**4.1.2 Capillary**

#### **Cardiopulmonary bypass**

As discussed, CPB causes pulmonary damage during surgery through different mechanisms, potentially leading to PH but, more frequently, it contributes to the exacerbation of PH caused by other factors during the surgical procedure. In this context, patients can benefit from PH-specific medical therapy (Table **2**) and prophylactic treatments for PH use in cardiac surgery, which will be discussed later in this chapter.

In 62 patients with preoperative PH (PVR > 125 dyn·sec·cm-5 immediately before induction of anesthesia) Solina *et al*. (Solina et al., 2001) explored the dose-responsiveness of 10, 20, 30 and 40 ppm of iNO administered upon termination of CPB in comparison to an intravenous bolus of 50 mg/kg of milrinone given 15 minutes before separation from CPB followed by a 0.5 mg/kg/min regimen administered in the operating room thereafter. Treatment with iNO was associated with significant reductions in PVR at all doses but no improved benefit was observed for doses higher than 10 ppm. No significant difference was observed between iNO and milrinone in terms of reduction in PVR and inotropic requirement.

The same team compared 20 and 40 ppm of iNO to the same dose of intravenous milrinone in 45 patients after cardiac surgery (Solina et al., 2000). Study drugs were administered upon termination of CPB for a 24h-period in the intensive care unit (ICU). The group receiving 20 ppm iNO had a significantly higher MAP while the group receiving 40 ppm had higher right ventricular ejection fraction (RVEF) on arrival in the ICU. The milrinone group required significantly more phenylephrine in the ICU with a trend towards higher heart rates.

In a crossover study, Schmid *et al*. (Schmid et al., 1999) compared iNO, PGE1 and NTG in 14 adult patients with severe PH (MPAP > 30 mmHg; PVR > 300 dyn·sec·cm-5) after cardiac surgery. The investigation was performed in the ICU within the first 24 h after the procedure. The generalization of results obtained from this study was limited, since it only included patients in stable postoperative circulatory conditions. However, in contrast to PGE1 and NTG, iNO decreased PVR without exerting concomitant systemic vasodilatory effects. In addition, iNO did not affect the right coronary perfusion pressure and increased oxygen transport.
