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Our data demonstrate that perioperative mortality is mainly dependent on the extent of surgery, the presence of CAD and provision of adequate medical and nursing care. Preoperative testing and interventions to reduce the cardiovascular risk factors may help to further improve perioperative outcome.

Postoperative RD(0.5) (Delta Creat >0.5 mg/dl) occurs in 15% of vascular patients and carries a bad prognosis. Preoperative renal insufficiency and factors related to the complexity of surgery are the main predictors of renal dysfunction.

Hemodilution is not an effective means to lower the risk of allogeneic blood transfusion in elective cardiac surgical patients with normal cardiac function and in the absence of high risk for coronary ischemia, provided standard intraoperative cell saving and high-dose aprotinin are used.

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Purpose: To investigate the effects of chronic ACE inhibition on cardiac neural function following induction of general anesthesia in patients with underlying coronary artery disease. Method:In a prospective case-control study, heart rate variability (HRV) and baroreflex control were compared preoperatively and 30 min after anesthesia induction in patients receiving, or not, ACEI (n=16, control group and n=16, ACEI group). All patients had normal cardiac function and anesthesia consisted of a fixed dose regimen of fentanyl and midazolam. Anesthesia-related hypotension was defined by systolic blood pressure < 90 mmHg. Spectral density of HRV was calculated for low frequency and high frequency bands (LF, from 0.05 to 0.15 Hz and HF, from > 0.15 to 0.6 Hz). Baroreflex sensitivity was estimated after blood pressure changes induced by injections of phenylephrine (PHE) and nitroglycerin (NTG). Results:The HRV parameters and baroreflex sensitivity were not different between groups, during the awake and anesthesia periods. Anesthesia produced similar reduction in total HRV in the Control and ACEI groups (-93 ± 28% vs -89 ± 32%,) and in baroreflex sensitivity during NTG (-64 ± 21% vs -54 ± 17%) or PHE tests (-74 ± 25% vs -72 ± 22%). Anesthesia-related hypotension occurred in nine patients in the ACEI group (vs two controls). Although the hypertensive response to phenylephrine was greater after anesthesia in both groups, the sensitivity to phenylephrine was attenuated in those patients experiencing hypotension in the ACEI group. Conclusions: Chronic preoperative treatment with ACEIs does not influence cardiac autonomic regulation and anesthetic-induced hypotensive episodes are mainly attributed to decreased -adrenergic vasoconstrictive response.Objectif : Rechercher les effets d'une inhibition chronique de l'ECA sur la fonction neurale cardiaque à la suite de l'induction d'une anesthésie générale chez des patients qui présentent une cardiopathie ischémique sous-jacente.Méthode : Lors d'une étude prospective cas-témoins, la variabilité de la fréquence cardiaque (VFC) et le contrôle baroréflexe ont été comparés avant l'opération et 30 min après l'induction de l'anesthésie chez des patients qui reçoivent, ou non, un IECA (groupe témoin : n = 16, groupe IECA : n = 16). Tous les patients présentaient une fonction cardiaque normale et l'anesthésie comprenait un schéma posologique fixe de fentanyl et de midazolam. On a défini l'hypotension reliée à l'anesthésie comme la tension artérielle systolique < 90 mmHg. La densité spectrale de la VFC a été calculée pour des bandes de basses et de hautes fréquences (BF, de 0,05 à 0,15 Hz et HF, de > 0,15 à 0,6 Hz). La sensibilité baroréflexe a été évaluée après les changements de pression sanguine induits par les injections de phényléphrine (PHE) et de nitroglycérine (NTG).Résultats : Les paramètres de la VFC et la sensibilité baroréflexe n'ont pas présenté de différence intergroupe pendant les périodes d'éveil et d'anesthésie. L'anesthésie a produit une réduction similaire de la VFC total...

PRIMARY pulmonary hypertension (PPH) is an uncommon, almost uniformly fatal disease that generally affects young adults. 1 The risk of death is best correlated with right ventricular hemodynamic indices and New York Heart Association functional class.2 Although anticoagulants, calcium-channel blockers and prostacyclin have shown great promise, lung transplantation remains the only viable treatment option in patients who remain symptomatic and deteriorate during treatment. 3We describe a patient with severe PPH in whom general anesthesia and mechanical ventilation precipitated the onset of cardiac failure and necessitated urgent cardiopulmonary bypass. Case ReportA 48-yr-old man with PPH was scheduled to undergo lung transplantation after a 3-yr history of progressive dyspnea with home oxygen therapy. Right-sided heart catheterization showed elevated pulmonary artery pressures (125/59 mmHg) with normal cardiac output (4.5 l/min) and mixed venous oxygen saturation (Smv O 2 ) of 74%. Pulmonary hypertension was unresponsive to inhaled nitric oxide, and treatment trials with calcium antagonists and prostacyclin failed to improve dyspnea and exercise tolerance. Twelve-lead electrocardiography (ECG) showed sinus tachycardia with right-axis deviation and right atrial and right ventricular hypertrophy. Lung volumes were within normal values, and resting arterial partial pressure of oxygen (Pa O 2 ) was 57 mmHg while breathing room air.Before surgery, electrocardiography leads and a pulse oximeter probe were placed, and arterial and pulmonary artery catheters were inserted during local anesthesia for continuous monitoring of mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP) and central venous pressure. After a 3-min oxygenation period, arterial oxygen saturation (Sp O 2 ) and Smv O 2 increased (Sp O 2 from 91 to 95% and Smv O 2 from 72 to 78%), with no change in systemic and pulmonary artery pressures (150/100 mmHg and 130/62 mmHg, respectively).General anesthesia was induced with incremental doses of fentanyl (250 g) and midazolam (3.5 mg). Succinylcholine (75 mg) was given to facilitate airway intubation with a double-lumen tracheobronchial tube, and controlled mechanical ventilation was initiated using low tidal volumes (5-7 ml/kg). Anesthesia was maintained with 0.5-1% isoflurane in oxygen.As shown in figure 1, anesthesia induction was associated with a marked decrease in MAP (from 125 to 85 mmHg). A large increase in MPAP (from 80 to 115 mmHg) occurred in response to tracheal intubation, with MPAP exceeding the level of MAP. Within 2 min after the start of positive-pressure ventilation, right ventricular failure developed, as indicated by high end-expiratory central venous pressure, a dramatic decrease in cardiac output (from 3.9 to 1.2 l/min) and by low Sp O 2 (Ͻ 85%), Smv O 2 (30%), and expired carbon dioxide values (Ͻ 2%). Hemodynamics and gas exchange improved transiently with the administration of epinephrine (two repeated doses of 50 g followed by an infusion of 0.01 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ). At...

Commentary P A CorrisOne of the inevitable consequences of success in a new clinical procedure would appear to be a slow but steady relaxation of strict guidelines pertaining to patient selection as familiarity increases. Nowhere has this been more evident than in the field of lung transplantation. After two decades of failure, the early 1980s were characterised by the cautious introduction of heart and lung transplantation for pulmonary vascular disease and single lung transplantation for fibrosing lung disease with clinical success. 1Transplant surgeons and, indeed, their physician colleagues were, however, blessed with a pioneering spirit and were keen to take on new challenges. This manifest itself by the development of a flood of ever increasing indications for lung transplantation. In this respect the decision to perform heart lung transplantation in a patient with respiratory failure due to cystic fibrosis was a milestone. The idea of transplanting an essentially septic recipient with a systemic disease flaunted the received wisdom at the time. Nevertheless, this brave decision has been proved an inspired one with the excellent results obtained oVering hope for a new life for many patients with advanced cystic fibrosis.The two case reports by Licker et al 2 and Hill et al 3 are based on a common theme and illustrate the points above because it is unlikely that either of the patients would have been considered for transplantation in the early 1980s. Results have been successful, at least in the medium term, and the transplant teams are to be congratulated on their success. What conclusions, however, can we draw? In essence both cases revolved around patients whose risk for a successful long term outcome would have to be estimated as less than average at the time the decision to transplant was made. Both cases have been reported as a direct result of success "in adversity" and this success has been used to justify the decision to transplant.Would the cases have been reported if both patients had died? Lung transplantation has become a victim of it's own success by failing to deliver an adequate service for well characterised lower risk patients with respiratory failure due to cystic fibrosis, emphysema and pulmonary fibrosis. A shortfall in donor organs has led to most centres experiencing a 50% mortality amongst patients on the active transplant waiting list. Transplant centres must make the best use of a rare resource and, whilst a pioneering spirit must be allowed to flourish, it should not do so if the cost is failure to deliver a service for ever increasing numbers of patients with established indications for whom success is more likely. Perhaps one way forward is for more transplant centres to try to expand the donor lung pool by the use of marginal donors for high risk cases 4 and good donor lungs for recipients who represent a lower risk. The introduction of successful lung xenografting in the future remains a tangible but distant prospect.