Pulmonary Ventilation - Mechanism; Positive Pressure Breathing

(Guyton and Hall, Textbook of Medical Physiology, Chapter 38)

A. Mechanism of Pulmonary Ventilation

• Inspiration (active process): The diaphragm contracts and flattens, pulling the lower surfaces of the lungs downward, and the external intercostals lift the rib cage forward and upward (increasing anteroposterior chest diameter by ~20%). Accessory muscles (sternocleidomastoid, anterior serrati, scaleni) assist in deep/forced inspiration.
• Expiration (largely passive at rest, due to elastic recoil of lungs and chest wall): During forced expiration, the internal intercostals and abdominal recti (which also compress abdominal contents upward against the diaphragm) contract.

• Pleural pressure: The pressure of fluid in the thin space between visceral and parietal pleura. It is normally slightly negative (about -5 cm H2O at the start of inspiration, becoming more negative, about -7.5 cm H2O, during inspiration), holding the lung "floated" against the chest wall.
• Alveolar pressure: Pressure inside the alveoli. During inspiration it falls to about -1 cm H2O (below atmospheric), driving air inward; during expiration it rises to about +1 cm H2O, driving air outward.
• Transpulmonary pressure: The difference between alveolar and pleural pressure; it is the measure of elastic recoil forces of the lung tending to collapse it at any instant, and it opposes lung expansion.

B. Positive Pressure Breathing

• Manual and mechanical resuscitators, and modern positive-pressure ventilators that intermittently apply pressure to the airway (mouth, nose, or endotracheal tube) to inflate the lungs, after which the lung deflates passively by its own elastic recoil (the reverse of normal quiet breathing where inspiration is the active phase).
• Intermittent positive-pressure breathing (IPPB) devices, and continuous positive airway pressure (CPAP), where a constant positive pressure is maintained throughout the respiratory cycle.

1. Reverses the normal pressure gradient: Instead of subatmospheric alveolar pressure causing air entry, supra-atmospheric pressure is applied at the airway opening, pushing air in; expiration occurs passively as pressure is released.
2. Effect on venous return and cardiac output: Because intrathoracic (and hence pleural and right atrial) pressure becomes positive instead of negative, venous return to the right heart is impeded. This can reduce cardiac output and arterial pressure, particularly if intrathoracic pressure remains persistently elevated (as with PEEP/CPAP) or if the patient is hypovolemic.
3. Effect on lymph flow: Normally, slightly negative pleural/interstitial pressures assist lymphatic drainage from the lungs; sustained positive pressure can reduce this lymphatic pump effect.
4. Clinical use: Used in artificial respiration/resuscitation (e.g., for respiratory paralysis, drowning, anesthesia, or respiratory failure) and forms the basis of modern mechanical ventilators used in ICU care, in contrast to older "tank respirators" (iron lung), which used negative pressure applied around the body to expand the chest.
5. Caution: Excessive or prolonged positive pressure can overdistend alveoli (barotrauma) and, by raising intrathoracic pressure, can significantly compromise venous return, especially in hypovolemic or cardiac patients.