Modified from Roizen MF, Beaupre PN, Alpert RA, et al. Monitoring with two-dimensional transesophageal echocardiography: comparison of myocardial function in patients undergoing supraceliac, suprarenal-infraceliac, or infrarenal aortic occlusion. J Vasc Surg 1984;1(2):300-305.
Patients with ischemic heart disease or ventricular dysfunction are unable to fully compensate as a result of the hemodynamic alterations. The increased wall stress attributed to aortic cross-clamp application may contribute to decreased global ventricular function and myocardial ischemia. Clinically, these patients experience increases in PAOP in response to aortic cross-clamping. Aggressive pharmacologic intervention is required for restoration of cardiac function during this time.
5. Metabolic alterations
After the application of an aortic cross-clamp, the lack of blood flow to distal structures makes these tissues prone to developing hypoxia. In response to hypoxia, metabolites (e.g., lactate) accumulate.
The release of arachidonic acid derivatives may also contribute to the cardiac instability that is observed during aortic cross-clamping. Thromboxane A2
synthesis, which is accelerated by the application of an aortic cross-clamp, may be responsible for the decrease in myocardial contractility and cardiac output that occurs.
Traction on the mesentery is a surgical maneuver used for exposing the aorta. Decreases in blood pressure and SVR, tachycardia, increased cardiac output, and facial flushing are common responses to mesenteric traction.
The neuroendocrine response to major surgical stress is believed to be mediated by cytokines such as interleukin 1-beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α), as well as plasma catecholamines and cortisol. These mediators are thought to be responsible for triggering the inflammatory response that results in increased body temperature, leukocytosis, tachycardia, tachypnea, and fluid sequestration.
6. Effects on regional circulation
Structures distal to the aortic clamp are underperfused during aortic cross-clamping. Renal insufficiency and renal failure have been reported to occur after abdominal aortic reconstruction.
Suprarenal and juxtarenal cross-clamping may be associated with a higher incidence of altered renal dynamics; however,
reductions in renal blood flow can occur with any level of clamp application.
Infrarenal aortic cross-clamping is associated with a 38% decrease in renal blood flow and a 75% increase in renal vascular resistance. These effects may lead to acute renal failure, which is fatal in 50% to 90% of patients who have undergone aneurysmectomies.
Preoperative evaluation of renal function is one of the most significant predictors of postoperative renal dysfunction. Therefore, a complete evaluation of renal function is required in the preoperative period.
Spinal cord damage is associated with aortic occlusion. Interruption of blood flow to the greater radicular artery (artery of Adamkiewicz) in the absence of collateral blood flow has been identified as a causative factor in paraplegia.
The incidence of neurologic complications increases as the aortic cross-clamp is positioned in a higher or more proximal area.
Ischemic colon injury is a well-documented complication that is associated with abdominal aortic resections. Ischemia of the colon is most frequently attributed to manipulation of the inferior mesenteric artery, which supplies the primary blood supply to the left colon. This vessel is often sacrificed during surgery, and blood flow to the descending and sigmoid colon depends on the presence and the adequacy of the collateral vessels. Mucosal ischemia occurs in 10% of patients who undergo AAA repair. In fewer than 1% of these patients, infarction of the left colon necessitates surgical intervention.
7. Aortic cross-clamp release
While the aorta is occluded, metabolites that are liberated as a result of anaerobic metabolism, such as serum lactate, accumulate below the aortic cross-clamp and induce vasodilation and vasomotor paralysis.
As the cross-clamp is released, SVR decreases, and blood is sequestered into previously dilated veins, which decreases venous return.
Reactive hyperemia causes transient vasodilation secondary to the presence of tissue hypoxia, the release of adenine nucleotides, and the liberation of an unnamed vasodepressor substance that acts as a myocardial depressant and a peripheral vasodilator.
This combination of events results in decreased preload and afterload. The hemodynamic instability that may ensue after the release of an aortic cross-clamp is called declamping shock syndrome
Evidence demonstrates that venous endothelin (ET)-1 may be partially responsible for the hemodynamic alterations that accompany declamping shock syndrome. Venous ET-1 has a positive inotropic effect on the heart as well as a vasoconstricting and vasodilating action on blood vessels.
The most frequently observed hemodynamic responses to aortic declamping are listed in the table below.
Hemodynamic Responses to Aortic Declamping
|Response to Clamp Release|
|Mean arterial pressure|
|Systemic vascular resistance|
|No change or increase|
|Pulmonary artery occlusion pressure|
The magnitude of the response to unclamping the aorta may be manipulated. Although SVR and MAP decrease, intravascular volume may influence the direction and the magnitude of change in cardiac output.
Restoration of circulating blood volume is paramount in the provision of circulatory stability before release of the aortic clamp.
The site and the duration of cross-clamp application, as well as the gradual release of the clamp, influence the magnitude of circulatory instability. Partial release of the aortic cross clamp over time frequently results in less severe hypotension.
8. Surgical approach
The standard approach for elective abdominal aortic reconstruction is the transperitoneal incision. The advantages of this route include exposure of infrarenal and iliac vessels, ability to inspect intraabdominal organs, and rapid closure. Unfavorable consequences associated with this approach include increased fluid losses, prolonged ileus, postoperative incisional pain, and pulmonary complications.
The retroperitoneal approach has gained popularity as an alternative to the standard route. Its advantages include excellent exposure (especially for juxtarenal and suprarenal aneurysms), decreased fluid losses, less incisional pain, and fewer postoperative pulmonary and intestinal complications. After implantation with a synthetic graft, the aortic adventitia is closed. In addition, the retroperitoneal approach does not elicit mesenteric traction syndrome. The reported limitations of this approach are unfamiliarity of surgeons with this technique, poor right distal renal artery exposure, and inability to inspect the integrity of the abdominal contents.
9. Management of fluid and blood loss
Extreme loss of extracellular fluid and blood should be expected with abdominal aortic aneurysmectomies. Evaporative losses and third spacing occur, with the magnitude of loss depending on the surgical approach, the duration of the surgery, and the experience of the surgeon.
Most blood loss occurs because of back bleeding from the lumbar and inferior mesenteric arteries after the vessels have been clamped and the aneurysm is opened.
The use of heparin also contributes to blood loss. Excessive bleeding, however, can occur at any point during surgery, and blood replacement is commonly administered during abdominal aortic resections.
Because of the heightened awareness of transfusion-related morbidity, the use of autologous blood has generated increasing interest. Presently, three options are available for the use of autologous transfusions: preoperative deposit, intraoperative phlebotomy and hemodilution, and intraoperative blood salvage.
10. Preoperative assessment
The presence of underlying CAD in patients with vascular disease has been well documented. CAD is reported to occur in more than 50% of patients who require abdominal aortic reconstruction and is the single most significant risk factor influencing long-term survivability. MIs are responsible for 40% to 70% of all fatalities that
occur after aneurysm reconstruction. In the presence of such threatening mortality rates, the extent of CAD and the subsequent functional limitations should be clearly defined and cardiac function optimized preoperatively before elective aortic vascular reconstruction is performed.
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