Respiratory Function in Anesthesia
Anesthesiologists directly manipulate pulmonary function, so it is important to have a thorough knowledge of pulmonary physiology for the safe conduct of anesthesia (Tamul PC, Ault ML. Respiratory function in anesthesia. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Ortega R, Stock MC, eds. Clinical Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 2013: 263–286).
I. Functional Anatomy of the Lungs
Muscles of Ventilation
The muscles of ventilation are endurance muscles that are adversely affected by poor nutrition, chronic obstructive pulmonary disease (COPD), and increased airway resistance.
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.
Lung Structures
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.
The lung parenchyma is subdivided into three airway categories based on functional lung anatomy (Table 11-1).
Large airways with diameters of 2 mm or larger create 90% of total airway resistance.
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 m2 of surface area for gas exchange.
An 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 (which 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.
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.
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.
Respiratory Airways and the Alveolar–Capillary Membrane
The alveolar–capillary membrane is important for transport of alveolar gases (O2, CO2) and metabolism of circulating substances.
Type I alveolar cells provide the extensive surface for gas exchange, and these cells are susceptible to injury (acute respiratory distress syndrome).
Type III alveolar cells are macrophages. They provide protection against infection and participate in the lung inflammatory response.
Pulmonary Vascular Systems
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.
Anatomic connections between the bronchial and pulmonary venous circulations create an absolute shunt of about 2% of the cardiac output (“normal or physiologic shunt”).
Table 11-1 Functional Airway Divisions | ||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
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.
Elastic Work
The lung’s natural tendency is to collapse (elastic recoil) such that normal expiration at rest is passive.
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.
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).
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.
Resistance to Gas Flow. Both laminar and turbulent flow exist within the respiratory tract.
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.
Turbulent flow is audible and is almost invariably present when high resistance to gas flow is problematic (helium improves flow).
Increased Airway Resistance
The normal response to increased inspiratory resistance is increased inspiratory muscle effort.
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.
An increased PaCO2 in the setting of increased airway resistance may signal that the patient’s compensatory mechanisms are nearly exhausted.
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.
Table 11-2 Physiologic Changes in Respiratory Function Associated with Aging | |
|---|---|
|
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).
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.
Generation of a Ventilatory Pattern (Table 11-3)
The medulla oblongata contains the most basic ventilatory control centers in the brain.
The pontine centers process information that originates in the medulla.
The reticular activating system in the midbrain increases the rate and amplitude of ventilation.
The cerebral cortex can affect the breathing pattern.
Reflex Control of Ventilation
Reflexes that directly influence the ventilatory pattern (swallowing, coughing, vomiting) usually do so to prevent airway obstruction.
The Hering-Breuer reflex (apnea during sustained lung distention) is only weakly present in humans.
Chemical Control of Ventilation
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).
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.
Patients who depend on hypoxic ventilatory drive have PaO2 values around 60 mm Hg.
Potent inhaled anesthetics depress hypoxic ventilatory responses by depressing the carotid body response to hypoxemia.
Central Chemoreceptors
Approximately 80% of the ventilatory response to inhaled CO2 originates in the central medullary centers.
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.)
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.)
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.
Breath-Holding
