Explain the hemodynamic consequences of aortic cross-clamping.
The most consistent hemodynamic response to acute aortic occlusion is an abrupt increase in afterload with a resultant increase in proximal aortic pressure. During supraceliac aortic occlusion, there is an increase in preload due to volume redistribution from veins distal to the site of aortic occlusion. The increases in afterload, preload, and possibly contractility resulting from aortic occlusion may exacerbate myocardial oxygen demand and possibly result in myocardial ischemia. Because of the expected increases in preload from aortic occlusion, the pre-occlusion preload should be maintained low. Venodilators such as nitroglyc-erin (NTG) may be titrated in order to further decrease preload and arterial dilators may be used to control increases in afterload. During aortic occlusion, attention should be directed toward maintaining preload, which may be complicated by continued blood loss.
Intraoperative hypotension may result from multiple causes. Hypovolemia, myocardial depression, and decreases in afterload should be considered. Reperfusion is associated with hypotension. Hypotension may be caused by central hypovolemia due to blood pooling in reperfused tissues, hypoxia-mediated vasodilation, and accumulation of vasoac-tive or myocardial-depressant metabolites, such as lactate. Treatment should be directed toward rapid correction of hypovolemia, acidosis, and hypocalcemia, as well as the judi-cious administration of vasoactive drugs. If there is difficulty obtaining hemodynamic stability, the aorta can be temporar-ily re-occluded while resuscitation continues (Table 36.2).
Renal insufficiency may occur as a result of abdominal aortic reconstruction. It is possible that pharmacologic agents may provide renal protection during repair. Although mannitol may result in greater diuresis on post-operative day 1 and has less subclinical glomerular and renal tubular damage, it most probably has no effect on postoperative blood urea levels, serum creatinine concen-tration, or creatinine clearance. There is little evidence of the effectiveness of furosemide as a renal protective agent.
Theoretically, the perioperative use of low doses of dopamine may confer renal protection in high-risk individuals. Low-dose dopamine (1–3 μg/kg/min) dilates renal afferent arterioles and increases renal blood flow, independent of its cardiac effects. Dopamine infusion during aortic clamping results in a significant rise in urine sodium output, potassium output, creatinine clearance, and urine volume. The use of perioperative dopamine during aortic surgery is associated with increases in effective renal plasma flow and glomerular filtration rate as well as fractional excre-tion of sodium during the postoperative period; however, no studies have demonstrated a renal protective effect of low-dose dopamine. It is most likely that renal-dose dopamine administration during the perioperative period confers no advantage over the maintenance of euvolemia in most vascu-lar patients during infrarenal AAA repair.
Visceral ischemia (which does not occur with infrarenal aortic clamping) may initiate fibrinolysis. Antifibrinolytic agents should be strongly considered if supraceliac occlusion is anticipated. Aminocaproic acid, tranexamic acid, and aprotinin are all effective in decreasing fibrinolytic activity.