Mechanics of breathing

Mechanics of breathing:

1. Muscles of respiration: The diaphragm is the most important muscle for respiration. Contraction of the diaphragm increases the intrathoracic volume and lowers the intrathoracic pressure. This helps in inspiration. External intercostal muscles and accessory muscles like scalene, pectorals etc. are important for inspiration when the respiratory rate and effort of breathing increases and in respiratory distress. When more effort is needed in exhalation, the abdominal muscles like the rectus abdominis, internal and external obliques along with the internal intercostals are used.

2. Transpulmonary pressure: When the lungs fill with air, the pressure inside the alveoli becomes more positive while the pressure outside is negative. The outside negative pressure distends the alveoli and helps it to fill with air. If the outside pressure becomes positive, the alveoli will collapse.

   Ptp = Palv – Pip. (where Ptp is transpulmonary pressure, Palv is alveolar pressure, and Pip is intrapleural pressure)

   Under physiological conditions the transpulmonary pressure is always positive; intrapleural pressure is always relatively negative and large, while alveolar pressure moves from slightly negative to slightly positive as a person breathes. Due to inherent elasticity, the natural tendency of the lung is to recoil inward while the chest wall tends to recoil outwards. These two opposing forces lead to a relatively negative intrapleural pressure. The negative intrapleural pressure is one of the important factors that keep the patency of small airways, which lack cartilaginous support. During inspiration, the Pip becomes more negative, causing the Palv to be lower than the atmospheric pressure. This causes air to flow into the alveoli. On the other hand, expiration is a passive process aided by elastic recoil of the lung.

"Intrapulmonary and Intrapleural Pressure Relationships: Alveolar pressure changes during the different phases of the cycle. It equalizes at 760 mm Hg but does not remain at 760 mm Hg. "

3. Compliance of the lung: Lung compliance is the change in the volume of the lung per change in the transpulmonary pressure or Ptp. When Ptp is zero, the lung can neither inflate or deflate. At functional respiratory capacity or FRC, P alv equals the atmospheric pressure. At FRC, the inward recoil tendency of the lungs is equal to the outward recoil tendency of the chest wall. Compliance is lowest at extremes of FRC. It implies that an expanded lung and a completely deflated lung have lower capacity to distend to a given pressure. Compliance can be estimated by the slope of the pressure-volume loop of the lung. Steeper slope (increase in slope) corresponds to increased compliance and vice versa.

4. The work of breathing: The work of breathing is usually estimated by the area under the dynamic pressure volume curve of the lungs. Under physiological conditions the work needed for inspiration is more than that needed for expiration.

5. Restrictive lung diseases like interstitial lung diseases, pneumonia and surfactant deficiency e.g. acute respiratory distress syndrome, hemothorax, pneumothorax, empyema, pleural effusion or thickening, respiratory muscles weakness, chest deformities, cardiomegaly etc. are associated with decreased compliance of the lungs, chest wall or both. This results in a rightward shift of static and dynamic pressure volume loop of the lungs, chest wall or both. FRC will be lower.

6. In obstructive lung diseases like bronchial asthma, emphysema, chronic bronchitis and bronchiectasis, pulmonary compliance is normal or increased especially if emphysematous lung changes co-exist. Dynamic lung compliance curves are either not displaced or shifted leftward if emphysematous lung changes developed. FRC will be higher. The main defect is increased airways resistance, especially during expiration.

7. Surfactant: It is synthesized by type II alveolar epithelial cells. Its primary component is a phospholipid called dipalmitoyl phosphatidylcholine (DPPC) which reduces the surface tension in the alveoli. Without surfactant small alveoli will collapse as they have a higher collapsing pressure. Surfactant reduces the alveolar collapsing pressure, increases compliance and reduces the work of breathing. Glucocorticoids increase surfactant production. In intrauterine life, surfactant is produced after 24 weeks of age. Premature infants are predisposed to respiratory distress syndrome from lack of sufficient surfactant. Pulmonary edema, pulmonary hemorrhage and meconium aspiration can inactivate surfactant and cause respiratory distress.

   Airway resistance: Resistance is indirectly proportional to the fourth power of radius. The medium sized airways (not small airways) are the site of greatest resistance. This is because even though the small airways have a smaller diameter, they are arranged in parallel, which decreases total resistance. Parasympathetic stimulation increases while sympathetic stimulation decreases airway resistance.

   Ventilation and perfusion of the lung (V/Q): Perfusion of the lung depends on three factors - alveolar pressure (Palv), pulmonary arterial pressure (Pa) and pulmonary venous pressure (Pv). Higher Palv can compromise blood flow in the local pulmonary circulation as the vessels are thinner walled and under lower pressure. On the basis of the influence of gravity, perfusion of lung is divided into three zones superior to inferior - I, II and III. In zone I, which is at the apex, Palv >Pa >Pv. Hence, arterial blood flow is very low and it adds to the physiological dead space. It is not normally seen in healthy individuals but under conditions of positive pressure ventilation, hemorrhage etc zone I conditions persist and add to the dead space. In middle zone or zone II, Pa >Palv >Pv. In the lower zone or zone III, Pa >Pv >Palv and perfusion is higher. During exercise Pa increases eliminating any existing zone I. Ventilation and perfusion both increase from top to bottom in the lung but perfusion increases more compared to ventilation. The average V/Q ratio for the lung is 0.8. V/Q ratio is higher in the apex and lowest at the base of the lung. In zone I, where V/Q is highest, PaO2 is highest and PaCO2 is lowest while in zone III, the PaO2 is lowest and PaCO2 is highest.

   A mismatch of ventilation and perfusion is called V/Q defect. When perfusion stops e.g. in pulmonary embolism, the V/Q becomes infinity and dead space increases; when the ventilation is obstructed V/Q becomes 0 and blood is shunted away from the non- ventilated regions to the ventilated regions of the lung. Accordingly, depending on the severity of ventilation and/or perfusion defect the V/Q ratio will change.