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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...

This study was designed to compare the anesthetic properties of hypobaric bupivacaine with those of isobaric and hyperbaric solutions when administered in the supine position in an elderly population undergoing hip surgery using continuous spinal anesthesia. Plain bupivacaine (0.5%) was mixed with equal volumes of 10% dextrose (hyperbaric), 0.9% NaCl (isobaric), or distilled water (hypobaric) to obtain 0.25% solutions. In a double-blind fashion, all patients received 3 mL (7.5 mg) of their particular solution injected through the spinal catheter in the horizontal supine position. The sensory level obtained in the hyperbaric group (median, T4; range, T3-L3) was significantly higher than in both the isobaric (median, T11; range, T6-L1) and hypobaric (median, L1; range, T4-L3) groups. A motor blockade of grade 2 or 3 was obtained in 14 of 15 and 12 of 15 patients in, respectively, the hyperbaric and isobaric groups, but only in 8 of 15 patients in the hypobaric group. After the initial injection of 3 mL (7.5 mg), a sensory level of T10 and a motor blockade of grade 2 or 3 was obtained in 14 of 15, 5 of 15, and 3 of 15 patients in the hyperbaric, isobaric, and hypobaric groups, respectively. All remaining patients received 1 or 2 additional milliliters (2.5-5 mg) and achieved these required anesthetic conditions, except for one patient in the hyperbaric group and eight patients in the hypobaric group in whom anesthesia was achieved with hyperbaric tetracaine. The decrease in mean arterial pressure was significantly more severe in the hyperbaric (30%) than in either the isobaric (18%) or hypobaric (14%) groups.(ABSTRACT TRUNCATED AT 250 WORDS)