Pro: A hematocrit of 20% is adequate to wean a patient from cardiopulmonary bypass

Pro: A hematocrit of 20% is adequate to wean a patient from cardiopulmonary bypass

PRO AND CON Paul G. Barash, MD, Section Editor A HEMATOCRIT OF 20% IS ADEQUATE TO WEAN A PATIENT FROM CARDIOPULMONARY BYPASS Pro: A H e m a t o c r i...

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PRO AND CON Paul G. Barash, MD, Section Editor

A HEMATOCRIT OF 20% IS ADEQUATE TO WEAN A PATIENT FROM CARDIOPULMONARY BYPASS Pro: A H e m a t o c r i t of 20% Is A d e q u a t e to W e a n a P a t i e n t F r o m Cardiopulmonary Bypass Raymond J. Martmeau, MD, FRCPC N THE E A R L Y development of cardlopulmonary bypass (CPB), generation of an adequate blood flow, design of an efficient blood gas exchange system, and control of the coagulation cascade were the major techmcal challenges resolved before their clinical use. Because there were no animal models, CPB was introduced m the field of cardiac surgery with a relatively poor knowledge of its physiologic effects. Because of blood viscosity changes caused by hypothermia, a certain degree of hemodilutaon was accepted to ophmize blood flow. However, red blood cells were frequently used to prime CPB, and surgical blood loss was replaced as necessary. Recently, because of the increased concern for blood product safety, the practice of blood product transfusion during surgery has been placed under intense scrutiny ~By allowing lower levels of hematocrit during CPB, it is expected that reqmrements for blood transfusion would be reduced during cardiac surgery. However, the lowest safe level of hematocrit that can be allowed during CPB has not been determined. Unfortunately, scientific data and clinical reformation available to resolve this question are scarce. In deciding what is the lowest safe level of hematocrit that can be allowed during CPB, the practmoner must balance the risks associated with transfusion of red blood cells against the risks of not transfusing red blood cells Withholding blood transfusion may cause inadequate oxygen delivery, which may result In organ dysfunction, and, if severe and prolonged, metabolic acidosis and death may occur. Furthermore, the present monitoring technology may be inadequate to detect subclinical manifestations of organ dysfunction. Within the body, the brain, the heart, and the splanchnic organs are probably the most sensitive organs to hypoxic damage owing to their large blood supply requirements and increased oxygen extraction ratio. 2 Therefore, oxygen delivery must meet oxygen requirements for these organs throughout cardiac surgery. During CPB, clinical practitioners can influence several parameters to ensure an adequate balance between oxygen supply and demand. Blood flow and hematocrlt levels are the main determinants of oxygen supply and delivery,3 while lowering body temperature, 4 and use of anesthetic drugs 5 can reduce oxygen demand. In addition, the body itself can compensate by increasing oxygen extraction and possibly,

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on a regional basis, by regulation of local blood flow) However, the effects of hypothermia on the oxygen dissociation curve are qmte complex. 6 Blood flow during CPB is usually maintained at 2.2 L / m m / m 2, a flow sufficient to meet total body requirements. Because blood flow is controlled, oxygen supply is correlated with hemoglobin levels in a hnear fashion. To maintain the same oxygen dehvery to peripheral tissues, blood oxygen extraction ratio must be increased. A simple equation can be used to calculate that, if hemoglobin concentration is decreased by half, the oxygen extraction must be doubled to provide a similar oxygen delivery. Because of great concern related to the effects of increased turbulence, higher than recommended blood flows must be used very cautiously to increase oxygen delivery during CPB. Local regulation of blood flow may enhance oxygen delivery in specific organs, such as the brain. Techniques known to preserve or enhance cerebral blood flow such as alpha-stat management 7 and maintenance of an adequate perfuslon pressure should be used. 8 Finally, total metabohc requirements are reduced by using hypothermla and by anesthetic drugs. 9 These effects are particularly important in lowering the oxygen demand within the central nervous system (CNS), where it has been shown that hypothermla 4 and anesthetic drugs 5 are both protective against hypoxic damage. During hypothermic CPB, blood viscosity is mcreased 1° and may cause a sigmficant impairment of perfusion in capillary beds. Lower hematocrit levels sigmficantly decrease viscosity in hypothermic conditions and may enhance perfuslon in areas of high resistance to flow. It ~s eshmated that the cerebral metabolic rate may be reduced from a normal level of 3.4 to 3.5 mL/100 g/mln to 1.0 mL/100 g/rain or less 9 by a combination of hypothermia and intravenous anesthetic drugs (ie, benzodlazepines,

From the Department of Anesthesia, Instttut de Cardtologte de Montreal, QuObec, Canada Address reprint requests to Raymond J Mamneau, MD, FRCPC, Department of Anesthesia, Instltut de Cardtologle de Montreal, 5000 est, rue B~langer, Montreal, QuObec, H1 T 1CB. Copyright © 1996 by W B Saunders Company 1053-0770/96/1002-002253.00/0 Key words hemoddutlon, transfusion, cardiac surgery

JournalofCardlothoractc and VascularAnesthesta, Vo110, No 2 (February), 1996. pp 291-293

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propofol, or barbiturates). Gwen the reduced metabolic requirements and provided that cerebral blood flow and regulation mechanisms are maintained, it can be calculated that the oxygen supply provided by a hematocnt of 20% would be sufficient to meet the oxygen requirements. Using the standard equation for blood oxygen content with a hemoglobin concentration at 6.6 gm% and PO2 of 300 mmHg, arterial oxygen content would be estimated to be between 10 and 10.5 mL%, a level sufficient to allow sufficient oxygen delivery even in the normal range of 30% of oxygen extraction in the cerebral circulation. The protective effects of hypothermia in reducing cerebral metabohc rate are important. At normothermia, the cerebral metabolic rate may be increased by up to 1.0 mL/100 g/min, and this may result in jugular venous oxygen desaturatmn m 17% to 23% of patients, t1 Furthermore, thas degree of desaturation was associated with a greater incidence of cognitive dysfunction after CPB. The heart has the greatest oxygen requirements, as demonstrated by its high extraction ratio and its low coronary sinus oxygen saturation. 2 Therefore, lower hemoglobin levels might be associated with decreased myocardial oxygen supply and may result in myocardial dysfunction, particularly in the presence of coronary artery disease. 12,a3 During CPB when the heart is arrested by cardioplegm, this is not a concern. However, after CPB, myocardial oxygen demands are rapidly increasing and sufficient oxygen delivery must be ensured. Lower hematocrit levels may be associated with an increased incidence of myocardial dysfunction. Interestingly, a recent study suggests that levels of hemoglobin are not associated with increased myocardml lactate flux after CPB m cardmc surgery patients. Nevertheless, hematocrit levels should be maintained in the range between 25% and 30% after CPB to reduce the work of the heart after cardiac surgery. 14 Inadequate delivery of oxygen m other organs, such as the liver, kidneys, and intestine remains a concern during CPB35 However, present knowledge of the splanchnic circulation suggests that regulation of splanchnic blood flow is strongly affected by the hormonal stress response during CPB On a speculative basas, hemodilution may actually improve oxygen dehvery by increasing splanchnic blood flow caused by lower viscosity16 and local vasodilatation potentmlly mediated by nitric oxide. 17 Techniques that can be used to monitor adequacy of oxygen supply include measurement of blood lactate levels and measurement of venous blood oxygen saturation or

partial pressure, ls,~9 Although this technology may be useful for assessing whole body demands, it does not provide reformation on oxygen supply and demand balance for each specific organ. Because of its clinical importance, monitoring of central nervous dysfunction has been of particular interest. However, the available technology for monitoring CNS global or regional function is still imprecise or too cumbersome to be of climcal use. 2° The lowest acceptable hematocrit level during CPB remains an unresolved issue. Accepting lower levels of hematocrit levels down to 20% during CPB does reduce the cllmcal margin of safety for oxygen delivery in the whole body and for each specific organ. Raising hematocrlt levels with red cell transfusions would increase this margin of safety but would expose patients to other potential comphcations. In clinical practice, lower hematocrit levels have been used by many clinicians during CPB and an unacceptable incidence of comphcations has not been reported. However, there are no prospective clinical studies that have been designed to specifically answer the safety issue of this chnical practice. To establish its safety beyond doubt, it should be demonstrated that it is not associated with increased mortality or morbidity. Furthermore, climcal conditions that may be associated with increased comphcatlons should be identified. Given the complexity of clinical interactions taking place during cardiac surgery, this may be a difficult study to undertake and would require a large population sample. In conclusion, allowing lower hematocnt levels (down to 20%) during CPB remains a clinical decision that must be made by practitioners for each patient. Present knowledge of the physiology of oxygen delivery and demand suggests that this practice is safe during hypothermia m low-risk patients. Cautmn should be exercised in the following clinical conditions: older patients, 21 patients with neck vessel disease, patients undergoing prolonged CPB, and patients kept at normothermia during CPB. In addition, in patients with low preoperatwe hemoglobin levels or patients with a small blood volume, the dilution effect of CPB priming should be anticipated and blood transfusions should be administered as required to avoid a decrease of the hematocm level below 20%. At lower hematocrit levels, it may be wise to add colloid solutions such as pentastarch or albumin to the CPB priming solution m order to maintain intravascular oncotlc pressure. At this institution, hematocrit levels down to a minimum of 20% in low-risk patients have been allowed for several years.

REFERENCES

1 Robblee JA, Crosby E. Transfusion medacme issues m the practice of anesthesiology.Transfusion medicine rewews 9:60-78,1995 2 Finch CA, Lenfant C Oxygen transport m man. N Engl J Med 286:407-415, 1972 3 Nunn JF Apphed physiology(ed 2). London, Butterworths, 1977 4 Krlvosic-Horber R' Mild to moderate hypothermla and brain protection Ann Fr Anesth Reanmm 14 122-128, 1995 5. Tempelhoff R, Cheng MA, Boulard G, et al Cerebral protection' Role of intravenous anaesthetic agents. Ann Fr Anesth R6amm. 14.129-133, 1995

6 Wfllford DC, Hall EP, Moores WY Theoretical analysis of oxygen transport during hypothermla J Chn Momt 2 30-43, 1986 7 Murkm JM, Farrar JK, Tweed WA, et al Cerebral autoregulatlon and flow/metabohsm coupling during hypothermxc cardlopulmonary bypass. The mfluence of PaCO2. Anesth Analg 66:665-672, 1987 8 Schawartz AE, Sandhy AA, Kaplon RJ, et al Cerebral blood flow is determined by arterial pressure and not cardiopulmonary bypass flow rate. Ann Thorac Surg 60 165-170, 1995 9. Prough DS, Rogers AT What are the normal levels of

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cerebral blood flow and cerebral oxygen consumption during car&opulmonary bypass in humans? Anesth Analg 76:690-693, 1993 10. Gordon RJ, Ravin M, Rawltscher RE, et al' Changes m arterial pressure, viscosity and resistance during car&opulmonary bypass. J Thorac Cardiovasc Surg 69:552-561, 1975 11. Croughwell ND, Newman MF, Bhumenthal JA, et al Jugular bulb saturation and cognitive dysfunction after cardlopulmonary bypass. Ann Thorac Surg 58:1702-1708, 1994 12. Parsloe MR, Wyld R, Fox M, et al: Silent myocardial lschemla m a patient with anaemia before operation. Br J Anaesth 64.634-637, 1990 13 Spalm DR, Leone BJ, Reves JG, et al: Car&ovascular and coronary physiology of acute lSovolemlc hemodilutlon--A review of nonoxygen-carrymgand oxygen-carrying solutions. Anesth Analg 78:1000-1021, 1994 14. Hall TS' The pathophyslology of car&opulmonary bypass. The risks and benefits of hemodllutlon. Chest 107.1125-1133, 1995 15. Landow L' Splanchmc lactate production in cardiac surgery patients. Cnt Care Med 21:$84-$91, 1993 16. Noldge GFE, Pneve H-J, Bohle W, et al. Effects of acute

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normovolemlc hemodilutlon on splanchnic oxygenation and on hepatic histology and metabolism in anesthetized pigs. Anesthesiol 74:908-918, 1991 17 Doss DN, Estafanous FG, Ferrarlo CM, et al: Mechanism of systemic vasodilatatlon during normovolemlchemodilution Anesth Analg 81:30-34, 1995 18. Baraka A, Baroody M, Garoum S, et al: Continuous venous oximetry during cardiopulmonary bypass: influence of temperature changes, perfusion flow, and hematocrit levels. J Cardiothar Anesth 4:35-38, 1990 19. Baraka A: Continuous blood gas monitoring should be a standard during cardiopulmonary bypass. Pro: Continuous venous oximetry should be used routinely during cardlopulmonary bypass. J Car&othor Vasc Anesth 6:105-108, 1992 20. McCormick PW: Monitoring cerebral oxygen delivery and hemodynamics Curr Opin Anaesthesiol 4:657-661, 1991 21. Newman MF, Croughwell ND, Blumenthal JA, et al: Effect of aging on cerebral autoregulation during car&opulmonary bypass. Association with postoperatwe cognitive dysfunction. Circulation 90:11-243-I1-249,1994 (part 2)