Table 4-1.
Current Therapies for Primary Pulmonary Hypertension
| Therapy | Advantages | Disadvantages |
|---|---|---|
| Nitric oxide (NO) | Pulmonary circulation with selective vasodilation; increased Pao2 | Possible formation of toxic byproducts; prolonged bleeding times; expensive |
| Prostaglandins (epoprostenol, treprostinil, iloprost) | Potent vasodilation; inhibits platelet aggregation and smooth muscle cell proliferation | Not selective for pulmonary circulation; systemic hypotension; headaches; expensive; requires continuous infusion or inhalation |
| Phosphodiesterase-5 inhibitors (dipyridamole, sildenafil) | Possible synergy with NO therapy inhibitors | — |
| Endothelin receptor antagonist (Bosentan) | FDA approval | Limited data available |
| Calcium channel blockers | High efficacy; inexpensive | Less effective in severe cases; negative inotropic effects can worsen right ventricular failure |
| Oxygen | Directly reduces pulmonary vascular resistance in cases of hypoxia | None |
| Warfarin (Coumadin) | Improved long-term survival; decreases risk of intrapulmonary thrombosis | Increased bleeding risk |
| Magnesium | Vasodilation through blockage of Ca2+ channels; enhance NO synthase activity; releases prostaglandin I | Risk of magnesium toxicity: weakness, sedation, ECG changes |
ECG, Electrocardiographic; Pao2, arterial oxygen tension (partial pressure).