Open repair of an abdominal aortic aneurysm in a patient with coronary artery disease
The following case will emphasize the care of a patient with vascular disease for a major operation.
· pre-operative evaluation of the patient with cardiovascular disease
· cardiovascular physiology
· invasive hemodynamic monitoring
· intra-operative myocardial ischemia.
A 70-year-old man is scheduled for open repair of an abdominal aortic aneurysm.
Based on the shape of the aneurysm, he was unsuitable for an endovascular stent procedure. Instead, he requires a highly invasive, open intra-abdominal proce-dure that involves cross-clamping the aorta for a time, with substantial implica-tions for blood pressure management and potential for uncontrolled blood loss.
History. The aneurysm has been followed for 3 years after detection during coronary angio-graphy. Its diameter has increased recently by 10 mm, and requires repair.
The location and extent of the aneurysm determine the level of the aortic cross-clamp. We are particularly concerned with the relationship of the clamp to the renal arteries, as supra-renal clamping requires renal protective maneuvers such as administration of mannitol. High clamp location may also endanger perfusion of the lower 2/3 of the spinal cord, which is supplied by the artery of Adamkiewicz arising from the aorta somewhere between T8 and L4.
Review of systems: Chronic hypertension; myocardial infarction (MI) 3 years ago with sub-sequent 3 vessel coronary artery bypass graft (CABG); currently he has stable angina with exertion, but walks 1 mile three times per week without chest pain. History of congestive heart failure (CHF), last exacerbation 6 months ago, now without orthopnea.
Apatient rarely has vascular disease in only one vessel and we worry about cerebral as well as more coronary arterial disease.
Medications: ACE inhibitor, beta-blocker, diuretic.
We will ask this ASA IV patient to discontinue the ACE inhibitor the day of surgery, but to take his diuretic and beta-blocker.
Physical examination. African American man in no distress; weight 90 kg; height 6 (180 cm)
BP 160/90 mmHg (equal in both arms); HR 70 beats/min; respiratory rate 12 breaths/min
Airway: Mallampati II; 3fb mouth opening; 4fb thyromental distance; full neck extension
CV: S1, S2, no S3, S4 or murmur
Resp: Lungs clear to auscultation
Lower extremities: mild edema.
In patients with vascular disease, we check blood pressure in both arms because it can vary significantly between them. We accept the higher one.
Pre-operative studies. Hgb 15 g/dL; Hct 45%; Plt 300,000/µL; Na 140 mEq/L; K 4.2 mEq/L; ECG: NSR at 90 beats/min, Q waves present in II, III and aVF; ST segments at baseline Echo (6 months old): left ventricular ejection fraction 35% (normal >50%); decreased wall motion inferiorly; normal valves.
Not only would we like to know his starting hematocrit, we should insist on a “type and cross” for four units of blood for two reasons: first, because this procedure can result in significant blood loss and second, because this patient has a history of coronary artery disease and, in case of hemorrhage, we may need to increase his oxygen carrying capacity. Measurement of electrolyte levels is indicated in a patient taking diuretics, as these drugs can wreak havoc on the electrolyte balance. The presented cardiac evaluation suffices if we go by the “Eagle criteria.” We might ask for a chest radiograph to rule out pulmonary edema if we are uncertain about the results of our auscultation of the lungs.
Preparation for anesthesia. We plan to use a combined epidural and general endotracheal anesthetic, placing the epidural catheter pre-operatively under sedation.
Because of his cardiac history and anticipated hemodynamic swings associated with aor-tic clamping and unclamping, we plan to place pressure catheters in a radial artery and pulmonary artery.
Epidural anesthesia may help us both as a means to buffer the wildly varying after-load from cross clamp application and removal (see below), and to improve post-operative pain management. While we worry that the anticoagulation required for this operation increases the risk of epidural hematoma, this complication occurs primarily at placement and removal of the catheter, neither of which we will do during the period of anticoagulation.
With the arterial catheter, we can monitor the blood pressure literally beat-by-beat. It also provides a conduit for repeated arterial blood gas and acid-base determinations. We can use the pulmonary artery catheter (PAC) to assess cardiac output and ventricular filling.
Induction of anesthesia. We place the arterial catheter awake with sedation and local anesthesia.
Before inducing general anesthesia, we dose the epidural catheter with 2% lidocaine with 1:200 000 epinephrine to obtain a T6 level.
Following pre-oxygenation, we induce the patient with fentanyl, etomidate, vecuronium, and esmolol. We successfully intubate the trachea with minimal hemodynamic swings. We place a PAC via the right internal jugular vein and record a wedge pressure of 15 mmHg and cardiac output of 5 liters/min.
We choose etomidate for induction because of its minimal cardiac depression, and employ fentanyl and esmolol to reduce the tachycardic response to direct laryngoscopy. Vecuronium has few side effects in the patient with normal hepatic and renal function.
The wedge pressure and cardiac output are in the expected range for this patient.
Maintenance of anesthesia. We maintain anesthesia with isoflurane in air enriched with 50% oxygen combined with a fentanyl infusion, titrating the isoflurane to keep hemodynamics stable, and the BIS between 40 and 60. We re-dose the epidural anesthetic every 60–90 minutes depending on the clinical situation.
Because the procedure requires an intra-abdominal approach, we avoid nitrous oxide. Isoflurane depresses the cardiovascular system so we give as little as possi-ble, relying on the hemodynamic changes and a “depth-of-anesthesia monitor” to guide us. By using the epidural for operative anesthesia, we limit the requirement for both volatile anesthetic and muscle relaxants, but its effects on the sympa-thetic nervous system must be considered.
Intra-operative event – Cross-clamping of the aorta. In addition to the vasodilation obtained from the epidural-induced sympathectomy, we administer a vasodilator such as nitroglyc-erin before aortic cross-clamping. Infra-renal clamp placement confers less risk of kidney problems, but still warrants consideration of mannitol. Before the cross-clamp is placed, we administer heparin 5000 u i.v.
Cross-clamping the aorta causes a sudden increase in afterload, which often but not invariably dramatically increases the blood pressure. While the epidural can buffer the increase by vasodilating the splanchnic bed, we administer vasodilators to lower the blood pressure just before cross-clamping. An anticoagulating dose of heparin prevents thrombosis below the cross-clamp.
Intra-operative event – Removing the cross-clamp. We prepare by increasing venous capac-itance with nitroglycerin, filling up this new capacity with i.v. fluids or blood. Immediately before removal of the clamp, we stop the nitroglycerin infusion, acutely decreasing venous capacitance. The resulting transient volume overload quickly dissipates following release of the cross clamp.
During the period of cross-clamp, veins distal to the clamp recoil, returning much of their blood to the heart. Subsequently, hypoxia causes both vasodilation (increasing venous capacity in this area) and the accumulation of many vasodila-ting and cardiac depressant metabolites. Thus, removal of the cross-clamp opens up this large vascular bed, causing a massive shift in blood volume. A major decrease in blood pressure may follow, unless we plan ahead to fill that space with additional fluid and/or blood.
Following removal of the cross clamp, we document the presence of distal pulses via Doppler, and administer protamine to reverse the anticoagulant effect of heparin. We might test the adequacy of reversal with an ACT.
Intra-operative complication – Ischemia. BP 90/50 mmHg; HR 110 beats/min; SpO2 95%;
ST segments 3 mm downward sloping in V5;
PCWP 20 mmHg; cardiac output 2.3 liters/min
Hemoglobin 7 g/dL.
The ST segment changes suggest ischemia, and increased PCWP indicates ven-tricular dysfunction and decreased compliance.
Management of ischemia. Transesophageal echocardiography: new anterolateral wall motion abnormality
We titrate esmolol to HR 70–80 beats/min and add a nitroglycerin infusion as tolerated.
We begin to transfuse packed red cells.
Using transesophageal echocardiography, we look for regional wall motion abnor-malities, ventricular volume and function. Treatment must improve the myocar-dial oxygen supply : demand balance by reducing heart rate and wall tension, increasing coronary perfusion pressure (diastolic blood pressure), and increasing oxygen carrying capacity. Normalization of the ST segments and PCWP indicate successful treatment.
Emergence from anesthesia. Following conclusion of the operation we leave the patient’s trachea intubated and him sedated for transport to the Intensive Care Unit where weaning from mechanical ventilation would occur over a day or two.
Transport of the intubated patient requires manual ventilation and continuous monitoring. We also bring along the equipment necessary to ventilate his lungs in case the endotracheal tube becomes dislodged (mask, laryngoscope, extra ETT).
Though not necessary for this operation, with a suprarenal clamp endangering perfusion of the distal spinal cord, we might awaken the patient immediately post-operatively to document neurologic function of the lower extremities.
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