Intrathoracic Pressure During Positive Pressure Ventilation
During positive pressure ventilation, intrathoracic pressure is actually closest to atmospheric at end-expiration, not end-inspiration. At end-inspiration, intrathoracic pressure reaches its peak and is furthest from atmospheric pressure. 1, 2
Physiological Mechanism
The respiratory cycle during positive pressure ventilation creates predictable pressure changes:
During inspiration with positive pressure ventilation, airway pressure increases and is transmitted to the pleural space (intrathoracic pressure), raising it above atmospheric pressure 1, 2
Approximately 50% of alveolar pressure changes are transmitted to pleural pressure in normal lungs during positive pressure ventilation 2
In diseased lungs with reduced compliance, less airway pressure is transmitted to the pleural space, but intrathoracic pressure still increases during inspiration 1, 3
At end-inspiration, intrathoracic pressure reaches its maximum value during the respiratory cycle, representing the point furthest from atmospheric pressure 1, 4
End-Expiratory Pressure Dynamics
At end-expiration, intrathoracic pressure returns toward baseline:
Without PEEP, intrathoracic pressure at end-expiration approaches atmospheric pressure as the positive pressure dissipates 1
When PEEP is applied, the pressure gradient for venous return remains decreased throughout the entire ventilatory cycle, meaning intrathoracic pressure stays elevated even at end-expiration 1, 5
End-expiratory measurements are standardly referenced against atmospheric pressure in clinical practice 6
Hemodynamic Implications
The inspiratory increase in intrathoracic pressure has significant cardiovascular effects:
Increasing intrathoracic pressure during inspiration transiently decreases venous return to the right ventricle by raising right atrial back pressure 1, 2
The inspiratory increase in intrathoracic pressure decreases left ventricular afterload by reducing transmural pressure (the difference between intracavitary pressure and surrounding intrathoracic pressure) 1, 2, 4
Despite reduced venous return, left ventricular stroke volume may paradoxically increase during inspiration due to decreased afterload and other mechanisms 4
The "reverse pulsus paradoxus" observed during positive pressure ventilation reflects both transmission of increased intrathoracic pressure to the thoracic aorta and changes in left ventricular stroke volume 4
Clinical Pitfalls
Common misconceptions about pressure transmission:
The assumption that low lung compliance completely protects against hemodynamic effects of positive pressure ventilation is incorrect—cardiac output can be equally depressed despite reduced fractional pressure transmission because absolute inspiratory pleural pressure remains elevated due to higher airway pressures required 3
Measurements made only at end-expiration may have serious limitations for understanding the full hemodynamic impact of positive pressure ventilation 4
Transmitted airway pressure only slightly affects intra-abdominal pressure (approximately 8% transmission), so concerns about pressure transmission to the abdomen are generally overstated 6