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      Anesthesia advanced circulatory life support Translated title: Réanimation circulatoire avancée en anesthésie

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          Abstract

          Purpose

          The constellation of advanced cardiac life support (ACLS) events, such as gas embolism, local anesthetic overdose, and spinal bradycardia, in the perioperative setting differs from events in the pre-hospital arena. As a result, modification of traditional ACLS protocols allows for more specific etiology-based resuscitation.

          Principal findings

          Perioperative arrests are both uncommon and heterogeneous and have not been described or studied to the same extent as cardiac arrest in the community. These crises are usually witnessed, frequently anticipated, and involve a rescuer physician with knowledge of the patient’s comorbidities and coexisting anesthetic or surgically related pathophysiology. When the health care provider identifies the probable cause of arrest, the practitioner has the ability to initiate medical management rapidly.

          Conclusions

          Recommendations for management must be predicated on expert opinion and physiological understanding rather than on the standards currently being used in the generation of ACLS protocols in the community. Adapting ACLS algorithms and considering the differential diagnoses of these perioperative events may prevent cardiac arrest.

          Résumé

          Objectif

          Le grand ensemble d’événements liés à la réanimation cardiaque avancée (ACLS) tels que les embolies gazeuses, les surdosages d’anesthésiques locaux et la bradycardie sinusale dans un contexte périopératoire est différent des événements que l’on observe à l’extérieur de l’hopital. En conséquence, une modification des protocoles traditionnels d’ACLS permet une réanimation plus spécifique, en fonction de l’étiologie.

          Constatations principales

          Les arrêts cardiaques en période périopératoire sont à la fois rares et hétérogènes; ils n’ont pas été décrits ou étudiés avec la même ampleur que les arrêts cardiaques survenant hors de l’hôpital. Ces crises sont habituellement vécues en direct, souvent anticipées et impliquent l’intervention d’un médecin connaissant les comorbidités du patient ainsi que la physiopathologie en rapport avec l’intervention et les anesthésiques utilisés. Lorsque le professionnel de la santé identifie la cause probable de l’arrêt cardiaque, le praticien a la possibilité d’entreprendre rapidement une prise en charge médicale.

          Conclusions

          Des recommandations pour la prise en charge doivent être fondées sur les avis d’experts et sur la compréhension de la physiologie plutôt que sur des normes actuellement utilisées pour la création de protocoles d’ACLS hors du milieu hospitalier. L’adaptation des algorithmes d’ACLS et la prise en compte des diagnostics différentiels de ces événements périopératoires peuvent prévenir les arrêts cardiaques.

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          Most cited references 115

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          Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature.

          : A systematic review of the literature to determine the ability of dynamic changes in arterial waveform-derived variables to predict fluid responsiveness and compare these with static indices of fluid responsiveness. The assessment of a patient's intravascular volume is one of the most difficult tasks in critical care medicine. Conventional static hemodynamic variables have proven unreliable as predictors of volume responsiveness. Dynamic changes in systolic pressure, pulse pressure, and stroke volume in patients undergoing mechanical ventilation have emerged as useful techniques to assess volume responsiveness. : MEDLINE, EMBASE, Cochrane Register of Controlled Trials and citation review of relevant primary and review articles. : Clinical studies that evaluated the association between stroke volume variation, pulse pressure variation, and/or stroke volume variation and the change in stroke volume/cardiac index after a fluid or positive end-expiratory pressure challenge. : Data were abstracted on study design, study size, study setting, patient population, and the correlation coefficient and/or receiver operating characteristic between the baseline systolic pressure variation, stroke volume variation, and/or pulse pressure variation and the change in stroke index/cardiac index after a fluid challenge. When reported, the receiver operating characteristic of the central venous pressure, global end-diastolic volume index, and left ventricular end-diastolic area index were also recorded. Meta-analytic techniques were used to summarize the data. Twenty-nine studies (which enrolled 685 patients) met our inclusion criteria. Overall, 56% of patients responded to a fluid challenge. The pooled correlation coefficients between the baseline pulse pressure variation, stroke volume variation, systolic pressure variation, and the change in stroke/cardiac index were 0.78, 0.72, and 0.72, respectively. The area under the receiver operating characteristic curves were 0.94, 0.84, and 0.86, respectively, compared with 0.55 for the central venous pressure, 0.56 for the global end-diastolic volume index, and 0.64 for the left ventricular end-diastolic area index. The mean threshold values were 12.5 +/- 1.6% for the pulse pressure variation and 11.6 +/- 1.9% for the stroke volume variation. The sensitivity, specificity, and diagnostic odds ratio were 0.89, 0.88, and 59.86 for the pulse pressure variation and 0.82, 0.86, and 27.34 for the stroke volume variation, respectively. : Dynamic changes of arterial waveform-derived variables during mechanical ventilation are highly accurate in predicting volume responsiveness in critically ill patients with an accuracy greater than that of traditional static indices of volume responsiveness. This technique, however, is limited to patients who receive controlled ventilation and who are not breathing spontaneously.
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            The respiratory variation in inferior vena cava diameter as a guide to fluid therapy.

            To investigate whether the respiratory variation in inferior vena cava diameter (DeltaD(IVC)) could be related to fluid responsiveness in mechanically ventilated patients. Prospective clinical study. Medical ICU of a non-university hospital. Mechanically ventilated patients with septic shock (n=39). Volume loading with 8 mL/kg of 6% hydroxyethylstarch over 20 min. Cardiac output and DeltaD(IVC) were assessed by echography before and immediately after the standardized volume load. Volume loading induced an increase in cardiac output from 5.7+/-2.0 to 6.4+/-1.9 L/min (P or =15% (responders). Before volume loading, the DeltaD(IVC) was greater in responders than in non-responders (25+/-15 vs 6+/-4%, P<0.001), closely correlated with the increase in cardiac output (r=0.82, P<0.001), and a 12% DeltaD(IVC) cut-off value allowed identification of responders with positive and negative predictive values of 93% and 92%, respectively. Analysis of DeltaD(IVC) is a simple and non-invasive method to detect fluid responsiveness in mechanically ventilated patients with septic shock.
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              Passive leg raising predicts fluid responsiveness in the critically ill.

              Passive leg raising (PLR) represents a "self-volume challenge" that could predict fluid response and might be useful when the respiratory variation of stroke volume cannot be used for that purpose. We hypothesized that the hemodynamic response to PLR predicts fluid responsiveness in mechanically ventilated patients. Prospective study. Medical intensive care unit of a university hospital. We investigated 71 mechanically ventilated patients considered for volume expansion. Thirty-one patients had spontaneous breathing activity and/or arrhythmias. We assessed hemodynamic status at baseline, after PLR, and after volume expansion (500 mL NaCl 0.9% infusion over 10 mins). We recorded aortic blood flow using esophageal Doppler and arterial pulse pressure. We calculated the respiratory variation of pulse pressure in patients without arrhythmias. In 37 patients (responders), aortic blood flow increased by > or =15% after fluid infusion. A PLR increase of aortic blood flow > or =10% predicted fluid responsiveness with a sensitivity of 97% and a specificity of 94%. A PLR increase of pulse pressure > or =12% predicted volume responsiveness with significantly lower sensitivity (60%) and specificity (85%). In 30 patients without arrhythmias or spontaneous breathing, a respiratory variation in pulse pressure > or =12% was of similar predictive value as was PLR increases in aortic blood flow (sensitivity of 88% and specificity of 93%). In patients with spontaneous breathing activity, the specificity of respiratory variations in pulse pressure was poor (46%). The changes in aortic blood flow induced by PLR predict preload responsiveness in ventilated patients, whereas with arrhythmias and spontaneous breathing activity, respiratory variations of arterial pulse pressure poorly predict preload responsiveness.
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                Author and article information

                Contributors
                +773-702-0182 , +773-834-0063 , moc5@dacc.uchicago.edu
                Journal
                Can J Anaesth
                Can J Anaesth
                Canadian Journal of Anaesthesia
                Springer-Verlag (New York )
                0832-610X
                1496-8975
                21 April 2012
                21 April 2012
                June 2012
                : 59
                : 6
                : 586-603
                Affiliations
                [1 ]Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, NY USA
                [2 ]Anesthesia Department, University of Florida, Gainesville, FL USA
                [3 ]American Anesthesiology of North Carolina/MEDNAX, Raleigh, NC USA
                [4 ]Department of Anesthesia and Critical Care, University of Chicago, 5841 S Maryland Ave, MC 4028, Chicago, IL 60637 USA
                Article
                9699
                10.1007/s12630-012-9699-3
                3345112
                22528163
                © The Author(s) 2012
                Categories
                Special Article
                Custom metadata
                © Canadian Anesthesiologists' Society 2012

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