inherently insensitive to mild hypoxemia because relatively large changes in PaO₂ in the flat upper portion of the curve cause very small changes in blood SaO₂.

Advantages of pulse oximetry include that it is noninvasive, simple, and can be used to evaluate trends (evaluation of oxygenation during exercise, sleep, during procedures).

Disadvantages of pulse oximetry include that it cannot be used to assess oxygen delivery (anemia) or adequacy of ventilation (PaCO₂) and that accuracy is lessened in the presence of elevated dysfunctional hemoglobin levels (CoHb, metHb), with a tendency to overestimate SaO₂ by an average of 2-3%.

Overestimation of SaO₂ is possible with bright sunlight on the probe, fluorescent lights, operating room lights, infrared heat lamps, elevated CoHb, elevated metHb, anemia, and motion artifact if the actual SaO₂ is less than 85%.

Underestimation of SaO₂ is possible because intravascular dyes, such as methylene blue and indocyanine green, produce transient reductions in SpO₂. Fingernail polish, increased venous pressures, and motion artifact if the actual SaO₂ is greater than 85% also can cause underestimation of the SaO₂.

Diagnose asthma, confirm diagnosis of asthma, document severity of hyperresponsiveness, and follow changes in hyperresponsiveness

Absolute contraindications include FEV₁ less than 1.5 L in adults, less than 1 L in children, recent severe acute asthma, myocardial infarction or cerebral vascular accident within 3 months, and arterial aneurysm.

Relative contraindications include moderate baseline airway obstruction, spirometry-induced bronchoconstriction, recent upper respiratory tract infection (URI), exacerbation of asthma, hypertension, pregnancy, and epilepsy.

The following medications are withdrawn before a methacholine challenge test for the specified period:

The following list shows the most common schedule of methacholine dosing in use in the United States today. Some labs begin with the lowest strength methacholine solution immediately after baseline; others advocate the use of a diluent stage between baseline and methacholine. This allows identification of a small percentage of individuals who exhibit significant bronchoconstriction in response to the diluent itself, suggestion, or repeated spirometry efforts. Abbreviated protocols that start with higher concentrations of methacholine should be used cautiously, if at all.

Methacholine challenge schedule: After establishing baseline spirometry measurements, the patient inhales 5 breaths of saline or diluent aerosol and then 5 breaths of each of the following strengths of aerosolized methacholine in solution: 0.0625 mg/mL, 0.25 mg/mL, 1 mg/mL, 4 mg/mL, and 16 mg/mL.

An alternative longer (10-stage) dosing schedule that may yield a more precise assessment of airway hyperreactivity calls for the patient to inhale 5 breaths of methacholine aerosol in the following strengths: 0.031 mg/mL, 0.0625 mg/mL, 0.125 mg/mL, 0.25 mg/mL, 0.5 mg/mL, 1 mg/mL, 2 mg/mL, 4 mg/mL, 8 mg/mL, and 16 mg/mL.

The following dosing schedule is approved by the US Food and Drug Administration and also may be used, although the ATS guidelines for methacholine challenge testing recommend 1 of the 2 schedules outlined above because the dosing steps are more even: 0.025 mg/mL, 0.25 mg/mL, 2.5 mg/mL, 10 mg/mL, and 25 mg/mL.

Methacholine aerosol is delivered in a standardized fashion by using a dosimeter, a device that applies a 0.6-second burst of compressed air to the nebulizer at the start of the inhalation from FRC to TLC. Subjects should hold their breath for 5 seconds. Spirometry is performed 30-90 seconds after the end of the last breath of each stage of the challenge. Symptoms volunteered by the subject are recorded. The challenge is discontinued when a fall in FEV₁ of greater than 20% is observed upon repeat efforts or a final cumulative dose of 188.64 cumulative dose units is received. Administration of a bronchodilator should immediately follow the final postmethacholine assessment.

Results are presented as both a table of spirometry parameters for each stage of the challenge and as a dose-response curve plotting the fall in FEV₁ against the methacholine concentration. The reporting of the PC20 (provocative concentration in mg/mL causing a 20% fall in FEV₁ from baseline) is the usual method of expressing the results of a positive test.

A 20% fall in FEV₁ generally is considered a positive test. One scheme for using the PC20 FEV₁ to characterize the severity of clinical hyperreactivity has been used by Hargreave et al.

PC20 FEV₁ severity is assessed as follows: 0.03-0.124 is considered severe, 0.125-1.99 is considered moderate, 2.00-7.99 is considered mild, and 8-25 is considered an increased hyperresponsive reaction (however, clinically significant disease is not common).

Spurious nonreproducible falls should not be considered valid. Continuation of the challenge beyond 25 mg/mL has little clinical value because responses of some healthy patients who are nonasthmatic begin at this level.

Failure to demonstrate bronchial hyperreactivity does not totally exclude asthma, particularly asthma triggered by occupational exposure to chemicals (eg, methylene diisocyanate, toluene diisocyanate).

Nonspecific bronchial hyperreactivity is characteristic of asthma but can persist for some months after a viral respiratory illness.

Nonspecific bronchial hyperreactivity also can be found in chronic obstructive pulmonary disease, cystic fibrosis, and bronchiectasis.

CPX test is used for evaluation of dyspnea that is out of proportion to findings on static pulmonary function tests, preoperative evaluation of operative risk when lung function is compromised or removal of lung segments is contemplated, evaluation of disability, identification of exercise-induced asthma, and evaluation of therapy.

Absolute contraindications include unstable angina, aortic stenosis, uncontrolled hypertension, uncontrolled asthma, hypoxemia (SaO₂ <85% at rest), and febrile illness.

Relative contraindications include hypertension, cardiac disease, epilepsy, and locomotor disorder (inability to exercise).

Perform calibration of the volume-measuring device and gas analyzers. Patients should avoid eating a heavy meal 1-2 hours before the test. Patients should wear loose comfortable clothing and athletic shoes. If exercise-induced bronchoconstriction is considered, withhold medications as with the methacholine challenge. ECG electrodes/leads are applied. Adjustment of the seat height on a bicycle ergometer is made to permit near-full leg extension when one pedal is at its lowest position (slight bend at knee). Airtight fitting of a low dead-space mask or mouthpiece/nose clips is applied. Apply and correctly position a blood pressure cuff. A pulse oximeter probe is applied securely. Insertion of an indwelling arterial canula for arterial blood sampling is optional.

The cardiopulmonary exercise test is a means of measuring the integrated response of the pulmonary, cardiovascular, and muscular systems to a steadily increasing workload. The test may be performed on a bicycle ergometer or treadmill. Resting measurements are made for 3-5 minutes. Three minutes of unloaded cycling is performed as a warmup period. The workload is incremented at a rate designed to allow reaching maximum work capacity in 8-12 minutes. The test continues to a point of symptom limitation (severe dyspnea, chest pain, faintness, pallor, inability to continue pedaling or walking) or discontinuation by medical staff for one of the following conditions: significant ECG abnormalities, fall in systolic or diastolic blood pressure (BP) greater than 20 mm Hg below resting value, rise in systolic BP to greater than 250 mm Hg, rise in diastolic BP to greater than 120 mm Hg, severe oxygen desaturation ( <80%), or achievement of maximum predicted heart rate.

Determining the proper rate of workload incrementation: The workload incrementation rate should be chosen to produce a test of 8-12 minutes in length. If the workload incrementation is too high, the test will be too brief. In this circumstance, the patient should be allowed to recover and should be retested. If the workload incrementation is too small, fatigue may prevent a valid second test. Below is Wasserman's method for estimating the workload increment size for cycle ergometry:

Patients with significant reductions in the predicted VEmax (FEV₁ below 50% of predicted) should use an increment of 10 watts/min or less. Patients with severe obstruction resulting in a preexercise maximum voluntary ventilation (MVV) of less than 40 L/min should use a 5-watt/min incrementation rate.

The following parameters are measured or calculated on a breath-by-breath basis: minute ventilation (V_E, LPM), tidal volume (V_T, mL/breath), respiratory rate (RR, mL/breath), oxygen uptake (VO₂, mL/min and mL/min/kg), carbon dioxide production (VCO₂, mL/min), respiratory exchange ratio (RER, VCO₂-to-VO₂), SpO₂, heart rate (HR, beats/min), oxygen pulse (mL VO₂/min/heartbeat), and BP (mm Hg). If ABG determinations are obtained, discrete values for the ratio of dead space to tidal volume (VD-to-V_T) and alveolar to arterial oxygen gradient (A-a-to-O₂) can be calculated for that interval of exercise.

The assessment of a normal work capacity is made by evaluation of the peak oxygen uptake (VO₂ peak). The normal value for oxygen uptake is based on sex, age, and weight.

The predicted peak VO₂ is determined by the patient's age and sex. This value can be further refined for sedentary individuals by a 3-step process (see below) that adjusts the predicted value up or down based on a comparison of the patient's weight and their ideal body weight.

A normal CPX test demonstrates a normal peak VO₂, the peak HR at or below the predicted maximum HR, and demonstration of ventilatory reserve (peak ventilation/predicted maximum ventilation <65-70%). When the VO₂ peak is low, the peak HR is compared to the predicted maximum HR to determine cardiovascular reserve. A ratio of HR peak to HR predicted maximum that approaches or exceeds 1 indicates a clear cardiovascular limitation to exercise.

Likewise, the peak expired volume (minute ventilation, V_E) is compared to the larger of a pretest MVV or FEV₁ multiplied by 40 to determine the pulmonary reserve. A ratio of V_E peak to V_E predicted maximum that approaches or exceeds 1 is a clear indication of pulmonary limitation. A VO₂ peak below 15 mL/min/kg often is used as an indication of disability. Pulmonary limitation also may cause significant oxygen desaturation due to the reduction of the transit time of the pulmonary capillary blood to a point where diffusion limitation can occur. In the absence of cardiovascular or pulmonary limitation, peripheral circulatory or skeletal muscle limitation may exist. This must be distinguished from poor effort or malingering.

The anaerobic threshold is defined as the workload (expressed as VO₂) in which blood lactate levels rise significantly, indicating that a significant fraction of the work is being accomplished by anaerobic metabolic sources. The establishment of the anaerobic threshold may have clinical importance, particularly when the evaluation seeks to determine the presence of an occupational disability.

Identifying the anaerobic threshold noninvasively: The noninvasive determination of the anaerobic threshold can be accomplished by analyzing time averaged (20- to 30-s intervals) plots of parameters measured or calculated during the CPX test. Two methods can be used, the V-slope method and the ventilatory equivalent method. Both methods allow determination of the same physiologic event, the increased production of carbon dioxide by isocapnic buffering of lactic acid produced by anaerobic metabolism and yield comparable estimations.

V-slope method: The V-slope method of determining the anaerobic threshold makes use of the fact that carbon dioxide production (VCO₂) plotted against oxygen consumption (VO₂) shows a slope of slightly less than 1 for work below the anaerobic threshold. A line of best fit for points obtained from the start of exercise is drawn through this plot to obtain the initial slope (S1). When this slope changes to a steeper slope (S2), it indicates an increase in carbon dioxide production from the isocapnic buffering of lactic acid. The intersection of S1 and S2 mark the anaerobic threshold, typically reported as either the absolute value of the oxygen uptake (VO₂, mL/min) at that point or as the percentage of the predicted peak VO₂.

Ventilatory equivalent method: The ventilatory equivalent method of determining the anaerobic threshold makes use of the derived values known as the ventilatory equivalents for oxygen and carbon dioxide. Carbon dioxide production (VCO₂) and oxygen consumption (VO₂) divided into the minute ventilation (V_E, L/min) are known as the ventilatory equivalents for carbon dioxide (V_E/VCO₂) and oxygen (V_E/VO₂). When time averaged (20- to 30-s intervals) plots of V_E/VO₂ and V_E/VCO₂ are plotted against time, the point at which the V_E/VO₂ is seen to increase without a simultaneous increase in the V_E/VCO₂ marks the anaerobic threshold.

Normal male: This 46-year-old man who previously smoked (smoking history of 30 pack-years) is evaluated as a biological control in the authors' laboratory. He has no health complaints.

The patient stopped the exercise test citing leg fatigue and dyspnea as the reasons for terminating the test. The results reveal a normal oxygen uptake with a normal cardiovascular limitation to exercise (predicted maximum HR was exceeded). Significant ventilatory reserve existed at the end of exercise.

Ventilatory limitation: A 55-year-old man with a smoking history of 35 pack-years and a diagnosis of emphysema was referred for cardiopulmonary exercise testing to evaluate the complaint of dyspnea upon exertion. The patient uses an inhaled beta-agonist as needed.

The patient terminated the procedure citing dyspnea as the sole reason for stopping the test. The results show moderate impairment of the peak oxygen consumption with a clear ventilatory limitation to exercise. Significant cardiovascular reserve existed at the end of exercise, and the ventilatory reserve was below normal. Pulse oximetry readings are suggestive of exercise desaturation.

Cardiac limitation: This 48-year-old woman was referred for a cardiopulmonary exercise testing to evaluate her shortness of breath upon exertion over the last 6 months. Pulmonary function tests reveal a mild restrictive ventilatory defect with a normal DLCO, suggesting no active parenchymal disease.

The patient terminated the exercise test citing shortness of breath. The results reveal a moderately reduced oxygen consumption with a cardiovascular limitation (HR maximum exceeded the predicted maximum HR) and adequate ventilatory reserve. The oxygen pulse did not increase normally during the study, with near-peak values observed during unloaded cycling and very little increase during the work phase of the study. Cardiac function studies demonstrated left ventricular failure secondary to mitral insufficiency.

VO₂ maximum values greater than 20/mL/kg/min or 75% of predicted indicate the ability to withstand pneumonectomy when the cardiac history is negative.

A VO₂ maximum between 10 and 20 mL/kg/min and 40-75% of predicted require prediction of postoperative FEV₁, DLCO, and VO₂. Prediction of postoperative function is calculated by multiplying the preoperative value by the fraction of total perfusion ascribed to the remaining lung, as follows:

When the FEV₁ PPO and DLCO PPO are greater than 40% and the VO₂ PPO is greater than 10 mL/kg/min and 35% of predicted, resection up to the calculated extent is feasible.

A VO₂ maximum of less than 40% or 10 mL/kg/min or VO₂ maximum PPO of less than 35% or 10 mL/kg/min strongly suggest inoperability for lung resection candidates.

Because motion artifact typically causes an estimation of SpO₂ of 85%, care should be taken to differentiate oxygen desaturation from motion artifact, particularly if circulation to the oximeter probe site is compromised by pressure on a treadmill handrail or ergometer handgrip. If arterial blood is sampled at peak exercise, it should be obtained while exercising because PaO₂ values can recover in as little as 15-30 seconds after cessation of exercise.

ABGs are used in the evaluation of ventilation, oxygenation, and acid-base status.

No contraindications exist, although some sampling sites may be deemed unsuitable for use secondary to peripheral circulatory disorders.

Assess collateral circulation. If a baseline room air oxygen level is desired, patients should discontinue use of supplemental oxygen for 20 minutes. If the patient is receiving anticoagulant therapy, extra care must be taken to continue pressure on the sampling site until bleeding has stopped. Personnel obtaining and/or analyzing the sample should don rubber gloves and take appropriate infection control measures.

The sampling site of choice is the radial artery, unless tests of collateral circulation indicate otherwise. Samples also may be obtained from the brachial and femoral arteries.

Measured: pH, PaCO₂ (mm Hg or kilopascal), PaO₂ (mm Hg or kilopascal), and, if hemoximetry is performed, total hemoglobin (tHb, g/dL), oxyhemoglobin (O₂Hb [%]), and metHb (%)

Calculated: Total bicarbonate (HCO₃ [mEq/L]), base excess or deficit (mEq/L), oxygen content (CO₂ [mL] O₂/dL or volume%)

ABGs provide 3 assessments of the function of the respiratory system: evaluation of oxygenation (PaO₂ [mm Hg] and A-a oxygen gradient PO₂), evaluation of the adequacy of ventilation (PaCO₂ [mm Hg]), and evaluation of the lung's role in acid-base balance of the arterial blood (pH, PaCO₂).

In healthy subjects breathing room air at sea level, the normal PaO₂ (mm Hg) is affected by age, body mass index (BMI), PaCO₂ (mm Hg), and posture (upright vs supine). An average decline in PaO₂ of 10 mm Hg occurs for each decade of life up to approximately 75 years.

Low levels of arterial oxygen can be attributed to 1 or more of 5 categories, as follows: (1) ventilation/perfusion (V/Q) mismatching, (2) alveolar-capillary diffusion limitation, (3) hypoventilation, (4) anatomic right-to-left shunts, and (5) low inspired oxygen partial pressures (eg, altitude).

Evaluation of hypoventilation as a cause for a reduced PaO₂ can be made using the ideal alveolar air equation, which allows computation of an alveolar oxygen tension and calculation of an A-a oxygen gradient.

PaO₂ is the ideal alveolar oxygen tension, PIO₂ is partial pressure of inspired oxygen, PaCO₂ is partial pressure of arterial carbon dioxide, and R is the ratio of carbon dioxide production to oxygen consumption (generally assumed to be 0.8 at rest).

The measured partial pressure of oxygen in the arterial blood is subtracted from the ideal alveolar oxygen tension to calculate the A-a PO₂ gradient. This gradient can be compared to a normal age-adjusted gradient (normal resting, room air A-a oxygen gradient = (age + 4)/4) to determine the effects of hypoventilation and hyperventilation. Reduced arterial oxygen tension secondary to pure hypoventilation exhibits a normal A-a PO₂ gradient.

Determination of right-to-left shunt by blood gases: The fraction of the cardiac output that bypasses normal circulatory pathways can be estimated by obtaining an ABG sample after 20 minutes of breathing 100% oxygen from a large reservoir bag. This period of oxygen breathing should wash out all of the nitrogen from all ventilated alveoli. This makes the measured oxygen gradient (A-a PO₂) independent of V/Q inequalities. While the true shunt requires a measurement of a mixed venous oxygen level, this often is not practical, and an estimated arterial-to-mixed venous oxygen content difference of 5 volume percent often is assumed, as shown.

Qs/Qt is the calculated right-to-left shunt fraction, 0.0031 is the solubility coefficient of oxygen in blood, (A-a) PO₂ is the gradient of alveolar to arterial oxygen partial pressure after 20 minutes of breathing 100% oxygen, and 5 is the assumed difference in resting arterial-to-mixed venous oxygen content. States of low and high cardiac output may invalidate the assumed arteriovenous oxygen (A-VO₂) difference and cause significant error in the calculated shunt fraction.

Causes of increased right-to-left shunting may be intrapulmonary, such as pulmonary arteriovenous malformations, dilated capillaries in hepatopulmonary syndrome, lobar collapse or consolidation, or extrapulmonary conditions (eg, right-to-left intracardiac shunts, bronchial artery-to-pulmonary vein connections.

Samples must be mixed with an anticoagulant, preferably heparin (if liquid, dead space volume of syringe and needle should be filled before sampling with 1000 U/mL heparin) to avoid clotting before or during analysis. If analysis is not performed immediately, samples should be placed in an ice-water solution.

Pulmonary Function Testing

AUTHOR AND EDITOR INFORMATION

SPIROMETRY

LUNG VOLUMES DETERMINATION

DIFFUSING CAPACITY OF THE LUNG FOR CARBON MONOXIDE

ASSESSMENT OF RESPIRATORY MUSCLE STRENGTH

PULSE OXIMETRY

METHACHOLINE CHALLENGE TESTING

CARDIOPULMONARY STRESS TESTING

ARTERIAL BLOOD GASES

MULTIMEDIA