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Year : 2010
| Volume
: 13 | Issue : 1 | Page
: 74-76 |
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Phlebotomy for the purpose of optimising myocardial stress in coronary artery disease: A questionable modality |
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Abhinav Gupta, Yatin Mehta
Department of Anaesthesia and Critical Care, Indraprastha Apollo Hospitals, New Delhi, India
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Date of Web Publication | 11-Jan-2010 |
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How to cite this article: Gupta A, Mehta Y. Phlebotomy for the purpose of optimising myocardial stress in coronary artery disease: A questionable modality. Ann Card Anaesth 2010;13:74-6 |
How to cite this URL: Gupta A, Mehta Y. Phlebotomy for the purpose of optimising myocardial stress in coronary artery disease: A questionable modality. Ann Card Anaesth [serial online] 2010 [cited 2021 Jan 18];13:74-6. Available from: https://www.annals.in/text.asp?2010/13/1/74/58845 |
The Editor,
The recommendation of phlebotomy to optimize myocardial stress in a patient of coronary artery disease (CAD), recently published as a case report in the journal, was not substantiated with any supporting reference or clinical evidence. [1] There were a few contradictions, not only regarding the patient's medical condition but also the suitability of the author's recommendations, in such circumstances.
The 65-year-old patient who was described in the report had stable angina with ST-T changes in inferior leads. As per the evidence provided in the 2007 guidelines by American Heart Associtaion (AHA) guidelines, the horizontal or down sloping ST-segment depression greater than 0.5 mm is associated with decreased life expectancy and ST-segment depression on a preoperative 12-lead electrocardiogram predicts adverse perioperative cardiac events. [2] 'In patients with known coronary artery disease, as well as those with previously occult coronary disease, the questions that become apparent are: 1) What is the amount of myocardium in jeopardy? 2) What is the ischemic threshold, i.e., the amount of stress required to produce ischemia? 3) Is the patient receiving optimal medical regimen? Clarification of these questions is an important goal of the preoperative history and physical examination. Poor a functional capacity in patients with chronic coronary artery disease or those convalescing after an acute ischemic coronary event is associated with an increased risk of subsequent cardiac morbidity and mortality.' [2] The authors have not made any mention of statins among the preoperative medications. Statins are Class IIa indication in stable cardiac patients undergoing vascular surgery. [3] Hindler and colleagues conducted a meta-analysis to evaluate the overall effect of preoperative statin therapy on postoperative outcomes. Preoperative statin therapy was associated with 59% reduction in the risk of mortality after vascular surgery (1.7% versus 6.1%; P=0.0001). [4]
The hemoglobin at which the autologous blood was withdrawn could have been mentioned. We are also interested in the intraoperative hemoglobin. One should not forget the intraoperative blood loss of 500 ml and the associated 450 ml withdrawn via autologous technique. Reduced hemoglobin in patients with ischemic heart disease is associated with increased risk of developing AMI. [5] The anemia associated with perioperative blood conservation has raised concerns regarding the safety of autologous blood donation in patients with ischemic cardiovascular disease. [6] A hematocrit level <28% is independently associated with risk for myocardial ischemia during and after noncardiac surgery. Avoidance of cardiac complications may require higher transfusion thresholds. [6]
The authors used sodium nitroprusside during cross clamping while the patient had impaired myocardial circulation. It's administration may produce myocardial ischemia when administered in doses sufficient to reduce mean arterial pressure to 80 mmHg or less presumably due to decreased coronary perfusion pressure, metabolite induced toxicity or a direct coronary vasodilatory steal effect. Nitroglycerine infusion is favored if there is impaired myocardial contractility and tissue oxygenation or signs of myocardial ischemia develop following aortic cross clamp application. This therapy may decrease arterial pressure, systemic vascular resistance and myocardial oxygen consumption. [7] Nitroglycerin administration maintains transmural distribution of flow favoring the endocardium. [8]
The increased sympathetic response accompanying surgical stress (incision and dissection) is most probably due to inadequate analgesia. We would appreciate that instead of suggesting phlebotomy to attenuate the consequences of increased sympathetic stimulation, the patient is provided with adequate analgesia.
During infraceliac aortic cross-clamping, blood volume may be redistributed from the distal venous vasculature either to the heart increasing pre-load (as in a case of supraceliac aortic cross-clamping) or to the splanchnic vasculature, without an increase in preload. The distribution of blood volume between the heart and the splanchnic vasculature depends on many factors, including overall sympathetic tone. Therefore, not all patients may have increased preload following aortic cross clamp, and draining them may rather lead to hypovolemia. [9]
Though the concerns for epidural analgesia with heparinization exist, there are many centres in the world publishing ample studies and series of reports regarding Epidural analgesia for CAD patients for coronary artery bypass grafting . Continuous epidural anesthesia has been frequently used either with general anesthesia or as primary anesthetic technique for patients undergoing vascular surgery. [10] Even for abdominal aortic aneurysm surgery, there are some advantages of epidural analgesia to make the postoperative period smoother and allowing earlier mobilization of patients. [11] Neuraxial anesthesia may help control pain and may reduce pulmonary and thrombotic complications, making this approach attractive even if it does not lower cardiac index. Risk of epidural hematoma for cardiac surgery mentioned is 1:12000. [12]
There are several case reports of combined CABG and abdominal aortic aneurysm (AAA) repair; the authors could have considered such a technique, as it could have been better for a single stage procedure, though the risks and benefits need to be weighed. [13]
Phlebotomy for autologous blood transfusion is recognized for decreasing the requirement for blood transfusion. However, in our opinion the suggestion of phlebotomy to decrease preload for optimizing myocardial stress in CAD patients, is not supported by evidence by the authors and in our opinion, is not acceptable as a good clinical practice.
References | |  |
1. | 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 Cardiac Anaesth 2009;12:133-5. |
2. | Lee AF, Joshua AB, Kenneth AB. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2007;116:418-500. |
3. | Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): Executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll Cardiol 2006;47:1239-312. [PUBMED] [FULLTEXT] |
4. | Hindler K, Shaw AD, Samuels J, Fulton S, Collard CD, Riedel B. Improved postoperative outcomes associated with preoperative statin therapy. Anesthesiology 2006;105:1260-72. [PUBMED] [FULLTEXT] |
5. | Hahn RG, Nilsson A, Farahmand BY, Persson PG. Blood hemoglobin and the long-term incidence of acute myocardial infarction after transurethral resection of the prostate. Eur Urol 1997;31:199-203. [PUBMED] [FULLTEXT] |
6. | Hogue CW Jr, Goodnough LT, Monk TG. Perioperative myocardial ischemic episodes are related to hematocrit level in patients undergoing radical prostatectomy Transfusion 2003;38:924-31. |
7. | Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 1995;82:1026-57. [PUBMED] [FULLTEXT] |
8. | Hummel BW, Raess DH, Gewertz BL, Wheeler HT, Fry WJ. Effect of nitroglycerin and aortic occlusion on myocardial blood flow. Surgery 1982;92:159-66. [PUBMED] [FULLTEXT] |
9. | Pottecher T, Meloche R. The use of aminophylline for correction of haemodynamic repercussions of clamping of the aorta. Can Anaesth Soc J 1977;24:162-74. [PUBMED] [FULLTEXT] |
10. | Cunningham AJ. Anaesthesia for abdominal aortic aneurysm surgery: A review (Part II). Can J Anaesth 1989;36:568-77. [PUBMED] [FULLTEXT] |
11. | Thomson DA. Anaesthesia for patients with abdominal aortic aneurysm. Best Pract Clin Anaesthesiol 2000;14:187-97. |
12. | Bracco D, Hemmerling T. Epidural analgesia in cardiac surgery: An updated risk assessment. Heart Surg Forum 2007;10:E334-7. [PUBMED] [FULLTEXT] |
13. | Kameda Y, Taniguchi S, Kawata T, Tabayashi N, Kimura M. Minimally invasive direct coronary artery bypass combined with abdominal aortic aneurysm repair. Ann Thorac Surg 1999;68:1537-9. [PUBMED] [FULLTEXT] |

Correspondence Address: Yatin Mehta Department of Anaesthesia and Critical Care, Indraprastha Apollo Hospitals, New Delhi India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0971-9784.58845

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This article has been cited by | 1 |
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| Kawamura, I., Takemura, G., Kanamori, H., Takeyama, T., Kawaguchi, T., Tsujimoto, A., Goto, K., (...), Minatoguchi, S. | | American Journal of Physiology - Heart and Circulatory Physiology. 2010; 299(2): h372-h378 | | [Pubmed] | | 2 |
Authorsę reply |
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| Neema, P.K., Vijayakumar, A., Manikandan, S., Rathod, R.C. | | Annals of Cardiac Anaesthesia. 2010; 13(1): 76-77 | | [Pubmed] | |
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