DefinitionAn AAA (abdominal aortic aneurysm) is defined as an enlargement of at least 3 cm of the abdominal aorta. The majority of abdominal aortic aneurysms begin below the renal arteries and end above the iliac arteries. The exact cause of (AAA) is unknown. However, this is thought to be due to a degenerative process in the abdominal aorta caused by atherosclerosis. Atherosclerosis represents a response to vessel wall injury caused by inflammation, genetically regulated defects in collagen and fibrillin, increased protease activity in the arterial wall, and mechanical factors (Stoelting p. 143). Pathophysiology The abdominal aorta consists of three distinct tissue layers, including: Intima, Media, and Adventicia. There is a reduction in the medial layers of elastin from the thoracic region to the abdominal portion in a normal aorta. Aneurysms are caused by dilation of all layers of the vessel wall. AAAs generally grow on average by 0.2 to 0.8 mm/year and eventually rupture (Gupta and Narani). Genetics, inflammation, immune responses, cell wall stress, and proteolytic degradation all contribute to AAA formation. Proteolytic degradation of extracellular matrix proteins and elastins is the primary event in the development of abdominal aortic aneurysm. Collagen and elastin content is reduced from the proximal to the distal aorta. Fragmentation and degeneration are detrimental to the aneurysm walls because elastin is the main load-bearing element of the aorta. These changes, along with changes in the protein matrix of aneurysms, may contribute to the propensity for aneurysm formation in the infrarenal aorta. Oxidative stress, lymphocytic and moncytic infiltration with immunoglobulin deposition middle of paper ......treat aortic dissection. Verapamil and diltazem are used because of their negative vasodilator and inotropic effects (Coughlin). A dopamine infusion may be used throughout the case to improve renal perfusion. Heparin is administered before cross-clamping the aorta to reduce the risk of clotting disorders. Mannitol may be administered before cross-clamping to prevent renal failure during AAA resection. Furosemide can be used after cross-clamp release to improve urine flow (LaMuralgia, Musch). The secret to successful management of these cases is preparation. Early involvement in anesthesia management and a thorough understanding of AAA pathophysiology (including rupture and dissection) as well as the surgical and anesthetic implications of treatment will improve morbidity and mortality outcomes in this population. of patients..