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DK2985_C000 1..28 - AlSharqia Echo Club

DK2985_C000 1..28 - AlSharqia Echo Club

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296 Transesophageal <strong>Echo</strong>cardiography(A)TMF(B)PVFSDEAPPV INSPIRATIONPPV INSPIRATION(C)RVOT(D)TAVS tE tA tPPV INSPIRATIONPPV INSPIRATIONFigure 13.14 Effect of positive-pressure ventilation (PPV) on the Doppler transmitral flow (TMF) (A), pulmonary venous flow (PVF)(B), right ventricular outflow tract (RVOT) velocity obtained from a deep transgastric view (C) and tricuspid annular velocities (TAV)(D) in a 58-year-old man. Note the reduction in systolic velocities in all four Doppler signals with positive-pressure inspiration displayedfrom simultaneous respirograms.agents and intravenous anesthetics, as they may influencecardiac function and echocardiographic measurements.Reduction in myocardial contractility induced by theadministration of volatile anesthetic agents may not bedetected with the conventional ventricular performanceindices such as FAC and circumferential fiber shortening(Vcf). The use of pressure–dimension indices such asthe end-systolic elastance (Ees) and preload recruitablestroke force (PRSF) are more sensitive to reductions inmyocardial contractility, but their measurements are considerablymore complex than the traditional indices ofmyocardial performance (30).1. Inhalation AgentsAll the inhalation anesthetics produce dose-related negativeinotropic effects. Enflurane and halothane depressmyocardial contractility to a similar extent but moreseverely than isoflurane, desflurane and sevoflurane. Arapid increase in desflurane concentration may howeverstimulate the sympathetic nervous system and temporarilymask its negative inotropic effect, inducing an increase inheart rate. Moreover, enflurane and halothane also inducean increase in left ventricular filling pressure. (Effects ofinhalational anesthetics on systemic hemodynamics andthe coronary circulation. In: Kaplan JA, ed. CardiacAnesthesia. 4th ed. Chapter 16. WB Saunders Company,1999.) In abnormal hearts, indices of contractility appearmore sensitive to a given concentration of a volatileanesthetic than in normal hearts. Nitrous oxide has aweak direct myocardial depressant action that may becounterbalanced by sympathetic activation.There is a lack of noninvasive-derived data regardingthe effects of potent volatile anesthetic agents on diastolicfunction. Using invasive measurements of diastolicfunction, halothane and enflurane seem to prolong the isovolumicrelaxation period and increase chamber stiffnesswhile isoflurane, sevoflurane and desflurane prolong the

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