d. 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.

e. 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.

3. Respiratory Airways and the Alveolar–Capillary Membrane

a. The alveolar–capillary membrane is important for transport of alveolar gases (O₂, CO₂) and metabolism of circulating substances.

b. Type I alveolar cells provide the extensive surface for gas exchange, and these cells are susceptible to injury (acute respiratory distress syndrome).

c. Type III alveolar cells are macrophages. They provide protection against infection and participate in the lung inflammatory response.

4. Pulmonary Vascular Systems

a. 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 O₂ to the conductive airways and pulmonary vessels) vascular networks.

b. Anatomic connections between the bronchial and pulmonary venous circulations create an absolute shunt of about 2% of the cardiac output (“normal or physiologic shunt”).

II. 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.

A. Elastic Work

1. The lung’s natural tendency is to collapse (elastic recoil) such that normal expiration at rest is passive.

2. 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.

3. Esophageal pressure is a reflection of the intrapleural pressure and allows an estimation of the patient’s work of breathing (elastic work and resistive work to overcome resistance to gas flow in the airway).

4. Patients with low lung compliance typically breathe with smaller tidal volumes at more rapid rates. Patients with diseases that increase lung compliance (gas trapping caused by asthma or COPD) must use the ventilatory muscles to actively exhale.

B. Resistance to Gas Flow. Both laminar and turbulent flow exist within the respiratory tract.

1. Laminar flow is not audible and is influenced only by viscosity. Helium has a low density, but its viscosity is close to that of air.

2. Turbulent flow is audible and is almost invariably present when high resistance to gas flow is problematic (helium improves flow).

C. Increased Airway Resistance

1. The normal response to increased inspiratory resistance is increased inspiratory muscle effort.

2. 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.

3. An increased PaCO₂ in the setting of increased airway resistance may signal that the patient’s compensatory mechanisms are nearly exhausted.

D. 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.

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).

A. 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.

B. Generation of a Ventilatory Pattern (Table 11-3)

1. The medulla oblongata contains the most basic ventilatory control centers in the brain.

2. The pontine centers process information that originates in the medulla.

3. The reticular activating system in the midbrain increases the rate and amplitude of ventilation.

4. The cerebral cortex can affect the breathing pattern.

C. Reflex Control of Ventilation

1. Reflexes that directly influence the ventilatory pattern (swallowing, coughing, vomiting) usually do so to prevent airway obstruction.

2. The Hering-Breuer reflex (apnea during sustained lung distention) is only weakly present in humans.

D. Chemical Control of Ventilation

1. 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).

a. 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.

b. Patients who depend on hypoxic ventilatory drive have PaO₂ values around 60 mm Hg.

c. Potent inhaled anesthetics depress hypoxic ventilatory responses by depressing the carotid body response to hypoxemia.

2. Central Chemoreceptors

a. Approximately 80% of the ventilatory response to inhaled CO₂ originates in the central medullary centers.

b. The chemosensitive areas of the medullary ventilatory centers are exquisitely sensitive to the extracellular fluid hydrogen ion concentration. (CO₂ indirectly determines this concentration by reacting with water to form carbonic acid.)

c. Increased PaCO₂ is 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.)

d. 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.

E. Breath-Holding

1. The rate of increase in PaCO₂ in 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.

2. The rate of increase in PaCO₂ in 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 anesthetized compared with awake patients.

3. 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.

F. Quantitative Aspects of Chemical Control of Breathing (Fig. 11-2)

1. The CO₂ response curve approaches linearity at PaCO₂ values between 20 and 80 mm Hg (>100 mm Hg; CO₂ acts as a ventilatory depressant).

2. The slope of the CO₂ response curve is considered to represent CO₂ sensitivity (normally 0.5–0.7 L/min/mm Hg CO₂).

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