Respiratory System

97% of alveolar surfaces. Line the alveoli. Squamous; thin for optimal gas diffusion

Secrete surfactant from lamellar bodies (arrow in A ) -> ↓ alveolar surface tension, prevents alveolar collapse, ↓ lung recoil, and ↑ compliance. Cuboidal and clustered B . Also serve as precursors to type I cells and other type II cells. Proliferate during lung damage.

Phagocytose foreign materials, release cytokines
and alveolar proteases.

• Large airways consists of nose, pharynx, larynx, trachea, and bronchi. Small airways consist of bronchioles.
• Warms, humidifies, and filters air but does not participate in gas exchange p “anatomic dead space.” Cartilage and goblet cells extend to end of bronchi.
• Airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point).

• Airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point).
• Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli.
• Cilia terminate in respiratory bronchioles.
• Alveolar macrophages clear debris and participate in immune response.

• Inspiratory reserve volume
  • Air that can still be breathed in after normal inspiration
• Tidal volume
  • Air that moves into lung with each quiet inspiration, typically 500 mL
• Expiratory reserve volume
  • Air that can still be breathed out after normal expiration
• Residual volume
  • Air in lung after maximal expiration; RV and any lung capacity that includes RV cannot be measured by spirometry
• Inspiratory capacity
  • IRV + TV
  • Air that can be breathed in after normal exhalation
• Functional residual capacity
  • RV + ERV
  • Volume of gas in lungs after normal expiration
• Vital capacity
  • TV + IRV + ERV
  • Maximum volume of gas that can be expired after a maximal inspiration
• Total lung capacity
  • IRV + TV + ERV + RV
  • Volume of gas present in lungs after a maximal inspiration

The expiratory upslope in normal conditions is nearly vertical. If obstruction occurs in the patient’s airway, endotracheal tube or sampling site, upslope is slanted. Expiratory plateau is nearly horizontal. In cases of expiratory airway or mechanical obstruction, a steeper slope is present. Inspiratory downslope produces a steep decline in the CO2 concentration. Incompetent inspiratory valve causes a prolonged downslope. Airway leakage causes hypoventilation of patient resulting in elevated CO2 concentrations (i.e. hypercapnea).

Hb exhibits positive cooperativity and negative allostery. Sigmoidal shape due to positive cooperativity (ie, tetrameric Hb molecule can bind 4 O2 molecules and has higher affinity for each subsequent O2 molecule bound). Myoglobin is monomeric and thus does not show positive cooperativity; curve lacks sigmoidal appearance.

• Deoxygenated form has low affnity for O2, thus promoting release/unloading of O2.
• Oxygenated form has high affnity for O2 (300×). Hb exhibits positive cooperativity and negative allostery.

Right shift (↑ O2 unloading)—ACE BATs right handed:

• Acid
• CO2
• Exercise
• 2,3-BPG
• Altitude
• Temperature

• Obstructive lung volumes > normal (↑ TLC, ↑ FRC, ↑ RV)
• Obstruction of air flow -> air trapping in lungs.
• PFTs: ↓↓ FEV1, ↓ FVC -> ↓ FEV1/FVC ratio (hallmark), V/Q mismatch.
• Chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale.
• COPD, chronic bronchitis, emphysema, asthma, Bronchiectasis
• Chronic obstructive bronchitis is referred to as “blue bloater”. The disease is characterized by obstruction of small airways secondary to mucus and inflammation. Patients with chronic bronchitis have significant decreases in PaO2 (< 65 mmHg is typical.) Compensatory consequences include erythrocytosis. PaCO2 is also chronically elevated. This results in pulmonary hypertension and cor pulmonale.
  • FEV1/FVC of 70% – mild obstruction
  • <60% moderate obstruction
  • <50% severe obstruction
• Emphysema causes destruction of lung parenchyma, enlargement of airway spaces, loss of lung elasticity and closure of small airways. Rapid, shallow respirations generally result in a PaCO2 which is normal to slightly decreased and a PaO2 > 65 mmHg. This disease is categorized as “pink puffer” and is generally not associated with cor Pulmonale.

• Restricted lung expansion causes ↓ lung volumes (↓ FVC and TLC).
• PFTs: FEV1/FVC ratio ≥ 80% (FVC is more reduced or close to same compared with FEV1 )
• Patient presents with short, shallow breaths.
• Poor breathing mechanics (extrapulmonary, peripheral hypoventilation, normal A-a gradient)
• Interstitial lung disease (↓ pulmonary diffusion capacity, ↑ A-a gradient)
  • Acute respiratory distress syndrome
  • Neonatal respiratory distress syndrome
  • Pneumoconioses
  • Sarcoidosis
  • Idiopathic pulmonary fibrosis: ↑ collagen deposits; honeycomb lung appearance and digital clubbing
  • Goodpasture syndrome
  • Granulomatosis with polyangitis (Wegener)
  • Pulmonary Langerhans cell histiocytosis (eosinophilic granuloma)

• Endothelial damage -> ↑ alveolar capillary permeability -> protein-rich leakage into alveoli -> diffuse alveolar damage and noncardiogenic pulmonary edema (normal PCWP .
• Results in formation of intraalveolar hyaline membranes. Initial damage due to release of neutrophilic substances toxic to alveolar wall and pulmonary capillary endothelial cells, activation of coagulation cascade, and oxygen-derived free radicals.
• Management: mechanical ventilation with low tidal volumes, address underlying cause.

Accumulation of air in pleural space (A) . Dyspnea, uneven chest expansion. Chest pain, ↓ tactile fremitus, hyperresonance, and diminished breath sounds, all on the affected side.

Air enters pleural space but cannot exit. Increasing trapped air -> tension pneumothorax. Trachea deviates away from affected lung (B). Needs immediate needle decompression and chest tube placement.

This is a classic tension pneumothorax and treatment is a clinical diagnosis with immediate needle decompression of the second intercostal space, midclavicular line. Tension pneumothorax can cause decreases in pulse pressure and muffled heart sounds, but also is accompanied by ipsilateral chest resonance and decreased breath sounds, and often with tracheal shift to the contralateral side.

• Increase peak airway pressure
• Hypotension
• Hypoxemia
• Decreased breath sounds
• Decreased tidal volume on side of pneumothorax
• Treatment: needle decompression in the second intercostal space in the mid-clavicular line

• Obesity: decreases FRC, ERV, TLC
• Morbid obesity is characterized by reductions in functional residual capacity (FRC= volume remaining in the lungs after a normal quiet expiration), expiratory reserve volume (ERV=volume of air that can forcefully expired after a normal resting expiration) and total lung capacity (TLC). These changes have been attributed to mass loading and splinting of the diaphragm. Anesthesia compounds these problems and impairs the ability of the obese to tolerate periods of apnea. Residual volume consists of the gases remaining in the lung after a forced expiration and is less variable than other parameters. FEV1 is the forced expiratory volume in 1 second and is most often used as a determinant of inflammation and small airway obstruction in obstructive lung diseases such as asthma.
• Patients who are morbidly obese have increased minute ventilation at rest to meet the metabolic needs of the increased tissue mass. Changes in lung volumes at rest include reduced FRC, vital capacity, and total lung capacity. Closing volume is unchanged and reduced FRC can result in lung volumes below closing capacity in normal tidal ventilation. Anesthesia compounds these problems with greater reductions in FRC in obese patients compared to nonobese patients of the same age. As a result, obese patient’s ability to tolerate periods of apnea is reduced.

• Functional residual capacity is the volume of lung after the end of a normal TV expiration. A smaller volume will reach a higher anesthetic concentration more quickly than a larger volume. A small functional residual capacity will allow the alveolar concentration to quickly approach the inspired concentration, speeding up induction.
• Pediatric patients have a small FRC and high alveolar ventilation resulting in more rapid inhalation induction compared to adults. Increasing alveolar ventilation will replace more anesthetic taken up by the pulmonary bloodstream, maintaining a higher alveolar concentration and thus speeding induction. An agent with low blood gas solubility will equilibrate rapidly resulting in a more rapid induction.
• While undergoing a general anesthetic, children without lung disease may lose as much as 45 percent of their FRC. Owing to a higher oxygen consumption and greater loss of FRC in children during general anesthesia, hypoxia develops in a matter of seconds. To compensate for the higher oxygen consumption, children have a higher blood volume per kg or compared to adult-(80-100 cc/kg children and 65-70cc/kg for adults). Children should have their ventilation controlled during anesthesia because hypoventilation exacerbates their tendency toward hypoxia. Atelectasis may occur in mechanically ventilated children, but is more likely to occur in children who breathe spontaneously. Children with pulmonary diseases may lose even more of the FRC, exposing them to increasing ventilation-perfusion mismatch and hypoxia. An increased inspired oxygen concentration and application of positive end-expiratory pressure (PEEP) may partially restore FRC. However, PEEP must be applied carefully.