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CASE REPORT Table of Contents   
Year : 2009  |  Volume : 12  |  Issue : 2  |  Page : 133-135
Infrarenal abdominal aortic aneurysm repair in presence of coronary artery disease: Optimization of myocardial stress by controlled phlebotomy

Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India

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Date of Web Publication21-Jul-2009


The repair of abdominal aortic aneurysm (AAA) in the presence of significant coronary artery disease (CAD) carries a high-risk of adverse peri-operative cardiac event. The options to reduce cardiac risk include perioperative β-blockade, preoperative optimization by myocardial revascularization and simultaneous (combined) coronary artery bypass grafting and aneurysm repair. We describe intra-operative controlled phlebotomy to optimize myocardial stress during repair of infrarenal AAA in a patient with significant stable CAD.

Keywords: Coronary artery disease, infrarenal abdominal aortic aneurysm, phlebotomy

How to cite this article:
Neema PK, Vijayakumar A, Manikandan S, Rathod RC. Infrarenal abdominal aortic aneurysm repair in presence of coronary artery disease: Optimization of myocardial stress by controlled phlebotomy. Ann Card Anaesth 2009;12:133-5

How to cite this URL:
Neema PK, Vijayakumar A, Manikandan S, Rathod RC. Infrarenal abdominal aortic aneurysm repair in presence of coronary artery disease: Optimization of myocardial stress by controlled phlebotomy. Ann Card Anaesth [serial online] 2009 [cited 2022 Jan 24];12:133-5. Available from:

   Introduction Top

The repair of abdominal aortic aneurysm (AAA) in presence of significant coronary artery disease (CAD) carries a high-risk of adverse perioperative cardiac event. The measures to reduce cardiac risk include perioperative β-blockade, [1] preoperative optimization by myocardial revascularization and simultaneous (combined) coronary artery bypass grafting and aneurysm repair. The intraoperative measures to optimize myocardial stress focus on afterload and preload reduction by inhalation anesthetics, regional anesthesia, and vasodilators; however, various hemodynamic effects are associated with these techniques that may adversely affect the myocardial perfusion. Moreover, the vasodilator effect of inhalation anesthetics and regional anesthetic blockade is not rapidly reversible and may aggravate hypotension that invariably occurs at the time of aortic declamping. We describe intraoperative controlled phlebotomy for optimizing myocardial stress in a patient with significant stable CAD undergoing repair of IAAA. With controlled phlebotomy the hemodynamics remained stable and intraoperatively as well as postoperatively the 'ST' segment remained unchanged and there was no suggestion of myocardial ischemia or dysfunction.

   Case Report Top

A 65-year-old man with stable angina presented for surgical repair of IRAAA. His medication included atenolol 50-mg, nicardipine 20-mg, and sorbitrate 30-mg. Resting ECG showed ST-T changes in inferolateral leads. Transthoracic echocardiography showed hypokinesia of interventricular septum and adjacent anterior wall. The left ventricular ejection fraction was 52%. Coronary angiogram showed total occlusion of right coronary artery and left circumflex artery at the origin of OM1.

The patient was premedicated with inj morphine 7.5 mg, inj glycopyrrolate 0.2 mg and tab atenolol 50-mg. Anesthesia was induced with fentanyl 100-µg, thiopentone 200-mg and pancuronium 6-mg and maintained with isoflurane (0-1.5%), nitrous-oxide in oxygen (60:40) and fentanyl, 200-µg. Monitoring included ECG (lead II, III, V5), ST-segment analysis, heart rate, pulse oximetry, End-tidal carbon dioxide, and arterial (ABP), central venous (CVP), and pulmonary artery (PA) pressures. During dissection of the aneurysm and the iliac arteries (about 45-minutes), approximately 450-ml blood was withdrawn in a blood collection bag (CPD preservative). After dissection and anti-coagulation with heparin 55 mg, ABP was lowered to 100/70-mmHg by sodium nitroprusside (SNP) infusion, 0.5-µg/kg/min, to facilitate aortic-cross-clamping (ACC). The aneurysm was isolated by clamping infrarenal aorta and iliac arteries; the systolic ABP increased marginally to 120-140 mmHg, and the ST segment remained unchanged. The SNP was gradually discontinued. The aneurysm was repaired in 57-minutes of aortic clamping. The patient received about 800-ml Ringer lactate solution until repair of aneurysm. After aneurysm repair, transfusion of collected blood was started; thereafter, gradually and sequentially, the ACC and clamps on left and right common iliac arteries were released. Nor-epinephrine infusion was kept ready to support acute decrease in ABP, if required. A fall in ABP to 96/50-mmHg occurred, it returned to normal within few minutes after transfusion of the collected autologous blood and 200-ml of Ringer lactate solution. The ST segment analysis during the entire procedure showed no significant change. Estimated blood loss was about 500-ml. Urine output was around 1-ml/kg/hr during the procedure. Troponin-t test in the immediate postoperative period and on subsequent day was negative. The post-operative stay was uneventful; however, the patient required myocardial revascularization after three months.

   Discussion Top

The myocardial stress during ACC is mainly because of two reasons - increased afterload secondary to reduced vascular bed and increased preload due to mobilization of blood from the vascular compartment below the level of ACC. [2],[3] The heart responds to these changes with increases in myocardial contractility and cardiac output provided coronary arteries are capable to increase myocardial blood flow commensurate to increased demand; however, if the coronary arteries are diseased myocardial ischemia, or dysfunction may follow. [4] One study reported a 30% incidence of myocardial ischemia after infrarenal ACC in patients with CAD. [5] The measures utilized to optimize myocardial stress generally focus on afterload and preload reduction by inhalation anesthetics, regional anesthesia, and vasodilators; [6] however, various hemodynamic effects associated with these techniques adversely affect the myocardial perfusion. Saada et al . [7] observed deterioration in regional myocardial function in patients with CAD after lumbar epidural analgesia and considered it secondary to reduced coronary perfusion. It should be noted that the vasodilatation and hypotension secondary to epidural block is not titrable. Further, in the presence of anti-coagulation, epidural instrumentation carries a risk of hematoma. According to Dodds et al. in view of exquisite ability to manipulate loading conditions, heart rate, contractility and perfusion pressure with optimal fluid loading, vasodilators, vasopressors, β-blockade and inotropic agents, epidural blockade must be considered a blunt instrument for manipulating the circulation. [8] Volatile anesthetics, such as isoflurane have useful vasodilator effects that can favorably modify responses to ACC; however, it attains significant tissue concentrations that precludes rapid reversal of its effects after clamp release. SNP effectively reduces aortic pressure but it can aggravate myocardial ischemia in patients with CAD. [9] Nitroglycerin reduces the increment in preload and promote subendocardial vasodilatation but poorly attenuates the largely increased vascular resistance. [10]

Surgical stimulation (incision and dissection) is invariably accompanied by hypertension. The pathophysiologic mechanism of hypertension are mediated by sympathetic stimulation and includes venoconstriction (increased preload), increases in systemic vascular resistance (increased afterload), myocardial contractility and heart rate; because of these changes cardiac output increases. The technique of controlled phlebotomy will attenuate the increase in preload that occur during surgical dissection and a part of the myocardial stress that occurs because of increased preload during aortic clamping. Dorje et al . [11] considered ACC as a means of changing a large vascular bed into a small one, into which the heart generates too large a flow relative to the size, thereby shifting the focus of attention from afterload to volume and flow as the cause of hypertension and left ventricular strain. Evidently, the myocardial ischemia of ACC is due to volume loading of the heart and increased afterload secondary to too large a flow in a relatively small vascular bed. It is conceivable that the intra-operative controlled phlebotomy would favorably affect O2 demand-supply by achieving normalization of volume (preload) and flow proportionate to vascular bed during ACC. Further, major vascular surgery is often associated with significant blood loss; in such events, intact sympathetic vasoconstriction is the mechanism that instantly restores the perfusion pressure. Apparently, normalization of myocardial stress and preservation of responsive vascular tree that can ensure myocardial perfusion are the logical goals for patients undergoing vascular surgery.

The phlebotomy amount is based on - 1) the fact that 450 ml blood can be withdrawn safely in adult patients, 2) autologous blood collection is often practiced in patients of CAD undergoing CABG, [12] and 3) surgical stimulation is accompanied by vasoconstriction (relative hypervolemia). Therefore, 450-ml blood was withdrawn over 45 minutes before ACC and only 500-ml Ringer lactate was administered aiming to keep hematocrit close to preoperative levels and to maintain normovolemia while aneurysm was dissected. Isoflurane was continued for maintenance of anesthesia and for fine control of arterial pressure. During entire surgical procedure, the ST segment remained unchanged, and there was no suggestion of myocardial ischemia or dysfunction. At the end of surgical repair and before release of cross-clamps, transfusion of autologous blood was started. The rate of transfusion was targeted to achieve PA diastolic pressure of 15-18 mm Hg. The technique should not be confused with isovolemic hemodilution and blood conservation, the aim of the technique is to optimize myocardial stress and to maintain hematocrit close to preoperative values that is why only 500 ml of Ringer's solution was administered in the period before ACC. However, blood conservation is an added advantage.

The declamping of aorta results in hypotension; the pathophysiology include 1) ischemia and acidosis-induced vasoplegia below the level of ACC [9] 2) central hypovolemia because of pooling of blood into reperfused tissues, and 3) myocardial depression due to accumulated vasoactive metabolites. [5] Precautionary measures employed are discontinuation of vasodilators and inhalation anesthetics, preloading, gradual unclamping of the aorta and major vessels, and infusion of vasoconstrictors.[13] In our patient, ABP recovered rapidly after cross-clamp release, this could be related to 1) preloading, 2) preservation of responsive vasculature, and 3) unstressed myocardium during aortic clamping.

Major blood loss is a possibility during dissection and opening of aneurysm; therefore, while collecting blood, the surgical field should be observed constantly, and in case of significant blood loss, the rate of collection should be modified. In the event of significant hypotension, the blood collected can be returned. The major benefits noticed with the technique were 1) prevention of myocardial ischemia and dysfunction, 2) rapid recovery of ABP on unclamping of aorta, and 3) reduced blood loss and requirement of allogenic blood.

To summarize, the technique of controlled phlebotomy was utilized to optimize myocardial stress during cross clamping of aorta in a patient of stable CAD who underwent repair of IRAAA. The patient well tolerated the procedure. The technique was found to be an effective alternative to normalize the intra-operative myocardial stress.

   References Top

1.Poldermans D, Boresma E, Bax JJ, Thomson IR, van de Ven LL, Blankensteijn JD, et al . The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. N Eng J Med 1999;341:1789-94.  Back to cited text no. 1    
2.Roizen MF, Beaupre PN, Alpert RA, Kremer P, Cahalan MK, Shiller N, 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;1:300-5.  Back to cited text no. 2    
3.Gelman S. Venous function and central venous pressure. A physiologic story. Anesthesiology 2008;108:735-48.  Back to cited text no. 3    
4.Sprung J, Abdelmalak B, Gottlieb A, Mayhew C, Hammel J, Levy PJ, et al . Analysis of risk factors for myocardial infarction and cardiac mortality after major vascular surgery. Anesthesiology 2000;93:129-40.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Attia RR, Murphy JD, Snider M, Lappas DG, Darling RC, Lowenstein E. Myocardial ischemia due to infrarenal aortic cross clamping during aortic surgery in patients with severe coronary artery disease. Circulation 1976;53:961-5.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Poli de Figueiredo LF, Mathru M, Tao W, Solanki D, Uchida T, et al . Hemodynamic effects of isovolemic hemodilution during descending thoracic aortic cross clamping and lower torso reperfusion. Surgery 1997;122:32-8.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Saada M, Duval AM, Bonnet F, Rey B, Castillon G, Macquin-Mavier I, et al . Abnormalities in myocardial segmental wall motion during lumbar epidural anesthesia. Anesthesiology 1989;71:26-32.  Back to cited text no. 7  [PUBMED]  
8.Dodds TM, Burns AK, Deroo DB, Plehn JF, Haney M, Griffin BP, et al . Effects of anesthetic technique on myocardial wall motion abnormalities during abdominal aortic surgery. J Cardiothorac Vasc Anesth 1997;11:129-36.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Gelman S. The pathophysiology of aortic cross clamping and unclamping. Anesthesiology 1995;82:1026-60.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Zaidan JR, Guffin AV, Perdue G, Smith R, McNeill DC. Hemodynamics of intravenous nitroglycerin during aortic clamping. Arch Surg 1982;117:1285-8.  Back to cited text no. 10    
11.Dorje P, Adhikary G, Baliga N, Hugunin R, Paxton LD, Stoneham MD. Hemodynamics of aortic cross-clamping. J Cardiothorac Vasc Anesth 1997;11:921-2.  Back to cited text no. 11    
12.Yoda M, Nonoyama M, Shimakura T. Autologous blood donation before elective off- pump coronary artery bypass grafting. Surg Today 2004;34:21-3.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Wozniak MF, LaMuraglia GM, Musch G. Anesthesia for open abdominal aortic surgery. Int Anesthesiol Clin 2005;43:61-77.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]

Correspondence Address:
Praveen Kumar Neema
B-9, NFH, Sree Chitra Residential Complex, Poonthi Road, Kumarpuram, Trivandrum - 695 011, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.53445

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