Aortic Clamping

Hemodynamic response: Hypertension is the primary hemodynamic response typically seen with aortic cross-clamp application that results from an increase in afterload. Blood volume redistributes after aortic cross-clamping such that venous capacitance decreases below the clamp, expelling blood from the splanchnic and nonsplanchnic vascular beds, and increases above the clamp. The increase in upper body blood volume results in increased central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), and left ventricular end-diastolic pressure (LVEDP). Differences in hemodynamic responses are observed with occlusion at different levels of the aorta and can be the result of different patterns of blood volume distribution. Supraceliac cross-clamp application results in the most consistent redistribution of blood flow as described in the previous section(s). With infraceliac aortic cross-clamping, blood volume shifts into the splanchnic system and reduces preload if the splanchnic venous tone is low or, alternatively, it can be expelled into the vasculature of other tissues proximal to the clamp to increase preload. Variability in blood volume redistribution and splanchnic vascular tone also result from differences in fluid loading, depth of anesthesia, or anesthetic pharmacodynamics.

Oxygen consumption: Oxygen consumption decreases both proximal and distal to the aortic occlusion. The reason for the paradoxical decrease in oxygen consumption above the cross-clamp is unknown but might be related to sympathetic discharge from the adrenal glands that decreases capillary flow, increased arteriovenous shunting, or microcirculatory disturbances that compromise oxygen exchange due to proximal hypervolemia. Mixed venous oxygen saturation increases during aortic cross-clamp, indicating decreased extraction. A reduction in oxygen consumption and cardiac output reflects reduced global oxygen uptake and perfusion.

Coronary blood flow and contractility: Aortic cross-clamping results in increased myocardial oxygen demand. In an intact coronary blood supply, an increase in demand would lead to coronary artery vasodilation and a concomitant increase in oxygen supply. When coronary blood flow increases, the subendocardium is perfused and contractility will increase in response to aortic cross-clamping, which is also known as the Anrep effect. In the presence of inadequate coronary blood flow, the LVEDP increases and an increase in contractility does not manifest since the subendocardium is not perfused, thereby leading to decreased cardiac output. The beneficial effect of vasodilators on myocardial function during aortic cross-clamping is attributable to a decrease in preload resulting from an increase in venous capacitance, a decrease in afterload resulting from vasodilation, dilation of the coronary arteries with an increase in coronary blood flow, and facilitation of the Anrep effect.

Level and duration of aortic cross-clamp: As discussed in the previous section(s), the level of the aortic cross-clamp affects the hemodynamic response observed. Changes in MAP, filling pressures, ejection fraction, and wall motion are minimal during infrarenal aortic cross-clamping but exaggerated during supraceliac aortic cross-clamping. With increased duration of aortic cross-clamping, SVR increases and cardiac output decreases, which remains incompletely understood. Elevated proximal aortic pressure may ultimately increase fluid extravasation into the interstitial space, resulting in a decrease in circulating blood volume and a compensatory increase in SVR.

Renal effects: Cross-clamping of both the suprarenal and infrarenal aorta results in an increase in renin and angiotensin, which contributes to hypertension. Cross-clamping of the thoracic aorta is associated with severe decreases in renal blood flow, glomerular filtration rate, and urine output. Ischemia-reperfusion injury to the kidneys plays a central role in renal dysfunction after aortic surgery and is also present after infrarenal cross-clamping. Although mannitol is still often used to help maintain renal perfusion, it has not been consistently shown to reduce the incidence of renal failure. The use of dopamine, furosemide, and fenoldopam has also not been found to preserve renal function.

Effects on spinal cord: Cross-clamping of the aorta is associated with a decrease in distal aortic pressure and possibly ASA pressure, depending on the anatomy and presence of collateral blood supply, as well as an increase in CSF pressure and a decrease in the compliance of the spinal fluid space. Vasodilators used to decrease proximal aortic pressure should ideally possess minimal cerebral vasodilating properties that would decrease SCPP by decreasing distal aortic pressure and increasing CSF pressure. Sodium nitroprusside, which decreases distal aortic pressure and increases CSF pressure, and nitroglycerin, which predominantly decreases distal aortic pressure, can both decrease SCPP. However, unlike nitroglycerin, nitroprusside has the undesirable effect of causing vascular steal, which has the potential to worsen both spinal cord and myocardial ischemia during cross-clamping by diverting flow from maximally vasodilated ischemic regions to nonischemic regions.

Aortic Unclamping

Hemodynamic response: Unclamping of the thoracic aorta leads to a sudden decrease in SVR with a resultant decrease in arterial blood pressure. Cardiac output can increase, decrease, or remain the same. Myocardial blood flow increases and LVEDP decreases. Hypotension results from central hypovolemia that develops due to pooling of blood into reperfused tissues distal to the aortic occlusion, as well as hypoxia-mediated vasodilation and accumulation of myocardial-depressant metabolites. The metabolism of oxygen free radicals can also lead to an increase in microvascular permeability and loss of intravascular volume that lead to central hypovolemia, arterial hypotension, and ischemia-reperfusion injury.

Acidosis: Hypoperfusion of tissues distal to the aortic cross-clamp leads to the accumulation of vasoactive and myocardial-depressant metabolites, such as lactate, which contribute to metabolic acidosis after release of the aortic cross-clamp. The degree of acidosis present depends on the underlying pathology. Aortic cross-clamping in patients with aneurysmal disease was associated with more dramatic increases in lactate concentration and lactate-pyruvate ratio relative to patients with concomitant occlusive aortic disease, presumably due to the presence of collateral vessels and better tissue perfusion distal to the cross-clamp. Cross-clamp removal is also associated with a transient increase in carbon dioxide release and oxygen consumption.

Renal effects: Unclamping of the aorta results in a significant increase in renin and angiotensin that lasts for 6 hours but is unrelated to hypertension. Maldistribution of renal blood flow is seen, with a decrease in renal cortical blood flow. Glomerular filtration rate and renal plasma flow can remain at decreased values even 6 months following surgery. Optimization of circulating blood volume is thought to be protective from renal complications associated with aortic cross-clamp-induced ischemic insult, possibly due to inhibition of the production of certain vasoconstrictive compounds by volume loading.

References

• Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology. 1995;82:1026-1060.
• Lester LC, Kostibas MP. Anesthetic management for open thoracoabdominal and abdominal aortic aneurysm repair. Anesthesiol Clin. 2022;40:705-718.
• Vaughn SB, LeMaire SA, Collard CD. Case scenario: anesthetic considerations for thoracoabdominal aortic aneurysm repair. Anesthesiology. 2011;115:1093-1102.