Ventilator Effects on Right Ventricular (RV) Function

Mechanical ventilation has profound and often under-recognized effects on right ventricular (RV) performance. The RV is particularly vulnerable because it is a thin-walled, volume-sensitive, afterload-intolerant chamber. Positive pressure ventilation (PPV) alters preload, afterload, interventricular interactions, and coronary perfusion, which together determine RV output.


1. Basic RV Physiology Relevant to Ventilation

Unique features of the RV

  • Thin-walled, compliant chamber
  • Designed to pump against low pulmonary vascular resistance (PVR)
  • Poor tolerance to acute increases in afterload
  • RV output is highly preload dependent
  • RV perfusion occurs throughout the cardiac cycle, but is sensitive to increased wall tension

β€”> Any ventilatory strategy that increases PVR or reduces venous return can precipitate RV failure


2. Effects of Positive Pressure Ventilation (PPV) on RV Preload

Mechanism

  • PPV β†’ ↑ intrathoracic pressure (ITP)
  • ↑ ITP β†’ ↓ pressure gradient between systemic veins and right atrium
  • Result: ↓ venous return β†’ ↓ RV preload

Clinical impact

  • Reduced RV filling
  • Decreased RV stroke volume
  • More pronounced in:
    • Hypovolemia
    • High PEEP
    • Low chest wall compliance

Key concept

PPV unloads the RV by reducing preload – beneficial in RV volume overload, harmful in preload-dependent states


3. Effects of Mechanical Ventilation on RV Afterload (Most Critical)

RV afterload = Pulmonary Vascular Resistance (PVR)

Factors increasing PVR during ventilation

  1. High Lung Volumes
    • Overdistension compresses alveolar capillaries
    • ↑ alveolar pressure β†’ ↑ PVR
  1. High PEEP
    • Excessive PEEP β†’ ↑ transpulmonary pressure
    • Capillary compression β†’ ↑ RV afterload
  1. Hypoxia
    • Hypoxic pulmonary vasoconstriction (HPV)
  1. Hypercapnia & Acidosis
    • Potent pulmonary vasoconstrictors
  1. Pulmonary vascular disease
    • ARDS
    • Pulmonary embolism
    • Pulmonary hypertension

Result

  • ↑ RV systolic pressure
  • RV dilation
  • RV ischemia
  • Reduced RV output β†’ reduced LV preload

!!!Acute rise in PVR is the single most important mechanism of ventilator-induced RV failure


4. Lung Volume–PVR Relationship (U-Shaped Curve)

Lung Volume

Effect on PVR

Low lung volume (atelectasis)

↑ PVR (extra-alveolar vessel collapse)

Optimal FRC

Lowest PVR

High lung volume (overdistension)

↑ PVR (alveolar capillary compression)

β€”>Both atelectasis and overdistension increase RV afterload
β€”> Lung-protective ventilation aims for optimal FRC


5. Interventricular Interdependence & Septal Shift

Mechanism

  • RV dilation β†’ ↑ RV end-diastolic pressure
  • Interventricular septum shifts toward LV
  • LV diastolic filling ↓
  • Cardiac output ↓

Exacerbated by

  • High PEEP
  • Acute pulmonary hypertension
  • ARDS

!!This explains hypotension in RV failure despite β€œnormal” LV contractility


6. Effects of PEEP on RV Function

Beneficial effects (context-dependent)

  • Improves oxygenation β†’ ↓ hypoxic pulmonary vasoconstriction
  • Reduces atelectasis β†’ ↓ PVR
  • Decreases LV afterload (indirect benefit)

Harmful effects

  • ↑ Intrathoracic pressure β†’ ↓ venous return
  • ↑ Transpulmonary pressure β†’ ↑ PVR
  • RV dilation β†’ septal shift

Clinical pearl

Moderate PEEP may unload the RV, excessive PEEP precipitates RV failure


7. Tidal Volume (VT) and Driving Pressure Effects

High VT

  • Alveolar overdistension
  • ↑ PVR
  • ↑ RV afterload

High Driving Pressure (Ξ”P = Pplat βˆ’ PEEP)

  • Strong predictor of RV dysfunction
  • Correlates with mortality in ARDS

β€”> Low VT (6 mL/kg PBW) + low driving pressure protects the RV


8. Impact of Hypercapnia (Permissive Hypercapnia)

Mechanism

  • Hypercapnia β†’ pulmonary vasoconstriction
  • Respiratory acidosis β†’ ↑ PVR

Result

  • RV pressure overload
  • RV dilation and dysfunction

πŸ“Œ Permissive hypercapnia is not benign in patients with RV dysfunction


9. Spontaneous Breathing vs Controlled Ventilation

Spontaneous breathing

  • Negative intrathoracic pressure
  • ↑ Venous return
  • ↓ RV afterload
  • But excessive effort β†’ large swings in transpulmonary pressure β†’ RV stress

Controlled ventilation

  • Predictable pressures
  • Risk of excessive PEEP/VT

Balanced approach: Avoid both vigorous spontaneous effort and injurious controlled ventilation


10. Ventilator-Induced RV Failure (Acute Cor Pulmonale)

Common in

  • Moderate–severe ARDS
  • Pulmonary embolism
  • Severe pneumonia
  • Pulmonary hypertension

Diagnostic clues

  • Sudden hypotension
  • Rising CVP
  • Echo: RV dilation, septal flattening, ↓ TAPSE
  • Worsening oxygenation after ↑ PEEP


11. Ventilator Strategies to Protect the RV (RV-Protective Ventilation)

Core principles

  1. Low tidal volume (6 mL/kg PBW)
  2. Limit plateau pressure (<30 cmHβ‚‚O)
  3. Minimize driving pressure
  4. Avoid excessive PEEP
  5. Prevent hypoxia
  6. Avoid severe hypercapnia/acidosis
  7. Prone positioning (reduces PVR and RV afterload)
  8. Optimize fluid status
  9. Use pulmonary vasodilators when indicated (inhaled NO, epoprostenol)


12. Summary Table – Ventilator Effects on RV

Ventilator Factor

Effect on RV

Positive pressure

↓ Preload

High PEEP

↑ Afterload

High VT

↑ PVR

Hypoxia

↑ PVR

Hypercapnia

↑ PVR

Optimal PEEP

↓ PVR

Prone position

↓ RV afterload

Lung overdistension

RV failure