Search

Objective: Almitrine enhances hypoxic pulmonary vasoconstriction (HPV) and can improve hypoxemia related to one-lung ventilation (OLV). Studies using almitrine have been conducted without inhaled anesthetics because they could inhibit HPV, counteracting the effect of almitrine. This hypothesis, however, has not been confirmed. This study's aim was to evaluate whether almitrine could improve oxygenation when administered during OLV with sevoflurane anesthesia., Design: A prospective, randomized, double-blind, placebo-controlled trial., Setting: A tertiary care, university teaching hospital., Participants: Thirty adult patients undergoing open-chest thoracic surgery., Interventions: Patients were assigned randomly to receive almitrine or placebo during OLV. Respiratory and hemodynamic variables were recorded continuously. Anesthesia was maintained with sevoflurane and remifentanil. Intraoperative techniques and medical teams were the same all over the study., Measurements and Main Results: Respiratory and hemodynamic variables were measured during two-lung ventilation and during open-chest OLV. Two-way repeated-measures analysis of variance was used to compare the effects of almitrine and placebo. During OLV, PaO2 and shunt fraction worsened in all patients without significant differences between groups. At 30-minutes of OLV, PaO2 was 184±67 mmHg in the almitrine group and 145±56 mmHg in the placebo group, while shunt fraction were 31%±6% and 36%±13%, respectively. Mean pulmonary artery pressure was higher in the almitrine group (31±5 v 24±5 mmHg, p<0.001)., Conclusions: During anesthesia with sevoflurane for open-chest OLV, almitrine failed to improve oxygenation and increased pulmonary artery pressure. The combination of sevoflurane and almitrine should, therefore, be avoided., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Almitrine combined with inhaled nitric oxide (NO) can prevent hypoxia during one-lung ventilation (OLV). The optimal dose of almitrine that would provide therapeutic advantage with few side-effects during open-chest OLV has not been established., Methods: Forty-two patients undergoing thoracotomy were randomly allocated to three groups: placebo, almitrine 4 microg kg(-1) min(-1) and inhaled NO 10 p.p.m. (ALM4+NO), and almitrine 16 microg kg(-1) min(-1) and inhaled NO 10 p.p.m. (ALM16+NO). Gas exchange, haemodynamic and respiratory variables and plasma concentrations of almitrine and lactate were monitored. Measurements were obtained with the patient awake (baseline), after induction of anaesthesia with two-lung ventilation (control 2LV), 20 min after treatment (2LV+T), and then at 10, 20 and 30 min of OLV (OLV10', OLV20' and OLV30') with FI(O2)1., Results: In the placebo group, OLV impaired Pa(O2) and increased pulmonary shunt [16 (SD 7) kPa and 42 (10)% respectively]. These improved with ALM4+NO [26 (10) kPa and 31 (7)%; P<0.001]. ALM16+NO further improved PaO2) to 36 (13) kPa (P<0.0001) but gave no improvement in the shunt. Mean pulmonary artery pressure was similar in the placebo and ALM4+NO groups [20 (4) vs 23 (5) mm Hg], whereas it was increased in the ALM16+NO group to 28 (8) mm Hg (P<0.01). Plasma concentrations of almitrine and lactate were unaltered by the treatments., Conclusions: Low-dose almitrine (4 microg kg(-1) min(-1)) together with inhaled NO significantly improves oxygenation during open-chest OLV, without modifying pulmonary haemodynamics. An increased dose of almitrine (16 microg kg(-1) min(-1)) with inhaled NO further improves arterial oxygenation, but also increases mean pulmonary artery pressure.

New drugs that improve arterial oxygenation (nitric oxide, almitrine, inhaled prostacyclin and cyclooxygenase inhibitors) are useful in the treatment of severe hypoxemia unresponsive to conventional treatment that is mainly seen in patients with acute respiratory distress syndrome (ARDS). By acting selectively on pulmonary blood flow and redistributing it, these drugs achieve effects unattainable until now. Thus, they decrease perfusion in non-ventilated zones (V/Q = O) responsible for shunt, or increase perfusion in well ventilated zones, guaranteeing adequate oxygenation. To apply these drugs the physician must understand their mechanism of action, guidelines for dosing, constraints on their use and side effects.

The purpose of the study was to analyze the hemodynamic response to hypoxemia induced during the first postoperative hour. We studied 151 patients who underwent general anesthesia for elective surgery. Arterial saturation of oxyhemoglobin (SpO2), heart rate (HR), and systolic arterial pressure (SAP) during respiration with atmospheric air were measured 20 min and 80 min after admission at the recovery room. We compared HR and SAP between hypoxemic (SpO2 less than or equal to 90%) and non-hypoxemic patients (SpO2 greater than 90%) and we did not find significant differences. SpO2 failed to correlate with HR or with SAP in any of the time samples. This lack of correlation was also observed between patients with or without halogenated anesthetic treatment. Our results indicate that the possible inhibitory effect of anesthesia on hemodynamic response to hypoxemia lasts at least during the first postoperative hour and it does not depend on the administration of halogenated anesthetics. We also conclude that postoperative hemodynamic stability is not an accurate index of the status of arterial oxygenation.