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