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1.
Anesth Analg ; 109(6): 1823-30, 2009 Dec.
Article in English | MEDLINE | ID: mdl-19923509

ABSTRACT

BACKGROUND: The intravascular volume of surgical patients should be optimized to avoid complications associated with both overhydration and underresuscitation. In patients undergoing intraoperative acute normovolemic hemodilution, we investigated whether stroke volume variation (SVV) derived from an arterial pressure-based cardiac output (CO) monitor system (FloTrac/Vigileo, Edwards Lifesciences, Irvine, CA) tracked the changes associated with blood removal and replacement. We further evaluated the correlations between SVV and 3-dimensional (3D) transesophageal echocardiographic (TEE) left ventricular (LV) volume measurements. METHODS: Twenty-five patients had procedures during which acute normovolemic hemodilution was a planned part of the intraoperative management. We defined 7 measurement timepoints: baseline, after the removal of 5%, 10%, and 15% of the estimated blood volume (EBV) and after replacement with an equal volume of 6% hetastarch to -10%, -5%, and baseline EBV. At each timepoint, heart rate and systolic, diastolic, and mean arterial blood pressure were obtained from standard monitors, CO and SVV measurements were obtained from the FloTrac/Vigileo monitor, and TEE images were recorded for subsequent off-line reconstruction and determination of LV end-systolic and end-diastolic volumes. For statistical evaluations, we used a mixed models analysis of variance and Dunnett's test for post hoc comparisons with baseline values. Pearson's correlation was used to examine the relationships between SVV and LV volume. RESULTS: Analysis of variance demonstrated no significant change in heart rate or mean arterial blood pressure over the duration of study. CO decreased from 4.9 +/- 0.3 to 4.5 +/- 0.3 L/min after removal of 15% of the EBV and then increased to a final value of 5.4 +/- 0.3 L/min after replacement of 15% of the EBV. SVV increased from 9.2% +/- 0.9% to 20.3% +/- 2.0% (P < 0.001) after removal of 15% of the EBV and returned to a final value of 7.2% +/- 0.9% after replacement of 15% of the EBV. The indexed LV end-diastolic volume decreased from 42.1 +/- 8.3 to 36.9.3 +/- 8.3 mL/m(2) (P < 0.001) after removal of 15% of the EBV and then returned to a final volume of 45.9 +/- 10.3 mL/m(2) after replacement of 15% of the EBV. The measurements of SVV correlated inversely with the 3D TEE LV volume measurements. CONCLUSIONS: The SVV derived from the FloTrac/Vigileo system changes significantly as blood is removed and replaced during hemodilution. These changes correlate with 3D TEE measurements of LV volume. The utility of SVV in guiding optimization of intravascular volume merits further study.


Subject(s)
Hemodilution , Hydroxyethyl Starch Derivatives/administration & dosage , Monitoring, Intraoperative , Plasma Substitutes/administration & dosage , Stroke Volume/drug effects , Ventricular Function, Left/drug effects , Blood Pressure/drug effects , Blood Pressure Determination , Blood Pressure Monitors , Cardiac Output/drug effects , Echocardiography, Transesophageal , Elective Surgical Procedures , Electrocardiography , Female , Heart Rate/drug effects , Heart Ventricles/diagnostic imaging , Heart Ventricles/drug effects , Humans , Intraoperative Care , Male , Middle Aged , Monitoring, Intraoperative/instrumentation , Monitoring, Intraoperative/methods , Predictive Value of Tests , Prospective Studies , Time Factors
2.
Anesth Analg ; 108(5): 1531-7, 2009 May.
Article in English | MEDLINE | ID: mdl-19372332

ABSTRACT

BACKGROUND: We investigated the actions of propofol and isoflurane on nociceptive responses of neurons in the spinal cord. METHODS: We determined nociceptive responses of lumbar neurons in the dorsal horn (<1200 microm) and ventral horn (>1200 microm) of decerebrate rats before and during propofol (1 effective dose, ED(50)) or isoflurane (1 minimum alveolar concentration) anesthesia. During recording of ventral horn neurons, we administered picrotoxin by infusion to determine whether isoflurane and propofol differed in their effects at the gamma aminobutyric acid (GABA) Type A receptors. We also determined whether decerebration altered propofol requirements to produce immobility. RESULTS: Decerebration did not affect propofol requirements. The ED(50) for propofol was 497 +/- 58 microg x kg(-1) x min(-1) in intact rats and 420 +/- 65 microg x kg(-1) x min(-1) in decerebrated rats (P > 0.05), with corresponding propofol blood concentrations of 8.1 +/- 1.1 microg/mL and 7.3 +/- 1.1 microg/mL, respectively (P > 0.05). Propofol did not significantly depress dorsal horn neurons, but isoflurane depressed the responses to 56% of control (P < 0.05). Propofol depressed ventral horn neurons to 47% of control, whereas isoflurane depressed ventral horn neurons to 20% of control. Picrotoxin significantly reversed the depressant effect of propofol on ventral horn neuronal responses (79% of control, not significantly different from control). Pic- rotoxin, however, had no effect on isoflurane's depression of ventral horn neuronal responses (26% of control). CONCLUSIONS: Propofol acts in the spinal cord to produce immobility. This depressive effect occurs in the ventral horn and is mediated mainly by GABA(A) receptors. Isoflurane also depresses neurons in the ventral horn; however, isoflurane actions at the GABA(A) receptor are either weak or overridden by other effects in the ventral horn.


Subject(s)
Anesthetics, Intravenous/administration & dosage , Anterior Horn Cells/drug effects , Immobilization , Movement/drug effects , Propofol/administration & dosage , gamma-Aminobutyric Acid/metabolism , Action Potentials , Anesthetics, Inhalation/administration & dosage , Animals , Anterior Horn Cells/metabolism , Decerebrate State , GABA Antagonists/administration & dosage , Isoflurane/administration & dosage , Male , Pain Threshold/drug effects , Picrotoxin/administration & dosage , Posterior Horn Cells/drug effects , Posterior Horn Cells/metabolism , Rats , Rats, Sprague-Dawley , Receptors, GABA-A/drug effects , Receptors, GABA-A/metabolism
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