What is the mechanism of breathing in a healthy individual and how is it affected in patients with respiratory conditions such as Chronic Obstructive Pulmonary Disease (COPD) or pneumonia?

Mechanism of Breathing in Health and Respiratory Disease

Normal Breathing Mechanics

In healthy individuals, breathing is driven by the diaphragm and intercostal muscles creating negative intrathoracic pressure during inspiration, with passive elastic recoil of the lungs driving expiration. 1

The respiratory control centers in the brainstem and carotid body chemoreceptors regulate ventilation primarily through carbon dioxide sensing, with CO₂ being highly soluble and carried in blood as bicarbonate (70-85%), dissolved CO₂ (5-10%), and bound to hemoglobin (10-20%). 1 Increased CO₂ levels stimulate ventilation to maintain pH balance, with normal PaCO₂ ranging from 4.6-6.1 kPa (34-46 mmHg). 1

During exercise in healthy individuals, end-expiratory lung volume (EELV) actually decreases, allowing for more efficient ventilation. 1 Oxygen uptake increases linearly with work rate at approximately 10 mL·min⁻¹·W⁻¹ during cycle ergometry. 1

Altered Mechanics in COPD

Airflow Obstruction and Dynamic Hyperinflation

COPD fundamentally alters breathing mechanics through expiratory flow limitation, which forces patients to adopt two compensatory strategies: increasing end-expiratory lung volume (dynamic hyperinflation) and increasing inspiratory flow rate with decreased inspiratory time. 1

• Expiratory flow becomes limited during tidal breathing, initially during exercise but eventually at rest as disease progresses. 1
• The rate of lung emptying slows dramatically, and the interval between inspiratory efforts does not allow expiration to the relaxation volume of the respiratory system, creating intrinsic positive end-expiratory pressure (PEEPi). 1, 2
• PEEPi acts as an inspiratory threshold load that contracting inspiratory muscles must overcome before creating negative alveolar pressure to initiate airflow. 1, 2
• Dynamic hyperinflation places the diaphragm at severe mechanical disadvantage, though the diaphragm adapts by developing greater resistance to fatigue. 1

Ventilation-Perfusion Mismatch

Ventilation-perfusion (V'/Q') inequality is the major mechanism impairing gas exchange in COPD at all stages, regardless of emphysema presence. 1

• Some lung units develop very high V'/Q' ratios (emphysematous regions with destroyed alveoli and lost vasculature), receiving up to 50% of alveolar ventilation but only 5% or less of cardiac output. 1
• Other areas have very low V'/Q' ratios representing partially blocked airways. 1
• This mismatch retards carbon dioxide elimination kinetics, as the bulk of CO₂ comes from relatively poorly ventilated areas. 1
• Hypoxic pulmonary vasoconstriction and collateral ventilation remain efficient, preventing significant shunt. 1

Carbon Dioxide Retention

Between 20-50% of patients with acute exacerbations of COPD are at risk of carbon dioxide retention if given excessively high oxygen concentrations, but the mechanism is far more complex than simple loss of hypoxic drive. 1

• Oxygen administration corrects hypoxemia but worsens V'/Q' mismatch and contributes to increased PaCO₂. 2, 3
• The appropriate target oxygen saturation for COPD patients is 88-92%, not the 94-98% used for other patients. 1, 2, 3
• Increased airway resistance and respiratory muscle weakness restrict the normal ventilatory response to elevated CO₂. 1

Respiratory Muscle Dysfunction

Despite diaphragmatic adaptation to chronic overload, both functional inspiratory muscle strength and endurance are compromised in COPD due to static and dynamic hyperinflation. 1

• At identical absolute lung volumes, inspiratory muscles can generate more pressure than healthy controls, but hyperinflation negates this advantage. 1
• Respiratory muscle weakness contributes to hypercapnia, dyspnea, nocturnal oxygen desaturation, and reduced exercise performance. 1
• The oxygen cost of breathing per unit ventilation increases substantially due to airway obstruction requiring more effort to move air. 1

Altered Mechanics in Pneumonia

Gas Exchange Impairment

Pneumonia causes hypoxemia primarily through V'/Q' mismatch from poor aeration of consolidated lung areas, which is the easiest form of hypoxemia to treat with oxygen therapy. 1

• Consolidated areas create regions of low V'/Q' where perfusion continues but ventilation is impaired. 1
• Unlike COPD, hypoxic vasoconstriction may not fully compensate for this mismatch during acute pneumonia. 1

Combined COPD and Pneumonia

When pneumonia complicates COPD, patients face compounded respiratory mechanics problems with significantly worse outcomes. 4

• Coexisting pneumonia increases mortality risk by 85% in hospitalized COPD patients (RR=1.85). 4
• These patients require mechanical ventilation 48% more often (RR=1.48) and have 58% more ICU admissions (RR=1.58). 4
• Intubated COPD patients develop substantial increases in intrinsic PEEP and end-expiratory lung volume during acute respiratory failure. 2
• Patients needing mechanical ventilation have mild to moderate intrapulmonary shunt, suggesting complete airway occlusion by bronchial secretions. 2

Mechanical Ventilation Considerations

For mechanically ventilated COPD patients with pneumonia, prolonging expiratory time by reducing respiratory rate to 10-15 breaths/min and adjusting I:E ratio to 1:2-1:4 allows complete exhalation and reduces gas trapping. 2

• External PEEP at 4-8 cmH₂O can offset iPEEP and reduce work of breathing, but never set PEEP greater than iPEEP as this worsens hyperinflation. 2, 3
• Target tidal volumes of 6-8 mL/kg predicted body weight to minimize ventilator-induced lung injury. 2, 3
• Maintain plateau pressure below 30 cmH₂O, employing permissive hypercapnia if pressures exceed this threshold. 2, 3
• Target SpO₂ of 88-92% specifically in COPD patients to avoid worsening hypercapnia from excessive oxygen. 2, 3

Common Pitfalls

• Never use high respiratory rates in mechanically ventilated COPD patients - this prevents adequate expiratory time and worsens dynamic hyperinflation. 2
• Avoid excessive FiO₂ - oxygen administration corrects hypoxemia but worsens V'/Q' mismatch and increases PaCO₂ in COPD. 2, 3
• Do not aggressively normalize PaCO₂ in chronic CO₂ retainers - permissive hypercapnia with pH >7.2 is well tolerated. 2, 3
• Never ignore unilateral findings - asymmetric examination in a ventilated patient demands investigation for pneumothorax, mucus plug, or mainstem intubation. 2