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J Thorac Cardiovasc Surg 1994;107:644-0646
© 1994 Mosby, Inc.
Letters to the Editor |
Department of Surgery
University of Michigan Medical Center
Ann Arbor, MI 48109
To the Editor:
In the December 1992 issue of the JOURNAL, Minami, Vyska, and Körfer
1 reported yet another study comparing pulsatile with nonpulsatile perfusion. Just when we thought this issue was finally settled, another group of investigators has added another bit of information to the huge body of data on this subject. There are two notable factors in this study. First, the physiologic experiments are carefully done, eliminating the heart and lungs entirely from the circulation, maintaining perfusion at normothermia, denervating the aortic arch baroreceptors by a proximal vagotomy, and focusing attention precisely on the carotid sinus baroreceptors. Second, through clever use of the extracorporeal circuit, the investigators quantitated an increase in venous capacitance blood volume during nonpulsatile perfusion, which they speculate is due to muscular spasm in large veins. The investigators maintained blood flow constant in the normal range for the dog (120 to 130 ml/kg per minute). They then varied the pulse contour from pulsatile to nonpulsatile, with a stabilization period of 15 to 30 minutes. The full range of systolic and diastolic pressures during pulsatile perfusion is not stated in the article, but the mean arterial pressure increased significantly during nonpulsatile perfusion. The effect on mean pressure was ablated by denervating the carotid sinuses and by combined 
- and ß-adrenergic blockade. Intracorporeal blood volume increased by approximately 100 ml during nonpulsatile perfusion and decreased by a similar amount when pulsatile perfusion was reestablished. This effect was also ablated by denervation or adrenergic blockade.
The role of carotid sinus baroreceptors, increasing sympathetic tone during constant flow but nonpulsatile perfusion, was previously described by Harrison, Chawla, and Seaton 2 and Harrison and Seaton. 3 Increased blood volume during nonpulsatile perfusion has been reported by Minami and coworkers. 4 This specific article documents the increase in capacitance blood volume and the fact that this effect is ablated by denervation or sympathoadrenergic blockade. Although the authors undertook this study to examine mechanisms by which systemic edema might accumulate during nonpulsatile perfusion, the periods of pulsatile and nonpulsatile perfusion were not long enough to examine this question. With the demonstration that increased sympathetic tone increases venous as well as arteriolar resistance, however, it is reasonable to think the systemic capillaries would be more likely to leak. It is equally likely that the arteriolar spasm is greater than the venous spasm, resulting in no net change in the Starling forces in the peripheral circulation. The significance of this observation to clinical perfusion is therefore uncertain. Nonetheless, this study adds one more bit of information to our understanding of the physiology of pulsatile flow.
The question of the clinical relevance of nonpulsatile flow for normal animals at normal flow and normal temperature was answered years ago by the experiments of Bernstein and associates, 5 who demonstrated that there is no significant difference between pulsatile and nonpulsatile perfusion when such other variables as hypothermia, total cardiopulmonary bypass, anesthesia, and hemodilution are eliminated. The Bernstein experiments simply substituted a centrifugal pump for the left ventricle; Golding and colleagues 6, 7 corroborated and extended these experiments to biventricular nonpulsatile perfusion, showing that the initial increase in systemic vascular resistance quickly subsided and animals remained essentially normal with nonpulsatile flow for 2 to 93 days. Specifically, there was no edema or ascites. Clinical experience with the use of centrifugal pumps or roller pumps during biventricular or total cardiopulmonary bypass for cardiac support supports these observations. Consequently, any study of the effects of nonpulsatility under normal physiologic conditions is interesting but clinically unimportant.
Perfusion for cardiac surgery, and in many instances perfusion for long-term cardiac support, however, is maintained below normal perfusion pressure or flow rate. Most of the experiments comparing pulsatile and nonpulsatile perfusion have been conducted at total blood flow in the range of 50 to 100 ml/kg per minute, well below the normal flow for the various animals under investigation. 8-12 Moreover, many of these experiments are complicated by hypothermia, hemodilution, anesthetics, and other drugs. Clinical studies are further complicated by the effects of coronary suction, steroids, mannitol, and the cardiac operation itself. 12, 13 The recent study by Minami, Vyska K, and Körfer, 1 the studies of Harrison, Chawla, and Seaton 2 and Harrison and Seaton, 3 and the excellent studies of Boucher, Rudy, and Edmunds 14 and Harken 15 are examples of excellent methodology, all of which demonstrated increased sympathetic tone but no deleterious effects on circulation or oxygen kinetics between pulsatile and nonpulsatile flow.
Why then, do most published studies and clinical experience indicate that pulsatile flow decreases or ablates the "poor perfusion" deleterious effects of nonpulsatile perfusion? Certainly every cardiac surgeon and perfusionist has witnessed the phenomenon of progressive metabolic acidosis, systemic capillary leakage, decreasing urinary output, and cold blue extremities during and after a long, difficult pump run. In the recovery room, the blood pressure is normal or high, the cardiac output is low, the calculated systemic resistance is therefore extremely high, and the syndrome looks exactly like norepinephrine overdose. Those who have experience with intraoperative pulsatile flow, have used an intraaortic balloon pump to augment pulsatile flow, or have used -adrenergic blockade in this circumstance have all witnessed the prompt lysis of sympathetic overload. Such clinical observations would seem to support the clinical relevance of the study of Minami, Vysla, and Körfer, 1 sending us all looking for suitable pulsatile pumps for short-term or long-term perfusion. This apparent paradox is explained when all of the various studies are compared with each other on the basis of total blood flow.
When total blood flow is normal in relationship to the metabolic requirements and to normal hemodynamics, there is indeed a small increase in sympathetic tone mediated by carotid sinus baroreceptors, but the effect is relatively small and short-lived and there is no practical difference between pulsatile and nonpulsatile perfusion. When systemic flow is progressively decreased from the normal level, the sympathetic response is greater when the flow is nonpulsatile. To state it another way, pulsatile perfusion blunts the sympathetic response to pathologically low blood flow. At extremely low blood flow, the sympathetic response is maximal whether or not the flow is pulsatile. This interpretation of the literature on the subject is summarized in Fig. 1.
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-adrenergic blockade. All of this discussion relates to the hemodynamic effects of pulsatile and nonpulsatile flow. Of equal importance for prolonged perfusion is the effect on coagulation, fibrinolysis, platelets, and white blood cells. The role of pulsation (or more accurately, periodic surges in flow affecting shear stress at blood-surface interfaces) may be an important reason to provide pulsatile flow for long-term perfusion, even in the absence of a hemodynamic rationale.
References
This article has been cited by other articles:
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  P. M. Pego-Fernandes, N. A.G. Stolf, L. F. P. Moreira, H. A. Fabri, A. A. Leirner, S. A. Oliveira, and A. D. Jatene Influence of biopump with and without intraaortic balloon on the coronary and carotid flow Ann. Thorac. Surg., February 1, 2000; 69(2): 536 - 540. [Abstract] [Full Text] [PDF]
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