Fig. 3

iNO reversal of hypoxemia and pulmonary hypertension during HPV. iNO is a pulmonary selective vasodilator. It diffuses selectively from ventilated alveoli to the adjacent pulmonary capillaries. This reduces PVR and the right ventricle afterload. The selective vasodilation of oxygenated vessels diverges pulmonary blood flow towards the ventilated alveoli. As a consequence, pulmonary shunt is reduced and arterial oxygenation is increased. In physiologic conditions, most of the alveoli are well ventilated and perfused, as low PVR ensures that a wide pulmonary capillary bed is recruited (A). If some of the alveoli are poorly or not ventilated (e.g., atelectasis, pneumonia), the pulmonary capillaries that perfuse those alveoli constrict because of HPV. The increased PVR leads to a consequent reduction of the available pulmonary vascular bed. This limits the blood perfusion of the poorly/not ventilated lung areas then limiting V/Q mismatch and pulmonary shunt (B). The administration of iNO in the presence of HPV increased the vasodilation of pulmonary vessels that are normally ventilated. This condition reduces PVR and reverses hypoxemia by diverging the blood flow to ventilated areas, thus reducing V/Q mismatch and pulmonary shunt (C). The P_AO₂-P_ACO₂ graph below, represents the partial pressure of the alveolar gases in each of the conditions previously described. In physiologic conditions, the V/Q is optimal (A arrow); when some the alveoli are not ventilated, hypoxemia emerges because of pulmonary shunt despite the compensatory mechanism of HPV (B arrow). This condition may be partially reverted by the administration of iNO (C arrow). The bottom panel was adapted from West JB, Luks AM. West’s Respiratory Physiology. The Essentials. Tenth Edition. Wolters Kluwer, 2015. PAO₂: alveolar pressure of O₂; PACO₂: alveolar pressure of CO₂; V/Q: ventilation–perfusion ratio; PVR: pulmonary vascular resistance; HPV: hypoxic pulmonary vasoconstriction