Annals of Cardiac Anaesthesia Annals of Cardiac Anaesthesia Annals of Cardiac Anaesthesia
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LETTER TO EDITOR Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 1  |  Page : 76-77
Authors' reply

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

Click here for correspondence address and email

Date of Web Publication11-Jan-2010

How to cite this article:
Neema PK, Vijayakumar A, Manikandan S, Rathod RC. Authors' reply. Ann Card Anaesth 2010;13:76-7

How to cite this URL:
Neema PK, Vijayakumar A, Manikandan S, Rathod RC. Authors' reply. Ann Card Anaesth [serial online] 2010 [cited 2022 Nov 29];13:76-7. Available from:

We appreciate the interest of the authors [1] in our article. [2] Since the preparation and publication of the case report, we have successfully utilized controlled phlebotomy in 20 more patients during repair of Infrarenal abdominal aortic aneurysm (IRAAA). We agree that patients with poor left ventricular function or those having significant myocardium at risk are poor candidates for extensive vascular surgery and in such patients, prior myocardial revascularization or simultaneous IRAAA repair and myocardial revascularization is a safer option. Please note that the reported patient had significant stable coronary artery disease; however, the left ventricular function was normal (ejection fraction 52%). Earlier, Poldermans et al.[3] and several others [4] have shown improved outcome with perioperative β- blockade in high-risk cardiac patients undergoing vascular or noncardiac surgery. Apparently, the ACC/AHA guidelines and the above mentioned study aim to optimize the myocardial O 2 demand-supply balance either by preventing unacceptable increases in myocardial O 2 demand by controlling heart-rate and myocardial contractility or by increasing the myocardial O 2 supply (myocardial revascularization). Our case report and subsequent experience strengthens our conviction; the myocardial stress of aortic cross clamping during surgical repair of IRAAA can be easily optimized by reducing the preload and afterload by optimizing the circulating blood volume (controlled phlebotomy).

The concerns regarding preoperative statins, Sodium Nitroprusside (SNP), and decrease in circulating hemoglobin are relevant. We agree, statins are recommended for patients undergoing vascular surgery; presently, we regularly use statins in all such patients. As we have described, the blood was collected slowly and not replaced by colloids, the aim was not to dilute the circulating hemoglobin and to achieve restoration of blood volume by mobilization of blood stored in liver and spleen on sympathetic stimulation. The preoperative hemoglobin of the patient was 15.4 gm/dl and the repeat hemoglobin after surgery and on postoperative day one was 13.1 and 12.2 gm/dl respectively. We generally transfuse patients with coronary artery disease if their hemoglobin falls below 12 gm/dl. We are aware that SNP administration may impair myocardial circulation; however, we administered it for a few minutes only for lowering the systolic arterial blood pressure to ~100 mmHg so as to facilitate safe application of the aortic cross clamp; it should be noted that the monitored ECG remained unchanged during its administration. In our present practice, we deepen the level of anesthesia a few minutes before application of aortic cross clamp by increasing inspired concentration of isoflurane (2-3%); and now we do not administer SNP for reducing the systolic arterial pressure. One can administer nitroglycerine also; however, its arterial pressure lowering effect is very weak as compared to SNP. Additionally, we monitor these patients for regional wall motion abnormality by transesophageal echocardiography (TEE).

The issue of sympathetic stimulation accompanying surgical stimulation is highly complex and does not necessarily indicate inadequate analgesia; one can attenuate sympathetic responses by opioids, by β- blockade, by neuraxial blockade, or by inhalation anesthetics, etc. The attenuation of sympathetic responses by epidural blockade or by high dose opioids can effectively prevent the increases in preload that accompany the cross-clamping of aorta but potentially results in paralyzed vascular system. As we have stated, 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. Conceivably, preservation of responsive vascular tree that can ensure myocardial perfusion and normalization of myocardial stress are the logical goals for patients undergoing vascular surgery.

Lastly, it should be appreciated that the case reports are not recommendations and there are several ways of managing a patient; what is most important is to know the intricacies of the method one is practicing and ensure safety of the patient.

   References Top

1.Gupta A, Mehta Y. Phlebotomy for the purpose of optimizing myocardial stress in coronary artery disease: A questionable modality. Ann Cardic Anaesth 2010;13:74-6.  Back to cited text no. 1      
2.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 Cardic Anaesth 2009;12:133-5.  Back to cited text no. 2      
3.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. 3      
4.Lindenauer PK, Pekow P, Wang K, Mamidi DK, Gutierrez B, Benjamin EM. Perioperative beta blocker therapy and mortality after major noncardiac surgery. N Eng J Med 2005;353:349-61.  Back to cited text no. 4      

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: 10.4103/0971-9784.58846

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