Evaluation of pimobendan effect on sublingual microcirculation in an experimental pharmacology induced hypotension porcine model.

New therapeutic approaches are needed to simultaneously resuscitate macro- and microcirculation during circulatory shock. The aims of this study were to explore the microcirculatory and macrocirculatory effects of pimobendan, an inodilator with dual phosphodiesterase 3 inhibitor and calcium-sensitizing effects, in an experimental porcine model of pharmacologically induced hypotension associating vasoplegia and decreased cardiac output. Eight piglets were anesthetized and monitored for their hemodynamic parameters. Hypotension was induced by sevoflurane overdose until a mean arterial pressure between 40 and 45 mmHg was reached. A bolus of pimobendan (0.25 mg/kg) was administered intravenously thereafter. Sublingual microcirculation was evaluated using a Sidestream Dark Field imaging device. Hemodynamic and microcirculatory parameters were recorded at the baseline period (A), immediately before pimobendan administration (B) and after pimobendan administration (C). Induction of hypotension was associated with a decreased cardiac index and microcirculation alterations. Pimobendan administration was associated with a significant increase in heart rate, cardiac index and decrease in systemic vascular resistance index. A significant increase in proportion of perfused vessels for all vessels (+8%, [2; 14], P = 0.01) and small vessels (+8% [1; 14], P = 0.03), in microvascular flow index (+0.31 AU, [0.04; 0,58], P = 0.03) were noticed, as well as a decrease in heterogeneity index (-0.34 [-0.66; -0.03], P = 0.04) and De Backer score for all vessels (-1.04, [-1.82; -0.25], P = 0.02). In conclusion, in a simple model of pharmacologically induced hypotension, pimobendan was associated with an improvement in several microcirculatory parameters.

Evaluation of gastric and bladder tonometry as indicators of tissue perfusion in induced hypotension in dogs.

OBJECTIVE: To evaluate the use of gastric (PgCO2 ) and bladder (PbCO2 ) tonometry for assessing tissue hypoperfusion in dogs during sevoflurane-induced hypotension, and to compare these measurements with delivery of oxygen, arterial oxygen content, and plasma lactate concentration. DESIGN: Prospective experimental trial. SETTING: University veterinary teaching hospital. ANIMALS: Fourteen adult Beagle dogs. INTERVENTIONS: Anesthetic induction was performed by mask with sevoflurane and oxygen. Heart rate, direct arterial pressures, respiratory rate, and end-tidal carbon dioxide were recorded; arterial blood samples were taken to measure blood gases, and venous samples were sampled to measure plasma lactate. A tonometric catheter was introduced into the stomach to measure PgCO2 . Samples of saline from the balloon of a Foley catheter placed in the bladder were collected every 10 minutes and used to measure PbCO2 by gas analysis. Tonometry measurements, plasma lactate, and oxygen delivery and consumption were compared at 3 time points: at baseline, during hypotension, and during treatment periods. A hypotensive period (mean arterial pressure (MAP) < 60 mm Hg) of 15 minutes was induced by an overdose of sevoflurane, whereas during the treatment period, a constant-rate infusion of dopamine (10 µg/kg/min) was administered intravenously for 40 minutes. MEASUREMENTS AND MAIN RESULTS: Values for PgCO2 and PbCO2 increased significantly during the hypotensive period, and correlations were found between these values and the delivery of oxygen. Gastric tonometry values had stronger correlations compared with bladder tonometry values. CONCLUSIONS: Gastric and bladder tonometry can be used to detect hypoperfusion. Further studies are warranted to determine the potential use of gastric and bladder tonometry in assessing dogs in clinical situations.

Fluid Management in Patients with Trauma: Restrictive Versus Liberal Approach.

Massive hemorrhage remains a major cause of traumatic deaths. The ideal fluid resuscitative strategy is much debated. Research has provided inconsistent results regarding which fluid strategy is ideal; the optimum fluid type, timing, and volume remains elusive. Aggressive large-volume resuscitation has been the mainstay based on controlled hemorrhage animal models. For uncontrolled hemorrhagic shock, liberal fluid resuscitative strategies exacerbate the lethal triad, invoke resuscitative injury, and increase mortality while more restrictive fluid strategies tend to ameliorate trauma-induced coagulopathy and favor a greater chance of survival. This article discusses the current evidence regarding liberal and restrictive fluid strategies for trauma.

Resucitación hipotensiva en el paciente politraumatizado con shock hemorrágico / Hypotensive resuscitation of the polytrauma patient with hemorrhagic shock

El shock hemorrágico constituye una importante causa de mortalidad en nuestro medio. A pesar de ello en los últimos 40 años ha habido pocos cambios en su tratamiento en el periodo previo a la hemostasia quirúrgica definitiva. El actual estándar de tratamiento, la reanimación con fluidos que busca la normotensión y normovolemia, se basa en trabajos con modelos animales de los años 50 y 60, que se resumen en esta publicación. En las últimas tres décadas han surgido nuevos modelos de shock hemorrágico experimentales más parecidos a las situaciones reales, basados en una hemorragia “incontrolada”. Estos estudios han demostrado un aumento de la supervivencia cuando se permite una hipotensión moderada durante este tipo de shock en pacientes politraumatizados. Esta terapéutica se denomina reanimación (resucitación) hipotensiva. Finalmente se revisan los ensayos clínicos publicados sobre la reanimación hipotensiva en el shock hemorrágico, así como otros indirectamente relacionados. Los autores consideramos la reanimación hipotensiva como una opción de tratamiento tanto extrahospitalaria como intrahospitalaria, prometedora en el shock hemorrágico, pero creemos necesarios más ensayos clínicos sobre el tema para convertirla en un estándar de tratamiento(AU)

Hemorrhagic shock is a significant cause of death in hospital practice, yet the management of this event in the period prior to definitive surgical hemostasis has changed little in 40 years. Currently, the standard treatment of resuscitation by means of fluid therapy to re-establish normal pressure and volume is based on animal models from the 1950s and 1960s; these studies will be reviewed in this article. However, new experimental models of hemorrhagic shock that have emerged in the last 3 decades are based on uncontrolled bleeding and are more similar to real-life situations. Recent studies using these models have demonstrated increased survival when polytrauma patients with hemorrhagic shock are deliberately allowed to remain in a moderate level of hypotension, a strategy referred to as hypotensive resuscitation. Finally, we review clinical trials of hypotensive resuscitation in hemorrhagic shock as well as studies indirectly related to this management approach. We conclude that hypotensive resuscitation is a promising treatment for use in cases of hemorrhagic shock that occur either in or out of hospital; however, we believe that more trials should be done before it can be considered a standard treatment(AU)

Induction of equine postanesthetic myositis after halothane-induced hypotension.

Wick catheters were used to measure intracompartmental pressures of the extensor carpi radialis muscles and long heads of the triceps brachii muscles of 7 horses maintained under halothane anesthesia during controlled ventilation. Horses were positioned in left lateral recumbency on a water bed for 4 hours. Using a crossover design, 6 of the 7 horses were subjected to normotensive and hypotensive anesthesia on separate occasions. Hypotension was achieved by increasing the inspired halothane concentration. Hematologic and biochemical measurements were determined at designated intervals before, during, and for 7 days after each anesthetic episode. Under hypotensive conditions, 2 horses developed severe generalized myositis and were euthanatized. Three of the 5 other horses developed swelling of the downside masseter muscle, 4 demonstrated mild extensor deficits of the downside forelimb, and 1 had a severe extensor deficit of the uppermost hind limb. As a group, the hypotensive horses had markedly increased activities of serum enzymes (creatine kinase, aspartate transaminase, and blood lactate) and abnormalities in calcium-phosphorus homeostasis. Lameness or enzyme alterations were not observed in normotensive horses. Although the intracompartmental pressure values were markedly increased in the muscle bellies of the compressed limbs of all horses, there was a statistically significant difference in intracompartmental pressures between the downside or compressed muscle compartments of the extensor carpi radialis of hypotensive and normotensive horses. High concentrations of halothane may predispose anesthetized horses to postanesthetic myositis, even when protective padding is used. Intracompartmental muscle pressure, as measured by the wick catheter, may not be a reliable predictor of equine postanesthetic lameness.

Effects of dexamethasone and surgical hypotension on the stomach of dogs: clinical, endoscopic, and pathologic evaluations.

Effects of dexamethasone and surgical hypotension on the gastric mucosa of 15 dogs was evaluated by clinical, endoscopic, and pathologic studies. Dexamethasone produced acute reddening of the gastric mucosa with frank hemorrhage, digested blood, and possible gastric erosions, whereas dogs treated by surgical hypotension did not have marked changes in the gastric mucosa. Gastrointestinal disease observed in dogs with spontaneous spinal cord injury that were given dexamethasone and decompressive spinal surgery was not produced. The role of corticosteroids and surgical hypotension in the pathogenesis of gastric lesions and the potential for spinal cord injury to produce gastrointestinal disease is discussed.