Does Positive Pressure Ventilation Increase Pulmonary Vascular Resistance?
Yes, positive pressure ventilation (PPV) consistently increases pulmonary vascular resistance (PVR), with the magnitude of increase directly proportional to mean airway pressure, particularly through the effects of tidal forces and positive end-expiratory pressure (PEEP). 1
Mechanisms of PVR Increase
The increase in PVR during PPV occurs through two primary physiologic mechanisms:
Transpulmonary Pressure Effects
Changes in transpulmonary pressure (the difference between alveolar and pleural pressure) are the primary driver of increased RV afterload during PPV. 1 When alveolar pressure rises with positive pressure ventilation:
- Microvascular collapse occurs when pleural pressure exceeds pulmonary venous pressure, creating West Zone 2 conditions 1
- Complete vascular obstruction develops when regional pressures exceed pulmonary arterial pressure (West Zone 1) 1
- Under both conditions, alveolar pressure becomes the effective outflow pressure for the right ventricle, considerably increasing RV afterload 1
Mean Airway Pressure Relationship
During controlled ventilation, tidal forces and PEEP increase PVR in direct proportion to their effects on mean airway pressure (mPaw). 1 This relationship is critical because:
- PEEP is the prominent but not sole determinant of mPaw 1
- Higher tidal driving pressures and longer duty cycles also increase mPaw and thus PVR 1
- At high levels of mPaw, the net effect encourages West Zone 2 conditions, raising effective vascular resistance within aerated lung compartments 1
Quantitative Evidence
Research demonstrates that PEEP elevation from 5 to 13 cmH₂O increases PVR by 32% in ARDS patients, with corresponding increases in right atrial pressure of 34%. 2 This occurs even when tidal volume and plateau pressure are limited to lung-protective levels.
In neonatal models, ventilation at 15 cmH₂O positive pressure significantly increases PVR compared to lower pressures at all inspired oxygen concentrations. 3
Clinical Context and Right Ventricular Impact
The increased PVR has direct hemodynamic consequences:
- Cardiac output decreases by approximately 13% with PEEP elevation due to increased RV afterload 2
- The right ventricle is particularly sensitive to afterload changes because of its limited myocardial thickness and contractile power 1
- In ARDS patients, acute cor pulmonale develops in 20-25% of cases, driven partly by mechanical ventilation effects 1
Special Populations at Higher Risk
Patients with pre-existing pulmonary hypertension, single-ventricle physiology (particularly post-Fontan), and right-sided heart disease are at substantially higher risk for hemodynamic compromise from PPV-induced PVR increases. 1 In these populations:
- Passive pulmonary blood flow (as in Fontan circulation) is critically dependent on low PVR 1
- Positive pressure ventilation can impede pulmonary blood flow and decrease cardiac output 1
- Alveolar hypoxia and acidosis must be aggressively avoided as they compound PVR increases 1
Lung Compliance Considerations
An important caveat: diseased lungs with reduced compliance transmit less alveolar pressure to pleural pressure. 1 In normal subjects, approximately 50% of alveolar pressure change transmits to pleural pressure, but stiffer ARDS lungs transmit less 1. Despite this, PVR escalates progressively in ARDS even though pleural pressure rises relatively little as mPaw increases. 1
Mitigating Strategies
While PPV inherently increases PVR, certain approaches can minimize this effect:
- In highly recruitable ARDS lungs, maintaining an open lung while limiting overdistention can improve vascular resistance 1
- Volume loading can partially reverse PVR increases: passive leg raising at high PEEP decreases PVR by 21% by recruiting collapsed pulmonary microvessels 2
- High-frequency positive pressure ventilation reduces PVR compared to conventional IPPV by lowering peak airway pressures 4