Mechanism of respiration and Clinical co relation with anaesthesia
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Mechanism of Respiration & Clinical Correlation with Anaesthesia
1. OVERVIEW
Respiration involves two inseparable components: ventilation (moving air in/out) and gas exchange (O₂/CO₂ transfer). Understanding these mechanisms is foundational for anaesthetic practice, since adverse respiratory events during anaesthesia can be catastrophic.
"A thorough understanding of the physiology of the respiratory system and how anesthesia affects breathing is fundamental to safe and effective practice in our specialty." — Barash's Clinical Anaesthesia, 9e
2. MUSCLES OF BREATHING
Inspiration (Active Process)
- Diaphragm — the primary muscle. On contraction, it pushes abdominal contents downward and lifts ribs upward/outward, increasing intrathoracic volume → lowers intrapleural pressure → air flows in
- External intercostals and accessory muscles (scalenes, sternomastoid) — recruited during increased demand (exercise, obstructive disease)
Expiration (Passive at Rest)
- Normally passive — elastic recoil of lungs drives air out
- Active expiration (exercise, asthma, COPD): abdominal muscles compress the abdomen and push the diaphragm up; internal intercostals pull ribs downward and inward
— Costanzo Physiology, 7e
3. RESPIRATORY MECHANICS — EQUATION OF MOTION
The total airway pressure (P_aw) needed for air movement during inflation reflects two opposing forces:
P_aw = P_res + P_el + PEEP
or more fully:
P_aw = Vt × E_RS + R_aw × V̇ + PEEP + PEEPi
Where:
- E_RS = respiratory system elastance (stiffness)
- R_aw = airway resistance
- V̇ = inspiratory flow
- Vt = tidal volume
- PEEPi = intrinsic PEEP (auto-PEEP)
The higher the resistance and/or the stiffer the lungs/chest wall, the higher the airway pressure required to achieve adequate lung volume.
— Barash's Clinical Anaesthesia, 9e
4. COMPLIANCE
Compliance = ΔVolume / ΔPressure
- Inversely related to elastance (stiffness)
- Increased compliance → lungs distend easily (e.g., emphysema)
- Decreased compliance → stiff lungs requiring more pressure (e.g., fibrosis, ARDS, atelectasis)
Transpulmonary pressure = intra-alveolar pressure − intrapleural pressure (key driving pressure)
Surfactant reduces surface tension at the alveolar air-liquid interface → prevents alveolar collapse → maintains compliance
— Costanzo Physiology, 7e
5. LUNG VOLUMES & CAPACITIES
| Volume/Capacity | Value (approx.) | Clinical Significance |
|---|---|---|
| Tidal Volume (VT) | 500 mL | Normal breath |
| IRV | 3000 mL | Reserve for deep breath |
| ERV | 1200 mL | Forced expiration reserve |
| RV | 1200 mL | Cannot be expelled; not measurable by spirometry |
| FRC (ERV + RV) | 2400 mL | Resting equilibrium volume; critical in anaesthesia |
| VC (IC + ERV) | 4700 mL | Decreases in restrictive disease |
| TLC | 5900 mL | Total lung capacity |
FRC is the most clinically important volume in anaesthesia — it acts as an oxygen reservoir during apnoea.
6. VENTILATION & DEAD SPACE
Alveolar Ventilation (V̇A):
V̇A = (VT − VD) × Respiratory Rate
- VD = dead space (~30% of VT in healthy adults)
- Physiologic dead space = anatomic + alveolar dead space (alveoli ventilated but not perfused)
Alveolar Ventilation Equation:
PAco₂ = (V̇CO₂ × K) / V̇A
- If CO₂ production is constant, PaCO₂ varies inversely with alveolar ventilation
- Hypoventilation → ↑ PaCO₂ (hypercapnia)
- Hyperventilation → ↓ PaCO₂ (hypocapnia)
7. GAS EXCHANGE — DIFFUSION
Alveolar Gas Equation:
PAO₂ = FiO₂ × (Patm − PH₂O) − PaCO₂ × (VO₂/VCO₂)
Transfer of O₂ across the alveolar-capillary membrane depends on:
- Partial pressure gradient
- Surface area available for diffusion
- Membrane thickness
- Diffusion coefficient (CO₂ diffuses 20× faster than O₂)
8. VENTILATION-PERFUSION (V/Q) MATCHING
| Condition | Effect |
|---|---|
| V/Q = 1 (normal) | Optimal gas exchange |
| V/Q → 0 (shunt) | Blood passes unventilated alveoli → hypoxaemia, not correctable with O₂ |
| V/Q → ∞ (dead space) | Ventilated alveoli not perfused → wasted ventilation, ↑ PaCO₂ |
Under anaesthesia, V/Q mismatch worsens significantly (see below).
9. CONTROL OF BREATHING
- Central chemoreceptors (medulla): primary sensor for CO₂/H⁺ — most potent stimulus to breathe
- Peripheral chemoreceptors (carotid and aortic bodies): respond to hypoxia (PaO₂ < 60 mmHg), hypercapnia, and acidosis
- Respiratory centres (medulla + pons): set rate and rhythm — pre-Bötzinger complex (rhythm generator), apneustic and pneumotaxic centres
10. CLINICAL CORRELATION WITH ANAESTHESIA
10.1 Effects of General Anaesthesia on Respiratory Mechanics
| Change | Mechanism | Consequence |
|---|---|---|
| ↓ Diaphragm & intercostal tone | Drug effect (inhalational & IV agents) | ↓ FRC by ~20% |
| Cephalad diaphragm shift | Loss of muscle tone | Dependent atelectasis within 10 minutes |
| ↓ Transverse thoracic diameter | Muscle relaxation | Compressive atelectasis |
| Shunt fraction up to 15% | Atelectatic areas still perfused | Hypoxaemia |
"Administration of general anaesthesia, whether by the inhaled or intravenous route, results in an almost immediate loss of diaphragmatic and intercostal muscle tone, a cephalad shift of the diaphragm, and a decrease in the transverse thoracic diameter... resulting in a 20% reduction in FRC and in the development of compressive atelectasis." — Fishman's Pulmonary Diseases & Disorders
Notable exception: Ketamine — uniquely maintains respiratory muscle tone; atelectasis is less likely.
10.2 Atelectasis under Anaesthesia
- Crescent-shaped atelectasis in dependent lung zones within 10 minutes of induction (seen on CT)
- Constitutes 2–10% of total lung volume
- Abolished with PEEP (positive end-expiratory pressure)
- Occurs regardless of spontaneous vs. mechanical ventilation
- Worsened by high FiO₂ pre-oxygenation (absorption atelectasis)
10.3 Impairment of Hypoxic Pulmonary Vasoconstriction (HPV)
- Volatile anaesthetic agents inhibit HPV
- HPV normally diverts blood away from poorly ventilated alveoli
- Inhibition → blood continues to perfuse atelectatic zones → ↑ shunt → hypoxaemia
10.4 Infant/Paediatric Considerations (Miller's Anaesthesia)
- Compliant chest wall (cartilaginous ribs) + poorly compliant lungs → tendency for alveolar collapse and lower resting FRC
- Infants lack fatigue-resistant muscle fibres (only 10–25% type I fibres in diaphragm vs. 60% in adults) → vulnerable to respiratory muscle fatigue
- Narrowest airway in children <5 years is at the cricoid (not the cords) → ETT selection is critical
- Dynamic FRC maintained via rapid respiratory rate, laryngeal braking, and increased intercostal tone during exhalation
10.5 Neuraxial Anaesthesia & Pulmonary Function
- Spinal/Epidural → intercostal and abdominal muscle block → reduced expiratory reserve, impaired cough
- High spinal (T4 or above) → diaphragmatic compromise → respiratory failure risk
- Epidural analgesia post-operatively: improves respiratory mechanics by reducing splinting from pain → reduces atelectasis, pneumonia risk
10.6 Postoperative Respiratory Complications
| Complication | Key Risk Factor | Prevention/Management |
|---|---|---|
| Atelectasis/pneumonia | Upper abdominal/thoracic surgery | Incentive spirometry, early mobilisation |
| Respiratory depression | Opioids → ↓ CO₂ sensitivity | Monitoring, naloxone, titrated dosing |
| Residual neuromuscular block | Inadequate reversal | TOF monitoring, sugammadex, neostigmine |
| OSA (Obstructive Sleep Apnoea) | Obesity, redundant pharyngeal tissue | Pre-op CPAP, careful opioid dosing |
| Bronchospasm | Reactive airways, active smoking | Pre-op bronchodilators, avoid irritant triggers |
| Persistent pulmonary hypertension (neonates) | Acidosis, cold, hypoxia post-delivery | Avoid hypoxia, maintain warmth |
10.7 Work of Breathing & Lung-Protective Ventilation
Under anaesthesia with neuromuscular blockade, the anaesthetist fully controls ventilation. Key principles:
- Driving pressure (plateau pressure − PEEP) should be minimised — high driving pressure correlates with postoperative pulmonary complications
- Low tidal volumes (6–8 mL/kg IBW) — lung-protective strategy
- PEEP (5–8 cmH₂O) — prevents atelectasis, restores FRC
- Recruitment manoeuvres — periodic sustained inflations to reopen collapsed alveoli
10.8 Smoking & Perioperative Risk
- ↑ Airway secretions, impaired mucociliary clearance
- Elevated carboxyhemoglobin → ↓ O₂ delivery
- Risk of prolonged ventilatory support
- Minimum 8 weeks of cessation required for meaningful reduction in pulmonary complications
- Preoperative preparation for COPD: bronchodilators, antibiotics if purulent secretions, short-course steroids for bronchospastic component
— Fishman's Pulmonary Diseases & Disorders
SUMMARY TABLE
| Physiologic Parameter | Normal | Under GA |
|---|---|---|
| FRC | 2400 mL | ↓ ~20% (to ~1900 mL) |
| Shunt fraction | <5% | Up to 15% |
| Compliance | Normal | ↓ due to atelectasis |
| V/Q matching | Normal | Worsened |
| HPV | Intact | Inhibited by volatiles |
| Respiratory drive | CO₂-driven | Blunted (dose-dependent) |
Key Sources:
- Barash, Cullen & Stoelting's Clinical Anaesthesia, 9e
- Costanzo Physiology, 7e
- Miller's Anaesthesia, 2-Volume Set, 10e
- Fishman's Pulmonary Diseases & Disorders
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