Acute Hypotension Research Articles

Blood flow in internal carotid and vertebral arteries during orthostatic stress

It remains unclear whether orthostatic stress evokes regional differences in cerebral blood flow. The present study compared blood flow in the internal carotid (ICA) and vertebral arteries (VA) during orthostatic stress (60 deg head-up tilt; HUT) in six healthy young men. The ICA and VA blood flow were measured using Doppler ultrasonography. Dynamic cerebral autoregulation was also determined during supine (Supine) and HUT conditions, from the rate of regulation (RoR) in cerebrovascular conductance of the ICA and VA during acute hypotension induced by the release of bilateral thigh-cuffs. The HUT decreased ICA blood flow by -9.4 ± 1.7% (P < 0.01 versus Supine), leaving ICA conductance unchanged. In contrast, there was no significant difference in VA blood flow between Supine and HUT, and VA conductance increased (+12.9 ± 0.8%, P < 0.01). In addition, dynamic cerebral autoregulation in both the ICA and VA was attenuated during HUT, and the magnitude of the attenuation in RoR was greater in the VA [0.25 ± 0.03 s(-1) Supine versus 0.16 ± 0.02 s(-1) HUT (-33.9 ± 5.8%); P < 0.05] compared with the ICA [0.23 ± 0.02 s(-1) Supine versus 0.20 ± 0.03 s(-1) HUT (-10.6 ± 13.4%); P > 0.05]. These data indicate that orthostatic stress evokes regional differences in cerebral blood flow and possible differences in dynamic cerebral autoregulation between two main brain vascular areas in response to an acute change in blood pressure during orthostatic stress.

Tonsillar carcinoma metastatic to the spleen presenting as trauma: A case report

Cancers of the head and neck rarely metastasize to the spleen. To the best of our knowledge, there is no reported case of a tonsillar carcinoma metastasizing to the spleen. This patient had a splenic capsular rupture likely related to his metastases that presented as a traumatic splenic injury. The patient had received neoadjuvant chemotherapy followed by concurrent chemoradiotherapy. Two months after completion of radiotherapy, he fell out of bed. The next day he had acute abdominal pain and hypotension. CT findings were consistent with splenic rupture, and he underwent splenectomy. Pathologic assessment of the specimen showed metastatic SCC. New splemic lesions in patients with head and neck cancer should be investigated.

Decreased expression of neuronal nitric oxide synthase in the nucleus tractus solitarii inhibits sympathetically mediated baroreflex responses in rat

Despite numerous studies it remains controversial whether nitric oxide (NO·) synthesized by neuronal NOS (nNOS) plays an excitatory or inhibitory role in transmission of baroreflex signals in the nucleus tractus solitarii (NTS). In the current studies we sought to test the hypothesis that nNOS is involved in excitation of baroreflex pathways in NTS while excluding pharmacological interventions in assessing the influence of nNOS. We therefore developed, validated and utilized a short hairpin RNA (shRNA) to reduce expression of nNOS in the NTS of rats whose baroreflex activity was then studied. We demonstrate downregulation of nNOS through transduction with adeno-associated virus type 2 (AAV2) carrying shRNA for nNOS. When injected bilaterally into NTS AAV2nNOSshRNA significantly reduced reflex tachycardic responses to acute hypotension while not affecting reflex bradycardic responses to acute increases of arterial pressure. Control animals treated with intravenous propranolol to block sympathetically mediated chronotropic responses manifested the same baroreflex responses as animals that had been treated with AAV2nNOSshRNA. Neither AAV2 eGFP nor AAV2nNOScDNA affected baroreflex responses. Blocking cardiac vagal influences with atropine similarly reduced baroreflex-mediated bradycardic responses to increases in arterial pressure both in control animals and in those treated with AAV2nNOSshRNA. We conclude that NO· synthesized by nNOS in the NTS is integral to excitation of baroreflex pathways involved in reflex tachycardia, a largely sympathetically mediated response, but not reflex bradycardia, a largely parasympathetically mediated response. We suggest that, at the basal state, nNOS is maximally engaged. Thus, its upregulation does not augment the baroreflex.

Atrial Fibrillation in Two Jet Pilots During Aircrew Periodical Medical Examination

Atrial fibrillation (AF) unfavorably affects cardiac output and may cause acute incapacitation in flight due to loss of the atrial systole, which mainly contributes to the diastolic filling of the ventricles. Although it is the most common type of arrhythmia, it is rare in pilots and not compatible with aviation. We present two AF cases incidentally detected in two jet pilots. The first case was a 39-yr-old male jet pilot with a lone AF. Since there was no structural abnormality or thrombus in the left atrial appendage on transesophageal echocardiography (TEE), the patient was converted to sinus rhythm via direct current cardioversion (DCC). The pilot returned to flying duties after a follow-up period without any recurrent arrhythmia. The second case was a 23-yr-old male jet pilot who had suffered six attacks of paroxysmal AF. Conversion to sinus rhythm was provided by DCC at once and the second via pharmacological cardioversion. Also, spontaneous conversion to sinus was observed during two attacks of AF during the follow-up period. There were no abnormalities on physical examination, echocardiography, and laboratory tests. Although the cardiac ablation procedure was applied, the patient couldn't be treated successfully. Thereafter the pilot was treated with sotalol and warfarin and was permanently disqualified from flying duties. Arrhythmia is among the frequent causes for aviators to be disqualified from flying duties. AF particularly should not be overlooked due to its potential for sudden incapacitation during flight via acute hypotension or thromboembolic events.

Effects of transient change in carotid arterial stiffness on arterial baroreflex during mild orthostatic stimulation

Stiffening of central conduit arteries –areas where the mechanoreceptors are embedded (e.g., ascending aorta and carotid artery) – is considered to be associated with the impaired baroreflex control in response to hypotensive stress. Arterial stiffness is modulated by vascular tone transiently and dynamically, however, it is unknown whether a transient change in the carotid artery stiffness influences the cardiac baroreflex response to a rapid hypotension. We measured (n = 11) carotid arterial stiffness (via concurrent applanation tonometory and ultrasound imaging) at supine rest and during 20-degree head-up tilt (HUT). To evaluate the cardiac baroreflex response, acute hypotension was evoked by releasing bilateral thigh cuffs after 3 min of suprasystolic resting ischemia at each posture; cardiac baroreflex sensitivity (e.g., change in heart rate for a given change in mean arterial pressure, ΔHR/ΔMAP) and latency (e.g., the time to peak HR response) was estimated. Carotid β-stiffness index, a measure of arterial stiffness, was reduced by 14% during HUT (P < 0.05 vs. supine position). Although cardiac baroreflex responses were unaltered, the within-group biological variability in the cardiac baroreflex sensitivity and latency from the supine to HUT was correlated with the corresponding changes in carotid arterial stiffness (r = 0.66 and r = 0.64, respectively, both P < 0.05). These findings suggest that a transient change in carotid arterial stiffness, at least in part, influences changes in the cardiac baroreflex response to a rapid hypotension.

Spontaneous Retroperitoneal Hemorrhage in a Dialysis Patient

BackgroundPatients with end-stage renal disease (ESRD) often present to the Emergency Department with a multitude of complaints. Abnormal vital signs and a chief complaint of pain can produce a diagnosis ranging from a cardiac etiology to an infectious source. ObjectivesOur goal is to discuss a case in which an ESRD dialysis patient presented with a rare, life-threatening emergency. Case ReportA 55-year-old man with ESRD presented with acute abdominal pain and hypotension caused by a spontaneous retroperitoneal hemorrhage. ConclusionThis case report demonstrates the necessity of having broad differential diagnoses when evaluating patients with ESRD.

The effect of metanephros transplantation on blood pressure in anephric rats with induced acute hypotension

The kidney is an important organ for maintaining blood pressure. We have previously reported that transplanted metanephroi can reproduce some kidney functions. The aim of the present study was to determine the metabolic function of transplanted metanephroi with particular reference to maintaining blood pressure. Male Wistar rats were transplanted with metanephroi (transplanted group, n = 28), following unilateral nephrectomy. For comparison, we performed unilateral nephrectomy without transplantation in 32 rats (non-transplanted group, n = 18; haeminephrectomy control group, n = 14). The remaining kidney was removed 2 weeks after the initial operation, while control rats had a sham operation. Hypotension was induced by intravenous infusion of diltiazem hydrochloride or rapid withdrawal of blood. Mean arterial blood pressure (MAP) was invasively monitored and plasma renin activity (PRA) was analysed at multiple time points. Renin expression by metanephroi was evaluated by real-time polymerase chain reaction and immunohistochemistry. Metanephroi in the transplanted group expressed renin messenger RNA. Metanephros transplantation significantly raised PRA and maintained MAP compared with the non-transplanted group. No significant differences between the transplanted and control groups were found with respect to PRA or MAP. PRA was positively correlated with metanephroi weight as well as MAP in the transplanted group. The present study shows that transplantation of metanephroi produces PRA and contributes to raising MAP in a rat model of acute hypotension.

Excessive Fall of Blood Pressure During Maintenance Hemodialysis in Patients With Chronic Renal Failure Is Induced by Vascular Malfunction and Imbalance of Autonomic Nervous Activity

Acute hypotension during maintenance hemodialysis (HD) is not only a critical complication, but also an independent risk factor for mortality in patients with chronic renal failure (CRF). This study was designed to clarify the mechanisms underlying excessive fall of blood pressure during HD. Fifty-six CRF patients with HD thrice a week were divided into two groups according to the intradialytic hypotension episodes after 4 weeks of the observation period; the hypotension group, showing four or more episodes of intradialytic hypotension, and the non-hypotension group, showing three episodes of intradialytic hypotension or less. The intradialytic hypotension was defined as a fall of ≥30 mm Hg in the systolic blood pressure during HD. The brachial-ankle pulse wave velocity (ba-PWV), serum high-sensitivity (hs)-CRP, reactive oxygen species (ROS) generation, and serum malondialdehyde-modified LDL (MDA-LDL) were measured before HD. The high- frequency (HF) and low-frequency components (LF) of the heart rate variability and entropy were analyzed by the maximal entropy method. The ba-PWV, hs-CRP, ROS generation, and MDA-LDL were significantly higher in the hypotension group than in the non-hypotension group. HF, LF/HF, and entropy during HD increased significantly in the non-hypotension group, while entropy during HD decreased significantly in the hypotension group as compared with the baseline. LF/HF and entropy during HD were significantly lower in the hypotension group than in the non-hypotension group. These findings suggest that the major factors causing excessive fall of blood pressure during HD in patients with CRF might be vascular malfunction and imbalance of autonomic nervous activity.

Nimodipine-Induced Hypotension but Not Nitroglycerin-Induced Hypotension Preserves Long- and Short-Term Memory in Adult Mice

Acute hypotension may be implicated in cognitive dysfunction. L-type calcium channel blockers in the setting of hypoxia are protective of learning and memory. We tested the hypothesis that hypotension induced by nimodipine (NIMO) and nicardipine (NICA) would be protective of long- and short-term memory compared to hypotension induced by nitroglycerin (NTG). Forty Swiss-Webster mice (30 to 35 g, 6 to 8 weeks) were randomized into 4 groups for i.p. injection immediately after passive avoidance (PA) learning on day 0: (1) NTG (30 mg/kg); (2) NICA (40 mg/kg); (3) NIMO (40 mg/kg); and (4) saline. PA training latencies (seconds) were recorded for entry from a suspended platform into a Plexiglas tube where a shock (0.3 mA; 2-second duration) was automatically delivered. On day 2 latencies were recorded during a testing trial during which no shock was delivered. Latencies >900 seconds were assigned this value. Lower testing latency is indicative of an impairment of long-term associative memory. Forty-nine additional mice were randomized into similar groups for object recognition testing (ORT) and given i.p. injections on day 0. ORT measures short-term memory by exploiting the tendency of mice to prefer novel objects where a familiar object is present. On day 5 during training, 2 identical objects were placed in a circular arena and mice explored both for 15 minutes. A testing trial was conducted 1 hour later for 3 minutes after a novel object replaced a familiar one. Mice with intact memory spend about 65% of the time exploring the novel object. Mice with impaired memory devote equal time to each object. Recognition index (RI) is defined as the ratio of time spent exploring the novel object to time spent exploring both objects was the measure of memory. Mean arterial blood pressure (MAP), cerebral bloodflow, and body and brain oxygenation (PO(2)) studies were done in separate groups of mice to determine the dosages for matched degrees of hypotension and the physiological profile of each treatment. The median PA latencies for the different conditions were as follows: NTG (219.5 ± 93.5 second semi-interquartile range [SIQR]), NICA (372.5 ± 75.5 second SIQR), NIMO (540 ± 200 second SIQR) and saline (804 ± 257.5 second SIQR). Rank methods were used to analyze the PA latencies for significant differences. NTG latency was significantly shorter than NIMO latency (P = 0.012) and saline latency (P = 0.006), but not NICA latency (P = 0.126). ORT RI values showed a similar pattern. We found that NTG RI (47.2 ± 5.9% SEM) was different from NIMO RI (60.2 ± 4.6% SEM, P = 0.031) and different from saline RI (66.9 + 3.7% SEM, P = 0.006). Physiological experiments showed that MAP decreased to 45 to 50 mm Hg in all animals who became minimally responsive to external stimuli within 10 to 15 minutes of injection. Intergroup differences for MAP, body and brain oxygenation, and cerebral bloodflow were not statistically significant. Acute hypotension induced by NIMO was protective of 2 categories of memory formation relevant to the clinical posttreatment period. Both immediate long-term associative memory consolidation as measured by the PA learning paradigm and delayed short-term working memory function as measured by the ORT paradigm were significantly improved compared to matched levels of hypotension induced by NTG. These results indicate the utility of further investigation of l-type calcium channel blockers as a potential means of preserving cognition in the setting of hypotensive and low flow states.

Mechanism of glutamate receptor for excitation of medial vestibular nucleus induced by acute hypotension

In the vestibular nuclei, acute hypotension induces excitation of electrical activity and expression of c-Fos protein and phosphorylated extracellular signal-regulated kinase (pERK). Expression of c-Fos protein and pERK is mediated by the excitatory neurotransmitter, glutamate. We investigated the signaling pathway of glutamate and its receptors in the vestibular nuclei following acute hypotension in conscious rats. Glutamate release and the expression of c-Fos protein in the medial vestibular nuclei (MVN) were measured by microdialysis and immunohistochemical analysis, respectively. We compared the responses of rats with unilateral labyrinthectomy to unaltered controls. Acute hypotension was induced by infusing sodium nitroprusside (SNP) into the femoral vein. In the control group, glutamate release and the expression of c-Fos protein increased in the bilateral MVN following acute hypotension. In the unilateral labyrinthectomy group, glutamate release and the expression of c-Fos protein increased in the MVN contralateral to the lesion, but did not change in the ipsilateral MVN following acute hypotension. Microinjection of NMDA or AMPA into the lateral ventricle increased the expression of c-Fos protein in the bilateral MVN of conscious intact labyrinthine rats. However, after intracerebroventricular microinjection of MK-801 or CNQX little c-Fos protein was expressed in the bilateral MVN of these rats following acute hypotension. These results suggest that in response to acute hypotension, excitatory afferent signals from the peripheral vestibular receptors release glutamate into postsynaptic neurons in the vestibular nuclei. These excitatory signals are transmitted through the NMDA receptors and AMPA receptors of glutamate in the vestibular system.

Melatonin does not attenuate dynamic cardiovascular and cerebrovascular reflex responses to acute hypotension in healthy men

BackgroundMelatonin has been shown to attenuate the reflex sympathetic increases that arise in response to orthostatic challenges. We tested the hypothesis that the attenuated sympathetic increase induced by melatonin premedication may weaken the arterial blood pressure (ABP) preserving the capability during acute hypotension, thereby altering dynamic cerebral autoregulation and causing a further decrease in cerebral blood flow (CBF).MethodsAcute hypotension was induced in 12 healthy subjects by releasing bilateral thigh cuffs before and after an oral dose of melatonin (0.2 mg/kg). Heart rate (HR), arterial blood pressure (ABP), Modelflow estimate of cardiac output (CO), total peripheral resistance (TPR) and cerebral blood flow velocity (CBFV) by transcranial Doppler were measured.ResultsSteady state HR, the mean arterial pressure and CBFV were not altered 60 minutes after melatonin ingestion. Reduced systolic arterial pressure (ΔSAP), changes in HR (ΔHR), CO (ΔCO), and TPR (ΔTPR), ΔHR/ΔSAP and percentage restoration of SAP were not affected after a temporal decrease in ABP induced by thigh cuff release. In the cerebral circulation, melatonin did not affect changes in CBFV, cerebrovascular resistance index, the rate of regulation and percentage restoration of CBFV following a sudden decrease in ABP.ConclusionsContrary to our hypothesis, melatonin did not affect the rapid vasodilatory and recovery responses of cardiovascular and dynamic cerebral autoregulation. These results suggest that melatonin premedication may not impair ABP and CBF preserving capability induced by sudden postural changes or hemorrhage.

Effectiveness of using automated external defibrillator by trained healthcare professionals on survival outcomes among adult patients after in-hospital cardiac arrest: a systematic review.

Review question/objective The objective of this review is to synthesise the best available evidence of the effectiveness of using automated external defibrillator by trained healthcare professionals on survival outcomes in adult patients after in-hospital cardiac arrest. More specifically, the objectives are to identify: the effectiveness of using automated external defibrillator by trained healthcare professionals on return of spontaneous circulation and survival to hospital discharge in adult patients after in-hospital cardiac arrest. Inclusion criteria Types of participants This review will consider studies that include adults 18 years old and above; suffering from cardiac arrest requiring chest compression in in-patient wards, emergency department and out-patient procedures in hospital; presenting with an initial index pulseless (for example, but not limited to, ventricular fibrillation and pulseless ventricular tachycardia, asystole or pulseless electrical activities); presence or absence of co-morbidities such as congestive heart failure, myocardial infarction, diabetes mellitus, renal, hepatic or respiratory insufficiency, motor, cognitive or functional deficits, acute stroke, acute non-stroke neurological disorder, pneumonia, hypotension, sepsis, major trauma, metabolic or electrolyte abnormality, metastatic or haematology malignancy. The exclusion criteria are any age group who suffered out-of-hospital cardiac arrest or adults 18 years old and above suffered in-hospital cardiac arrest with a ‘do not resuscitate’ order (DNR). Types of intervention(s) This review will consider as interventions any use of commercially available automated external defibrillator by trained healthcare professionals for in-hospital cardiac arrest. The comparator of interest is use of manual/standard external defibrillator by trained healthcare professionals for in-hospital cardiac arrest. Types of outcomes This review will consider studies that include the following outcome measures: 1. survival with a return of spontaneous circulation for at least 20 minutes during resuscitation 2. survival to hospital discharge regardless of time to discharge 3. initial cardiac arrest rhythms

Cardiovascular adverse effects of metoclopramide: Review of literature

Articles pertaining to reports and clinical or pharmacological research for cardiovascular adverse effects of metoclopramide were identified via a search of MEDLINE (1966-February 2012), SCOPUS, and Google Scholar. To review the reports in literature of patients receiving metoclopramide who sufferred from cardiac arrest, bradycardia, total heart block, acute hypotension, supraventricular tachycardia, circulatory collapse, QT prolongation, Torsade de Pointes, ST depression, and congestive heart failure. In most cases the reactions occurred immediately after administration of metoclopramide, were associated with normal doses administered via intravenous or central lines, and resolved. Rechallenge occurred in several cases. The likelihood of these events occurring and the mechanism by which metoclopramide affects the cardiovascular system is unclear, however, it has been shown to have a direct effect on the heart, block presynaptic autoreceptors and enhance catecholamine release, enhance cholinergic neurotransmission and cause 5-HT3 receptor blockade and 5-HT4 receptor antagonism. Conclusion: Due to cardiovascular risks associated with the use of IV metoclopramide, recommendations are to monitor patients and report these events.

Acute right and left heart failure caused by an intrathoracic stomach

Hiatus hernia (HH) is a frequent condition and is asymptomatic most of the time. Common symptoms can include epigastric pain, postprandial fullness, and nausea. We report a case of postprandial acute right and left heart failure caused by an intrathoracic stomach in a previously asymptomatic woman. Clinical manifestations included acute pulmonary edema and severe hypotension after administration of vasodilators for treatment of acute left heart failure. Chest computed tomography images showed a pre- and afterload compromise caused by a large compressive HH with massive gastric distension. To the best of our knowledge, ours is the first report of both acute right and left heart failure due to an HH. The prompt placement of a nasogastric tube was lifesaving. We believe that the diagnosis of HH ought to be taken into consideration by emergency physicians and included in the differential diagnosis for acute postprandial heart failure.

Acute systemic hypotension after arteriovenous fistula construction in a patient with severe aortic stenosis

We report the case of a 53-year-old hemodialysis patient with severe aortic stenosis, who developed acute systemic hypoperfusion after arteriovenous fistula (AVF) construction. He presented with hypotension and repeated syncope soon after distal radiocephalic AVF construction, and finally developed a respiratory arrest. His blood pressure and hemodynamics recovered promptly by sub-emergent aortic valve replacement surgery. In the present case, the heart with severe aortic stenosis could not increase cardiac output in response to the reduction in peripheral vascular resistance caused by the AVF. High-output heart failure, a relatively rare AVF-associated disorder, occurs with an excessive AVF flow, usually more than 3L/min or 30% of cardiac output. However, heart failure may develop soon after construction of an AVF with a moderate blood flow if a patient's cardiac function is severely impaired. In addition, heart failure may improve with AVF preservation if the underlying heart disease is treatable.

Massive Portal Venous Gas Related to Small Bowel Ischemia

Purpose: Aim: To describe a case of massive portal venous gas (PVG) related to small bowel ischemia and highlight the radiographic findings related to this clinical entity. Case Report: A morbidly obese and diabetic 76 yo female presented with a 3 day history of constipation, mid abdominal pain and vomiting. Surgical history was significant for prior hysterectomy with partial colon resection, temporary colostomy placement and incidental appendectomy in the remote past (related to a migrated intrauterine device). Upon admission, CT of the abdomen/pelvis revealed dilated loops of small bowel and a ventral hernia which contained a loop of transverse colon. The latter had been seen on a CT scan performed 2 years previously. The primary care team believed symptoms were related to a fecal impaction, and the patient was treated with manual fecal disimpaction, tap water enemas and intravenous hydration. 72 hours following hospital admission, abdominal pain worsened and vomiting recurred. An obstruction series revealed dilated small intestine and stomach, and the radiologist interpreted it as also demonstrating either pneumobilia or portal venous gas (PVG). 12 hours later, GI consultation was sought after dark red-colored hematemesis occurred. At this point the patient became hypotensive and required vigorous intravascular fluid expansion and a vasopressor to maintain relative hypotension. Review of the recently performed plain abdominal radiograph suggested that massive PVG was undoubtedly present (branching air lucencies were noted to extend to the periphery of the liver). Intestinal ischemia was suspected, broad-spectrum antibiotics were started and immediate laparotomy was orchestrated (within 60 minutes of GI consultation). At laparotomy, the entire small bowel was severely ischemic-appearing, but it was macroscopically judged to be viable, after a pelvic adhesive band was lysed, which appeared to be the cause of intestinal obstruction and secondary ischemia (the ventral hernia which contained a loop of transverse colon was incidental). On the following day, hypotension persisted and both respiratory and renal failure ensued. Repeat laparotomy was declined by the patient and her family. The patient expired later that day. Conclusions: (1) Small intestinal obstruction should not be attributed to rectal fecal impaction, (2) PVG produces branching air lucencies which extend to the periphery of the liver, (3) In the setting of acute abdominal pain and hypotension, the finding of PVG suggests an intra-abdominal catastrophe which mandates emergent laparotomy.

Bilateral Bispectral Index (BIS)-VISTA monitoring of cerebral hypoperfusion in patients with carotid artery stenosis undergoing coronary artery bypass surgery

BackgroundCarotid stenosis is a frequent coexisting condition in patients undergoing Coronary Artery Bypass Graft (CABG) surgery. During cardiac surgery, acute hemodynamic changes can cause cerebral ischemia. When acute slowing of the Electroencephalography (EEG) develops because of cerebral ischemia, a profound reduction in Bispectral Index (BIS) is seen, although the depth of anesthesia does not change. We investigated the diagnostic value of bilateral BIS as an indicator of cerebral hypoperfusion during CABG surgery in patients with carotid artery stenosis and the incidence of left-right BIS differences.MethodsForty patients scheduled for elective CABG surgery were randomized into two groups according to preoperative Duplex carotid ultrasound; Group with Carotid Artery stenosis (CA-stenosis) (n = 23) and Group without stenosis (CA-normal) (n = 17). All patients underwent monitoring using bilateral BIS system. We analyzed BIS data at eight stages of the CABG procedure.ResultsMean BIS values recorded from left and right hemispheres declined significantly in comparison to steady state of anesthesia in both groups (T2), (p < 0.0001 for both). In CA-stenosis group only, there were significant interhemispheric differences during AXC apply (p < 0.01). Average BIS values of right and left hemispheres and parallel to it, SEF data decreased significantly in both groups during initiation of CPB-T3, during AXC application-T4 and during AXC removal-T6 (p < 0.001). Intergroup comparison showed significant decrease in BIS values in CA-stenosis group when compared to CA-normal group during induction of anesthesia-T1 and during AXC apply-T4 (both p < 0.001) and during AXC removal-T6 (p = 0.04).ConclusionOur findings suggest that an acute decrease in BIS which represent abrupt slowing of the EEG, reflects acute cerebral hypoperfusion particularly when it accompanies acute hypotension, as long as the changes in BIS is not drug induced.

Use of Ephedrine for the Short-Term Treatment of Postoperative Nausea and Vomiting: A Case Report

Ephedrine, a well-known sympathomimetic agent, is used in the perioperative setting to treat acute hypotension, especially hypotension related to anesthetic events. Ephedrine's unlabeled use as an antiemetic agent is less well known despite its efficacy and safety profile for short-term and/or prophylactic treatment. The following case report describes the benefits of using ephedrine to mitigate postoperative nausea and vomiting and associated dizziness while waiting for longer lasting therapy to take effect and/or use as a secondary agent.

Diagnostic Accuracy of HMGB-1, sTREM-1, and CD64 as Markers of Sepsis in Patients Recently Admitted to the Emergency Department

The objectives were to evaluate the diagnostic accuracy for sepsis in an emergency department (ED) population of the cluster of differentiation-64 (CD64) glycoprotein expression on the surface of neutrophils (nCD64), serum levels of soluble triggering receptor expressed on myeloid cells-1 (s-TREM-1), and high-mobility group box-1 protein (HMGB-1). Patients with any of the following as admission diagnosis were enrolled: 1) suspected infection, 2) fever, 3) delirium, or 4) acute hypotension of unexplained origin within 24 hours of ED presentation. Levels of nCD64, HMGB-1, and s-TREM-1 were measured within the first 24 hours of the first ED evaluation. Baseline clinical data, Sepsis-related Organ Failure Assessment (SOFA) score, Acute Physiology and Chronic Health Evaluation (APACHE II) score, daily clinical and microbiologic information, and 28-day mortality rate were collected. Because there is not a definitive criterion standard for sepsis, the authors used expert consensus based on clinical, microbiologic, laboratory, and radiologic data collected for each patient during the first 7 days of hospitalization. This expert consensus defined the primary outcome of sepsis, and the primary data analysis was based in the comparison of sepsis versus nonsepsis patients. The cut points to define sensitivity and specificity values, as well as positive and negative likelihood ratios (LRs) for the markers related to sepsis diagnosis, were determined using receiver operative characteristics (ROC) curves. The patients in this study were a prespecified nested subsample population of a larger study. Of 631 patients included in the study, 66% (95% confidence interval [CI] = 62% to 67%, n = 416) had sepsis according with the expert consensus diagnosis. Among these sepsis patients, SOFA score defined 67% (95% CI = 62% to 71%, n = 277) in severe sepsis and 1% (95% CI = 0.3% to 3%, n = 6) in septic shock. The sensitivities for sepsis diagnosis were CD64, 65.8% (95% CI = 61.1% to 70.3%); HMGB-1, 57.5% (95% CI = 52.7% to 62.3%); and s-TREM-1, 60% (95% CI = 55.2% to 64.7%). The specificities were CD64, 64.6% (95% CI = 57.8% to 70.8%), HMGB-1, 57.8% (95% CI = 51.1% to 64.3%), and s-TREM-1, 59.2% (95% CI = 52.5% to 65.6%). The positive LR (LR+) for CD64 was 1.85 (95% CI = 1.52 to 2.26) and the negative LR (LR-) was 0.52 (95% CI = 0.44 to 0.62]; for HMGB-1 the LR+ was 1.36 (95% CI = 1.14 to 1.63) and LR- was 0.73 (95% CI = 0.62 to 0.86); and for s-TREM-1 the LR+ was 1.47 (95% CI = 1.22 to 1.76) and the LR- was 0.67 (95% CI = 0.57 to 0.79). In this cohort of patients suspected of having any infection in the ED, the accuracy of nCD64, s-TREM-1, and HMGB-1 was not significantly sensitive or specific for diagnosis of sepsis.

Hydrogen supplemented air inhalation reduces changes of prooxidant enzyme and gap junction protein levels after transient global cerebral ischemia in the rat hippocampus

Transient global cerebral ischemia (TGCI) occurs during acute severe hypotension depriving the brain of oxygen and glucose for a short period of time. During reperfusion, several mechanisms can induce secondary neuronal damage, including the increased production of reactive oxygen species (ROS). Hydrogen gas-enriched air inhalation is a neuroprotective approach with proven antioxidant potential, which has not yet been examined in TGCI. Accordingly, we set out to describe the effect of inhalation of 2.1% hydrogen supplemented room air (H 2-RA) in comparison with a well studied neuroprotective agent, rosiglitazone (RSG) in a TGCI rat model. Male Wistar rats were exposed to TGCI (n = 26) or sham operation (n = 26), while a third group served as intact control (naive, n = 5). The operated groups were further divided into non-treated, H 2-RA, RSG (6 mg/kg i.v.) and vehicle treated animals. Tissue samples from the hippocampus and frontal cortex were taken 3 days following surgery. Western blot analysis was applied to determine the expressions of cyclooxygenase-2 (COX-2), neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively), manganese superoxide dismutase (MnSOD) and glial connexin proteins: connexin 30 and connexin 43. The expressions of COX-2, and connexin proteins were upregulated, while nNOS was downregulated 3 days after TGCI. Both RSG and H 2-RA prevented the changes of enzyme and connexin levels. Considering the lack of harmful side effects, inhalation of H 2-RA can be a promising approach to reduce neuronal damage after TGCI.