How does positive pressure ventilation (PPV) increase right ventricle (RV) afterload?

Mechanisms of Positive Pressure Ventilation on Right Ventricular Afterload

Positive pressure ventilation increases right ventricular afterload primarily by creating West zone 1 and 2 conditions in the lungs, where alveolar pressure exceeds pulmonary venous or arterial pressure, causing microvascular collapse and increased pulmonary vascular resistance. 1

Physiological Mechanisms

Direct Effects on Pulmonary Vasculature

• When pleural pressure (Ppl) increases during positive pressure ventilation, it can exceed pulmonary venous pressure, creating West zone 2 conditions 1
• In more extreme cases, when pleural and interstitial pressures exceed pulmonary arterial pressure, West zone 1 conditions develop 1
• Under both conditions, alveolar pressure becomes the effective outflow pressure for the right ventricle, significantly increasing RV afterload 1
• This mechanism is particularly important in patients with:
  • Sepsis
  • Post-cardiac surgery
  • ARDS
  • Decreased RV function
  • Low lung compliance 1

Impact of Mean Airway Pressure

• During controlled ventilation, tidal forces and PEEP increase pulmonary vascular resistance (PVR) proportionally to their effects on mean alveolar pressure 1
• Mean airway pressure (mPaw) is clinically used to approximate mean alveolar pressure 1
• PEEP is a major determinant of mPaw, but longer duty cycles and higher tidal driving pressures also contribute 1
• Higher mPaw has dual effects:
  • Distends already open lung units
  • Encourages microvascular closure 1

Lung Volume and Vascular Resistance

• At high levels of mPaw, West zone 2 conditions are promoted, which:
  • Raises effective vascular resistance in aerated lung compartments
  • Redirects blood flow toward poorly ventilated units
  • Increases dead space
  • Afterloads the RV 1, 2

Hemodynamic Consequences

RV Sensitivity to Afterload

• The normal right ventricle is highly compliant but has limited myocardial thickness and contractile power 1
• RV is more sensitive to changes in afterload than to variations in preload 1
• When RV afterload increases acutely, RV stroke volume decreases significantly and arterial elastance increases disproportionately to end-systolic elastance 1
• This makes RV function inefficient, requiring more energy to maintain adequate output 1

Ventricular Interdependence

• RV dilation from increased afterload can cause:
  • Leftward shift of the interventricular septum
  • Increased LV end-diastolic pressure
  • Reduced LV transmural filling pressure
  • Impeded LV diastolic filling 1
• Overdistention of the afterload-sensitive RV functionally stiffens the left ventricle through shared septum, circumferential muscle fibers, and pericardial space 1

Risk of RV Ischemia

• Unlike LV coronary perfusion (primarily diastolic), normal RV perfusion occurs during both systole and diastole 1
• The pressure-overloaded RV is at increased risk for ischemia due to:
  • Decreased perfusion pressure
  • Increased RV intramural pressure
  • Decreased systemic arterial pressure 1
• End-diastolic pressure elevation leads to decreased RV coronary blood flow and potential subendocardial ischemia 1

Clinical Implications

Factors Affecting Severity

• The hemodynamic impact of positive pressure ventilation is magnified by:
  • Higher changes in lung volume
  • Greater increases in intrathoracic pressure
  • Reduced effective circulating blood volume
  • Decreased cardiac contractility 3
• In patients with lung injury, the effects are more pronounced due to:
  • Reduced capacity to accommodate blood flow (inflammation, consolidation)
  • Compressive vascular collapse
  • Microthrombosis 1

Management Considerations

• Use the lowest effective PEEP to maintain oxygenation 2
• Consider lower tidal volumes (6-8 mL/kg) to minimize increases in intrathoracic pressure 2
• Monitor for signs of decreased venous return (hypotension, tachycardia) 2
• Ensure adequate volume status before initiating positive pressure ventilation 2

Common Pitfalls and Caveats

• While positive pressure ventilation decreases LV afterload, this beneficial effect is often negated by the simultaneous decrease in venous return 1
• The pressure gradient driving venous return is normally only 4-8 mmHg, making it highly sensitive to small changes in pleural pressure 1
• In ARDS patients with highly recruitable lungs, maintaining a relatively open lung while limiting overdistention can actually improve vascular resistance, but excessive pressures will still increase RV afterload 1
• Patients with pre-existing RV dysfunction are particularly vulnerable to the afterload-increasing effects of positive pressure ventilation 4