Keywords
abdominal aortic aneurysm repair, aortic cross clamping, endovascular aortic aneurysm repair, infraceliac aortic cross clamping, supraceliac aortic cross clamping
Case Synopsis
A 74-year-old man with chronic stable angina, hypertension, and a previous myocardial infarction is undergoing an endovascular aneurysm repair (EVAR) of an infrarenal para-anastomotic aortic aneurysm under general anesthesia. Previous dipyridamole thallium testing revealed a large, fixed myocardial defect with no evidence of reversible disease. It has been 4 months since his prior open abdominal aortic aneurysm (AAA) repair in which his postoperative recovery involved a 1-week stay in the intensive care unit (ICU) and treatment for acute kidney injury (AKI). During deployment of the endovascular graft, there is mild hypertension that resolves quickly after balloon deflation. A total of 2 L of Plasmalyte was given during the case. The patient is successfully extubated at the end of the procedure and transported to the ICU.
Problem Analysis
Definition
EVAR is becoming a common approach for the treatment of both primary and reoperative AAAs ( Fig. 29.1 ). The anesthetic considerations for EVARs are quite different than for open AAA repairs. Understanding aspects of each technique will help develop an appropriate anesthetic plan when determining monitoring choices, anesthetic technique, and the anticipated intraoperative and perioperative complications.
Open surgical repair (OSR) of an AAA involves clamping of the infrarenal aorta. The surgical dissection leading up to aortic occlusion, the occlusion of the aorta itself, and the pathophysiologic events following release of the aortic clamp are associated with varying degrees of hemodynamic instability. Hypotension during the extensive surgical exposure is relatively common, although it is usually transient and well tolerated. Myocardial ischemia is sometimes encountered in patients with known or previously undiagnosed coronary artery disease (CAD) and may be accompanied by increased pulmonary capillary wedge pressure, reduced cardiac output, and transesophageal echocardiogram (TEE) evidence of regional wall abnormalities. During aortic occlusion hypertension and left ventricular (LV) dysfunction may occur. Table 29.1 compares the hemodynamic changes associated with aortic occlusion at different levels of the aorta. Hypotension after release of the aortic cross-clamp is a common and expected event.
| Level of Aortic Occlusion | |||
|---|---|---|---|
| Variable | Supraceliac | Suprarenal-Infraceliac | Infrarenal |
| Mean arterial blood pressure | +54 | +5 ∗ | +2 ∗ |
| Pulmonary capillary wedge pressure | +38 | +10 ∗ | 0 ∗ |
| End-diastolic area | +28 | +2 ∗ | +9 ∗ |
| End-systolic area | +69 | +10 ∗ | +11 ∗ |
| Ejection fraction | −38 | −10 ∗ | −8 ∗ |
| Patients with wall motion abnormalities | +92 | +33 | 0 |
| New myocardial infarction | +8 | 0 | 0 |
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