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Pulmonary hypertension is a common but underappreciated pathological condition in patients who undergo thoracic surgery, and being unaware of this condition or underestimating its severity can lead to significant perioperative complications. Management of this condition requires foresight and preparation as discussed in this chapter. Thus, this chapter will serve to: (1) review the pathogenesis of pulmonary hypertension, (2) describe the preoperative preparation and evaluation of patients with pulmonary hypertension who present for thoracic surgery, (3) explain the effects of anesthesia and surgery on the pulmonary vasculature, and (4) define the proper use of the pharmacological aids to control pulmonary hypertension.

At rest, the normal pulmonary vascular system is noted as a high-compliance, high-flow, low-pressure system. This stands in contrast to the systemic circulation, which has much higher resting level of arterial and venous tone. This difference stems partly from the anatomy because the pulmonary precapillary arterioles have a thinner media and less smooth muscle than their systemic counterparts. Furthermore, at rest, there are far more recruitable vessels in the pulmonary bed, which permits dramatic increases in flow with minimal impact on pressure.

The difference between the systemic and arterial systems is also due to the response of the pulmonary vascular endothelium to the challenges of hypoxia (hypoxic pulmonary vasoconstriction: HPV). This vasoconstriction is known as the Euler-Lijestrand reflex. Mitochondria play a key role as the primary sensor of hypoxia, with intracellular calcium increasing as a key response, but the basic mechanism is controversial.1 Figure 4–1 displays several of the key pathways for hypoxic vasoconstriction in which voltage gated potassium (K+) channels directly alter mitochondrial responses. L-type calcium (Ca2+) channels are facilitated by the depolarization of the K+ channels; they then directly increase intracellular Ca2+. Further, classical transient receptor potential channel 6 (TRPC6) also increases intracellular Ca2+ as do store operated channels (SOC) and sodium (Na+)/Ca2+ exchangers (NCX).1 This rise in intracellular Ca2+ also triggers release from sarcoplasmic reticulum via activation of the ryanodine receptors. The end result is constriction of the smooth muscle of the precapillary sphincters and pulmonary arterioles. This calcium-dependent vasoconstriction is the primary phase of HPV and lasts 15 to 30 minutes. The Ca2+ independent phase (the sustained phase) of pulmonary vascular constriction starts at 15 minutes and can last for hours. It is highly dependent on RhoA/Rho kinase (ROCK) mediated Ca2+ sensitization,2 and may be a key to the development of pulmonary hypertension.3 Interestingly, nitric oxide (NO)-induced relaxation and endothelin-1-induced vasoconstriction of pulmonary arteries have been shown to be due to regulation of ROCK-mediated Ca2+-sensitization, rather than altered Ca2+ metabolism.4,5 See Figure 4–1.

Figure 4–1.

Ca2+ mobilization in HPV: mechanisms that have been implicated in the hypoxia-induced elevation of [Ca2+], and their potential signaling pathways. Note that ...

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