Changes in Respiratory Function During Anesthesia and Factors Influencing Them

Overview

1. Changes in Lung Volumes

Functional Residual Capacity (FRC)

• Moving from upright to supine position reduces FRC by ~1 L
• Induction of general anesthesia further reduces FRC by ~0.5 L
• Net result: FRC falls from ~3.5 L to ~2 L (a ~20% reduction), approaching residual volume (RV)
• This reduction occurs with both inhalational and intravenous anesthetics, whether breathing is spontaneous or controlled
• Muscle paralysis in the context of general anesthesia does not cause additional FRC reduction beyond anesthesia alone

Other Lung Volumes

• Tidal volume (VT): Falls with decreased lung compliance or reduced ventilatory muscle strength
• Vital capacity (VC): Reduced by restrictive changes (atelectasis, effusion) and muscle weakness
• Total lung capacity (TLC): Generally reduced
• Closing capacity: May exceed FRC, especially in elderly and obese, causing airway closure during normal tidal breathing

2. Compliance and Airway Resistance

Compliance

• Static compliance of the total respiratory system (lungs + chest wall) is reduced on average from 95 to 60 mL/cmH₂O during anesthesia
• Lung (static) compliance decreases from ~190 to ~150 mL/cmH₂O
• The lungs become smaller and stiffer, primarily due to atelectasis

• Trendelenburg position
• Obesity (shifts pressure-volume curve of chest wall rightward - more severely affects lung compliance)
• Pneumoperitoneum (reduces chest wall compliance with relative preservation of lung compliance)
• Low tidal volume ventilation when FRC is already reduced

Airway Resistance

• Most studies suggest anesthesia increases respiratory resistance, especially during mechanical ventilation
• The mechanism is closely related to FRC reduction: lower lung volumes decrease airway dimensions, increasing raw resistance
• Intrinsic PEEP may develop in patients with high resistance (asthma) or high compliance (COPD) if expiratory time is insufficient

3. Atelectasis - The Central Phenomenon

• Atelectatic area typically constitutes 5-6% of total lung area in routine cases, but can exceed 20%
• Because atelectatic lung contains mostly tissue (not air), 15-20% of total lung tissue is collapsed during uneventful anesthesia
• After thoracic surgery or cardiopulmonary bypass, collapse can involve up to 50% of lung volume
• Postoperative atelectasis can persist for several days after abdominal surgery

Mechanisms of Atelectasis Formation

4. Distribution of Ventilation and Perfusion (V/Q Mismatch)

Distribution of Ventilation

Distribution of Blood Flow

Consequences

• Shunt (V/Q → 0): Persistent perfusion of non-ventilated atelectatic areas. Shunt fraction may approach 15% during routine anesthesia. Shunt is the primary cause of hypoxemia under anesthesia.
• Alveolar dead space (V/Q → ∞): Upper lung regions where alveolar pressure exceeds pulmonary vascular pressure (West Zone 1). Contributes to CO₂ elimination impairment.
• Overall: The V/Q distribution shifts from a narrow peak centered near 1.0 to a bimodal distribution with both shunt and dead space components.

5. Gas Exchange

Oxygenation

• Mild-to-moderate hypoxemia (SaO₂ 85-90%) is common during anesthesia
• Approximately 20% of patients may suffer SaO₂ < 81% for up to 5 minutes
• Supplemental O₂ (FiO₂ 0.3-0.5) is routinely required
• Shunt physiology (from atelectasis) is the primary etiology
• Hypoxic pulmonary vasoconstriction (HPV) - the normal defense against V/Q mismatch - is impaired by inhalational anesthetics, worsening the hypoxemia

CO₂ Elimination

1. Reduced alveolar ventilation: All anesthetic drugs (volatile agents, opioids, propofol) depress ventilatory control in a dose-dependent manner, reducing minute ventilation and causing hypoventilation. During apnea, PaCO₂ rises ~10 mmHg in the first minute, then ~3.5 mmHg/minute.
2. V/Q mismatch: Increased alveolar dead space, instrumental dead space from breathing circuits, and regional inhomogeneity all increase V̇D/V̇T. The increase in V̇D/V̇T is alveolar in nature (confirmed by MIGET scanning). High PEEP and inspiratory pressures can cause alveolar overdistension in nondependent regions, further widening the alveolar-arterial CO₂ gradient.
3. VCO₂ changes: Metabolic rate and CO₂ production are generally reduced during anesthesia. However, CO₂ can increase in hypermetabolic states - shivering, fever, malignant hyperthermia.

6. Control of Breathing

Chemical Feedback (Chemoreceptors)

• CO₂ response (hypercapnic drive): Volatile anesthetics depress the CO₂-ventilation response curve in a dose-dependent fashion. The PaCO₂-ventilation response curve shifts rightward (higher resting PaCO₂) and the slope decreases (reduced sensitivity). The apneic threshold rises. At low concentrations (emergence), the effect on hypercapnic response is negligible.
• O₂ response (hypoxic drive): Hypoxemic ventilatory drive is markedly attenuated even at subanesthetic concentrations of volatile agents. Because these agents distribute into fat and muscle, concentrations sufficient to depress hypoxic drive persist for several hours after anesthesia ends. This is especially dangerous in patients with chronic hypercapnia who depend on hypoxic drive to breathe (type II respiratory failure).
• Opioids cause a dose-dependent rightward shift of the CO₂-ventilation curve and raise resting PaCO₂, while also profoundly blunting hypoxic drive.
• Painful surgical stimulation can partially reverse the depression of ventilatory responses, to varying and unpredictable degrees.

Upper Airway Reflexes

• Protective reflexes (laryngeal, pharyngeal) are progressively obtunded
• Loss of upper airway dilator muscle tone contributes to obstruction
• Residual neuromuscular blockade in the recovery room markedly attenuates hypoxic ventilatory response and impairs upper airway dilator muscles

7. Factors Influencing Respiratory Changes During Anesthesia

Patient-Related Factors

Position-Related Factors

• Supine position: Reduces FRC by ~1 L even before induction; most anesthesia is administered in this position
• Trendelenburg (head-down): Abdominal contents push diaphragm cephalad, further reducing FRC and worsening atelectasis; major determinant of compliance reduction
• Lateral decubitus: Dependent lung more atelectatic; V/Q relationships complex; used for thoracic surgery
• Upright/semi-upright: Minimizes diaphragmatic pressure transmission; reduces atelectasis formation. Upright positioning can reduce the cranial diaphragm shift.

Anesthetic Technique and Drug Factors

• All volatile anesthetics and IV agents (except ketamine): Reduce FRC and cause atelectasis
• Ketamine: Uniquely maintains respiratory muscle tone - does not reduce FRC or cause atelectasis; if NMB added, atelectasis occurs like other agents
• Neuromuscular blocking agents: Residual blockade (33-64% of patients arriving in PACU have inadequate recovery by TOF monitoring) causes impaired hypoxic drive, reduced upper airway dilator tone, and postoperative hypoxemia
• High FiO₂ (preoxygenation): High inspired oxygen concentrations promote resorption atelectasis; 100% O₂ preoxygenation increases atelectasis significantly vs. 30% O₂

Surgical Factors

• Thoracic surgery / cardiopulmonary bypass: Atelectasis up to 50% of lung volume; persists hours postoperatively
• Upper abdominal surgery: Diaphragmatic dysfunction, pain, splinting; atelectasis persists days
• Abdominal surgery with pneumoperitoneum: Reduces chest wall compliance (not lung compliance), requiring higher airway pressures
• One-lung ventilation: Obligate shunt from non-ventilated lung; dependent lung also develops atelectasis

Ventilatory Management Factors

• PEEP: Recruits atelectasis, reduces shunt, restores compliance; PEEP of 7 cmH₂O in normal-weight patients recruits most collapsed lung. However, excessive PEEP reduces venous return and cardiac output, and may worsen dead space by overdistending nondependent alveoli.
• Recruitment maneuvers (VC maneuvers): Airway pressure of 30-40 cmH₂O required for significant atelectasis reversal; must be sustained (40 cmH₂O for 7-8 seconds opens nearly all anesthesia-induced atelectasis)
• Tidal volume: Low VT without adequate PEEP can worsen atelectasis; driving pressure (Pplat - PEEP) correlates better with postoperative pulmonary complications than VT alone
• FiO₂: Lower FiO₂ with adequate SpO₂ reduces resorption atelectasis; post-recruitment ventilation with 60% N₂ helps maintain recruited lung

8. Neuraxial Anesthesia

• Diaphragmatic function is preserved with low-to-mid spinal levels
• Intercostal and abdominal muscles are blocked, slightly reducing expiratory reserve volume and cough efficacy
• High thoracic blocks (T4 and above) can impair accessory respiratory muscles
• No significant FRC reduction; atelectasis is uncommon
• Postoperative analgesia from neuraxial techniques promotes better pulmonary toilet and reduces splinting

Summary Table