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Ann Thorac Surg 1995;60:549-550
© 1995 The Society of Thoracic Surgeons


Invited Commentary

Invited Commentary

Stephen Westaby, FRCS

Department of Cardiac Surgery, Oxford Heart Center, Oxford Radcliffe Hospital, The John Radcliffe, Headington, Oxford OX3 9DU England

See also page 544.

The importance of circuit priming volume, intraoperative hemodilution, and redistribution of fluid through the body compartments is understated. This article from Jansen and associates highlights the adverse physiologic effects of a large-volume circuit prime even in low-risk coronary bypass patients.

Hemodilution was a critical step in reducing the morbidity from a large priming volume of citrated donor blood. The degree of hemodilution is determined by bypass circuit volume and preoperative hemoglobin level. Blood transfusion may be needed to achieve a target hematocrit between 20% and 25%. Oxygen content is a linear function of hematocrit, but there is an exponential relationship between hematocrit and blood viscosity [1]. Consequently, a fractional fall in hematocrit produces an overall increase in oxygen transport. In contrast, cooling increases blood viscosity. In hypothermic perfusion hemodilution promotes microcirculatory flow so that reduced oxygen carrying capacity is offset by increased delivery [2]. This is partly due to dilution of fibrinogen down to a concentration that no longer causes the red cells to aggregate.

Different temperatures have their own optimal hematocrit. Optimal is defined as providing sufficient oxygen delivery to maintain normal mitochondrial oxygen tension levels of approximately 0.5 to 1.0 mL/mg and average intracellular oxygen tension levels of approximately 5 mL/mg. These values are reflected by a mixed venous oxygen content of about 40 mL/mg and mixed venous oxygen saturation of about 75%. At 32° to 37°C maximum oxygen carrying capacity occurs with a hematocrit of 30%, so less hemodilution is desirable. With extreme hemodilution increased blood flow may not compensate for decreased oxygen content [3]. There is a critical cell separation distance that, when exceeded for a given level of oxygen consumption, results in cessation of continuous oxygen delivery [4].

Fluid accumulation progresses with duration of cardiopulmonary bypass at a rate of 800 mL per m2 body surface area per hour. An adult patient may gain between 0.45 and 6.75 kg up to 150 mL fluid/kg body weight, or 2,500 mL/m2 body surface area. On the second postoperative day the extracellular fluid space is expanded by a third, with an increase in total body water of up to 13%. Many intraoperative variables affect fluid shift. These include reduced plasma colloid osmotic pressure, interstitial fluid pressure, capillary permeability, temperature, and urine output. Arguably the most important are reduced colloid osmotic pressure due to hemodilution and the effect of the systemic inflammatory response on endothelial permeability. Utley and colleagues [5] investigated the relative importance of reduced colloid osmotic pressure, hypothermia and the inflammatory response and concluded that hemodilution was the principal cause of fluid retention. As in Jansen and associates' study, decreased oxygen carrying capacity, reduced blood viscosity, and vasodilation produced high output failure. Although this is well tolerated by low-risk patients, fluid accumulation contributes to morbidity in those with poor respiratory function or renal impairment.

The patient's preoperative blood volume and body fluid composition also affect changes in fluid balance. Fluid retention during cardiopulmonary bypass is least in congenital heart patients with left to right shunts, intermediate in coronary, single-valve, or cyanotic congenital patients, and greatest in patients with multiple valve disease and biventricular failure [6]. Mean postoperative fluid accumulation ranges from around 700 mL/L2 in patients with left to right shunts to more than 2,000 mL/L2 in multiple-valve patients. Coronary patients with good left ventricular function tolerate hemodilution well because they already have a contracted plasma and red blood cell volume. The so-called empty heart phenomenon probably occurs in response to increased sympathetic activity (infusion of catacholemines decreases plasma volume) [7]. In contrast, coronary patients with poor left ventricular function already have expansion of all fluid compartments including blood volume.

Jansen and associates speculate on the influence of small volume circuits on time to extubation and cost of operation. Cardiopulmonary bypass in Oxford employs a 1,500-mL circuit with a membrane oxygenator and roller pump but no arterial line filter. Cardioplegic volume rarely exceeds 1 L, and cardiotomy suction is minimized to reduce bleeding complications. Most coronary and valve operations are performed at between 32° and 35°C with early rewarming.

My colleagues and I discovered that with membrane oxygenation, low-volume circuit prime, and perfusion at temperatures greater than 32°C, the majority of adult patients, irrespective of age, did not need ventilatory support postoperatively. Our early extubation policy resulted in median time to extubation for coronary bypass, aortic, mitral, and double-valve patients of 2.0, 2.5, 3.0, and 3.0 hours, respectively [8]. Cardiac recovery beds were reused and required lower levels of nurse staffing. Reintubation was required in only 0.1% of patients. In 1,000 consecutive patients the overall mortality was 1.4% and the mean postoperative stay was 6 days. For coronary patients similar to those in Jansen and associates' study, cardiac index was 2.75 L • min-1 • m-2 with systemic vascular resistance, pulmonary vascular resistance, and oxygen delivery directly equivalent to their small prime group. Despite a twofold increase in intrapulmonary shunt (18.5% ± 9.7% versus 9.6% ± 3.2% before operation), extubation of coronary patients within the first postoperative hour was uneventful [9]. Our favorable experience with low-volume circuits highlights the disadvantages of excessive priming volume in most pump oxygenator systems. Research efforts in the industry should be directed as much to reducing circuit volume as to moderating the systemic inflammatory response. Evidence suggests that this would expedite postoperative recovery and contribute to reduction in costs.

References

  1. Messmer K, Kessler M, Krumme A, et al. Microcirculatory changes during normovolaemic haemodilution: rheological changes during normovolaemic haemodilution. Arzneimittelforschung 1975;25:1670.
  2. Mirhastemi A, Erkefai S, Messmer K, Intaglietta M. Model analysis of the enhancement of tissue oxygenation by hemodilution due to increased microvascular flow velocity. Microvasc Res 1987;34;290–301.[Medline]
  3. Niinikoski J, Laaksonen V, Meretoja O, et al. Oxygen transport to tissue under normovolemic moderate and extreme hemodilution during coronary bypass operation. Ann Thorac Surg 1981;31:134–43.[Abstract]
  4. Federspeil WJ, Sarelius IH. An examination of the contribution of red cell sparing to the uniformity of oxygen flux at the capillary wall. Microvasc Res 1994;27:273–85.
  5. Utley JR, Wachtel C, Cain RB, Spaw EA, Collins JC, Stephens DB. Effect of hypothermia, hemodilution, and pump oxygenation on organ water content, blood flow and oxygen delivery, and renal function. Ann Thorac Surg 1981;31:121–33.[Abstract]
  6. Cohn LN, Angell WW, Shumway N. Body fluid shifts after cardiopulmonary bypass I. Effects of congestive heart failure and hemodilution. J Thorac Cardiovasc Surg 1971;62:423–30.[Medline]
  7. Wigboldus AH, Urzua J, Viljoen JF. The empty heart phenomenon. J Thorac Cardiovasc Surg 1973;66:807–12.[Medline]
  8. Westaby S, Pillai R, Parry A, et al. Does modern cardiac surgery require conventional intensive care? Eur J Cardiothorac Surg 1993;7:313–8.[Abstract]
  9. Butler J, Rocker GM, Westaby S, et al. Early extubation after coronary bypass surgery: effects on oxygen flux and haemodynamic variables. J Cardiovasc Surg 1992;33:276–80.[Medline]



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