Case scenario: Increased end-tidal carbon dioxide: a diagnostic dilemma.

Department of Anesthesiology, University of California-Davis, Davis, CA 95616, USA.
Anesthesiology (Impact Factor: 6.17). 02/2010; 112(2):440-6. DOI: 10.1097/ALN.0b013e3181ca7c38
Source: PubMed
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    ABSTRACT: /st>The objective of this study was to determine whether assessment of stroke volume (SV) and measurement of exhaled end-tidal carbon dioxide $({\small{\rm E}}{^{\prime}_{{\rm C}{{\rm O}_2}}})$ during an end-expiratory occlusion (EEO) test can predict fluid responsiveness in the operating theatre. /st>Forty-two subjects monitored by oesophageal Doppler who required i.v. fluids during surgery were studied. Haemodynamic variables [heart rate, non-invasive arterial pressure, SV, cardiac output (CO), respiratory variation of SV (ΔrespSV), variation of SV during EEO, and ${\small{\rm E}}{^{\prime}_{{\rm C}{{\rm O}_2}}}$] were measured at baseline, during EEO (ΔEEO), and after fluid expansion. Responders were defined by an increase in SV over 15% after infusion of 500 ml of crystalloid solution. /st>Of the 42 subjects, 28 (67%) responded to fluid infusion. A cut-off of >2.3% ΔSVEEO predicted fluid responsiveness with an area under the receiver-operating characteristic (AUC) curve of 0.78 [95% confidence interval (95% CI): 0.63-0.89, P=0.003]. The AUC of ΔrespSV was 0.89 (95% CI: 0.76-0.97, P<0.001). With an AUC of 0.68 (95% CI: 0.51-0.81, P=0.07), $\Delta {\small{\rm E}}{^{\prime}_{{\rm C}{{\rm O}_{2{\rm EEO}}}}}$ was poorly predictive of fluid responsiveness. /st>ΔSVEEO and $\Delta {\small{\rm E}}{^{\prime}_{{\rm C}{{\rm O}_2}}}$ were unable to accurately predict fluid responsiveness during surgery.
    BJA British Journal of Anaesthesia 03/2014; 112(6). DOI:10.1093/bja/aet582 · 4.35 Impact Factor
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    03/2013; 2013(1):44-62. DOI:10.5339/gcsp.2013.7
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    ABSTRACT: Malignant hyperthermia is a potentially lethal inherited disorder characterized by disturbance of calcium homeostasis in skeletal muscle. Volatile anesthetics and/or the depolarizing muscle relaxant succinylcholine may induce this hypermetabolic muscular syndrome due to uncontrolled sarcoplasmic calcium release via functionally altered calcium release receptors, resulting in hypoxemia, hypercapnia, tachycardia, muscular rigidity, acidosis, hyperkalemia, and hyperthermia in susceptible individuals. Since the clinical presentation of malignant hyperthermia is highly variable, survival of affected patients depends largely on early recognition of the symptoms characteristic of malignant hyperthermia, and immediate action on the part of the attending anesthesiologist. Clinical symptoms of malignant hyperthermia, diagnostic criteria, and current therapeutic guidelines, as well as adequate management of anesthesia in patients susceptible to malignant hyperthermia, are discussed in this review.
    Therapeutics and Clinical Risk Management 05/2014; 10:355-362. DOI:10.2147/TCRM.S47632 · 1.34 Impact Factor


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