Jean-François Hardy

Hemorrhage and the Use of Blood Products After Adult Cardiac Operations: Myths and Realities

BACKGROUNDnSeveral patient-, procedure-, and prescriber-related factors are thought to influence the decision to administer allogeneic blood products. We reexamine a number of assertions applied commonly to the practice of transfusion in cardiac operations.nnnMETHODSnMore than 50 original articles including a total of more than 10,000 patients from 70 centers were reviewed. Data from 5,426 patients operated on between 1990 and 1994 at the Montreal Heart Institute are presented.nnnRESULTSnFrom our review of the literature, we conclude that postoperative mediastinal fluid drainage averages 917 mL and that aspirin therapy increases drainage by less than 300 mL in most studies, which should not increase use of blood products, insofar as a strict transfusional protocol is adhered to. Across centers, transfusions can vary eightfold for the same postoperative drainage. Data from our institution show that postoperative mediastinal drainage per se is not influenced by reoperation or by the type of operation. However, total blood losses and transfusion requirements remain increased in reoperative and complex procedures. Excessive mediastinal drainage resulting in increased transfusions occurs in 29% of patients.nnnCONCLUSIONSnExposure to allogeneic transfusions remains institution dependent. Constant reevaluation of local practice is essential to implement efficient blood conservation strategies.

Simultaneous Determination of Aortic Valve Area by the Gorlin Formula and by Transesophageal Echocardiography Under Different Transvalvular Flow Conditions: Evidence That Anatomic Aortic Valve Area Does Not Change With Variations in Flow in Aortic Stenosis☆

OBJECTIVESnThe purpose of this study was to determine the impact of changes in flow on aortic valve area (AVA) as measured by the Gorlin formula and transesophageal echocardiographic (TEE) planimetry.nnnBACKGROUNDnThe meaning of flow-related changes in AVA calculations using the Gorlin formula in patients with aortic stenosis remains controversial. It has been suggested that flow dependence of the calculated area could be due to a true widening of the orifice as flow increases or to a disproportionate flow dependence of the formula itself. Alternatively, anatomic AVA can be measured by direct planimetry of the valve orifice with TEE.nnnMETHODSnSimultaneous measurement of the planimetered and Gorlin valve area was performed intraoperatively under different hemodynamic conditions in 11 patients. Left ventricular and ascending aortic pressures were measured simultaneously after transventricular and aortic punctures. Changes in flow were induced by dobutamine infusion. Using multiplane TEE, AVA was planimetered at the level of the leaflet tips in the short-axis view.nnnRESULTSnOverall, cardiac output, stroke volume and transvalvular volume flow rate ranged from 2.5 to 7.3 liters/min, from 43 to 86 ml and from 102 to 306 ml/min, respectively. During dobutamine infusion, cardiac-output increased by 42% and mean aortic valve gradient by 54%. When minimal flow was compared with maximal flow, the Gorlin area varied from (mean +/- SD) 0.44 +/- 0.12 to 0.60 +/- 0.14 cm2 (p < 0.005). The mean change in Gorlin area under different flow rates was 36 +/- 32%. Despite these changes, there was no significant change in the planimetered area when minimal flow was compared with maximal flow. The mean difference in planimetered area under different flow rates was 0.002 +/- 0.01 cm2 (p = 0.86).nnnCONCLUSIONSnBy simultaneous determination of Gorlin formula and TEE planimetry valve areas, we showed that acute changes in transvalvular volume flow substantially altered valve area calculated by the Gorlin formula but did not result in significant alterations of the anatomic valve area in aortic stenosis. These results suggest that the flow-related variation in the Gorlin AVA is due to a disproportionate flow dependence of the formula itself and not a true change in valve area.

Pathophysiology of rupture of the pulmonary artery by pulmonary artery balloon-tipped catheters.

High pressures have been reported in pulmonary artery catheter balloons. This study was undertaken to determine the in vitro rupturing pressures of human peripheral pulmonary arteries and to evaluate whether such pressures could be generated under clinical conditions. The in vitro model then was confirmed in vivo in the dog and the evolution of a rupture of a peripheral pulmonary artery studied. In vitro, pulmonary arteries of subjects under age 60 yr are remarkably resistant and tolerate intra-balloon pressures of 2700 mm Hg in the one mid-pulmonary artery studied and up to 4219 ± 720 mm Hg (mean ± SD) in the distal pulmonary artery. Subjects over the age of 60 yr have significantly lower rupturing pressures (1965 ± 540 mm Hg in the mid-pulmonary artery, and 2498 ± 600 mm Hg in the distal pulmonary artery), (P < 0.05). Thus overdistension by the balloon may explain most ruptures. Preexisting pulmonary hypertension did not affect in vitro rupturing pressures. Clinicians generated in traballoon mean pressures of 795 ± 130 mm Hg, with 20% of them generating higher and potentially dangerous pressures (1000 mm Hg or more). The in vitro model was confirmed by in vivo studies in dogs with pressures that cause pulmonary artery rupture. Furthermore, in normal dogs, rupture of a peripheral pulmonary artery was without complications. This suggests that rupture of the peripheral pulmonary artery may occur clinically more frequently than reported. The user of flotation pulmonary arterial catheters should be aware of the dangers associated with this diagnostic tool. In particular, liquids must never be used to inflate pulmonary arterial catheter balloons.

Prophylactic Tranexamic Acid and ϵ-Aminocaproic Acid for Primary Myocardial Revascularization

Abstract Background . The efficacy of prophylactic ϵ-aminocaproic acid and tranexamic acid to reduce transfusions after primary myocardial revascularization was evaluated in a teaching hospital context. Methods . Patients (n = 134) received either ϵ-aminocaproic acid (15-g bolus + infusion of 1 g/h), high-dose tranexamic acid (10-g bolus + placebo infusion), or normal saline solution in a double-blind fashion. Anticoagulation and conduct of cardiopulmonary bypass were standardized. Results . Tranexamic acid and ϵ-aminocaproic acid produced a significant reduction in postoperative blood loss compared with placebo (median loss, 438 mL, 538 mL, and 700 mL, respectively). Transfusion of red cells was similar in all three groups. Nonetheless, the percentage of patients receiving hemostatic blood products was significantly decreased in the ϵ-aminocaproic acid group compared with the placebo group (20% versus 43%; p = 0.03). Both tranexamic acid and ϵ-aminocaproic acid significantly decreased total exposure to allogeneic blood products compared with placebo ( p = 0.01 and p = 0.05, respectively), and this reduction was clinically important (median exposure, 2, 2, and 7.5 units, respectively). Fibrinolysis was inhibited significantly in both treatment groups. Conclusions . We conclude that either high-dose tranexamic acid or ϵ-aminocaproic acid effectively reduces transfusions in patients undergoing primary, elective myocardial revascularization.

Prevention and treatment of coagulopathy in patients receiving massive transfusions

Patients undergoing massive transfusions frequently develop a coagulopathy, which is already present in a considerable percentage of patients upon admission to the emergency room. This derangement of coagulation may aggravate the bleeding tendency and is associated with significant morbidity and mortality. Existing guidelines for optimal transfusion therapy in massively bleeding patients advocate early administration of crystalloid or colloid fluids in conjunction with transfusion of red cells. And, according to the guidelines, fresh frozen plasma (FFP) and platelets should only be administered when a whole blood volume or more has been replaced and then only in patients with excessive or microvascular bleeding and, at best, according to conventional laboratory coagulation analysis. However, this approach may cause dilution coagulopathy and a further impairment of hemostasis due to direct effects of plasma replacement treatment on platelet-vessel wall interaction and thus compromise haemostatic ability further in severely bleeding patients. In recent years, there has been increasing evidence, although mainly coming from non-randomized studies, that early and more intense replacement of coagulation factors and platelets may improve the outcome in patients undergoing massive transfusion. The recommendations in the existing guidelines are based on the results of conventional coagulation assays such as the activated partial thromboplastin time. However, these assays poorly correlate with clinically relevant coagulopathies [1, 2]. Cell-based whole blood viscoelastical assays such as thromboelastography (TEG) provide quantitative information of the haemostatic process and thus give a profile of the haemostatic changes that occur during clotting. Such tests may provide a better guide for blood component therapy for patients with massive bleeding, although also for these tests the clinical relevance has never been adequately validated [3–5]. It seemed of interest to obtain information on these issues by sending the following questions to experts in the field. Question 1: What is your definition of ‘massive blood transfusion’? Question 2: When treating a patient with massive bleeding, do you still follow the official guidelines i.e. restoration of blood volume initially with cristalloids or colloids followed by packed red cells and subsequently the use of FFP, platelets, cryoprecipitate, and other coagulation concentrates depending on the results of coagulation tests and platelet counts? If no: please explain. Question 3: Or do you follow a more aggressive regimen administering FFP and platelets as part of the standard transfusion program? If so, which FFP:RBC ratio do you apply? Please describe your transfusion policy in detail. Question 4: If you use coagulation parameters in your setting, which tests do you apply? Do you think that the conventional tests are satisfactory for this purpose? If not, please explain why. What would be an acceptable turn-around time for any test? Question 5: Have you evidence that a more aggressive regimen with regard to FFP and platelet transfusions improves outcome? Or do you think FFP and platelet transfusion may be harmful? We received 12 contributions to this Forum. Many of the answers are extensive and contain much detailed information. It is impossible to include all this information in an editorial. The reader is therefore strongly advised to read the answers. Although some participants still use the standard definition of massive transfusion, i.e. 10 units of RBC within 24 h, most now use a different definition. Most

A simple classification of the risk in cardiac surgery: the first decade

Since 1980, the operative risk in all our cardiac surgical patients has been assessed before surgery. In light of reports of changes in cardiac surgical populations, we reexamined our practice and risk classification. The purpose of this study was to compare the surgery performed, the characteristics of the patients operated upon and the hospital mortality in our institution in two epochs ten years apart. In 1989–90, the 2029 consecutive cardiac surgical patients who had the same operations as the 500 patients of a 1980 study in our institution were prospectively stratified using our risk classification based on the number of risk factors (RFs) present: normal-risk patient = no RF, increased risk = 1 RF, high risk ≥ 2 RFs. These two cohorts of patients were compared. From 1980 to 1990, the proportion of high-risk patients tripled whereas the proportion of normalrisk patients diminished by one third and the proportion of increased risks remained unchanged. The incidence of the following RFs increased: poor left ventricular function, advanced age, emergency surgery, reoperation and other systemic disorders. In coronary artery surgery patients, the incidence of unstable angina/ recent myocardial infarction and of obesity also increased. In noncoronary artery surgery patients, the incidence of heart failure increased while obesity remained unchanged. The difference in hospital mortality among the three risk classes was significant within both study periods. The mortality in each risk class and total mortality did not change between 1980 and 1990. Complex surgery carried a higher mortality than simple surgery (8.7% vs 2.6% in 1980 and 11.7% vs 4.1% in 1990). A stable hospital mortality and an increase in the proportion of high-risk patients in the more recent population may be attributed to recently improved therapeutic measures. The risk classification that we use remains a practical, reliable and simple clinical tool to estimate outcome and quality of care. The required data are readily available at the preanaesthetic visit. Complex surgery is a new RF.RésuméDepuis 1980, l’ anesthésiste évalue le risque de décès lors de la visite préopératoire chez tous nos opérés du coeur. Suite à diverses communications faisant état de changements des caractéristiques chez des patients subissant une chirurgie cardiaque, nous avons réexaminé notre pratique et notre classification du risque opératoire. Le but de cette étude était de comparer les interventions chirurgicales, les caractéristiques des opérés, et la mortalité durant l’ hospitalisation à deux époques séparées par une décennie. En 1989–90, 2029 patients consécutifs qui avaient subi les interventions décrites dans une étude portant sur 500 patients opérés en 1980, furent regroupés prospectivement selon notre classification basée sur la présence de facteurs de risques (FR): patient à risque habituel = aucun FR, risque accru = 1 FR, risque élevé ≥ 2 FRs. Les deux populations furent comparées. De 1980 à 1990, la proportion de patients à risque élevé a triplé alors que celle des patients à risque habituel a diminué du tiers et la proportion de patients à risque accrru n’ a pas changé. L’ incidence de la dysfonction ventriculaire gauche, de l’ âge supérieur à 65 ans, de la chirurgie urgente, de la réintervention, et d’ autres atteintes systémiques sévères a augmenté. Chez les patients de chirurgie coronarienne, l’ incidence de d’ angine instable/infarctus du myocarde récent et d’ obésité a augmente. Chez les opérés de chirurgie non coronarienne, l’ incidence d’ insuffisance cardiaque a augmenté tandis que l’ incidence d’ obésité n’ a pas changé. A chaque periode étudiée, la mortalité entre les classes de risque était significativement dijférente. La mortalité dans chaque classe ainsi que la mortalité totale n’ ont pas changé entre 1980 et 1990. La mortalité était plus grande dans le chirurgie complexe comparativement à la chirurgie plus simple (7, 8% vs 2, 6% en 1980 et 11,7% vs 4,1% en 1990). De 1980 à 1990, bien que l’ état de santé des opérés du coeur se soit détérioré, la mortalité est demeurée stable. L’ amélioration de la qualité des soins pourrait expliquer cet état de fait. Notre classification du risque demeure un outil clinique pratique et simple, ainsi qu’ un indicateur fiable du devenir des opérés du coeur. Cette classification peut également servir à évaluer la qualité des soins. La chirurgie complexe est identifiée comme un nouveau FR.

Natural and synthetic antifibrinolytics in adult cardiac surgery: efficacy, effectiveness and efficiency

Epsilon-aminocaproic acid and tranexamic acid, two synthetic antifibrinolytics, and aprotinin, an antifibrinolytic derived from bovine lung, are used to reduce excessive bleeding and transfusion of homologous blood products (HBP) after cardiac surgery. This review analyzes the studies on the utilization of antifibrinolytics in adult cardiac surgery according to the epidemiological concepts of efficacy, effectiveness and efficiency. A majority of published studies confirm the efficacy of antifibrinolytics administered prophylactically to reduce postoperative bleeding and transfusion of HBP. More studies are needed, however, to compare antifibrinolytics and determine if any one is superior to the others. Despite their demonstrated efficacy, antifibrinolytics are only one of the options available to diminish the use of HBP. Other blood-saving techniques, surgical expertise, temperature during cardiopulmonary bypass and respect of established transfusion guidelines may modify the effectiveness of antifibrinolytics to the point where antifibrinolytics may not be necessary. At this time, insufficient data have been published to perform a cost vs benefit analysis of the use of antifibrinolytics. This complex analysis takes into account not only direct costs (cost of the drug and of blood products), but also the ensuing effects of treatment such as: length of stay in the operating room, in the intensive care unit and in the hospital; need for surgical re-exploration; treatment of transfusion or drug-related complications, etc. In particular, the risk of thrombotic complications associated with antifibrinolytics is the subject of an ongoing, unresolved controversy. In conclusion, it is important for each institution to determine if their patient population (or a subset of this population) is likely to benefit from prophylactic treatment with antifibrinolytics, and to confirm that treatment is not associated with an increased incidence of untoward effects, before engaging in the routine use of any of these medications.RésuméTrois antifibrinolytiques sont présentement utilisés en chirurgie cardiaque afin de réduire le saignement postopératoire et la transfusion de produits sanguins homologues (PSH). Il s’agit de l’acide epsilon-aminocaproïque et de l’acide tranexamique, deux antifibrinolytiques de synthèse, ainsi que de l’aprotinine, un antifibrinolytique naturel isolé à partir de poumons de bovins. Cet article fait une revue de l’utilisation des antifibrinolytiques en chirurgie cardiaque de l’adulte en fonction des concepts épidémiologiques fondamentaux que sont l’efficacité expérimentale, l’efficacité clinique et l’efficience. La majorité des études publiées confirme l’efficacité expérimentale des antifibrinolytiques administrés prophylactiquement dans le but de diminuer le saignement postopératoire et la transfusion de PSH. Cependant, les études cherchant à comparer les antifibrinolytiques entre eux sont rares. Seuls d’autres travaux nous permettront d’établir l’efficacité comparée de ces médicaments. Malgré leur efficacité expérimentale, les antifibrinolytiques ne sont qu’une des options à notre disposition pour diminuer le recours à la transfusion. Ainsi, l’efficacité clinique des antifibrinolytiques sera modifiée par l’utilisation des autres technologies visant à minimiser les pertes sanguines et la transfusion, par l’expertise de l’équipe chirurgicale, par la température durant la perfusion extra-corporelle, ainsi que par le respect des indications bien établies de la transfusion. Ainsi, dans un contexte donné, l’utilisation de ces médicaments pourra même s’avérer superflue. Nous ne disposons pas actuellement de données suffisantes pour compléter une analyse coûts/ bénéfices des antifibrinolytiques en chirurgie cardiaque de l’adulte. Cette analyse complexe devra tenir compte non seulement des coûts directs (médicaments et produits sanguins), mais aussi des effets associés au traitement tels que: durée de séjour en salle d’opération, aux soins intensifs et à l’hôpital; nécessité d’une ré-exploration pour hémostase; traitement des complications secondaires aux transfusions ou aux médicaments, etc. Plus spécifiquement, le risque de complications thrombotiques secondaires aux antifibrinolytiques fait l’objet d’une controverse non résolue à ce jour. En conclusion, avant de procéder à l’administration routinière de ces médicaments, chaque institution devra déterminer, dans la population chirurgicale qui lui est propre (ou dans un sous-groupe de cette population), l’utilité et l’innocuité des antifibrinolytiques administrés prophylactiquement.

Amrinone, in combination with norepinephrine, is an effective first-line drug for difficult separation from cardiopulmonary bypass

A crucial element for weaning patients from cardiopulmonary bypass (CPB) rests on the selection of an appropriate therapeutic regimen. Amrinone, a phosphodiesterase III inhibitor, combines inotropic support with pulmonary and systemic vasodilatation, without increasing heart rate (HR) or myocardial oxygen consumption. These characteristics should be useful in the failing heart during weaning from CPB. Nineteen patients were included in this prospective, open-labelled, phase IV study when systolic blood pressure (SBP) <80 mmHg, and diastolic pulmonary artery pressure (DPAP) > 15 mmHg or central venous pressure (CVP) > 75 mmHg, during progressive separation from CPB. At that moment, CPB flow was increased to alleviate heart failure and amrinone administered as a bolus (0.75 mg · kg−1) followed by an infusion (10 μg · kg−1 · min−1). Weaning from CPB was then resumed and haemodynamic variables (SBP, DPAP, CVP and HR) were compared with those measured at CPB flow when failure had first occurred. Failure to wean from CPB occurred at 57 ± 25% of full pump flow. After the amrinone bolus, DPAP and CVP decreased by 20% and 21% respectively. Subsequently, 16 patients required the infusion of norepinephrine (4-8 fig-min−1) to maintain a SBP > 80 mmHg. Heart rate remained unchanged after the bolus of amrinone, after separation from CPB, and no arrhythmias were noted. Successful weaning from CPB was possible 12 ± 8 min after the amrinone bolus. Weaning resulted in a cardiac index similar to that measured pre-bypass. Amrinone is rapidly effective during weaning from CPB and, in combination with norepinephrine, provides the necessary inotropic support during this unstable period.RésuméLorsque le sevrage de la circulation extracorporelle (CEC) s’avère difficile, le choix d’un régime thérapeutique approprié est d’une importance capitale. L’amrinone, un inhibiteur de la phosphodiestérase de type III, augmente l’inotropie et dilate les circulations pulmonaire et systémique, sans augmenter la fréquence cardiaque ou la consommation d’oxygène du myocarde. Ces caractéristiques pharmacologiques devraient être bénéfiques durant le sevrage de la CEC. Furent inclus dans cette étude prospective de phase IV dix-neuf patients dont la pression artérielle systémique (PAS) était <80 mmHg alors que la pression diastolique de l’artère pulmonaire (PDAP) > 15 mmHg ou la pression veineuse centrale > 15 mmHg durant le sevrage lent et progressif de la CEC. Lors de l’échec du sevrage, le débit de la CEC était augmenté de façon à soulager la défaillance cardiaque et un bolus damrinone était administré (0.75 mg · kg−1), suivi d’une perfusion (10 μg · kg−1 · min−1). Le sevrage était alors repris et les paramètres hémodynamiques comparés au débit de CEC où l’échec était survenu initialement. L’échec du sevrage survint à 57 ± 25% du plein débit de CEC. Après le bolus d’amrinone, la PDAP et la PVC diminuèrent de 20% et de 21% respectivement. Par la suite, une perfusion de norépinéphrine (4–8 μg · min−1) fut requise chez 16 patients afin de maintenir la PAS > 80 mmHg. Le rythme cardiaque demeura stable après l’administration du bolus d’amrinone et après le sevrage de la CEC, et aucune arythmie ne fut notée. Les patients furent complétement sevrés de la CEC 12 ± 8 min après le bolus d’amrinone et leur index cardiaque après la CEC était superposable à celui mesuré avant la CEC. Ainsi, l’amrinone agit rapidement et efficacement durant le sevrage de la CEC et, en association avec la norépinéphrine, procure au myocarde le support inotrope nécessaire durant cette période de grande instabilité hémodynamique.

Low-dose aprotinin infusion is not clinically useful to reduce bleeding and transfusion of homologous blood products in high-risk cardiac surgical patients

A high-dose regimen of aprotinin 5–6 million KIU is effective in reducing bleeding and the need for homologous blood products (HBP) associated with cardiopulmonary bypass (CPB). These high doses aim at achieving plasmin and plasma kallikrein concentrations which in vitro are inhibitory but, theoretically, smaller doses could suffice in vivo. Also, aprotinin is an expensive drug, so efficiency requires using the smallest effective dose. Therefore, the efficacy of prophylactic aprotinin 1 million KIU (the maximal dose approved currently) was evaluated in a patient population at high risk of bleeding and of being transfused. Forty-one patients undergoing reoperation or a complex surgical procedure were included in a prospective, randomized, placebo-controlled, double-blind study. Before skin incision, a bolus of 200,000 KIU aprotinin was administered in 20 min, followed by an infusion of 100,000 KIU· hr−1 over eight hours. Control patients received an equal volume of saline. Dryness of the operative field, chest drainage, transfusion of HBP, haemoglobin concentrations, and coagulation variables (including bleeding time) were compared. There were no differences between aprotinin and placebo-treated patients for all clinical and laboratory variables. The apparent ineffectiveness of aprotinin may be explained by the use of an insufficient dose, by a different protocol of administration (e.g., no bolus in CPB prime), or by the inability of aprotinin to decrease bleeding and transfusions any further. Also, the number of patients studied does not exclude the possibility of a Type II error. However, based on the small differences observed, we conclude that low-dose aprotinin infusion is not useful clinically to reduce chest drainage and transfusions in a patient population at high risk of being exposed to HBP.RésuméUne posologie élevée d’aprotinine de 5–6 millions KIU diminue le saignement et le besoin de produits sanguins homologues utilisés pour la circulation extracorporelle (CEC). Ces doses élevées visent l’atteinte de concentrations de plasmine et de kallicréine plasmatique efficaces in vitro, mais théoriquement, de plus faibles doses devraient suffire in vivo. De plus, l’aprolinine est une produit coûteux et il est normal qu’on n’utilise que la plus petite dose efficace. C’est dans ce contexte que l’efficacité de l’aprolinine prophylactique 1 million KIU (la dose maximale actuellement approuvée) est évaluée sur une population à haut risque d’hémorragies et de transfusions subséquentes. Quarante-et-un patients soumis à une ré-opération ou à une intervention cardiaque complexe sont inclus dans une étude prospective à double aveugle, randomisée et contrôlée avec placebo. Avant l’incision de la peau, un bolus de 200000 KIU d’aprotinine est administré en 20 min, suivi d’une perfusion de 100 000 KIU · hr−1 répartie sur huit heures. Le groupe contrôle reçoit du soluté physiologique en volume égal. La quantité de sang du champ opératoire, l’importance des pertes par les drains thoraciques, les transfusions de produit sanguins homologues, la concentration de l’hémoglobine et les épreuves de coagulation (temps de saignement inclus) sont comparés. On ne trouve pas de différences entre le groupe aprotinine et le groupe placebo pour tous les paramètres cliniques et de laboratoire. L’inefficacité apparente de l’aprotinine peut s’expliquer par l’utilisation d’une dose insuffisante, par un protocole d’administration différent (v.g. absence de bolus dans l’amorce de CEC), ou par l’incapacité de l’aprotinine à diminuer encore plus le saignement et le besoin de transfusions. De plus le nombre de patients étudiés n’exclut pas la possibilité d’une erreur de type II. Toutefois, sur la base des différences minimes observées, nous concluons que l’aprotinine à faible dose en perfusion n’est pas utile cliniquement pour diminuer les pertes par les drains thoraciques et la quantité de sang transfusée chez une population de patients très susceptible de recevoir des produits de sang homologue.

Inotropic support of the heart that fails to successfully wean from cardiopulmonary bypass: The Montreal Heart Institute experience

The selection of an appropriate therapeutic regimen, especially in patients with preexisting cardiac dysfunction prior to surgery, is a crucial element for successful separation from cardiopulmonary bypass (CPB). At the present time there are no definitive studies to determine which treatment modality, or combination of treatments, is optimal in this patient population. A brief review of the literature is presented to answer the following questions: (1) Should inotropic support be administered in anticipation of failure to wean from CPB? and (2) Which inotrope or combination of drugs is best? There is no evidence at present that the prophylactic administration of inotropes to assist separation from CPB may result in damaging effects to the myocardium in humans. Inasmuch as tachycardia is avoided and coronary perfusion pressure is maintained within the normal range, prophylactic inotropes may be of benefit to patients with preexisting myocardial dysfunction during weaning from CPB by allowing a smoother separation and a shorter time on CPB. While no specific drug has been proven superior, the use of phosphodiesterase inhibitors as part of the regimen to provide inotropic support in these patients may exert a beneficial effect on myocardial ischemia and reperfusion injury. Prophylactic support of the circulation during separation from CPB, especially with phosphodiesterase inhibitors, may be indicated in this specific patient population as part of the strategy to ensure maximal preservation of myocardial function.