LITERATURE REVIEW Carol L. Lake, AID, Editor

Blumberg N, Laczin J, McMican A, et ah A critical survey of fresh-frozen plasma use. Trans- fusion 26:511-513, 1986

Although most blood banks consider that the major justification for the preparation of fresh frozen plasma (FFP) from whole blood is for the availability of factor VIII, this prospective review of FFP use in a university teaching hospital during 2 months in 1981 indicates that FFP and packed erythrocytes are being given as a replacement for or in preference to whole blood. Blood banks consider that the only clear indications for FFP are factor VIII, IX, or von Willebrand factor deficiencies; other congenital factor defi- ciencies for which factor concentrates are unavailable; and for acquired deficiencies of coagulation factors. In this study, only 27% of the FFP transfusions were for replacement of labile coagulation factors, with volume repletion, intraopera- tive bleeding or massive transfusion without coagulopathy, and miscellaneous needs as the indications for the remaining 73% of FFP transfusions. Because of the increased costs and risk of blood-borne infection, transfusion of FFP and packed erythrocytes when whole blood is indicated is an undesirable practice.

Mayer M, Finci Z, Chaouat M: Suppres- sion of plasminogen activator activity by dexa- methasone in cultured cardiac myocytes. J Mol Cell Cardiol 18:1117-1124, 1986

Rat myocardial cells contain two forms of active plasminogen activator; a membrane-bound form present in myocytes and fibroblasts, and a soluble, extracellular form secreted by myocytes. Both secreted and cell-associated forms were suppressed (inhibited) by the addition of dexa- methasone, 10 -7 mol/L. Plasminogen activator inhibition may result from the presence of an inactive proenzyme or formation of an inhibitor-plasminogen activator complex. These findings suggest the necessity to reexamine the con- comitant use of steroids during pharmacological vascular thrombolytic procedures.

Davies GG, Jebson P JR, Blasgow BM, et al: Continuous Fick cardiac output compared to thermodilution cardiac output. Crit Care Med 14:881-885, 1986

Because thermodilution cardiac output determina- tions provide only intermittent measurements and have intrinsic errors, the authors attempted to use continuous measurements of cardiac output by the Fick principle. A computer-based system that integrated measurement of oxy- gen consumption by a gas exchange analyzer with arteriove-

nous oxygen difference measured by pulse and fiberoptic pulmonary artery oximetry was used. A correlation of contin- uous Fick with thermodilution measurements of 0.86 was found. Although the continuous Fick measurements were consistently lower than thermodilution measurements and the differences augmented by low-flow states, the method was simple, scientifically sound, and contributed important information about overall cardiorespiratory function.

Baier H: Functional adaptation of the bron- chial circulation. Lung 164:247-257, 1986

The bronchial circulation has important functions aside from the nutrition of the pulmonary parenchyma as outlined in this excellent review. It actively participates in airway responses to both injurious and physiological stimuli.

Bronchial arteries in humans arise from the undersur- face of the thoracic aorta at T 5 and T 6. Although they anastomose extensively with the coronary, internal mamma- ry, esophageal, thyroid, thyrocervical, intercostal, thymic, subclavian, vertebral, and pericardiophrenic circulations, the bronchial arteries are end arteries. Bronchial flow drains into both the right heart and the pulmonary circulation. Normal bronchial flow is about 0.9% to 1.43% of the cardiac output. Bronchial flow depends upon arterial pressure and ceases at aortic pressures less than 40 mmHg.

Positive end-expiratory pressure decreases bronchial flow, as does sympathetic stimulation or administration of catecholamines. Parasympathetic or vagal stimulation increases bronchial flow, an effect blocked by atropine. Both hypercarbia and hypoxia increase bronchial flow. Chemical mediators such as histamine, prostaglandin Ez and F2~ decrease bronchial flow by contraction of bronchial arteries. Bronchial blood flow may also be important in the develop- ment of pulmonary edema.

Braude S, Nolop KB, Fleming JS, et al: Increased pulmonary transvascular protein flux after canine cardiopulmonary bypass. Am Rev Respir Dis 134:867-872, 1986

In a canine model of cardiopulmonary bypass, signifi- cant pulmonary sequestration of neutrophils was demon- strated. N eutrophils release proteolytic enzymes, oxygen free radicals, and arachidonate-derived products, all of which can cause lung injury. Products of peroxidation caused by the

From the Department of Anesthesiology, University of Virginia, Charlottesville.

© 1987 by Grune & Stratton, Inc. 0888-6296/87/0103-001453.00/0

Journal of Cardiothoracic Anesthesia, Vol I, No 3 (June), 1987: pp 263 -266 263

264 LITERATURE REVIEW

oxygen free radicals peroxidizing the lipids of the cell mem- brane are quantitated by the thiobarbituric acid reaction. Reperfusion after a period of cardiac asystole resulted in a central venous-toqeft atrial gradient for neutrophils and an increase in thiobarbituric acid reactivity. There was a corre- lation between lipid peroxidation and neutrophil sequestra- tion after cardiopulmonary bypass. Thus, it appears that the tissue oxidants are released by neutrophils sequestered in the lung. Associated with these findings was an increase in lung protein flux (measured by transvascular flux of labeled transferrin), which may result from changes in pulmonary vascular permeability induced by the oxidants.

Tuman K J, Ivankovich AD: Bronchospasm during cardiopuimonary bypass. Etiology and management. Chest 90:635-637, 1986

Some of the findings noted in the previous abstract may be applicable to the case report of severe bronchospasm noted at the resumption of ventilation during the later stages of cardiopulmonary bypass. Three case reports of patients without a history of bronchospasm who developed severe wheezing during cardiopulmonary bypass arc presented. None of the patients demonstrated cutaneous signs of allergic reactions. All responded to aggressive therapy with steroids, bronchodilators, anticholinergics, atropine, or halothane. Possible etiologies included cold urticaria, complement- mediated reactions, or other unidentified factors.

Huddleston CB, Stoney WS, Alford WC, et al: Internal mammary artery grafts: Technical factors influencing patency. Ann Thorac Surg 42:543-549, 1986

Life table analysis was used to evaluate the patcncy of the internal mammary artery as a conduit for coronary bypass grafting in a long-term study of 814 patients. Although three different methods, mobilization of the inter- nal mammary artery as a wide pedicle with 1 to 2 cm of cndothoracic fascia, skeletenization of the artery, or mobili- zation of the artery with surrounding fat and veins, were used to harvest the internal mammary artery, no differences in patency were attributable to method of harvest. The highest patency rates occurred when the internal mammary artery was anastomosed to the left anterior descending (LAD) coronary artery, with similar patency rates at 1 year, but markedly divergent rates at 5 years (89.2% patency of LAD v 84.2% patency of the diagonal). Left internal mammary grafts also had higher patency rates than saphenous vein grafts (51% v 20% at 10 years), although right internal mammary grafts had similar patency rates to saphcnous veins. As demonstrated by previous studies, higher initial flow rates through the mammary artery were associated with improved patency. Reasons suggested for the lower patency rates of the right internal mammary artery were its anasto- mosis to the diagonal coronary artery, and anastomosis of a more distal segment of the mammary artery because of the distance necessary to reach the diagonal.

Lang RM, Borow KM, Neumann A, et al: Systemic vascular resistance: An unreliable index

of left ventricular afterload. Circulation 74:1114- 1123, 1986

Systemic vascular resistance is frequently used clini- cally to estimate ventricular afterload. True ventricular afterload is the force opposing ventricular fiber shortening during left ventricular ejection. Afterload is essentially left ventricular wall stress, which includes peak systolic wall stress and the integral of left ventricular systolic wall stress over time. Geometric factors such as increasing wall thick- ness and decreasing ventricular size determine instantaneous wall stress. Left ventricular afterload peaks during the first one third of ventricular ejection and decreases throughout the rest of systole, even while ventricular pressure is increasing.

An experimental canine preparation was used to eval- uate the use of end-systolic wall stress to reflect the effects of left ventricular wall thickness, dimension, and chamber pres- sure as well as peripheral loading conditions rather than systemic vascular resistance to determine changes in after- load during pharmacological interventions. End-systolic pres- sure was measured with a catheter-tipped transducer, and end-systolic and diastolic dimensions and wall thicknesses were measured echocardiographically. Minimal changes in afterload associated with augmented contractility (norepi- nephrine administration) were inaccurately predicted by systemic vascular resistance. Similarly, when afterload alone was decreased with nitroprusside, systemic vascular resis- tance underestimated the decrease by 22%. It also underesti- mated an increased afterload produced by methoxamine by 54%. The combination of increased contractility and decreased afterload produced by dobutamine was also under- estimated. Thus, measurements of left ventricular afterload must take into account both myocardial and peripheral factors. Systemic vascular resistance reflects only peripheral arteriolar tone and neglects the ventricular component of afterload.

Demas K, Wyner J, Mihm FG, et ai: Anaes- thesia for heart transplantation. Br J Anaesth 58:1357-1364, 1986

Although cardiac transplantation is now being widely performed, the anaesthetic management of patients undergo- ing transplantation has not been extensively reviewed. The authors of this paper described a large series (261 patients) of cardiac transplantations at Stanford University. Although the majority were anesthetized with high-dose narcotic tech- niques, narcotic anesthesia was associated with a high inci- dence of dysrhythmias requiring either pharmacological or electrical conversion. In the 17% of patients receiving volatile anesthetics, hypotension to less than 90/50 mmHg (mean of 60) for longer than five minutes was the major problem. However, no morbidity was associated with this type of anesthesia.

The authors also detail the general management of patients undergoing transplantation. Fentanyl or sufentanil with diazepam is the recommended anesthetic regimen. In addition, the need to use sterile airway equipment, bacterial filters on both sides of the anesthetic circuit, and aseptic placement of intraarterial and central venous catheters is emphasized. Pulmonary artery catheters are not placed since