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OBJECTIVE@#To quantify the relationship between cerebral blood flow velocity and peripheral blood pressure during hypotension period, aiming to predict the brain hypotension before symptomatic occurrence.@*METHODS@#Twenty vasovagal syncope (VVS) patients who had a previous clinical history were selected in groups and 20 pair-matched control subjects underwent 70° tilt-up test. The subjects remained supine for 30 minutes before recordings when Doppler probes, electrodes and Finapres device were prepared. After continuous baseline recordings for 10 min, the subjects underwent head up tilt (HUT) test (70°), and were standing upright for 30 minutes or until syncope was imminent. For ethical reasons, the subjects were turned back to supine position immediately after SBP dropped to ≥20 mmHg, when their consciousness persisted. The point of syncope was synchronized for all the subjects by the point SBP reached the minima. Their beat-to-beat blood pressures (BP) were recorded continuously and bilateral middle cerebral artery (MCA) flow velocities were obtained with two 2 MHz Doppler probes from a transcranial Doppler ultrasonography (TCD) system. A nonlinear dynamic method--multimodal pressure flow (MMPF) analysis was introduced to access cerebral autoregulation during different time intervals. We introduced a new indicator--syncope index (SI), which was extracted from blood flow velocity (BFV) signal to evaluate the variation of cerebral vascular tension, and could reflect the deepness of dicrotic notch in BFV signal.@*RESULTS@#Compared with the syncope index of the baseline value at the beginning of the tilt test, SI in VVS group showed significantly lower when the VVS occurred (0.16±0.10 vs.0.27±0.10,P<0.01),while there was no significant difference in syncope index between the control group at the end of the tilt test and the baseline value at the beginning of the tilt test. For those VVS patients, pulse index and resistance index had no significant change. Syncope index decreased significantly 3 minutes before the point of syncope (0.23±0.07 vs.0.29±0.07,P<0.01).@*CONCLUSION@#Dynamic regulation is exhausted when vasovagal syncope occurred. Tension decrease of small vessels could have some relationship with loss of the cerebral autoregulation capability. The proposed syncope index could be a useful parameter in predicting syncope of VVS patients since it decreased significantly up to 3 minutes earlier from the point of syncope.
Subject(s)
Humans , Blood Pressure , Heart Rate , Nonlinear Dynamics , Syncope , Syncope, Vasovagal , Tilt-Table TestABSTRACT
Objective To observe the protective effect of dexmedetomidine(Dex)at different doses com-bined with ulinastatin in lung resection patients with one lung ventilation. Methods 80 patients having undergone unilateral lung resection were divided into four groups randomly:control group(C group)and groups Dex 1-3,20 cases in each group.One lung ventilation(OLV)was used in all the groups during operation.The patients in groups Dex 1-3 were treated with 0.5,1.0,2.0 μg/kg combined with ulinastatin,and the C group with amount of normal sa-line instead.The comparisons were done among the four groups in terms of SOD,L-6,IL-10,serum malondialde-hyde(MDA)concentration at 5 min after endotracheal intubation(T0),30 min(T1),60 min(T2),120 min (T3)as well as the levels of FVC,FEVl and FEVl/FVC at 24 h,48 h and 72 h after surgery. Results In the groups C and Dex 1,SOD decreased at T1-4 and IL-6,MDA and IL-10 at T2-4 rose.SOD decreased at T2-4 in groups Dex 2-3 and MDA,IL-6 and IL-10 rose.Compared with group C,the levels of SOD and IL-10 at T2-4 in groups Dex 1-2 and at T1-4 in group Dex 3 rose. In groups Dex 1-3,postoperative FVC,FEVl and FEVl/FVC rose.Compared with group Dex 1 or 2 respectively,SOD and IL-10 at T2-4 in group Dex 3 significantly rose,but MDA and IL-6 significantly declined;FVC,FEVl and FEVl/FVC significantly rose 48 h and 72 h after surgery (P<0.05). Conclusion Dex combined with ulinastatin has a protective effect for patients with one lung ventila-tion after lung resection,with the best-suggested dose of 1.0 μg/kg.
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<p><b>OBJECTIVE</b>To review the pathophysiology and study the diagnosis and clinical management of neurogenic pulmonary edema (NPE).</p><p><b>METHODS</b>The data of 5 patients who developed NPE after head injury treated in our hospital form December 1995 to May 2003 were collected and analyzed.</p><p><b>RESULTS</b>The patients developed dyspnea and respiratory failure 2-8 hours after neurologic event. Four of the 5 patients presented with pink frothy sputum. Chest radiography showed bilateral diffuse infiltrations in all the 5 patients. After supportive measures such as oxygen support and pharmacologic therapy, 4 patients recovered in 72 hours and one patient died.</p><p><b>CONCLUSIONS</b>The pathophysiologic mechanisms of NPE is unclear. In acute respiratory failure following head injury, NPE must be given much attention and timely and effective measures should be taken.</p>