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🫁 Respiratory System: Anatomy, Physiology & Anesthesia Implications

A Complete Lecture for the Anesthesia Trainee

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PART I — FUNCTIONAL ANATOMY OF THE RESPIRATORY SYSTEM

1. Overview and Structural Division

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2. The Upper Airway

• Lined with pseudostratified ciliated epithelium and a vascular submucosa → warms and humidifies inhaled gas
• Nasal turbinates create turbulent flow to trap particles
• Blood supply: branches of the internal and external carotid arteries (Kiesselbach's plexus anteriorly — epistaxis site)
• Anesthetic relevance: Nasal intubation risks bleeding (always have vasoconstrictors ready); nasopharyngeal airways can damage the adenoids or cause epistaxis

• Extends from base of skull to the lower border of C6
• Divided into naso-, oro-, and laryngopharynx
• The hypopharynx (laryngopharynx) is where the larynx and esophagus diverge — the piriform fossae flank the larynx and are a site for topical local anaesthetic injection

• Located at C3–C6 in adults (higher in children — infant larynx at C3, making it "anterior" and difficult to visualise)
• Key cartilages: Thyroid (largest), cricoid (only complete ring — the narrowest point in the pediatric airway), arytenoids, and epiglottis
• The cricothyroid membrane lies between the thyroid and cricoid cartilages — the preferred site for emergency surgical airway (cricothyrotomy)
• Vocal cords (true) form the glottic opening; the narrowest part of the adult airway is the glottis
• Innervation:
  • Superior laryngeal nerve (SLN) — internal branch (sensory above cords), external branch (motor to cricothyroid)
  • Recurrent laryngeal nerve (RLN) — motor to all intrinsic laryngeal muscles except cricothyroid; sensory below cords
• Anesthetic relevance: SLN and RLN blocks are used for awake fibreoptic intubation; RLN damage causes hoarseness/stridor

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3. The Tracheobronchial Tree

• Standard oral ETT placement: tip should be 4–6 cm above the carina (mid-tracheal position)
• Neck flexion → tube migrates distally (into the right main bronchus); neck extension → tube migrates proximally (may extubate)
• The cuff should sit below the vocal cords and above the carina

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4. The Lungs and Alveoli

• Right lung: 3 lobes (upper, middle, lower), 10 bronchopulmonary segments
• Left lung: 2 lobes (upper, lower), 8–9 segments; the lingula is the equivalent of the right middle lobe
• Alveoli: ~300–500 million; total surface area ~70 m²; wall thickness ~0.5 μm
• Type I pneumocytes (95% of surface): thin, for gas exchange
• Type II pneumocytes (5% of surface): cuboidal; produce surfactant (DPPC — dipalmitoylphosphatidylcholine), which reduces surface tension and prevents alveolar collapse

• Reduces alveolar surface tension → prevents collapse at end-expiration
• Begins production at ~24 weeks gestation (inadequate in preterm infants → Respiratory Distress Syndrome)
• Anesthetic relevance: High FiO₂ (oxygen toxicity), sepsis, and ARDS destroy surfactant → atelectasis

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5. Pleura and Mediastinum

• Visceral pleura covers lung parenchyma (no pain receptors)
• Parietal pleura lines chest wall (pain receptors — thoracic and phrenic nerve supply)
• Pleural space: normally contains ~10–20 mL fluid at −5 cmH₂O pressure (subatmospheric)
• Anesthetic relevance: Positive pressure ventilation can rupture blebs → pneumothorax; central line placement risks pneumothorax

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6. Innervation and Vascular Supply

• SNS (T1–T4 stellate ganglia): Bronchodilation + pulmonary vasoconstriction
• PNS (vagus nerve): Bronchoconstriction + increased secretion
• Vagal receptor endings in alveolar ducts regulate ventilatory reflexes

• Right ventricle → pulmonary artery → capillaries → pulmonary veins → left atrium
• Low-pressure, low-resistance circuit (PAP ~25/10 mmHg, mean ~15 mmHg)
• Bronchial circulation: High-pressure systemic circulation supplying airways and pleura (returns via pulmonary veins → small physiological shunt)

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PART II — RESPIRATORY PHYSIOLOGY

1. Ventilation Mechanics

• Pmus = muscle pressure (driving force in spontaneous breathing)
• Paw = airway pressure (driving force in mechanical ventilation)
• V·R = flow × resistance (resistive component)
• V·E = volume × elastance (elastic component = compliance⁻¹)

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2. Lung Volumes and Capacities

TOTAL LUNG CAPACITY (TLC) ─────────────────────────── ~6000 mL
  │
  ├── INSPIRATORY CAPACITY (IC) = TV + IRV ────────── ~3600 mL
  │     ├── Tidal Volume (TV/VT) ───────────────────── ~500 mL
  │     └── Inspiratory Reserve Volume (IRV) ──────── ~3100 mL
  │
  └── FUNCTIONAL RESIDUAL CAPACITY (FRC) ──────────── ~2400 mL
        ├── Expiratory Reserve Volume (ERV) ────────── ~1200 mL
        └── Residual Volume (RV) ──────────────────── ~1200 mL

• FRC is the volume of gas remaining after a normal passive expiration
• It is the oxygen reserve during apnoea (pre-oxygenation expands this)
• FRC decreases with:
  • General anaesthesia (↓ by ~20% or 400–500 mL) — most significant change
  • Supine positioning (↓ by 800 mL from standing)
  • Obesity (dramatically reduced — may approach RV, causing airway closure)
  • Pregnancy (elevated diaphragm)
  • Trendelenburg position + abdominal insufflation (laparoscopy)
• A reduced FRC → airway closure → atelectasis → hypoxaemia

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3. Dead Space and Alveolar Ventilation

• Anatomical dead space: ~150 mL (conducting airways, 1 mL/lb body weight rule)
• Alveolar dead space: ventilated alveoli with no perfusion (V/Q = ∞)
• Physiological dead space = anatomical + alveolar dead space
• Normal VD/VT ratio: ~0.33 (one-third of each breath is dead space)

• Endotracheal tubes, circuits, and masks all add instrumental dead space — critical in paediatrics (small VT)
• Dead space increases during anaesthesia (reduced cardiac output → more alveolar dead space)
• PEEP can reduce dead space by recruiting atelectatic zones

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4. Compliance and Resistance

• Pulmonary oedema, fibrosis, ARDS, pneumonia
• Anaesthesia (atelectasis formation → stiffer lungs)
• Obesity, ascites, pregnancy (external restriction)
• Loss of surfactant

• Normal: 0.5–2.0 cmH₂O/L/s
• Resistance ∝ length / r⁴ (Poiseuille's Law) — radius is the critical determinant
• Medium-sized bronchi (2–5 mm) contribute the most to total airway resistance

• Bronchodilation: β₂-agonists, SNS, volatile anaesthetics (at clinical doses), deep anaesthesia
• Bronchoconstriction: vagal stimulation, histamine, cold air, smoke, light anaesthesia with airway manipulation, neostigmine, morphine (histamine release)

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5. V/Q Matching — The Heart of Gas Exchange

• Normal V̇/Q̇ ratio ≈ 0.8 (overall)
• V̇/Q̇ = 0: Shunt (perfused but not ventilated) → hypoxaemia unresponsive to supplemental O₂
• V̇/Q̇ = ∞: Dead space (ventilated but not perfused) → hypercapnia
• V̇/Q̇ mismatch causes the majority of hypoxaemia in clinical anaesthesia

• A critical homeostatic reflex: local alveolar hypoxia (PO₂ < 70 mmHg) constricts pulmonary arterioles → diverts blood to better-ventilated regions
• HPV is inhibited by: Volatile anaesthetics (dose-dependent), vasodilators (SNP, GTN), pulmonary hypertension
• Anesthetic relevance: During one-lung ventilation (OLV), HPV is essential to reduce shunt through the non-ventilated lung; volatile agents blunt HPV, but in clinical doses (≤1 MAC) the effect is moderate

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6. Oxygen Transport and the Oxyhaemoglobin Dissociation Curve

• Sigmoid shape due to cooperative haemoglobin binding
• P50 = PaO₂ at which Hb is 50% saturated = 26.7 mmHg (normal)

• Hypothermia (common intraoperatively) → left shift → decreased tissue O₂ delivery despite normal SpO₂
• Stored blood has low 2,3-DPG → left shift → reduced O₂ offloading

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7. Carbon Dioxide Transport and Elimination

1. Dissolved in plasma (5–10%)
2. As bicarbonate (HCO₃⁻) — 60–70% (carbonic anhydrase catalysed)
3. Bound to haemoglobin as carbamino compounds (~25%)

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8. Control of Breathing

• Respond to changes in CSF pH (driven by CO₂)
• Primary drive to breathe in normal patients
• Depressed by: volatile agents, opioids, barbiturates, benzodiazepines

• Respond to hypoxia (PaO₂ < 60 mmHg), hypercapnia, acidosis
• Fast response (seconds)
• In patients with chronic hypercapnia (COPD), hypoxic drive becomes the primary stimulus

• Dorsal respiratory group (DRG, nucleus tractus solitarius) — inspiration
• Ventral respiratory group (VRG) — forced inspiration and expiration
• Pre-Bötzinger complex — rhythm generation (pacemaker)
• Pneumotaxic centre (pons) — fine-tunes timing

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PART III — ANESTHESIA IMPLICATIONS

1. Effects of General Anaesthesia on the Respiratory System

1. Compression atelectasis — loss of diaphragm muscle tone (cephalad displacement) compresses dependent lung regions
2. Absorption atelectasis — high FiO₂ promotes resorption of O₂ behind closed airways
3. Surfactant impairment — mechanical ventilation without physiological sighs, O₂ toxicity

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2. Volatile Anaesthetics and the Respiratory System

• Sevoflurane is the agent of choice for asthmatic patients and inhalational induction (non-pungent, bronchodilator)
• Desflurane causes airway irritation, cough, laryngospasm, bronchospasm especially on rapid concentration increases — avoid in asthmatics
• All volatile agents produce a dose-dependent decrease in tidal volume and respiratory rate, increasing PaCO₂

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3. Opioids and Respiratory Depression

• Opioids bind μ-receptors in the brainstem (pre-Bötzinger complex, DRG)
• Effects:
  • ↓ Hypercapnic drive (blunts CO₂ response curve slope)
  • ↓ Hypoxic drive (peripheral chemoreceptors)
  • ↓ Respiratory rate > tidal volume
  • Chest wall rigidity at high doses (fentanyl/remifentanil) → difficult ventilation
  • Cough suppression
• Reversed by naloxone (0.04–0.4 mg IV; short half-life — re-narcotisation risk)

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4. Neuromuscular Blocking Agents (NMBAs) and Ventilation

• Paralysis abolishes spontaneous breathing → mandatory IPPV
• Residual neuromuscular blockade (TOFR < 0.9) is a major cause of postoperative respiratory failure
  • Upper airway dysfunction precedes phrenic nerve recovery (pharyngeal muscles more sensitive to NMBAs)
  • Results in: inability to protect airway, atelectasis, silent aspiration
• Monitoring with train-of-four (TOF) is mandatory; TOFR ≥ 0.9 required before extubation
• Reversal agents: Neostigmine (ACh↑ → bronchoconstriction risk) vs. Sugammadex (encapsulates rocuronium/vecuronium — no pulmonary effects)

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5. Anaesthesia in Specific Respiratory Conditions

• Triggers: Light anaesthesia, airway manipulation (intubation, suctioning), neostigmine, β-blockers, NSAIDs, histamine-releasing drugs
• Preventive strategy: Deep anaesthesia before intubation, preoperative bronchodilators, avoid triggers
• Management of intraoperative bronchospasm:
  • Deepen anaesthesia (sevoflurane/propofol)
  • Salbutamol via ETT or IV
  • IV magnesium sulphate
  • IV hydrocortisone + adrenaline in severe cases
  • Rule out endobronchial intubation, pneumothorax

• Risk: Air trapping, dynamic hyperinflation, intrinsic PEEP (auto-PEEP)
• Ventilator strategy: ↓ respiratory rate, ↑ expiratory time (I:E = 1:3 or 1:4), minimal PEEP, tolerate permissive hypercapnia
• Avoid high FiO₂ in patients with chronic hypercapnia (blunts hypoxic drive)

• FRC severely reduced (may approach closing volume in supine position)
• Rapid desaturation during apnoea (reduced oxygen reserve)
• Pre-oxygenation strategy: Head-up 20–30°, PEEP/CPAP during mask ventilation
• Intraoperative PEEP 10 cmH₂O + recruitment manoeuvres

• Indication: Isolation of lungs (surgery, haemorrhage, infection, bronchopleural fistula)
• Device: Double-lumen tube (DLT) or bronchial blocker
• Physiology: 100% of cardiac output initially goes to both lungs; when one lung is collapsed, shunt ≈ 20–30% of CO (HPV reduces this)
• Management of hypoxaemia during OLV:
  1. ↑ FiO₂ to 1.0
  2. Apply CPAP (5–10 cmH₂O) to non-ventilated lung
  3. Apply PEEP (5–10 cmH₂O) to ventilated lung
  4. Reduce anaesthetic volatile concentration (allow HPV)
  5. Consider partial ventilation, intermittent re-inflation of collapsed lung

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6. Protective Lung Ventilation Strategy

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7. Pre-oxygenation (Denitrogenation)

• Standard: 100% O₂ via tight-fitting mask for 3 minutes of tidal breathing OR 4 vital capacity breaths in 30 seconds
• Target: EtO₂ ≥ 90% (confirms denitrogenation)
• Safe apnoea time (SpO₂ falls to 90%):
  • Healthy adult (upright): ~8 minutes
  • Obese patient: ~2–3 minutes
  • Pregnant patient: ~3 minutes
  • Child: ~3–4 minutes (high O₂ consumption/kg, reduced FRC/kg)
• NODESAT/THRIVE (High-Flow Nasal Oxygen): Extends safe apnoea time through apnoeic oxygenation

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8. Pulmonary Function Tests — Preoperative Assessment

• Pneumonectomy: predicted postop FEV₁ > 40%; ppoFEV₁ < 30% is prohibitive
• Lobectomy: ppoFEV₁ > 30–40%

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KEY ANESTHETIC TAKE-HOME POINTS

1. FRC is the cornerstone: GA reduces it → atelectasis → shunt → hypoxaemia. Every intervention (positioning, PEEP, recruitment, pre-oxygenation) targets FRC.
2. The right bronchus is the troublemaker: Shorter and more vertical → endobronchial intubation goes right; aspiration goes right (particularly into the right lower lobe).
3. Anaesthetics depress all aspects of breathing: Drive, mechanics, muscles, and protective reflexes — in a dose-dependent manner.
4. HPV is your friend in OLV: Blunting it with high-dose volatiles worsens hypoxaemia. Use lower MAC or switch to TIVA.
5. Driving pressure, not tidal volume, predicts lung injury: Target ΔP < 15 cmH₂O in all ventilated patients.
6. Residual paralysis is underdiagnosed: Qualitative TOF is insufficient — use quantitative acceleromyography (TOFR ≥ 0.9) before extubation.
7. Preoperative PFTs are targeted, not routine: Indicated for COPD staging, lung resection planning, and identifying reversible bronchospasm — not as a screening tool.

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What This Lecture Covers

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