Asthma and Chronic Obstructive Pulmonary Disease

Fun-Sun F. Yao

Angela R. Selzer

A. Medical Disease and Differential Diagnosis

What differential diagnosis is compatible with these symptoms?
What is the prevalence of asthma and chronic obstructive pulmonary disease (COPD)?
What is the etiology of asthma?
Discuss the pathogenesis of asthma. How is asthma distinguished from COPD?
What are the predisposing factors of bronchospasm?
What is the universal finding in ABGs during asthmatic attacks: hypoxemia or CO₂ retention?
Describe the abnormalities seen in spirometry, lung volumes, and lung capacities during an asthmatic attack.

B. Preoperative Evaluation and Preparation

How would you evaluate the patient preoperatively? What preoperative workup would you order?
How would you distinguish obstructive lung disease from restrictive lung disease by spirometry?
Define normal lung volumes and lung capacities. Give normal values for an average adult male.
What are flow-volume loops? Draw flow-volume loops for a healthy subject and patients with COPD, restrictive lung disease, fixed obstruction of the upper airway, variable extrathoracic obstruction, and variable intrathoracic obstruction.
Define closing volume (CV) and closing capacity (CC). What is the normal value of CV?
Why is the functional residual capacity (FRC) important in oxygenation?
How are FRC and CC affected by age and posture? How are they affected by anesthesia?
Give the equations for shunt (QS/QT) and dead space/tidal volume (VD/VT). What are their normal values?
Interpret the following ABG: pH, 7.36; PCO₂, 60 mm Hg; PO₂, 70 mm Hg; CO₂ content, 36 mEq per L.
What are the common physiologic causes of hypoxemia?
How would you prepare this asthmatic patient with COPD for surgery?
The patient comes to your perioperative clinic 2 weeks before surgery. He wants to know if his smoking puts him at increased risk during surgery. What do you tell him? Should he quit now?
You discover that the patient had a recent upper respiratory infection (URI), would you postpone surgery? For how long?
What medications would you expect the patient to have taken in the past or be taking at the present time?
Should the patient receive preoperative steroids? Why or why not?
What is the onset of action of intravenous steroid therapy in asthma?

C. Intraoperative Management

If the patient had a severe asthmatic attack in the operating room before the induction of anesthesia, would you proceed with the anesthetic or postpone the surgery?
The patient did not have an asthmatic attack in the operating room and you proceed with induction. How would you induce anesthesia? Would you use a supraglottic airway instead of an endotracheal tube?
Would you use propofol for induction of anesthesia?
Would you use thiopental, methohexital, etomidate, or ketamine for induction?
Would you administer lidocaine for intubation?
If this is an emergency surgery and rapid sequence induction is indicated, how would you induce anesthesia in this patient?
Could a regional technique be used for this surgery? Discuss the advantages and disadvantages of neuraxial anesthesia in this patient for this surgery.
Would you choose an inhalational or an intravenous technique for maintenance of anesthesia?
What mechanisms produce bronchodilation from volatile anesthetics?
Which muscle relaxants would you use? Why?
How will you ventilate the patient? Will you use positive end-expiratory pressure (PEEP)? How can you detect the presence of auto-PEEP on your ventilator?
In the middle of surgery, peak inspiratory pressures suddenly increase. How do you manage this?
How would you give β₂-agonists? What is their mechanism of action on asthma?
If the patient does not respond to the aforementioned treatment and becomes cyanotic, what would you do?
What are the differential diagnoses of intraoperative bronchospasm?
The asthmatic attack was relieved with your treatment and the surgery was completed. Following emergence, the patient was found to be hypoventilating. What are the common causes of hypoventilation? What will be your approach to treat hypoventilation?
Would you consider a deep extubation in this patient?
If the patient cannot be extubated, what measures can you take to reduce the likelihood of bronchospasm with an endotracheal tube in place?

D. Postoperative Management

In patients with asthma, are there special considerations for the use of opioids and nonsteroidal anti-inflammatory drugs (NSAIDs) for postoperative pain control?
Would you consider using a regional technique for analgesia?
The patient was breathing well and was extubated. Would you place this patient on supplemental oxygen in the recovery room? How much?

A. Medical Disease and Differential Diagnosis

A.1. What differential diagnosis is compatible with these symptoms?

The differential diagnoses of wheezing and dyspnea include bronchial asthma; COPD; acute left ventricular failure (cardiac asthma); upper airway obstruction by tumor or laryngeal edema; and endobronchial disease such as foreign body aspiration, neoplasms, bronchial stenosis, carcinoid tumors, recurrent pulmonary emboli, eosinophilic pneumonias, chemical pneumonias, and occasionally polyarteritis.

The triad of dyspnea, coughing, and wheezing, in addition to a history of periodic attacks, is quite characteristic of asthma. A personal or family history of allergic disease is valuable contributory evidence. The ability to trigger bronchospasm with histamine or methacholine administration is a hallmark characteristic of asthma. However, this airway hyperreactivity is typically present in patients with COPD as well. In patients such as this one, with a considerable smoking history, concomitant COPD and asthma is common, and airway obstruction with both reversible and irreversible components is frequently seen.

Severe COPD with systemic features is associated with a high perioperative mortality. The patient with advanced COPD has signs of wasting and nutritional deficiency. Signs of rightsided heart failure and cor pulmonale include jugular venous distension, a split second heart sound, tricuspid or pulmonary insufficiency murmurs, hepatic enlargement, and peripheral edema.

Cardiac asthma, on the other hand, is a misnomer and refers to acute left ventricular failure. Although the primary lesion is cardiac, the disease manifests itself in the lungs. The symptoms and signs may mimic bronchial asthma, but the findings of moist basilar rales, gallop rhythms, blood-tinged sputum, peripheral edema, and a history of heart disease allow the appropriate diagnosis to be reached.

American Thoracic Society/European Respiratory Society Task Force. Standards for the diagnosis and management of patients with COPD. Published 2004. Updated September 8, 2005. http://www.thoracic.org/go/copd. Accessed November 11, 2014.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2084-2087, 2102-2116, 2151-2160.

A.2. What is the prevalence of asthma and chronic obstructive pulmonary disease (COPD)?

Asthma is one of the most common chronic diseases globally and currently affects approximately 300 million people. The prevalence of asthma has risen in affluent countries over the last 30 years but now appears to have stabilized. The prevalence of asthma in the United States is 8.7% of the adult population and 8.2% of children. It occurs at all ages, with a peak in children aged 5 to 9 years. In childhood, there is a 10:7 male/female preponderance, which is reversed in adulthood (6.5:10 male/female).

The greatest modifiable risk factor for asthma is smoking. Nonmodifiable risk factors include income (inversely proportional), ethnicity (Whites and Hispanics have a reduced risk, increased prevalence in African Americans), and environmental exposure.

Although deaths from asthma are rare, the annual rate of death from asthma is approximately 15-fold higher in adults older than 65 years than in children (37.2 vs. 2.6 per million).

The estimated worldwide prevalence of COPD is 210 million. In the United States, 14.1% of smokers carry a diagnosis of COPD, 7.1% of former smokers, and 2.9% of never smokers. The majority (71.2%) of COPD patients carry the diagnosis of at least one
comorbidity and have a significantly higher rate of hyperlipidemia, hypertension, coronary artery disease, diabetes, cancer, stroke, and chronic kidney disease than patients without COPD.

Asthma Facts: CDC’s National Asthma Control Program Grantees. Published 2013. http://www.cdc.gov/asthma/reports_publications.htm. Accessed December 2, 2014.

Cunningham TJ, Ford ES, Rolle IV, et al. Associations of self-reported cigarette smoking with chronic obstructive pulmonary disease and co-morbid chronic conditions in the United States. COPD. 2015;12:276-286.

World Health Organization. Global Surveillance, Prevention and Control of Chronic Respiratory Diseases: A Comprehensive Approach. Geneva, Switzerland: World Health Organization; 2007.

A.3. What is the etiology of asthma?

Asthma is a heterogeneous disease with complex, multifactorial etiologies. The common denominator that underlies the asthmatic diathesis is a nonspecific hyperirritability of the tracheobronchial tree. Clinically, asthma is classified into two groups: allergic (extrinsic) and idiosyncratic (intrinsic). Allergic asthma is usually associated with a personal or family history of allergic diseases, positive skin reactions to extracts of airborne antigens, and increased levels of immunoglobulin E (IgE) in the serum. Immunologic mechanisms appear to be causally related to 25% to 35% of all cases and contributory in another 33%. Idiosyncratic asthma cannot be classified on the basis of immunologic mechanisms, and it is probably due to abnormality of the parasympathetic nervous system.

Bronchospasm is provoked when certain agents stimulate tracheobronchial receptors. Intraoperative bronchospasm is often cholinergically mediated. Afferent receptors in the bronchial mucosa can be an initiating event, although such an event is not always identifiable. Efferent parasympathetic fibers travel to bronchial smooth muscle where the stimulation of the M3 cholinergic receptors on bronchial smooth muscle results in bronchoconstriction. After release of acetylcholine (Ach) at the M3 receptor, the Ach will stimulate the M2 muscarinic receptor, an inhibitory receptor that limits further release of Ach. Alterations of M2 receptor function may contribute to bronchospasm.

Fanta CH. Asthma. N Engl J Med. 2009;360:1002-1014.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2102-2116.

A.4. Discuss the pathogenesis of asthma. How is asthma distinguished from COPD?

Asthma is a chronic disease characterized by reversible expiratory airflow obstruction resulting from narrowing of the airways in response to various stimuli and a nonspecific hyperirritability of the tracheobronchial tree.

COPD is characterized by mucous hypersecretion, ciliary dysfunction, lung hyperinflation, and irreversible expiratory airflow obstruction.

The underlying mechanism of both conditions is thought to be chronic airway inflammation. Bronchial biopsies of asthmatics reveal infiltration by inflammatory cells and epithelial shedding from the mucosa.

With asthma, exposure to an initiating stimulus triggers inflammatory cells (mast cells, eosinophils, T lymphocytes, macrophages, basophils, neutrophils, and platelets) and structural cells (epithelial cells, fibroblasts, and airway smooth muscle cells) to release various mediators that lead to bronchospasm, vascular congestion, increased capillary permeability (edema of bronchial mucosa), and thick tenacious secretions (Fig. 1.1).

The net result is a reduction in airway diameter, an increase in airway resistance, decreased forced expiratory volumes and flow rates, hyperinflation of the lungs and thorax, increased work of breathing, alterations in respiratory tract muscle function, mismatched ventilation/perfusion, and altered blood gases.

In COPD, goblet cell hypertrophy, activated inflammatory cells (lymphocytes, neutrophils, and macrophages), and alteration in function of structural cells lead to increased mucus production, airway fibrosis, loss of alveolar attachments, and pulmonary vascular remodelling. The net result is hypersecretion of mucus, emphysema with peripheral airway collapse, impaired gas exchange, pulmonary hypertension, and right ventricular dysfunction.
The minority of COPD cases are a result of a genetic deficiency in antitrypsin levels, leading to an imbalance between antiproteinases and increased lung parenchymal destruction.

FIGURE 1.1 The pathogenesis of bronchial asthma. IgE, immunoglobulin E; PAF, platelet-activating factor.

Fanta CH. Asthma. N Engl J Med. 2009;360:1002-1014.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2102-2116, 2151-2160.

A.5. What are the predisposing factors of bronchospasm?

Allergens. Inhaled allergens are common triggers of asthma. Airborne allergens are able to activate mast cells with bound IgE, immediately releasing bronchoconstrictor.
Infections. Respiratory tract infections are among the most common stimuli that evoke acute asthmatic attacks.
Pharmacologic stimuli. Drugs associated with bronchospasm include coloring agents such as tartrazine, β-adrenergic antagonists, acetylcholinesterase inhibitors, and sulfiting agents. Aspirin and other NSAIDs, such as indomethacin, mefenamic acid, ibuprofen, fenoprofen, flufenamic acid, naproxen, and phenylbutazone, can worsen asthma
via inhibition of prostaglandin G/H synthetase 1 (cyclooxygenase type 1). All nonspecific β-blockers should be avoided in asthmatics because their use can lead to severe bronchospasm. The ultra-short-acting β-1 selective antagonists landiolol and esmolol can be safely used perioperatively in patients with airway hyperreactivity. Intraoperative bronchospasm is more likely to occur after administration of acetylcholinesterase inhibitors for neuromuscular blockade reversal. Adequate dosing of a concomitant anticholinergic is necessary to avoid this complication, and some advocate avoiding reversal altogether in an asthmatic patient with adequate return of neuromuscular function.
Environment and air pollution. Some types of asthma, such as Tokyo-Yokohama or New Orleans asthma, tend to occur in individuals who live in heavy industrial or dense urban areas. Dry, cold air can also trigger bronchospasm in susceptible individuals.
Occupational factors. Various compounds used in industry can cause asthma in susceptible individuals. Various names have been applied to this condition, such as meat wrapper’s asthma, baker’s asthma, and woodworker’s asthma.
Exercise. Asthma can be induced or made worse by physical exertion. The mechanism is linked to hyperventilation, which results in increased osmolality in airway lining fluid and triggers mast cell mediator release, resulting in bronchoconstriction.
Emotional stress. Asthma can be induced by bronchoconstriction through the cholinergic reflex pathway.

Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-existing Disease. 6th ed. Philadelphia, PA: Churchill Livingstone; 2012:182-188.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2102-2116.

Yamakage M, Iwasaki S, Jeong SW, et al. Beta-1 selective adrenergic antagonist landiolol and esmolol can be safely used in patients with airway hyperreactivity. Heart Lung. 2009;38:48-55.

A.6. What is the universal finding in ABGs during asthmatic attacks: hypoxemia or CO₂ retention?

Hypoxemia is a universal finding during asthmatic attacks. Frank ventilatory failure with CO₂ retention is relatively uncommon because CO₂ has a diffusion capacity that is 20 times higher than that of oxygen. During acute asthmatic attacks, most patients try to overcome airway obstruction and hypoxia by hyperventilation. This results in hypocarbia and respiratory alkalosis. CO₂ retention is a late finding and indicates severe and prolonged airway obstruction, as in status asthmaticus.

Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-existing Disease. 6th ed. Philadelphia, PA: Churchill Livingstone; 2012:182-188.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2102-2116.

A.7. Describe the abnormalities seen in spirometry, lung volumes, and lung capacities during an asthmatic attack.

The forced vital capacity (FVC) is usually normal but may be decreased during a severe attack. The forced expiratory volume at 1 second (FEV₁) is sharply reduced, usually to less than 50% of the FVC, typically less than 40% of that predicted. The FEF_25%-75% is sharply reduced as well. FEF_25%-75% (also referred to as the maximum midexpiratory flow rate or MMEFR) is the forced expiratory flow rate during 25% and 75% of the vital capacity. Unlike the FEV₁, the FEF_25%-75% is independent of patient effort. Other classic spirometry findings include a maximum breathing capacity (MBC) that is sharply reduced and a moderately decreased expiratory reserve volume (ERV). Conversely, the residual volume (RV) markedly increases, frequently approaching 400% of normal. This results in a net increase in total lung capacity (TLC) and FRC, which frequently doubles.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2094-2116.

Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth. 2009;103(suppl 1):i57-i65.

B. Preoperative Evaluation and Preparation

B.1. How would you evaluate the patient preoperatively? What preoperative workup would you order?

A thorough history and examination provides crucial information to the anesthesiologist caring for a patient with COPD and asthma. A focused medical history should include physical status and exercise tolerance, recent or current presence of infectious symptoms, sputum quantity and quality, known triggers of attacks, most recent exacerbation, current medications and time of last use, last course of systemic steroids, recent medication changes, coexisting morbidities, oxygen dependence, presence of obstructive sleep apnea, smoking history, recent weight loss, previous surgery, and anesthesia.

A focused cardiopulmonary exam should occur. First, observe the patient’s breathing and look for use of accessory muscles, pursed-lip exhalation, or cyanosis. Auscultation of the lungs can reveal wheezing, adventitious lung sounds, and hyperinflation. Auscultation of the heart may reveal a split second heart sound typical of cor pulmonale or the murmur of tricuspid or pulmonary regurgitation present in some patients with long-standing pulmonary hypertension. Additionally, jugular venous distension, peripheral edema, and hepatic enlargement may be present. Cachexia may also be seen.

Laboratory testing should include a complete blood count, serum electrolytes, electrocardiogram, urinalysis, and coagulation screening. Additionally, these patients should have a chest radiograph, a room air Spo2, and spirometry. Although not necessary in every patient, a computed tomography scan of the chest, detailed lung volume testing (including diffusion capacity of the lung for carbon monoxide [DLCO]), and a room air ABG would certainly be informative if available.

Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-existing Disease. 6th ed. Philadelphia, PA: Churchill Livingstone; 2012:182-195.

Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth. 2009;103(suppl 1):i57-i65.

Yamakage M, Iwasaki S, Namiki A. Guideline-oriented perioperative management of patients with bronchial asthma and chronic obstructive pulmonary disease. J Anesth. 2008;22:412-428.

B.2. How would you distinguish obstructive lung disease from restrictive lung disease by spirometry?

Table 1.1 summarizes the distinctions between the two types of lung diseases. In restrictive lung disease (e.g., pulmonary fibrosis and ankylosing spondylitis), the FVC is low because of limited expansion of the lungs or chest wall, although the FEV₁ is often not reduced proportionately, because airway resistance is normal. Therefore, the FEV₁/FVC percentage is normal or high.

In obstructive lung disease, the FEV₁/FVC is grossly reduced because the airway resistance is high. Normally, FEV₁ is more than 80% of FVC, and VC should be more than 80% of predicted value. The predicted values depend on body size, age, and sex. The FEV₁/FVC is less than 0.70 in COPD. The severity of COPD is determined by the FEV₁. Patients with an FEV₁
greater than 80% of predicted are considered to have mild COPD. Those with FEV₁ greater than 50% but less than 80% of predicted are classified as having moderate COPD. Severe cases of COPD have an FEV₁ that is less than 50% of predicted.

TABLE 1.1 Differences between Obstructive and Restrictive Lung Diseases

	OBSTRUCTIVE	RESTRICTIVE
Vital capacity	N or ↓	↓
Total lung capacity	N or ↓	↓
Residual volume	↑	↓
FEV₁/FVC	↓	N or ↑
Maximum midexpiratory flow rate	↓	N
Maximum breathing capacity	↓	N
↓, decreased; ↑, increased; FEV₁, forced expiratory volume in 1 second; FVC, forced vital capacity; N, normal.

The TLC is increased in obstructive lung disease and decreased in restrictive lung disease. However, TLC cannot be obtained by routine screening spirometry.

Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:279-281.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2087-2094.

Rabe KF, Hurd S, Anzueto A, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. GOLD executive summary. Am J Respir Crit Care Med. 2007;176:532-555.

B.3. Define normal lung volumes and lung capacities. Give normal values for an average adult male.

There are four basic “volumes” and four derived “capacities” that are combinations of these volumes (Fig. 1.2).

Tidal volume (VT) is the volume of air inhaled or exhaled during normal breathing. Normal VT is 500 mL or approximately 6 to 8 mL per kg.

Inspiratory reserve volume (IRV) is the maximum volume of gas that can be inhaled following a normal inspiration while at rest. Normal IRV is 2,000 to 3,000 mL.

Expiratory reserve volume (ERV) is the maximum volume of gas that can be exhaled after a normal expiration. Normal ERV is 1,000 mL.

Residual volume (RV) is the volume of gas remaining in the lungs after a forced exhalation. Normal RV is 1,500 mL.

Vital capacity (VC) is the maximum amount of gas that can be exhaled after a maximum inhalation. VC is the sum of VT, ERV, and IRV. Normal VC is approximately 60 to 70 mL per kg.

Inspiratory capacity (IC) is the maximum amount of gas that can be inhaled from the resting expiratory position after a normal exhalation. It is the sum of VT and IRV. Normal IC is 3,500 mL.

Functional residual capacity (FRC) is the remaining lung volume at the end of a normal quiet expiration. It is the sum of RV and ERV. Normal FRC is 2,500 mL or 30 to 40 mL per kg.

FIGURE 1.2 Lung volumes and lung capacities.

Total lung capacity (TLC) is the lung volume at the end of a maximum inspiration. It is the sum of VC and RV. Normal TLC is 5,000 to 6,000 mL for an adult man and 4,000 to 5,000 mL for an adult woman.

Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:279-281.

Longo DL, Fauci AS, Braunwald E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2087-2094.

Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Philadelphia, PA: Butterworth-Heinemann; 2010:33-35.

B.4. What are flow-volume loops? Draw flow-volume loops for a healthy subject and patients with COPD, restrictive lung disease, fixed obstruction of the upper airway, variable extrathoracic obstruction, and variable intrathoracic obstruction.

Flow-volume loops provide a graphic analysis of flow at various lung volumes. To perform the test, subjects are asked to inhale maximally (to TLC) and then exhale as forcefully and maximally as possible (to RV). This cycle is repeated. The flow (L/sec) is plotted on the y-axis and volume (L) on the x-axis (Fig. 1.3A). The test requires a compliant patient for accurate results—the majority of the test is effort dependent, including the entire inspiratory curve and both ends of the expiratory curve (near TLC and RV). The forced expiratory flow during 25% to 75% of VC (FEF_25%-75%), is reflective of the small to medium sized airways and is considered a relatively effort-independent value.

Normal flow-volume loop (Fig. 1.3A). Inspiratory limb of loop is symmetric and convex. Expiratory limb is linear. Airflow at the midpoint of inspiratory capacity and airflow at the midpoint of expiratory capacity are often measured and compared. Maximal inspiratory flow (MIF) at 50% FVC is greater than maximal expiratory flow (MEF) at 50% FVC because dynamic compression of the airways occurs during exhalation.

Obstructive disorder (e.g., emphysema, asthma) (Fig. 1.3B). Although all airflow is diminished, expiratory prolongation predominates, and MEF < MIF. Peak expiratory flow (PEF) is sometimes used to estimate degree of airway obstruction but depends on patient effort.

Restrictive disorder (e.g., interstitial lung disease, kyphoscoliosis) (Fig. 1.3C). The loop is narrowed because of diminished lung volumes. Airflow is greater than normal at comparable lung volumes because the increased elastic recoil of lungs holds the airways open.

Fixed obstruction of the upper airway (e.g., tracheal stenosis, goiter) (Fig. 1.3D). The top and bottom of the loops are flattened so that the configuration approaches that of a rectangle. Fixed obstruction limits flow equally during inspiration and expiration, and MEF = MIF.

Variable extrathoracic obstruction (e.g., unilateral vocal cord paralysis, vocal cord dysfunction) (Fig. 1.3E). When a single vocal cord is paralyzed, it moves passively with pressure gradients across the glottis. During forced inspiration, it is drawn inward, resulting in a plateau of decreased inspiratory flow. During forced expiration, it is passively blown aside, and expiratory flow is unimpaired. Therefore, MIF 50% FVC < MEF 50% FVC.

Variable intrathoracic obstruction (e.g., tracheomalacia) (Fig. 1.3F). During a forced inspiration, negative pleural pressure holds the floppy trachea open. With forced expiration, loss of structural support results in tracheal narrowing and a plateau of diminished flow. Airflow is maintained briefly before airway compression occurs.

Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:280.

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