Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2003
Clinical TrialPulse contour analysis for cardiac output monitoring in cardiac surgery for congenital heart disease.
Conventional methods of cardiac output monitoring using pulmonary artery catheters may not be feasible in patients with congenital heart disease because of patients' small size or aberrant anatomy. We studied the accuracy of a new device, which uses pulse contour analysis to measure continuous cardiac output, in children and adults undergoing congenital heart surgery. Sixteen patients, median ages 7 yr old, were included in this prospective study. One-hundred-ninety-one data points were obtained in the pre- and postcardiopulmonary bypass periods and in the first 12 h after intensive care unit admission. We evaluated the relationship between cardiac index (CI) derived from transpulmonary thermodilution (TDCI) and CI derived from pulse contour analysis (PCCI). Bias and limits of agreement between TDCI and PCCI over all time periods were 0.1 +/- 1.94, indicating a wide dispersion of the data. Coefficient of correlation (r) between the TDCI and PCCI was 0.7. Although in previous studies, PCCI has been suggested to be accurate in adult cardiac surgery, we found it to be less reliable in our study patients, even after shunt correction. The relationships of the volume and pressure based measures of preload, intrathoracic blood volume index (ITBI), and central venous pressure with CI were also investigated. After repair, correlation (r) between PCCI or TDCI and ITBI (0.56 and 0.71, respectively) was better than that between PCCI or TDCI and CVP (0.16 and 0.11, respectively), indicating greater validity of ITBI as a measure of preload. ⋯ Our results suggest that the pulse contour analysis cardiac output (CO) monitoring in patients undergoing congenital heart surgery may not provide as accurate or reliable measures of CO as previously suggested. The volume-based variable of preload intrathoracic blood volume index (ITBI) has better correlation with cardiac index (CI) than the central venous pressure, suggesting that ITBI may be a better indicator of preload.
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Anesthesia and analgesia · Nov 2003
Case ReportsIntrathecal clonidine and severe hypotension after cardiopulmonary bypass.
The use of intrathecal clonidine as an adjunct for the management of chronic pain, intra- and postoperative analgesia is gaining an increase in popularity. However, antinociceptive doses of intrathecal clonidine may produce pronounced hemodynamic side effects, including hypotension and bradycardia. ⋯ We postulate that the intrathecally administered alpha 2-agonist clonidine reduced our patient's ability to tolerate the hemodynamic lability that is present during the separation from cardiopulmonary bypass by potentially inhibiting sympathetic nervous system activity, renin-angiotensin system, or vasopressin release. The authors report a case of severe hypotension after cardiopulmonary bypass in a patient receiving intrathecal clonidine infusion for chronic neuropathic pain.
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Anesthesia and analgesia · Nov 2003
The cardioprotective effect of sevoflurane depends on protein kinase C activation, opening of mitochondrial K(+)(ATP) channels, and the production of reactive oxygen species.
Several studies suggest that the cardioprotective effect of sevoflurane depends on protein kinase C (PKC) activation, mitochondrial K(+)(ATP) channel (mitoK(+)(ATP)) opening, and reactive oxygen species (ROS). However, evidence for their involvement was obtained in separate experimental models. Here, we studied the relative roles of PKC, mitoK(+)(ATP), and ROS in sevoflurane-induced cardioprotection in one model. Rat trabeculae were subjected to simulated ischemia by applying metabolic inhibition (MI) through buffer containing NaCN, followed by 60-min reperfusion. Recovery of active force (F(a)) was assessed as percentage of pre-MI force. In time controls, F(a) amounted 60% +/- 5% at the end of the experiment. The recovery of F(a) after MI was reduced to 28% +/- 5% (P = 0.045 versus time control), whereas sevoflurane reversed the detrimental effect of MI (F(a) recovery, 67% +/- 8%; P = 0.01 versus MI). The PKC inhibitor chelerythrine, the mitoK(+)(ATP) inhibitor 5-hydroxy decanoic, and the ROS scavenger N-(2-mercaptopropionyl)-glycine all completely abolished the protective effect of sevoflurane (recovery of F(a), 31% +/- 8%, 33% +/- 8%, and 24% +/- 9% for chelerythrine, 5-hydroxy decanoic, and N-(2-mercaptopropionyl)-glycine, respectively). In conclusion, PKC activation, mitoK(+)(ATP) channel opening, and ROS production are all essential for sevoflurane-induced cardioprotection. These signaling events are arranged in series within a common signaling pathway, rather than in parallel cascades. Our findings implicate that the perioperative use of sevoflurane preserves cardiac function by preventing ischemia-reperfusion injury. ⋯ Protein kinase C, mitochondrial K(+)(ATP) channels and reactive oxygen species act within one downstream signaling pathway in mediating the cardioprotective effect of sevoflurane.