Handbook of Clinical Anesthesia

Chapter 11

Respiratory Function

Anesthesiologists directly manipulate pulmonary function, so it is important to have a thorough knowledge of pulmonary physiology for the safe conduct of anesthesia (Ault ML, Stock MC: Respiratory function. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 233–255).

1. Functional Anatomy of the Lungs
2. Muscles of Ventilation
3. The muscles of ventilation are endurance muscles that are adversely affected by poor nutrition, chronic obstructive pulmonary disease (COPD), and increased airway resistance.
4. The primary ventilatory muscle is the diaphragm with minor contributions from the intercostal muscles. The muscles of the abdominal wall are important for expulsive efforts such as coughing.
5. Lung Structures
6. The visceral and parietal pleura are in constant contact, creating a potential intrapleural space in which pressure decreases when the diaphragm descends and the rib cage expands.
7. The lung parenchyma is subdivided into three airway categories based on functional lung anatomy (Table 11-1).
8. Large airways with diameters of above 2 mm create 90% of total airway resistance.
9. The number of alveoli increases progressively with age, starting at about 24 million at birth and reaching the final adult count of 300 million by age 8 or 9 years. There is an estimated 70 m²of surface area for gas exchange.

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3. The adult trachea is 10 to 12 cm long with an outside diameter of about 20 mm. The cricoid cartilage corresponds to the level of the sixth cervical vertebral body. Both ends of the trachea are attached to mobile structures, and in adults, the carina can move an average of 3.8 cm with flexion and extension of the neck. (This is important in intubated patients.) In children, tracheal tube movement is even more critical because displacement of even 1 cm can move the tube out of the trachea or below the carina.
4. In adults, the right mainstem bronchus leaves the trachea at approximately 25 degrees from the vertical tracheal axis; the angle of the left mainstem bronchus is approximately 45 degrees. (Therefore, accidental endobronchial intubation or aspiration is more likely to occur on the right side.) In children younger than age 3 years, the angles created by the right and left mainstem bronchi are approximately equal.
5. The right mainstem bronchus is approximately 2.5 cm long before its initial branching; the left mainstem bronchus is about 4.5 cm. In 2% to 3% of adults, the right upper lobe bronchus opens into the trachea above the carina, which is important to know during placement of a double-lumen tube.
6. Respiratory Airways and the Alveolar–Capillary Membrane
7. The alveolar–capillary membrane is important for transport of alveolar gases (O₂, CO₂) and metabolism of circulating substances.

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1. Type I alveolar cells provide the extensive surface for gas exchange, and these cells are susceptible to injury (e.g., acute respiratory distress syndrome).
2. Type III alveolar cells are macrophages. They provide protection against infection and participate in the lung inflammatory response.
3. Pulmonary Vascular Systems
4. Two major circulatory systems supply blood to the lungs: the pulmonary (which supplies gas exchange and metabolic needs of the alveolar parenchyma) and the bronchial (which supplies O₂to the conductive airways and pulmonary vessels) vascular networks.
5. Anatomic connections between the bronchial and pulmonary venous circulations create an absolute shunt of about 2% of the cardiac output (“normal or physiologic shunt”).
6. Lung Mechanics

Lung movement is entirely passive and responds to forces external to the lungs. (During spontaneous ventilation, the external forces are produced by ventilatory muscles.)

1. Elastic Work
2. The lung's natural tendency is to collapse (elastic recoil) such that normal expiration at rest is passive.
3. Surface tension at an air–fluid interface is responsible for keeping alveoli open. (During inspiration, surface tension increases, ensuring that gas tends to flow from larger to smaller alveoli, thereby preventing collapse.)
4. Esophageal pressureis a reflection of the intrapleural pressure and allows an estimation of the patient's work of breathing (i.e., elastic work and resistive work to overcome resistance to gas flow in the airway).
5. Patients with low lung compliance typically breathe with smaller tidal volumes at more rapid rates. Patients with diseases that increase lung compliance (e.g., gas trapping caused by asthma or COPD) must use the ventilatory muscles to actively exhale.

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1. Resistance to Gas Flow.Both laminar and turbulent flow exist within the respiratory tract.
2. Laminar flowis not audible and is influenced only by viscosity. Helium has a low density, but its viscosity is close to that of air.
3. Turbulent flowis audible and is almost invariably present when high resistance to gas flow is problematic. (Helium will improve flow.)
4. Increased Airway Resistance
5. The normal response to increased inspiratory resistance is increased inspiratory muscle effort.
6. The normal response to increased expiratory resistance is use of accessory muscles to force gas from the lungs. Patients who chronically use accessory muscles to exhale are at risk for ventilatory muscle fatigue if they experience an acute increase in ventilatory work, most commonly precipitated by pneumonia or heart failure.
7. An increased PaCO₂in the setting of increased airway resistance may signal that the patient's compensatory mechanisms are nearly exhausted.
8. Physiologic Changes in Respiratory Function Associated with Aging(Table 11-2). Despite changes, the respiratory system is able to maintain adequate gas exchange at rest and during exertion throughout life with only modest decrements in PaO₂ and no change in PaCO₂.

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III. Control of Ventilation

Mechanisms that control ventilation are complex, requiring integration of many parts of the central and peripheral nervous systems (Fig. 11-1).

1. Terminology.The terms breathing (the act of inspiring and exhaling), ventilation (movement of gas into and out of the lungs), and respiration (occurs when energy is released from organic molecules) are often used interchangeably. Breathing requires energy utilization for muscle work. When spontaneous, ventilation requires energy for muscle work and thus is breathing.
2. Generation of a Ventilatory Pattern(Table 11-3)
3. The medulla oblongata contains the most basic ven-tilatory control centers in the brain.
4. The pontine centers process information that originates in the medulla.

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4. The reticular activating system in the midbrain increases the rate and amplitude of ventilation.
5. The cerebral cortex can affect the breathing pattern.
6. Reflex Control of Ventilation
7. Reflexes that directly influence the ventilatory pattern (swallowing, coughing, vomiting) usually do so to prevent airway obstruction.
8. The Hering-Breuer reflex (apnea during sustained lung distention) is only weakly present in humans.
9. Chemical Control of Ventilation
10. Peripheral chemoreceptors include the carotid bodies (ventilatory effects characterized by increased breathing rate and tidal volume) and aortic bodies (circulatory effects characterized by bradycardia and hypertension).
11. Both carotid and aortic bodies are stimulated by decreased PaO₂(<60 mm Hg) but not by arterial hemoglobin saturation with O₂, arterial O₂ concentration (anemia), or PaCO₂.
12. Patients who depend on hypoxic ventilatory drive have PaO₂values around 60 mm Hg.
13. Potent inhaled anesthetics depress hypoxic ventilatory responses by depressing the carotid body response to hypoxemia.
14. Central Chemoreceptors
15. Approximately 80% of the ventilatory response to inhaled CO₂originates in the central medullary centers.

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1. The chemosensitive areas of the medullary ventilatory centers are exquisitely sensitive to the extracellular fluid hydrogen ion concentration. (CO₂indirectly determines this concentration by reacting with water to form carbonic acid.)
2. Increased PaCO₂is a more potent stimulus (increased breathing rate and tidal volume within 60 to 120 seconds) to ventilation than is metabolic acidosis. (CO₂ but not hydrogen ions can easily cross the blood–brain barrier.)
3. Normalization of the cerebrospinal fluid pH (active transport of bicarbonate ions) over time results in a decline in ventilation despite persistent increases in the PaCO₂. The reverse sequence occurs when acute ascent to altitude initially stimulates ventilation, leading to an abrupt decrease in PaCO₂.
4. Breath-Holding
5. The rate of increase in PaCO₂in awake, preoxygenated adults with normal lungs who hold their breath without previous hyperventilation is 7 mm Hg in the first 10 seconds, 2 mm Hg in the next 10 seconds, and 6 mm Hg thereafter.
6. The rate of increase in PaCO₂in apneic anesthetized patients is 12 mm Hg during the first minute and 3.5 mm Hg for every subsequent minute. This reflects a decreased metabolic rate and CO₂ production in the anesthetized compared with awake patients.
7. Hyperventilation is rarely followed by an apneic period in awake humans despite a decreased PaCO₂. In contrast, even mild hyperventilation during general anesthesia produces apnea.
8. Quantitative Aspects of Chemical Control of Breathing(Fig. 11-2)
9. The CO₂response curve approaches linearity at PaCO₂ values between 20 and 80 mm Hg (>100 mm Hg, CO₂ acts as a ventilatory depressant).
10. The slope of the CO₂response curve is considered to represent CO₂ sensitivity (normally 0.5–0.7 L/min/mm Hg CO₂).
11. The apneic threshold occurs at a PaCO₂of about 32 mm Hg.
12. Various events cause a shift in the position or change in the slope of the CO₂response curve (Table 11-4).

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1. Oxygen and Carbon Dioxide Transport
2. The movement of gas across the alveolar–capillary membrane depends on the integrity of the pulmonary and cardiac systems.

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1. Bulk Flow of Gas (Convection)
2. The greatest part of airway resistance occurs in the larger airways (>2 mm in diameter), where gas molecules travel more quickly.
3. During normal, quiet ventilation, gas flow within convective airways is mainly laminar, thus decreasing resistance to gas flow.
4. Gas Diffusion
5. Diffusion defects that create arterial hypoxemia are rare. The most common reason for a measured decrease in diffusing capacity is mismatching of ventilation to perfusion that functionally results in a decreased surface area available for diffusion.
6. Hypercarbia is never the result of diffusion defects. (CO₂is 20 times more diffusible than O₂.)
7. Distribution of Ventilation and Perfusion
8. The efficiency with which O₂and CO₂ exchange at the alveolar–capillary membrane depends on the matching of capillary perfusion and alveolar ventilation.
9. Distribution of blood flowwithin the lungs is mainly gravity dependent, depending on the relationship between pulmonary artery pressure, alveolar pressure, and pulmonary venous pressure (Fig. 11-3).
10. Distribution of ventilationis preferentially directed to more dependent areas of the lung.
11. The ideal matching of ventilation to perfusion (V/Q = 1) is believed to occur at approximately the level of the third rib. Above this level, ventilation

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occurs slightly in excess of perfusion; below this level, the ratio becomes less than 1 (Fig. 11-4).

1. Hypoxic pulmonary vasoconstrictiondecreases blood flow to unventilated (hypoxic) alveoli in an attempt to maintain a desirable V/Q ratio.
2. Whereas increases in dead space ventilation primarily affect CO₂elimination and have little effect on arterial oxygenation, physiologic shunt primarily affects arterial oxygenation with little effect on CO₂ elimination.
3. Physiologic Dead Space
4. Anatomic dead space(2 mL/kg) accounts for the majority of dead space ventilation and is attributable

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to ventilation of structures that do not participate in oxygenation (oronasopharynx to the terminal and respiratory bronchioles). Clinical conditions that modify anatomic dead space include tracheal intubation, tracheostomy, and large lengths of ventilatory tubing between the tracheal tube and the ventilator Y-piece.

2. Alveolar dead spacearises from ventilation of alveoli where there is little or no perfusion.
3. Increases in physiologic dead spaceare most often caused by increases in alveolar dead space (decreased cardiac output as may occur with decreased venous return after institution of positive pressure ventilation of the lungs, pulmonary embolism, and COPD). A decrease in pulmonary blood flow associated with pulmonary embolism is more often caused by reflex bronchoconstriction than mechanical obstruction to blood flow.
4. Assessment of Physiologic Dead Space.A comparison of the minute ventilation and PaCO₂ allows a gross qualitative assessment of physiologic dead space ventilation. The difference between pressure of end-tidal CO₂ (P_ETCO₂) and PaCO₂ is attributable to dead space ventilation.
5. Physiologic Shunt.The physiologic shunt is the portion of the cardiac output that returns to the left heart without being exposed to ventilated alveoli. (Absolute shunt and oxygenation cannot be improved by administration of supplemental O₂.)
6. An anatomic shunt arises from the venous return from the pleural, bronchiolar, and thebesian veins (2% to 5% of the cardiac output).
7. Anatomic shunts of the greatest magnitude are usually associated with congenital heart disease.
8. Shunt effect (venous admixture)occurs in areas where alveolar ventilation is deficient compared with perfusion. (Oxygenation is improved by administration of supplemental O₂.) Disease entities that tend to produce venous admixture include mild pulmonary edema, postoperative atelectasis, and COPD.
9. Assessment of Arterial Oxygenation and Physiologic Shunt.The simplest assessment of oxygenation is qualitative comparison of the patient's inspired O₂ concentration and resulting PaO₂. (Venous admixture magnifies the effect of a small shunt.)

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1. Physiologic shunt calculationincludes the contribution of mixed venous blood, which may be extremely desaturated in critically ill patients owing to low cardiac output, anemia, arterial hypoxemia, and increased metabolic O₂ requirements. This calculation is the best estimate of how well the lungs can oxygenate the arterial blood.
2. Pulmonary Function Testing (Table 11-5) (Fig. 11-5)
3. Lung Volumes and Capacities(Fig. 11-6)
4. Flow-Volume Loops.Imaging techniques (e.g., magnetic resonance imaging) provide more precise and useful information in the diagnosis of upper airway and extrathoracic obstruction and have replaced use of flow-volume loops.
5. Carbon Monoxide Diffusing Capacity
6. Whereas decreased hemoglobin concentration decreases the carbon monoxide diffusing capacity (DLCO), an increased P_ACO₂increases the DLCO.
7. DLCO is deceased by alveolar fibrosis associated with O₂toxicity and pulmonary edema.
8. Preoperative Pulmonary Assessment(Table 11-6)
9. Specific measurements of lung function do not predict postoperative complications.
10. History of smoking (>40 pack years), COPD, asthma, cough, and exercise intolerance (<one flight of stairs) are more predictive of postoperative complications.
11. Baseline pulmonary function data are reserved for patients with severely impaired preoperative

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pulmonary function (e.g., those with quadriplegia or myasthenia), so assessment of weaning from mechanical ventilation or tracheal extubation may be guided by preoperative values.

4. Arterial blood gases are not indicated unless patient's history suggests hypoxemia or CO₂retention (identify reversible disease or to define severity as a baseline).
5. Defining baseline PaO₂and PaCO₂ is important if it is anticipated that a patient with severe COPD will require postoperative mechanical ventilation (Table 11-7).
6. Anesthesia and Obstructive Pulmonary Disease
7. Patients with marked obstructive pulmonary disease are at increased risk for intraoperative (reflex bronchoconstriction during direct laryngoscopy and tracheal intubation) and postoperative complications.
8. Patients with asthma and COPD may benefit from preoperative bronchodilator therapy.
9. Controlled ventilation of the lungs at less than 10 breaths/min should prevent hypercarbia,

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minimize V/Q mismatch, and allow time for exhalation.

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3. Tidal volume and inspiratory flow rates are adjusted to keep peak airway pressure below 40 cm H₂O.
4. Tracheal extubation as soon as possible after the end of the operation is desirable in an attempt to decrease the risk of iatrogenic infection.

VII. Anesthesia and Restrictive Pulmonary Disease

1. These patients typically breathe rapidly and shallowly because more pressure is required to expand stiff lungs.
2. Positive end-expiratory pressure increases the functional residual capacity and reverses arterial hypoxemia.
3. High peak airway pressures may be required to expand stiffened lungs, but large tidal volumes are avoided because of the risk of barotrauma and volutrauma.
4. Arterial hypoxemia can develop rapidly (as during apnea for tracheal intubation or transportation from the operating room), reflecting the limited O₂stores in the lungs because of the decreased functional residual capacity.
5. General anesthesia further decreases the functional residual capacity that persists into the postoperative period (this is offset with positive airway pressure).
6. The most important aspect of postoperative pulmonary care is getting the patient out of bed, preferably walking.

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VIII. Effects of Cigarette Smoking on Pulmonary Function (Table 11-8)

1. Cessation of smoking for 12 to 24 hours is sufficient to decrease carboxyhemoglobin levels to near normal but does not predictably influence the incidence of postoperative pulmonary complications.
2. Normalization of mucociliary function requires 2 to 3 weeks of abstinence from smoking during which time sputum increases.
3. Smokers who decrease but do not stop cigarette consumption (change their smoking technique) continue to acquire the same amount of nicotine, and it is unlikely that postoperative pulmonary complications will be altered.
4. Patients who smoke should be advised to stop smoking 2 months before elective operations to maximize the effect of smoking cessation or for at least 4 weeks to gain some benefit from mucociliary function.
5. Smoking is one of the main risk factors associated with postoperative morbidity (pneumonia).
6. Postoperative Pulmonary Function
7. Postoperative Pulmonary Function
8. Changes in pulmonary function that occur after surgery are primarily restrictive (gauged by a decrease in functional residual capacity).

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3. The operative site is the single most important determinant of postoperative pulmonary restriction and pulmonary complications (Table 11-9).
4. Postoperative Pulmonary Complications
5. Atelectasis and pneumonia, as reflected by changes in the color and quantity of sputum, oral temperature above 38°C, and a new infiltrate seen on chest radiography, are the two most common postoperative complications.
6. The risk of postoperative pulmonary complications can be minimized by ensuring the absence of active pulmonary infection and use of therapeutic bronchodilation if reactive airway disease is associated with increased airway resistance.
7. Strategies to decrease the risk of postoperative pulmonary complications include the use of lung-expanding therapies, choice of analgesia, and cessation of smoking.
8. Stir-up regimens (e.g., walking) are as effective as incentive spirometry.
9. After median sternotomy, functional residual capacity does not return to normal for several weeks regardless of postoperative pulmonary therapy.
10. The most important aspect of postoperative pulmonary care is getting the patient out of bed, preferably walking.
11. Postoperative analgesia influences the risk of postoperative pulmonary complications (epidural analgesia, especially for abdominal and thoracic operations, decreases the risk).

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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