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Objectives: The objectives of the present study were to evaluate, in patients with persistent arterial hypotension in the immediate postcardiac surgery period, the effects of norepinephrine infusion on ventriculo-arterial coupling, its determinants: arterial elastance and end-systolic ventricular elastance, and to test the ability of arterial elastance to end-systolic ventricular elastance ratio to predict stroke volume increases., Design: Prospective observational study., Setting: Cardiac-vascular surgical ICU., Patients: Twenty-eight postoperative cardiac surgery patients, in whom physicians decided to administer norepinephrine infusion, were included., Measurements and Main Results: Arterial pressure, stroke volume index, cardiac index, indexed total peripheral resistance, arterial compliance, arterial elastance, and end-systolic ventricular elastance, were measured before and after norepinephrine infusion. We estimated ventriculo-arterial coupling by the arterial elastance to end-systolic ventricular elastance ratio and defined stroke volume responders by a stroke volume increase greater than or equal to 15%. Twenty-two of the 28 subjects had altered ventriculo-arterial coupling (1.87 [1.57-2.51] vs 1.1 [1-1.18]). Fifteen of the 28 subjects (54%) were stroke volume responders. At baseline, stroke volume responders had similar arterial pressure, higher indexed total peripheral resistance, arterial elastance, arterial elastance to end-systolic ventricular elastance ratio (2.21 [1.69-2.89] vs 1.33 [1.1-1.56]; p < 0.05), and lower arterial compliance, indexed total peripheral resistance and cardiac index. Norepinephrine significantly increased arterial pressure in all subjects. In stroke volume responders, norepinephrine increased arterial elastance, end-systolic ventricular elastance, cardiac index, and improved arterial elastance/end-systolic ventricular elastance coupling. The baseline arterial elastance to end-systolic ventricular elastance ratio predicted stroke volume responsiveness (area under the curve [95% CI], 0.87 [0.71-1]; p < 0.0001)., Conclusions: In patients with arterial hypotension norepinephrine increased end-systolic ventricular elastance and arterial elastance. The effects of norepinephrine on stroke volume depend on baseline ventriculo-arterial coupling. Although norepinephrine infusion corrects arterial hypotension in all subjects, increase of stroke volume occurred only in subjects with altered ventriculo-arterial coupling.

Background: In contrast to other types of shock, anaphylactic shock decreases cerebral blood flow more than would be expected from severe arterial hypotension, thus potentially affecting survival through brain ischaemia/hypoxia. We hypothesised that epinephrine (EPI) used as a first-line treatment of anaphylactic shock and arginine vasopressin (AVP) proposed in case of EPI refractoriness may have different effects on brain oxygenation., Objectives: To compare the effect of EPI and AVP on brain oxygenation under similar macro-haemodynamic target values in an anaphylactic shock model., Design: Prospective laboratory study., Setting: University laboratory., Animals: Male brown Norway rats (n = 27)., Interventions: Twenty-seven rats were sensitised with ovalbumin (OVA). Twenty rats had anaphylactic shock induced with OVA and were resuscitated with either 0.9% saline (OVA group), EPI (EPI group) or AVP (AVP group). Sensitised control rats received only 0.9% saline and no OVA (CON group)., Main Outcome Measures: Mean arterial pressure (MAP), carotid artery blood flow (CaBF), cerebral cortical blood flow (CBF) and hippocampal oxygen partial pressure (PtiO2) were recorded., Results: All rats in the OVA group died within 15 min. EPI and AVP restored comparable levels of MAP, carotid artery blood flow and CBF, and extended survival time. EPI was associated with biologically relevant and significantly (P < 0.05) higher PtiO2 values (nadir values at 20 min: 25.0 ± 2.2 mmHg) compared with the AVP group (14.9 ± 2.0 mmHg). The slopes of the correlations of MAP vs. PtiO2 and CBF were significantly steeper with AVP (more pressure dependence) compared with EPI. By the end of the experiment, hippocampal PtiO2 values between the EPI (24.1 ± 2.1 mmHg) and the AVP (20.8 ± 2.0 mmHg) groups were similar., Conclusion: At early, but not at late time points, resuscitation of anaphylactic shock with EPI or AVP to similar MAP and CBF endpoints resulted in hippocampal PtiO2 being significantly higher after EPI. In addition, the PtiO2 after EPI always remained above the threshold for brain hypoxia, whereas PtiO2 after AVP was below the hypoxic threshold most of the time. Because of this early brain hypoxia, AVP may not be the drug of first choice for resuscitation of anaphylactic shock.

Recently, three case reports have suggested the possible efficacy of sugammadex in anaphylactic shock refractory to conventional treatment induced by rocuronium. We report a new case of severe anaphylactic reaction to rocuronium treated with sugammadex. After 18 minutes of conventional treatment because of persistent cardiocirculatory failure and bronchospasm, a bolus of 2000 mg (18 mg/kg) of sugammadex was injected. This was associated with rapid correction of arterial hypotension and bronchoconstriction. The underlying pathophysiological mechanisms that explain the potential beneficial effect of sugammadex in this context are unknown but it is important to know that refractory anaphylactic shock to rocuronium can be potentially corrected with sugammadex., (Copyright © 2011 Société française d'anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.)

Recent findings in human septic shock suggest that glucocorticosteroids can limit and even reverse hemodynamic disturbances and dependence on catecholamines. In a rodent model of hypotensive and hypokinetic septic shock, we investigated the effects of early or late dexamethasone administration on hemodynamics, response to catecholamines, and cardiac beta-adrenergic signalling. As compared with sham-operated rats, the untreated septic rats displayed significant arterial hypotension and reduced aortic blood flow. However, in vivo pressor response to epinephrine and phenylephrine was not different among sham and septic animals. Conversely, the chronotropic response to isoproterenol was significantly attenuated in septic animals. Steroid-treated septic animals displayed complete reversal of hypotension, improvement in aortic blood flow, and reduced plasma lactate and nitrite/nitrate concentrations as compared with untreated septic animals. The number of myocardial beta-adrenergic receptors and in vivo isoproterenol-stimulated myocardial cAMP content were similar in sham and septic animals. Glucocorticosteroids, although not changing these patterns, significantly decreased the receptors affinity when administered late, but not early. In this model of septic shock, hemodynamic abnormalities may not be related to adrenergic receptor desensitization. That steroids can improve them suggests that they could act mainly distal to adrenergic receptors, for instance, on myocardial and vascular smooth fiber contraction properties through mechanisms probably including inducible nitric oxide synthase inhibition.

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Copyright of IRBM is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Résumé: Objectifs: Décrire les aspects pratiques de l’entraînement électrosystolique (EES) post-chirurgie cardiaque via les électrodes épicardiques temporaires. Méthodologie: Synthèse des données publiées durant les cinq dernières années sur l’EES épicardique temporaire (indications, modes de stimulation, électrodes et stimulateurs utilisés). Les bases de données ScienceDirect et Pubmed ont été utilisées et les publications en langue française ou anglaise ont été analysées. Synthèse des données: L’EES épicardique temporaire permet le traitement des troubles conductifs et/ou du rythme graves post-chirurgie cardiaque, mais aussi l’optimisation hémodynamique par la modification de certains paramètres de stimulation. En pratique, l’EES épicardique temporaire consiste à choisir le meilleur mode de stimulation compte tenu du contexte (patient, intervention, troubles de la conduction) et à régler les paramètres de l’EES pour assurer : i) un fonctionnement optimal du dispositif ; ii) la préservation de la durée de vie des électrodes ; iii) un bénéfice hémodynamique maximal. La connaissance des réglages de l’EES, ainsi que la vérification régulière, au moins quotidienne, de ces paramètres et leur ajustement en fonction de l’évolution des seuils des électrodes s’inscrivent dans les bonnes pratiques. La littérature française manque toutefois de recommandations officielles pour l’EES épicardique temporaire. Conclusion: L’EES épicardique temporaire post-chirurgie cardiaque est une technique simple, plus efficace que la stimulation transcutanée et plus rapidement disponible que la stimulation interne. Les modalités de bonnes pratiques de l’EES doivent être connues de tous les opérateurs amenés à l’initier (anesthésistes-réanimateurs, chirurgiens cardiaques), ainsi que du personnel paramédical, pour éviter les risques liés à un fonctionnement suboptimal. Un protocole de bonne utilisation est proposé. [ABSTRACT FROM AUTHOR]

Abstract: Recently, three case reports have suggested the possible efficacy of sugammadex in anaphylactic shock refractory to conventional treatment induced by rocuronium. We report a new case of severe anaphylactic reaction to rocuronium treated with sugammadex. After 18minutes of conventional treatment because of persistent cardiocirculatory failure and bronchospasm, a bolus of 2000mg (18mg/kg) of sugammadex was injected. This was associated with rapid correction of arterial hypotension and bronchoconstriction. The underlying pathophysiological mechanisms that explain the potential beneficial effect of sugammadex in this context are unknown but it is important to know that refractory anaphylactic shock to rocuronium can be potentially corrected with sugammadex. [Copyright &y& Elsevier]