The primary anesthetic used during vascular surgery  will depend on factors such as patient comorbidities, surgeon skill and comfort level, anatomic considerations, and the invasiveness of the surgical procedure. As such, anesthetic techniques for specific procedures are discussed in subsequent sections. Upon arrival to the operating room (OR), all patients should be placed on standard American Society of Anesthesiologists (ASA) monitors, including regular noninvasive blood pressure measurement, pulse oximetry, and continuous ECG. It is prudent to place an arterial catheter for invasive blood pressure monitoring for all but the most minor of vascular procedures because of the inherent risk for rapid hemodynamic changes and major blood loss. Patient comorbidities, cross-clamping on major vascular structures, and potential for hemorrhage all contribute to the hemodynamic instability frequently observed during these procedures. Invasive arterial monitoring also allows for frequent blood sampling to assess ventilation and oxygenation, ongoing blood loss and resuscitation needs, and overall metabolic milieu. Because induction of general anesthesia and endotracheal intubation are among the more hemodynamically labile periods, placing the arterial monitoring before induction of general anesthesia is wise.

Invasive monitoring with central venous or pulmonary arterial cannulation is not routine for most vascular procedures. Common exceptions include open aortic procedures or when patient comorbidities dictate utility. Large-bore intravenous (IV) access, either peripheral or central, is mandatory for any major vascular procedure because of the inherent risk of blood loss and need for resuscitation. An active type and screen and adequate blood product availability should be confirmed before undertaking any major vascular procedure.

Vascular repair in the cardiovascular system is a complex biological process involving orchestrated responses among and between the endothelium, smooth muscle cells, cardiac fibroblasts, and myocytes. The endothelium serves as a nexus for molecular signaling events that contribute to postinjury tissue remodeling. While cardiac tissue remodeling plays an initially protective role in response to injury, excessive activation of fibroblasts leads to adverse remolding and fibrosis that exacerbates heart failure. Endothelial cell-derived factors can both facilitate and inhibit vascular tissue repair, the balance of which ultimately determines the extent of fibrosis and cardiac dysfunction. A detailed description of all the known molecular factors of vascular injury and repair is beyond the scope of this article. Rather, a novel perspective is provided in which the roles of protease-activated receptors (PARs) and neuregulin-1 (NRG-1) in vascular repair are compared and contrasted, which is especially relevant given that both PARs and NRGs are promising therapeutic targets.

Vascular surgical procedures are associated with a two- to fourfold higher risk of adverse cardiac events (MI, cardiac death) compared with other types of noncardiac operations. Patients presenting for emergency vascular surgery have an even higher risk for perioperative morbidity and mortality. Many of these patients are at risk of having coexisting CAD.