Reclutamiento alveolar agresivo en el SDRA: más sombras que luces / Aggressive alveolar recruitment in ARDS: more shadows than lights

Reclutamiento alveolar en el síndrome de distrés respiratorio agudo (SDRA) se define como la entrada de gas en zonas previamente no ventiladas o en zonas pobremente ventiladas. El reclutamiento alveolar durante una maniobra de reclutamiento (MR) dependerá de la duración de la maniobra, del tejido pulmonar reclutable, del balance entre reclutamiento de áreas colapsadas y sobredistensión de las áreas ventiladas. La estimación del reclutamiento alveolar se realiza con la tomografía computarizada de tórax y,a pie de cama, con la construcción de curvas de volumen y presión, la ecografía pulmonar y la tomografía por impedancia. La evidencia científica nos indica que la utilización de las MR en pacientes con SDRA sigue sujeta a controversia. Estudios aleatorizados del SDRA o bien no han demostrado beneficio o bien han revelado un incremento de la mortalidad y, por ello, no se recomienda su uso rutinario. (AU)

Alveolar recruitment in acute respiratory distress syndrome (ARDS) is defined as the penetration of gas into previously unventilated areas or poorly ventilated areas. Alveolar recruitment during recruitment maneuvering (RM) depends on the duration of the maneuver, the recruitable lung tissue, and the balance between the recruitment of collapsed areas and over-insufflation of the ventilated areas. Alveolar recruitment is estimated using computed tomography of the lung and, at the patient bedside, through assessment of the recruited volume using pressure-volume curves and assessing lung morphology with pulmonary ultrasound and/or impedance tomography. The scientific evidence on RM in patients with ARDS remains subject to controversy. Randomized studies on ARDS have shown no benefit or have even reflected an increase in mortality. The routine use of RM is therefore not recommended. (AU)

The effect of cannabidiol on sevoflurane minimum alveolar concentration reduction produced by morphine in rats.

OBJECTIVE: To investigate the effect of cannabidiol (CBD) on sevoflurane minimum alveolar concentration (MACSEV) reduction produced by morphine in rats. STUDY DESIGN: Randomized, blinded trial. ANIMALS: A total of 75 male Wistar Han rats weighing 276 ± 23 g (mean and standard deviation), aged 3 months. METHODS: Cannabidiol (CBD) was prepared in an ethanol-solutol-saline vehicle. Animals were randomly divided into 15 groups and given an intraperitoneal bolus of 1, 3, 5, 6.5, 7.5 or 10 mg kg-1 of CBD alone (CBD1, CBD3, CBD5, CBD6.5, CBD7.5 and CBD10 respectively) or combined with 5 mg kg-1 of morphine (MOR+CBD1, MOR+CBD3, MOR+CBD5, MOR+CBD6.5, MOR+CBD7.5 and MOR+CBD10). While three controls groups: MOR+saline, MOR+vehicle and vehicle were given an intraperitoneal bolus of morphine with saline, morphine with vehicle or vehicle alone respectively. The MACSEV was determined from alveolar gas samples at the time of tail clamp application. The MACSEV reduction was analyzed using a one-way ANOVA followed by Tukey's test. Additionally, Kruskal-Wallis test for non-normally-distributed data was performed. Data are presented as mean ± standard deviation. P < 0.05 RESULTS: The mean MACSEV was not reduced by the action of CBD administered alone, but the addition of morphine to the different doses of CBD significantly reduced the MACSEV. That reduction was greatest in the MOR+CBD1, MOR+CBD7.5 and MOR+CBD10 groups (29 ± 5%, 32 ± 5% and 30 ± 6% respectively), less in MOR+CBD3 and MOR+CBD6.5 groups (24 ± 3% and 26 ± 4% respectively) and least in MOR+CBD5 group (17 ± 2%). However, only the MOR+CBD5 group was statistically significantly different from MOR+CBD1, MOR+CBD7.5 and MOR+CBD10 groups. CONCLUSIONS AND CLINICAL RELEVANCE: MACSEV in rat was unaltered by the action of CBD alone, the reduction in MACSEV produced by morphine was not enhanced by the addition of CBD at the doses studied.

Effect of the I/E ratio on CO2 removal during high-frequency oscillatory ventilation with volume guarantee in a neonatal animal model of RDS.

UNLABELLED: The objective of this study was to analyze the effect of I/E ratio on carbon dioxide (CO2) elimination during high-frequency oscillatory ventilation (HFOV) combined with volume guarantee (VG). Five 2-day-old piglets were studied before and after a bronchoalveolar lavage (BAL). The effect of an I/E ratio of 1:1 and 1:2 with (VG-ON) and without VG (VG-OFF) on PaCO2, as well as delta and mean airway pressures at the airway opening (∆Phf-ao, mPaw-ao) and at the tracheal level (∆Phf-t, mPaw-t) were evaluated at frequencies of 5, 8, 11, and 14 Hz. With the VG-ON, PaCO2 was significant lower with the I/E ratio of 1:2 at 5 Hz compared with the 1:1. mPaw-t was higher than mPaw-ao, with 1:1 I/E ratio, and on VG-ON, this difference was statistically significant. CONCLUSION: "In this animal study and with this ventilator, the I/E ratio of 1:1 compared to 1:2 in HFOV and VG-ON did not produce a higher CO2 lavage as when HFOV was used without the VG modality. Even more, a lower PaCO2 was found when using the lower frequency and 1:2 ratio compared to 1:1. So in contrast to non-VG HFOV mode, using a fixed tidal volume, no significant changes on CO2 elimination are observed during HFOV when the I/E ratios of 1:1 and 1:2 are compared at different frequencies." WHAT IS KNOWN: •The tidal volume on HFOV is determinant in CO 2 removal, and this is generated by delta pressure and the length of the inspiratory time. What is New: •HFOV combined with VG, an I/E ratio of 1:2 is more effective to remove CO 2 , and this is not related to the tidal volume.

Single-syringe ketamine-propofol for induction of anaesthesia in rabbits.

OBJECTIVE: To evaluate and compare three intravenous (IV) doses of a ketamine-propofol admixture (ketofol) for induction of anaesthesia in unpremedicated rabbits. STUDY DESIGN: Prospective, randomized 'blinded' trial. ANIMALS: Twenty-one healthy female New Zealand rabbits weighing 2.7 ± 0.1 kg. METHODS: Animals were allocated randomly into three groups of seven animals and received 1 (KP1), 3 (KP3) or 5 (KP5) mg kg(-1) of both ketamine and propofol in a 1:1 mg kg(-1) ratio admixture. Cardiorespiratory parameters and arterial blood gases were measured at baseline, 2 and 5 minutes after drug administration. The time to loss of the righting reflex (LORR) and the duration of action and apnoea were recorded. The quality of induction and intubation were scored. Data were compared using a two-way anova or a t-test for unpaired data, as relevant. RESULTS: The time to LORR was the shortest (11 ± 5 seconds) and the duration of action the longest (374 ± 26 seconds) in group KP5. Group KP1 did not lose the righting reflex; instead mild to moderate sedation was observed in this group. The quality of induction in group KP5 was smooth, but ranged from smooth to fair in group KP3. Intubation was not possible in the KP1 group, and 10 animals in the other two groups showed some resistance to intubation. At 2 and 5 minutes, the pulse rate was significantly higher in all three groups compared with baseline, but no statistical differences were seen in arterial blood pressures. Hypoxaemia and dose-dependent respiratory depression were observed in all groups, with periods of apnoea in the KP5 group. CONCLUSIONS AND CLINICAL RELEVANCE: The IV ketamine-propofol admixture had a dose-dependent effect. Haemodynamic function was well maintained in all groups but hypoxemia was observed at the highest doses and oxygen administration is recommended. Addition of premedication or topical lidocaine is advisable to make intubation easier.

Effects of intramuscular dexmedetomidine in combination with ketamine or alfaxalone in swine.

OBJECTIVE: To evaluate and compare the use of intramuscular (IM) premedication with dexmedetomidine in combination with ketamine or alfaxalone in pigs. STUDY DESIGN: Prospective, randomized, 'blinded' trial. ANIMALS: Fourteen healthy 2-month-old Landrace × Large White pigs weighing 21.5 ± 0.6 kg. METHODS: Animals were distributed randomly into two groups: group KD (n = 7) was given 10 mg kg(-1) IM ketamine + 10 µg kg(-1) IM dexmedetomidine; and group AD (n = 7) was given 5 mg kg(-1) IM alfaxalone + 10 µg kg(-1) IM dexmedetomidine mixed in the same syringe. Pain on injection, degree of sedation and quality of induction were scored. The time from induction of anaesthesia to recumbency was recorded. Once pigs were recumbent, reflexes were evaluated. Pulse and respiratory rates, end-tidal carbon dioxide and arterial oxygen saturation were recorded at 5 and 10 minutes after drug administration. Data were compared using a two-way anova or a t-test for unpaired data as relevant. Data are presented as the mean ± standard deviation (range). RESULTS: Two animals in both groups showed slight pain on drug injection. The time to lateral recumbency in group KD [187 ± 34 seconds (153-230)] was similar to group AD [206 ± 36 seconds (150-248)]. In group AD, sedation was deeper, and the quality of anaesthetic induction was smoother. When moved for anaesthesia, five pigs in group KD vocalized. There were no differences between groups in pulse rates, arterial oxygen saturation and end-tidal carbon dioxide; however, the respiratory rate at 10 minutes was significantly higher in group KD than in group AD. CONCLUSIONS AND CLINICAL RELEVANCE: IM dexmedetomidine in combination with ketamine in pigs induced moderate to deep sedation and fair to smooth induction of anaesthesia. When dexmedetomidine was combined with alfaxalone, sedation was deeper, and induction was of a better quality.

Effects of lidocaine, dexmedetomidine or their combination on the minimum alveolar concentration of sevoflurane in dogs.

The aim of this study was to determine the effects of lidocaine (LIDO) and dexmedetomidine (DEX) or their combination (LIDO-DEX), administered by constant-rate infusion (CRI), on the minimum alveolar concentration (MAC) of sevoflurane in dogs. Seven healthy mongrel dogs were used with a 2-week washout interval between treatments in this study. Anesthesia was induced with propofol and maintained with sevoflurane in oxygen, and MAC of sevoflurane was determined after 90 min equilibration period in the dogs (SEV-MACBASAL). Then, sevoflurane MAC was determined again in the dogs after 45 min equilibration period of one of the following treatments: an intravenous loading dose of lidocaine 2 mg/kg followed by 6 mg/kg/hr CRI (SEV-MACLIDO); an intravenous loading dose of dexmedetomidine 2 µg/kg followed by 2 µg/kg/hr CRI (SEV-MACDEX); or their combination (SEV-MACLIDO-DEX). These SEV-MACs were determined in duplicate. Data were analyzed using ANOVA and post hoc Tuckey test when appropriate. The SEV-MACBASAL was 1.82 ± 0.06%, SEV-MACLIDO was 1.38 ± 0.08%, SEV-MACDEX was 1.22 ± 0.10%, and SEV-MACLIDO-DEX was 0.78 ± 0.06%. The CRI administration of lidocaine, dexmedetomidine and their combination produced a significant reduction in the MAC of sevoflurane by 26.1 ± 9.0% (P<0.0001), 43.7 ± 11.8% (P<0.0002) and 54.4 ± 9.8% (P<0.0001), respectively. The MAC reduction was significantly greater after the CRI combination of lidocaine and dexmedetomidine when compared with lidocaine CRI (P<0.0001) or dexmedetomidine CRI treatments (P<0.025).

Evaluation of safety and pharmacokinetics of vancomycin after intraosseous regional limb perfusion and comparison of results with those obtained after intravenous regional limb perfusion in horses.

OBJECTIVE: To evaluate the clinical effects and pharmacokinetics of vancomycin in plasma and synovial fluid after intraosseous regional limb perfusion (IORLP) in horses and to compare results with those obtained after IV regional limb perfusion (IVRLP). ANIMALS: 6 horses. PROCEDURES: 1 forelimb of each horse received vancomycin hydrochloride (300 mg in 60 mL of saline [0.9% NaCl] solution) via IORLP; the contralateral limb received 60 mL of saline solution (control). Solutions were injected into the medullary cavity of the distal portion of the third metacarpal bone. Synovial fluid from the metacarpophalangeal (MTCP) and distal interphalangeal (DIP) joints and blood were collected prior to perfusion and 15, 30, 45, 65, and 90 minutes after beginning IORLP, and synovial fluid from the MTCP joint only and blood were collected 4, 8, 12, and 24 hours after beginning IORLP. Plasma urea and creatinine concentrations and clinical appearance of the MTCP joint region and infusion sites were determined daily for 7 days. Results were compared with those of a separate IVRLP study. RESULTS: Clinical complications were not observed after IORLP. Mean vancomycin concentration in the MTCP joint was 4 microg/mL for 24 hours after IORLP. Compared with IORLP, higher vancomycin concentrations were detected in the DIP joint after IVRLP. Compared with IVRLP, higher vancomycin concentrations were detected in the MTCP joint for a longer duration after IORLP. CONCLUSIONS AND CLINICAL RELEVANCE: IORLP with 300 mg of vancomycin in a 0.5% solution was safe and may be clinically useful in horses. Intravenous and intraosseous routes may be better indicated for infectious processes in the DIP and MTCP joints, respectively.

Cardiopulmonary effects of desflurane in horses.

OBJECTIVE: To determine the cardiopulmonary effects of desflurane (DES) in horses. ANIMALS: Six healthy adult horses, three males and three females, aged 9 +/- 4 (mean +/- SD) years and weighing 370 +/- 36 kg. MATERIALS AND METHODS: Anaesthesia was induced with an O2 (10 L minute(-1)) and DES mixture (vaporizer setting 18%). After oro-tracheal intubation, horses were positioned in right lateral recumbency. Anaesthesia was maintained with DES in O2 (20 mL kg(-1) minute(-1)) delivered through a large animal circle breathing system. The minimum alveolar concentration of DES (MAC(DES)) that prevented purposeful movement in response to 60 seconds of electrical stimulation of the oral mucous membranes was determined for each horse. The delivered concentration of DES was then increased to achieve end-tidal concentrations corresponding to 1.5 x MAC(DES), 1.75 x MAC(DES), and 2.0 x MAC(DES). Heart rate (HR), mean arterial blood pressure (MAP), respiratory rate (fr), tidal volume (VT), minute volume (VM) and core temperature were determined, and blood samples for arterial blood gas analysis taken at each DES concentration. All data were analysed by two-way anova for repeated measures and Fisher's test for multiple comparisons. A probability level of p < 0.05 was applied. RESULTS: Desflurane concentrations of 2.0 x MAC(DES) increased HR whereas lower concentrations did not. Mean arterial pressure was not affected by 1.0 x MAC(DES) 1.5 x MAC(DES) or 1.75 x MAC(DES), whereas it decreased at 2.0 x MAC(DES). All concentrations of DES examined significantly depressed fr, VT and VM. CONCLUSIONS AND CLINICAL RELEVANCE: Desflurane concentrations between 1.0 and 1.75 x MAC(DES) reduces fr and VM but does not affect HR or MAP in horses.

Large concentrations of nitrous oxide decrease the isoflurane minimum alveolar concentration sparing effect of morphine in the rat.

Many adjuvant drugs have demonstrated anesthetic-sparing properties when combined with volatile anesthetics. Nitrous oxide is combined with volatile anesthetics to reduce the concentrations of volatile anesthetics required to produce anesthesia. Analgesic doses of opioids clearly reduce the requirement for inhaled anesthetics in both human patients and experimental animals. We performed this study to determine whether the combination of nitrous oxide and morphine decreased isoflurane minimum alveolar anesthetic concentration (MAC) even further in the rat. Fifty-eight female rats were used. The rats were divided into 8 groups: isoflurane in 4 possible nitrous oxide concentrations (0%, 30%, 50%, or 70%) with saline or morphine (1 mg/kg). Then the MAC of isoflurane (MAC(ISO))was determined from alveolar gas samples at the time of tail clamp. The MAC of isoflurane was significantly different at each nitrous oxide concentration, and increasing nitrous oxide concentrations reduced anesthetic requirements for isoflurane. The administration of morphine reduced the MAC(ISO) when used with 0% or 30% nitrous oxide. This MAC(ISO) by morphine reduction was less with 50% nitrous oxide and nonexistent at 70% nitrous oxide. However, with morphine present the MAC(ISO) was independent of the nitrous oxide concentration in the 30%-70% range.

Inhaled nitric oxide affects endogenous surfactant in experimental lung transplantation.

BACKGROUND: Inhalation of nitric oxide (NO) has been proposed as a therapy to improve lung transplantation outcome. We investigated the effect that inhaled NO has on the surfactant system in the context of ischemia-reperfusion injury. METHODS: Single left-lung transplantation was performed in weight-matched pairs of Landrace pigs. A double-lung block from the donor animal was flushed with University of Wisconsin solution at 4 degrees C followed by immersion in cold University of Wisconsin solution for 22 hr. The left donor lung was transplanted into the recipient. Recipients were divided into two groups: (1) treated with inhaled NO (40 ppm) (n=6) immediately after initiating lung reperfusion and (2) without treatment (n=6). Lung function was measured during 2 hr of reperfusion. Surfactant components in small and large aggregates, isolated from cell-free bronchoalveolar lavages, and surfactant function were measured. RESULTS: NO inhalation significantly decreased arterial oxygenation. With respect to the surfactant system, NO inhalation worsened the surfactant adsorption rate to an air-liquid interface and affected levels of hydrophobic surfactant proteins (SPs), SP-B and SP-C, and phospholipids, which decreased in large surfactant aggregates but not in small surfactant aggregates. SP-A was reduced in large surfactant aggregates of transplanted lungs from both untreated and NO-treated groups. CONCLUSION: A decreased level of SP-A, SP-B, and SP-C in large surfactant aggregates of transplanted lungs treated with NO is a marker of lung injury. We conclude that treatment with inhaled NO after lung transplantation is deleterious for the surfactant system and causes a parallel worsening of arterial oxygenation.

Meloxicam, a specific COX-2 inhibitor, does not enhance the isoflurane minimum alveolar concentration reduction produced by morphine in the rat.

UNLABELLED: A synergistic effect of nonselective cyclooxygenase (COX) inhibitors on morphine-induced decrease of isoflurane minimum alveolar concentration (MAC(ISO)) has been observed in the rat. We studied the influence of specific COX-2 inhibitors on this decrease of MAC. Sixty-four female rats were anesthetized with isoflurane in oxygen. The animals were grouped into saline solution, aspirin (30 mg/kg), morphine (1 mg/kg), morphine (1 mg/kg) + aspirin (30 mg/kg), meloxicam (1 and 3 mg/kg), and morphine (1 mg/kg) + meloxicam (1 and 3 mg/kg). Then the MAC(ISO) was determined from alveolar gas samples at the time of tail clamp. The groups treated with saline solution, aspirin, and 1 and 3 mg/kg meloxicam did not express any statistically relevant changes among them. The administration of morphine + meloxicam 1 or 3 mg/kg significantly reduced the MAC(ISO) just as in the group where only morphine was administered (morphine 1.35% +/- 0.07%, morphine + 1 mg/kg meloxicam 1.36% +/- 0.04%, and morphine + 3 mg/kg meloxicam 1.37% +/- 0.08%). The greatest reduction of MAC(ISO) was after administration of morphine + aspirin (1.19% +/- 0.05%). The administration of meloxicam does not potentiate the morphine-induced decrease of MAC(ISO) in the rat. IMPLICATIONS: A synergistic effect between morphine and aspirin on isoflurane minimum alveolar concentration has been observed in the rat--an effect that does not occur between morphine and meloxicam.

Evaluation of the local analgesic effect of ketamine in the palmar digital nerve block at the base of the proximal sesamoid (abaxial sesamoid block) in horses.

OBJECTIVE: To evaluate the local analgesic effect of ketamine in a palmar digital nerve block at the base of the proximal sesamoid (abaxial sesamoid block) in horses. ANIMALS: 36 mature healthy Andalusian horses. PROCEDURE: Horses were randomly assigned to 4 groups of 9 horses each and received an abaxial sesamoid block in a randomly chosen forelimb with 1 of the following: saline (0.9% NaCl) solution, 1% ketamine solution, 2% ketamine solution, or 3% ketamine solution. To determine analgesia, the radiant heat lamp-hoof withdrawal model was used as a noxious thermal stimulus. Before each nerve block, baseline hoof withdrawal reflex latency (HWRL, time between lamp illumination and withdrawal of the hoof) was determined; after the nerve block, local analgesic effects were determined by measuring HWRL at 2 and 5 minutes after injection and then every 5 minutes for a total period of 1 hour. RESULTS: Significant differences in HWRL were found between baseline values and values at 2 to 15 minutes following a nerve block with ketamine. Significant differences were found between HWRL values at every time point from 2 to 10 minutes following a nerve block with saline solution, compared with 1 or 2% ketamine solution. Similarly, significant differences were found between HWRL values at every time point from 2 to 15 minutes following a nerve block with saline solution, compared with 3% ketamine solution. CONCLUSIONS AND CLINICAL RELEVANCE: Abaxial sesamoid block with ketamine ensures adequate analgesia in horses with an onset of action of 2 minutes and a maximal duration of action of 15 minutes.

Efeitos cardiovasculares e respiratórios em cães anestesiados com diferentes concentrações de isoflurano / Cardiovascular and pulmonary effects of different isoflurane concentrations in dogs

No presente trabalho foram analisados os efeitos sobre os aparelhos cardiovascular e respiratório da anestesia inalatória com isoflurano em 3 (três) concentrações fixas (1, 1 ,5 e 2 CAM) no cão. Foram utilizados 6 (seis) cães machos, pesando 25 ± 2, 7 kg, com valores hematológicos e bioquímicas dentro da faixa de normalidade. Os parâmetros analisados foram: frequência cardíaca (FC), pressão arterial sistólica (PS), diastólica (PD) e média (PM), débito cardíaco (DC), índice cardíaco (IC), frequência respiratória (FR),volume corrente (VC) e volume minuto (VM). Observou-se que, baixas concentrações de isoflurano (1 e 1,5 CAM) produziram um aumento de FC. Com relação à pressão arterial, verificou-se um decréscimo dose-dependente, causado pela diminuição da resistência vascular periférica, o que explicaria a manutenção do DC e IC em baixas concentrações (1 e 1,5 CAM). A 2 CAM de concentração, o aumento da FC não foi capaz de compensar o menor volume de ejeção do coração. Devido a isso, observou-se queda do DC e IC. No sistema respiratório, encontrou-se diminuição da FR, VC e VM, dose-dependente.

Cardiovascular and pulmonary effexts of isoflurane anesthesia at 1, 1 ,5 and 2 minimum alveolar concentration (MAC) were studies in 6 male dogs, healty, weighting 25 ± 2.7 kg. Heart rate (HR), systolic arterial pressure (SAP), dyastolic arterial pressure rate (RR), tidal volume (TV) and minute ventilation (MV) were measured. Low isoflurane concentrations (1 and 1,5 MAC) increased the heart rate (HR). Arterial blood pressure decreased as the MAC increased, explaining the maintenance of the CO and the Cl at low concentrations of isoflurane (1 and 1,5 MAC). At 2 MAC the increase of the HR is not enough to compensate the low heart stroke volume, soa drop of CO an Cl was obseved. A dose-dependent decrease of the RR, TV and MV was also obseved.