The correlation of heart rate between natural sleep and dexmedetomidine sedation / 대한마취과학회지

BACKGROUND@#Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation.@*METHODS@#The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection.@*RESULTS@#During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09).@*CONCLUSIONS@#There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.

Big data differential analysis of microglial cell responses in neurodegenerative diseases / 대한해부학회지

The correlation of heart rate between natural sleep and dexmedetomidine sedation / 대한마취과학회지

BACKGROUND: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. METHODS: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. RESULTS: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). CONCLUSIONS: There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.

A comparison of systolic and diastolic time variation with pulse pressure variation as a predictor of fluid responsiveness during pediatric liver transplantation

BACKGROUND: In pediatric patients, dynamic preload indices to predict fluid responsiveness remain controversial. Because each beat of blood pressure (BP) - waveform - contains evidence of a systolic and diastolic time interval (STI, DTI), we compared pulse pressure variation (PPV) with respiratory STI and DTI variation (STV, DTV) as predictors of fluid responsiveness during pediatric liver transplantation. METHODS: A total of 61 datasets from 16 pediatric liver transplant patients (age range one month to seven years), before and after an inferior vena cava clamp was applied, were retrospectively evaluated from electronically archived BP and central venous pressure (CVP) waveforms. STI and DTI were separated by a beat-to-beat blood pressure waveform. STV, DTV and PPV were calculated by averaging three consecutive respiratory cycles. Averaged CVP was used as a static preload index. A PPV threshold of > or =16%, a known cutoff value in pediatric surgery, was used to discriminate fluid responsiveness in the receiver operating characteristic (ROC) curve analysis. RESULTS: PPV showed correlations with STV and DTV (r = 0.65 and 0.57, P < 0.001, respectively), but not with CVP (r = -0.30, P = 0.079). The area under the ROC curves (AUC) of STV, DTV and CVP were 0.834, 0.872, and 0.613, respectively. Cut-off values of STV and DTV were 7.7% (sensitivity/specificity, 0.80/0.83) and 7.7% (sensitivity/specificity, 0.70/0.88), respectively. CONCLUSIONS: This study demonstrates that STV and DTV from a BP waveform showed the potential to predict fluid responsiveness as a surrogate of PPV during pediatric surgery.

Sudden cardiovascular collapse after platelet transfusion during liver transplantation: flat-line thromboelastometry and inferred pulmonary thromboembolism: A case report

Despite the well-known bleeding diathesis in patients with end-stage liver disease, inappropriate hypercoagulation is also emerging as a major concern. Pulmonary thromboembolism (PTE) is a major cause of perioperative morbidity and mortality during liver transplantation (LT). Flat-line thromboelastography is reported to predict PTE during LT. In this case, a 52-year-old woman with hepatocellular carcinoma underwent living-related LT. During the pre-anhepatic phase, one unit of apheresis platelets was transfused because of thrombocytopenia (32,000 /ml). After 20 minutes, blood pressure became unstable and circulatory collapse suddenly developed. In the middle of cardiopulmonary resuscitation, transesophageal echocardiography was immediately conducted, which revealed flail thrombi in the right atrium. Rotational thromboelastometry (ROTEM) conducted at that time was surprisingly flat in 4 channels, contradictory to the finding of hypercoagulation. This finding lead to a management dilemma during LT. Flattening in ROTEM requires caution in interpretation of severe hypocoagulation or ongoing PTE.

G protein-coupled receptor, family C, group 5 (GPRC5B) downregulation in spinal cord neurons is involved in neuropathic pain / 대한마취과학회지

BACKGROUND: G protein-coupled receptor, family C, group 5 (GPRC5B), a retinoic acid-inducible orphan G-protein-coupled receptor (GPCR), is a member of the group C metabotropic glutamate receptor family proteins presumably related in non-canonical Wnt signaling. In this study, we investigated altered GPRC5B expression in the dorsal horn of the spinal cord after spinal nerve injury and its involvement in the development of neuropathic pain. METHODS: After induction of anesthesia by intraperitoneal injection of pentobarbital (35 mg /kg), the left L5 spinal nerve at the level of 2 mm distal to the L5 DRG was tightly ligated with silk and cut just distal to the ligature. Seven days after nerve injury, animals were perfused with 4% paraformaldehyde, and the spinal cords were extracted and post-fixed at 4degrees C overnight. To identify the expression of GPRC5B and analyze the involvement of GPRC5B in neuropathic pain, immunofluorescence was performed using several markers for neurons and glial cells in spinal cord tissue. RESULTS: After L5 spinal nerve ligation (SNL), the expression of GPRC5B was decreased in the ipsilateral part, as compared to the contralateral part, of the spinal dorsal horn. SNL induced the downregulation of GPRC5B in NeuN-positive neurons in the spinal dorsal horn. However, CNPase-positive oligodendrocytes, OX42-positive microglia, and GFAP-positive astrocytes were not immunolabeled with GPRC5B antibody in the spinal dorsal horn. CONCLUSIONS: These results imply that L5 SNL-induced GPRC5B downregulation may affect microglial activation in the spinal dorsal horn and be involved in neuropathic pain.