What are the effects of positive pressure ventilation (PPV) on hemodynamic measurements?

Effects of Positive Pressure Ventilation on Hemodynamic Measurements

Positive pressure ventilation significantly impacts hemodynamics primarily by altering venous return and right ventricular afterload, which can lead to decreased cardiac output and potential hemodynamic instability in ARDS patients. 1

Physiological Mechanisms

• Positive pressure ventilation affects hemodynamics through two primary mechanisms: changes in pleural pressure (Ppl) and changes in transpulmonary pressure (TP) 1
• Transpulmonary pressure primarily affects right ventricular (RV) afterload, while changes in pleural pressure affect venous return 1
• Tidal forces and positive end-expiratory pressure (PEEP) increase pulmonary vascular resistance (PVR) in direct proportion to their effects on mean airway pressure 1
• The increased intrathoracic pressure reduces the pressure gradient for venous return to the heart, potentially decreasing cardiac output 1

Hemodynamic Effects

• Decreased venous return to the right ventricle due to increased pleural pressure, leading to reduced RV preload 2
• Increased RV afterload due to increased transpulmonary pressure and pulmonary vascular resistance 1
• Reduced left ventricular (LV) preload due to decreased RV output and ventricular interdependence 3
• Decreased LV afterload due to increased pleural pressure, which reduces transmural pressure 1
• Overall reduction in cardiac output, primarily through decreased stroke volume as heart rate usually remains unchanged 4

Monitoring Hemodynamic Effects

• Pulse pressure variation (PPV) during passive ventilation is a good predictor of fluid responsiveness when properly interpreted 1
• High PPV values (>12-13%) suggest that the patient is fluid responsive, even with low tidal volumes or low lung compliance 1
• Central venous pressure (CVP) is useful for monitoring RV function response to treatment, though it's a poor predictor of preload responsiveness 1
• Echocardiography should be performed early to assess ventricular dimensions, function, and to detect acute cor pulmonale (ACP), which occurs in 20-25% of ARDS cases 1
• Pulmonary artery catheter may be useful in severe cases to measure pulmonary artery pressure, vascular resistance, and cardiac output 1

Management Strategies

• Careful evaluation of fluid administration is crucial - while it may improve systemic perfusion, excessive fluids can worsen pulmonary edema and promote RV failure 1

• In patients with significant PPV, consider:

  • Judicious use of norepinephrine to improve RV function by restoring mean arterial pressure 1
  • Adaptation of respiratory settings (driving pressure, plateau pressure, PEEP) 1
  • Limiting hypercapnia which can worsen pulmonary hypertension 1
  • Prone positioning which may improve RV function 1

• For patients with ARDS who are not in shock, a fluid conservative protocol (FACTT-lite) is recommended as it increases ventilator-free days 1

Special Considerations

• PPV may not be reliable in cases of spontaneous breathing, low tidal volume, low lung compliance, or arrhythmias 5
• Continuous thermodilution-based and pulse contour analysis-based cardiac output monitoring are not recommended in patients treated with ECMO 1
• Negative pressure ventilation may be an alternative in select cases, as it has been shown to produce less cardiac depression compared to positive pressure ventilation 6

Pitfalls and Caveats

• High PEEP levels can significantly reduce cardiac output but may be necessary for oxygenation in ARDS 4
• Fluid responsiveness does not always mean fluid should be administered - the risk of worsening pulmonary edema must be considered 1
• In severe RV failure, high PPV may indicate RV afterload dependence rather than fluid responsiveness, requiring echocardiographic assessment 1
• Cardiac output measurements may be misleading in cases of tricuspid regurgitation associated with RV dilatation 1