Anatomy and Physiology for Anesthesia · 10 min read
Airway and Respiratory Anatomy and Physiology
This chapter covers the anatomy of the upper airway and larynx with its innervation, the differences between adult and pediatric airways, the tracheobronchial tree, lung volumes and mechanics, ventilation-perfusion relationships, oxygen and carbon dioxide transport, and the control of breathing under anesthesia.
Nose and Pharynx
The nasal cavity is innervated by branches of the trigeminal nerve (ophthalmic and maxillary divisions). The inferior turbinate is the largest, and a nasal tube passed along the floor of the nose under the inferior turbinate is least likely to cause bleeding. The pharynx is divided into the nasopharynx, oropharynx and hypopharynx (laryngopharynx). Under anesthesia, loss of genioglossus tone lets the tongue and soft palate fall back, which is the most common cause of upper airway obstruction.
The Larynx
The adult larynx lies opposite about C3-C6, with the glottis near C5. It contains three unpaired cartilages (thyroid, cricoid and epiglottis) and three paired cartilages (arytenoid, corniculate and cuneiform). The cricoid is the only complete cartilaginous ring in the airway, which is why it is used for cricoid pressure. The cricothyroid membrane, between the thyroid and cricoid cartilages, is the site for emergency front-of-neck access.
| Muscle | Action | Nerve |
|---|---|---|
| Posterior cricoarytenoid | Only abductor (opens cords) | Recurrent laryngeal |
| Lateral cricoarytenoid | Adducts cords | Recurrent laryngeal |
| Thyroarytenoid | Relaxes and shortens cords | Recurrent laryngeal |
| Cricothyroid | Tenses and lengthens cords | External branch of superior laryngeal |
The extrinsic laryngeal muscles (suprahyoid and infrahyoid groups) move the larynx as a whole during swallowing and phonation.
| Nerve | Sensory Area | Motor |
|---|---|---|
| Glossopharyngeal (CN IX) | Posterior third of tongue, vallecula, anterior epiglottis, pharyngeal walls, tonsils | Stylopharyngeus |
| Superior laryngeal, internal branch | Posterior epiglottis down to the vocal cords | None |
| Superior laryngeal, external branch | None | Cricothyroid |
| Recurrent laryngeal | Below the vocal cords, trachea | All intrinsic muscles except cricothyroid |
The glossopharyngeal nerve carries the afferent limb of the gag reflex. The internal branch of the superior laryngeal nerve carries the afferent limb of laryngospasm protection from the supraglottic larynx. These are the nerves blocked for awake intubation.
| Injury | Cord Position | Clinical Result |
|---|---|---|
| Unilateral | Paramedian on affected side | Hoarseness |
| Bilateral, acute | Both paramedian | Stridor, airway obstruction |
| Bilateral, chronic | Both paramedian | Aphonia, airway usually adequate at rest |
| Superior laryngeal, external | Cord lax | Weak, low-pitched voice, fatigue |
Adult Versus Pediatric Airway
Infants have a large occiput, a relatively large tongue, a floppy omega-shaped epiglottis, and a larynx that sits higher and more anterior (about C3-C4) than in adults. The narrowest functional region has traditionally been taught as the cricoid ring, while imaging studies show the glottic opening is narrowest in some children; the practical point is that the subglottic area is the least distensible, so a tight tube causes edema there. One millimeter of edema in a 4 mm infant airway reduces cross-sectional area by about 75% and increases resistance about 16-fold under laminar flow. Neonates are preferential (often called obligate) nasal breathers. The neonatal trachea is only about 4-5 cm long, so tube migration into a bronchus with head flexion is easy.
Tracheobronchial Tree
The adult trachea is about 10-15 cm long and divides at the carina, about T4-T5 (the sternal angle). The right mainstem bronchus is shorter, wider and more vertical (about 25 degrees from vertical) than the left (about 45 degrees), so endobronchial intubation and aspiration favor the right side. The right upper lobe bronchus arises only about 1.5-2.5 cm from the carina, which is why left-sided double-lumen tubes are preferred. The airway branches through about 23 generations: the conducting zone (anatomic dead space) runs through about generation 16, and the respiratory zone (respiratory bronchioles, alveolar ducts and alveoli) occupies generations 17-23.
Lung Volumes and Capacities
| Volume or Capacity | Definition | Approximate Value |
|---|---|---|
| Tidal volume | Normal breath | 500 mL (6-8 mL/kg) |
| Residual volume | Left after maximal exhalation | 1,200 mL |
| FRC | ERV + RV | 2,300-2,500 mL |
| Vital capacity | IRV + TV + ERV | 4,500-4,800 mL (about 65-70 mL/kg) |
| Total lung capacity | All volumes | 5,800-6,000 mL |
FRC is the volume at the end of a normal passive exhalation, where the inward recoil of the lung balances the outward recoil of the chest wall. It is the oxygen reservoir during apnea, which is why preoxygenation fills FRC with oxygen. FRC falls by about 0.8-1 L when moving from standing to supine and by another 15-20% with induction of general anesthesia, regardless of whether the patient breathes spontaneously or is paralyzed. Obesity, pregnancy, abdominal distension, Trendelenburg position and laparoscopy reduce it further; PEEP, the head-up position and recruitment maneuvers restore it.
Closing capacity is the lung volume at which small airways in dependent regions begin to close. It increases with age, smoking and lung disease. When closing capacity exceeds FRC, airway closure occurs during normal tidal breathing, producing shunt and hypoxemia. Closing capacity equals FRC at about age 44 in the supine position and about age 66 upright.
Compliance and Resistance
Compliance is change in volume per change in pressure. Total respiratory compliance is about 100 mL/cmH2O (lung and chest wall each about 200 mL/cmH2O).
Dynamic compliance = tidal volume / (peak pressure - PEEP)
Static compliance = tidal volume / (plateau pressure - PEEP)
Worked example: tidal volume 500 mL, peak pressure 30 cmH2O, plateau 25 cmH2O, PEEP 5 cmH2O. Dynamic compliance = 500 / 25 = 20 mL/cmH2O. Static compliance = 500 / 20 = 25 mL/cmH2O. The 5 cmH2O gap between peak and plateau reflects airway resistance. A rising peak with an unchanged plateau suggests a resistance problem (kinked tube, bronchospasm, secretions); a rise in both suggests a compliance problem (pneumothorax, endobronchial intubation, pulmonary edema, insufflation, inadequate relaxation).
Ventilation, Perfusion, Dead Space and Shunt
Normal alveolar ventilation is about 4 L/min and pulmonary blood flow about 5 L/min, so the overall V/Q ratio is about 0.8. In the upright lung, both ventilation and perfusion increase toward the base, but perfusion increases more, so V/Q is highest at the apex (about 3) and lowest at the base (about 0.6).
| Zone | Pressure Relationship | Meaning |
|---|---|---|
| 1 | PA > Pa > Pv | No flow, alveolar dead space |
| 2 | Pa > PA > Pv | Flow depends on arterial minus alveolar pressure |
| 3 | Pa > Pv > PA | Continuous flow, where a PA catheter tip should sit |
Hypovolemia and positive-pressure ventilation enlarge zone 1. Dead space is ventilation without perfusion. Anatomic dead space is about 2 mL/kg (about 150 mL in an adult); physiologic dead space (anatomic plus alveolar) is normally about 30% of tidal volume.
Bohr equation: VD/VT = (PaCO2 - PECO2) / PaCO2
Worked example: PaCO2 40 mmHg, mixed expired CO2 28 mmHg. VD/VT = (40 - 28) / 40 = 0.30. If a pulmonary embolus raises the ratio to 0.5, ETCO2 falls while PaCO2 rises, widening the arterial to end-tidal gradient.
Shunt is perfusion without ventilation. Normal anatomic shunt (bronchial and Thebesian veins) is about 2-5% of cardiac output. Hypoxemia from true shunt responds poorly to increased FiO2, while hypoxemia from low V/Q improves with oxygen.
Hypoxic pulmonary vasoconstriction (HPV) diverts blood away from poorly ventilated alveoli. It is inhibited by volatile anesthetics in a dose-dependent way (minimal below about 1 MAC), by vasodilators such as nitroprusside and nitroglycerin, by hypocapnia and alkalosis, by very high or very low pulmonary artery pressures and by pulmonary infection. Intravenous agents such as propofol do not inhibit HPV. HPV matters most during one-lung ventilation.
Oxygen Transport and the Dissociation Curve
Worked example: Hb 12 g/dL, SaO2 98% (0.98), PaO2 100 mmHg. CaO2 = (1.34 x 12 x 0.98) + (0.003 x 100) = 15.76 + 0.30 = 16.1 mL O2/dL. With a cardiac output of 5 L/min, oxygen delivery (DO2) = CaO2 x CO x 10 = 16.1 x 5 x 10 = 805 mL/min. Normal oxygen consumption is about 250 mL/min (about 3-4 mL/kg/min in adults).
The P50 (PaO2 at 50% saturation) is about 26.5-27 mmHg in adults. Saturation is about 75% at a PaO2 of 40 mmHg (mixed venous) and about 90% at 60 mmHg, the point below which saturation falls steeply.
| Right Shift (P50 higher, releases O2) | Left Shift (P50 lower, holds O2) |
|---|---|
| Acidosis, hypercarbia | Alkalosis, hypocarbia |
| Hyperthermia | Hypothermia |
| Increased 2,3-DPG | Decreased 2,3-DPG (stored blood) |
| Pregnancy, sickle hemoglobin | Fetal hemoglobin (P50 about 19), CO, methemoglobin |
The Bohr effect is the right shift caused by CO2 and hydrogen ion at the tissues. The Haldane effect is the increased ability of deoxygenated hemoglobin to carry CO2; giving high FiO2 to a patient with chronic CO2 retention displaces CO2 from hemoglobin and worsens V/Q matching by releasing HPV, which raises PaCO2.
Carbon Dioxide Transport
CO2 is carried in blood about 70% as bicarbonate (formed in red cells by carbonic anhydrase, with chloride shifting into the cell), about 20-23% bound to hemoglobin as carbamino compounds, and about 7-10% dissolved. During apnea, PaCO2 rises about 6 mmHg in the first minute and then about 3-4 mmHg each minute after.
Control of Breathing and Anesthetic Effects
Central chemoreceptors on the ventral surface of the medulla respond to hydrogen ion in cerebrospinal fluid, which reflects PaCO2 because CO2 crosses the blood-brain barrier easily. They provide about 80% of the response to CO2. Peripheral chemoreceptors in the carotid bodies (glossopharyngeal nerve) and aortic bodies (vagus nerve) respond mainly to PaO2 below about 60 mmHg, and also to pH and CO2.
| Drug | Effect |
|---|---|
| Volatile agents | Shift CO2 response curve right and flatten slope; depress hypoxic response even at about 0.1 MAC; rapid shallow breathing |
| Opioids | Shift CO2 response curve right; slow deep breathing; apnea at high doses |
| Propofol, barbiturates | Dose-dependent depression, apnea at induction doses |
| Ketamine, dexmedetomidine | Relatively preserved ventilation at usual doses |
The apneic threshold is the PaCO2 below which spontaneous breathing stops; under anesthesia it is a few mmHg below the resting PaCO2. Patients who are hyperventilated during the case may not breathe until PaCO2 rises back above that threshold.
Key Takeaways
- The posterior cricoarytenoid is the only vocal cord abductor; the recurrent laryngeal nerve supplies all intrinsic muscles except the cricothyroid.
- FRC (about 2,300-2,500 mL) falls with supine position, induction, obesity, pregnancy and laparoscopy; closing capacity rises with age.
- A rise in peak pressure with unchanged plateau pressure indicates increased resistance; a rise in both indicates decreased compliance.
- Dead space lowers ETCO2 relative to PaCO2; true shunt responds poorly to oxygen.
- CaO2 = (1.34 x Hb x SaO2) + (0.003 x PaO2); know the right-shift and left-shift causes.
- Volatile agents depress the hypoxic ventilatory response at very low concentrations and inhibit HPV at higher concentrations.
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