Anesth Analg 1999;88:329
© 1999 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Intracranial Pressure and Venous Cannulation for Cardiopulmonary Bypass
Walter Plöchl, MD*,
David J. Cook, MD ,
Thomas A. Orszulak, MD , and
Richard C. Daly, MD
*Department of Anaesthesiology and General Intensive Care, University of Vienna, Vienna, Austria; and Departments of
Anesthesiology and
Surgery, Mayo Clinic, Rochester, Minnesota
Address correspondence and reprint requests to David J. Cook, MD, Department of Anesthesiology, 200 First St. SW, Rochester, MN 55905. Address e-mail to cook.david{at}mayo.edu
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Introduction
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The onset of cardiopulmonary bypass (CPB) is a period of changing hemodynamics, and during this transition, the position of the aortic and venous cannulas is assessed. Increased arterial line pressures may indicate a malposition of the aortic cannula, whereas reduced venous return to the reservoir of the CPB circuit suggests suboptimal position of a venous cannula. Classically described signs of compromised venous drainage, such as engorgement of the head and neck, are rare, and incomplete obstruction of the superior vena cavae may be difficult to detect clinically but can significantly alter cerebral physiology. Impedance to superior vena caval (SVC) flow may increase intracranial pressure (ICP) and decrease cerebral perfusion pressure (CPP) (CPP = mean arterial pressure [MAP] - [ICP] (1). In the experimental setting, we have incidentally, but repeatedly, observed this effect. The same physiologic phenomenon is of relevance in the operating suite and may bear on practice. The purpose of this article is to briefly describe the influence of venous cannula position on ICP during CPB.
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Methods
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After review and approval by our animal care and use committee, we observed ICP changes on transition to CPB in 15 unmedicated, fasting adult mongrel dogs weighing 21 ± 2 kg. Anesthesia was established with halothane (3%–4% inspired) and was maintained with halothane (0.5–1% inspired), fentanyl (3 µg · kg-1 · min-1), and midazolam (9.6 µg · kg-1 · min-1).
Cannulae were surgically inserted into a femoral artery for MAP measurements and blood sampling. Central venous pressure monitoring was not obtained. For continuous ICP monitoring, a LADD fiberoptic epidural sensor (LADD Industries, Burlington, VT) was placed through a burr hole placed in the parieto-occipital region.
For CPB, a left-sided thoracotomy was performed. Heparin was given to maintain the celite-activated clotting time >500 s. The bypass machine was primed with approximately 750 mL of 6% Dextran 70. Venous drainage to the extracorporeal circuit was by a 10-mm inner diameter cannula placed in the right atrium via the right atrial appendage. The blood was circulated by a centrifugal pump through a combined heat exchanger-oxygenator (Bentley Spiral Gold, Irvine, CA) and returned via a cannula (4.5-mm inner diameter) into the root of the aorta. CPB temperature was set to approximate the animals' nasopharyngeal temperature at the time of aortic cannulation (34–35°C).
ICP and MAP were recorded before and each minute after the onset of CPB. ICP was displayed continuously on the LADD monitor. The surgeon was not aware of the ICP recording during cannulation or initiation of bypass. CPB was initiated and flows were adjusted to target a MAP of 50–65 mm Hg. If an acute increase in ICP to  15 mm Hg was identified, the surgeon was asked to reposition the venous cannula, and the effect of cannula repositioning was determined.
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Results
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In all 15 animals, the ICP was <15 mm Hg before the onset of bypass. In 5 of 15 animals, ICP increased to 15 mm Hg within the first 3 min of CPB and was associated with reduced venous return to the reservoir. Before CPB, the ICP of these five animals did not differ from those with normal ICPs after the initiation of bypass (Table 1). On CPB, the MAP in the 5 animals with increased ICP did not differ from the other 10 animals, and none had a MAP >86 mm Hg. The highest recorded ICP was 29 mm Hg. Repositioning of the venous cannula quickly returned the ICP to normal values in every animal and improved venous return to the reservoir. After cannula repositioning, the ICP values did not differ between animals in which the venous cannula had to be repositioned and those in which ICP was never increased. Figure 1 shows the changes in ICP with the onset of CPB and correction by venous cannula repositioning in one animal.
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Figure 1. Intracranial pressure (ICP) in the pre-cardiopulmonary bypass (CPB) period and during 30 min of CPB in one animal showing the effect of right atrial cannula position on ICP.
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Discussion
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The initiation of CPB is a dynamic period. If an asanguineous prime is used, the reduction in blood viscosity that occurs with the initiation of CPB reduces arterial resistance and MAP. This hypotension occurs when oxygen delivery is reduced because of the reduction in oxygen-carrying capacity. Additionally, even a normal MAP during CPB may be insufficient to support cerebral perfusion. This was emphasized by Lundar et al. (2,3), who examined the effect of changing MAP and PaCO2 on ICP and middle cerebral artery blood flow velocity. If MAP is decreased and superior vena caval pressure or ICP is high, then CPP may be compromized. In this study, we found that a third of animals had marked increases in ICP within the first 3 min after the onset of CPB. These increases were sufficient to reduce CPP to below what has been described as the critical CPP during tepid CPB in dogs (4).
Although ICP may increase gradually through CPB, the experimental literature indicates that it should remain normal (<15 mm Hg) (5,6). However, as we show, venous cannula malposition can dramatically increase ICP due to partial SVC obstruction. If immediately detected, repositioning of the venous cannula rapidly normalizes ICP. This is of greatest importance during early CPB when MAP is reduced and patients are relatively warm. However, it may also occur periodically during bypass with lifting of the heart or retraction of the right atrium during mitral valve procedures. Poor SVC drainage or partial obstruction may be insidious, and reduced venous return to the pump may be modest. Additionally, monitoring of right atrial pressure may not be sufficient to detect this because the monitoring port of a central venous line is typically in the right atrium.
Although this study can be criticized for not directly measuring internal jugular pressures, acute venous outflow obstruction is transmitted directly to the ICP (1). Furthermore, we observed improvement in venous return to the reservoir and normalization of ICP with repositioning of the right atrial cannula. Thus, we recommend that monitoring internal jugular pressure may be advantageous whenever reductions in venous return are identified.
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Conclusion
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We conclude that observation of internal jugular pressure may be advantageous during the initiation of CPB, especially in the context of bicaval cannulation or during any periods when reduced return to the venous reservoir is detected. Although compression of the SVC is sometimes unavoidable, patient care may be improved by awareness of this potential problem. If the cannula or heart cannot be promptly repositioned, increasing MAP with a vasoconstrictor may be indicated to maintain CPP. This physiology is at the intersection of surgical, anesthetic, and perfusion practice and can be most effectively identified and managed by communication among the specialties.
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References
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Ekstrom-Jodal B. On the relation between blood pressure and blood flow in the canine brain with particular regard to the mechanism responsible for cerebral blood flow autoregulation. Acta Physiol Scand Suppl 1970;350:1–61.[Medline]
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Lundar T, Lindegaard KF, Froysaker T, et al. Cerebral perfusion during nonpulsatile cardiopulmonary bypass. Ann Thorac Surg 1985;40:144–50.[Abstract]
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Lundar T, Froysaker T, Lindegaard KF, et al. Some observations on cerebral perfusion during cardiopulmonary bypass. Ann Thorac Surg 1985;39:318–23.[Abstract]
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Plochl W, Cook DJ, Orszulak TA, Daly RC. Critical cerebral perfusion pressure during tepid heart surgery in dogs. Ann Thorac Surg 1998;66:118–24.[Abstract/Free Full Text]
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Johnston WE, Vinten-Johansen J, DeWitt DS, et al. Cerebral perfusion during canine hypothermic cardiopulmonary bypass: effect of arterial carbon dioxide tension. Surg 1991;52:479–89.
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Cook DJ, Orszulak TA, Daly RC. Minimum hematocrit at differing cardiopulmonary bypass temperatures in dogs. Circulation 1998;98:II170–5.
Accepted for publication November 10, 1998.
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