Inhaled Pulmonary Vasodilators

Inhaled Pulmonary Vasodilators

David Ray Velez, MD

Beneficial Effects 

  • Inhalation Keeps Vasodilation Selective to the Pulmonary Vasculature that is Better Ventilated
  • Improved Ventilation-Perfusion (V/Q) Matching and Arterial Oxygenation
    • Blood Flow is Preferentially Directed to Better Ventilated Areas
  • Decreased Intrapulmonary (Right-to-Left) Shunting
  • Decreased Pulmonary Vascular Resistance, Reducing Right Ventricular Afterload

Side Effects

  • Typically Has Minimal Systemic Effects
  • Increased Preload Can Worsen Cardiogenic Pulmonary Edema from Left Heart Failure
  • Small Anti-Platelet Effect (Clinical Impact is Unclear)

Indications

  • ARDS with Worsening Oxygenation Despite Lung-Protective Ventilation Strategies
    • *Improves Oxygenation in Severe ARDS but No Proven Mortality Benefit
  • Decompensated Pulmonary Hypertension
  • Acute Right Heart Failure
  • Hypoxemia Due to Pulmonary Vasoconstriction

Contraindications

  • Left-Sided Heart Failure

Agents

  • Nitric Oxide
    • Potent Vasodilator
    • Starting Dose: 20 ppm (Initial and Maximal Dose) and Subsequently Weaned Down Over the Following Days Once Stabilized
  • Aerosolized Epoprostenol Sodium (Flolan/Veletri)
    • Synthetic Prostacyclin Causes Vasodilation
    • Generally Much Less Expensive than Nitric Oxide
    • Starting Dose: 50 ng/kg/min (Initial and Maximal Dose) and Subsequently Weaned Down Over the Following Days Once Stabilized
  • Less Common Agents:
    • Nitroglycerine – Metabolized to Nitric Oxide
    • Milrinone – Phosphodiesterase Inhibitor
  • *All Have Similar Efficacy but Nitric Oxide and Epoprostenol Can Be Precisely Titrated Making Them Better Suited for Prolonged Maintenance Therapy