Right Ventricular Afterload
The pulmonary arteries have a relatively high-density of alpha-1 receptors [Rudner XL et al. Circulation 100: 2336, 1999], second only to hepatic/omental arteries. The pulmonary arteries also contains alpha receptors [Troncy E et al. Br J Anaesth 79: 631, 1997; Blaise G et al. Anesthesiology 99: 1415, 2003]. Therefore, it should be assumed that alpha-agonists can profoundly increase RV afterload.
While pulmonary “vascular resistance” is ~ 20% of SVR, pulmonary vascular impedance is 50% of systemic vascular impedance. The difference in the two is most likely related to the increased intensity of pulse wave reflections in the pulmonary vascular tree (impedance is related to vascular resistance, vascular compliance, and wave reflections, all of which oppose pulsatile blood flow) [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 882, 2006]. Because SVR is such a poor indicator of afterload [Lang RM et al. Circulation 74: 1114, 1986], it may follow that PVR does not accurately predict right ventricular pressure volume work or myocardial consumption.
Furthermore, the relationship between pulmonary blood flow and calculated PVR is non-linear, most likely due to the recruitment of blood vessels when PA pressures rise (i.e. converting West Zone 2 to Zone 3) [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 882, 2006].
Metabolic Activities of the Pulmonary Endothelium
Pulmonary vascular endothelium metabolizes a variety of hormones and drugs, including norepinephrine (but not epinephrine or vasopressin), 5-HT, lidocaine, bupivacaine, and fentanyl.