Decrease In Cerebral Perfusion Research Articles

Epileptic Seizures Versus Syncope: Pathophysiology and Clinical Approach

<p>Generalised epileptic seizures and syncope are two syndromes with similar clinical manifestation and their differentiation can be quite challenging. The aim of this review is to use an evidence-based approach in differentiating these two syndromes through the comprehension of the pathophysiological mechanisms involved and their clinical signs. Both syndromes affect regions of the forebrain and consciousness level, although, different mechanisms are involved. Syncope is a paroxysmal event secondary to a short-term decrease in cerebral perfusion, oxygenation or essential nutrients delivery. Generalised epileptic seizure activity is defined as the clinical manifestation of transient paroxysmal disturbances in brain function secondary to an imbalance between excitatory and inhibitory neurotransmitters. Clinical criteria, including precipitating events, clinical signs preceding, during and following the episodes and event duration, can be used to differentiate the two syndromes. Although these criteria might be useful for the practitioner, definite conclusions should be precluded due to the lack of original research articles and weak evidence on this specific field.</p><p><strong>Application:</strong> The review might be a useful tool for the general practitioner and clinical scientist as it will aid towards the differentiation of two syndromes, i.e. generalised epileptic seizures and syncope, with similar clinical presentation.</p><br /> <img src="https://www.veterinaryevidence.org/rcvskmod/icons/oa-icon.jpg" alt="Open Access" /> <img src="https://www.veterinaryevidence.org/rcvskmod/icons/pr-icon.jpg" alt="Peer Reviewed" />

Perfusion Computed Tomography Study: A Utility Tool in Traumatic Cerebral Contusions

Aim To assess the usefulness of CT perfusion scans of the brain in patients with traumatic brain injury having cerebral contusion on CT scan. Material and Methods This prospective study included 76 patients with cerebral contusion on plain CT of the brain, aged 5 to 86 years, admitted in our institution. They underwent perfusion CT as part of their admission CT survey and follow-up scan 48 hours later. Clinical data, unenhanced CT brain findings, and perfusion CT scans were evaluated with respect to the postoperative GCS (Glasgow Coma Score) and neurologic deficit. Results Perfusion CT gave additional information when done with conventional unenhanced CT in the detection of cerebral contusions. Perfusion CT featured specific patterns with respect to patient outcome, patients with unfavorable outcome having significant decrease in cerebral perfusion. In patients having less GCS score, a significant decrease in cerebral blood flow and cerebral blood volume was detected. Conclusion Perfusion CT provides independent useful information regarding functional outcome. In the acute phase of mild head injury, disturbed cerebral perfusion is seen in patients with normal noncontrast CT correlating with evolution, severity of injury, and outcome.

Dynamics of intracranial pressure, mean arterial pressure and cerebral perfusion pressure at change of head-of-bad position for patients with non-traumatic intracranial hemorrhages

Introduction and purpose. Change of the «head-of-bed» position is a routine and simple method of correction of intracranial hypertension. There is still no consensus what exactly situation most effectively reduces intracranial pressure and doesn't compromise a cerebral blood flow. The purpose of the conducted research was the assessment influence of positioning on intracranial pressure and system hemodynamic at patients with a hemorrhagic stroke. Methods. 80 patients with a hemorrhagic stroke entered research. All of the patient carried out continuous monitoring of intracranial and system arterial pressure, transcranial doppler was daily carried out. To each patient was carried out «head-of-bed position» test (30°-0°-60°). Results. Despite various mechanism of hemorrhage in two studied groups in the first three days from the beginning of a disease similar tendencies to the progressing increase of intracranial pressure and decrease in mean arterial and cerebral perfusion pressure were observed. Only for the fifth days there were essential distinctions of the studied indicators. At consecutive «head-of-bed» changes are received the essential distinctions in the studied groups which aren't allowing to apply to them uniform algorithm of positioning. Conclusions. Positioning of patients with subarachnoid hemorrhages has no essential impact on the studied parameters. For patients with parenchymatous hemorrhages is preferable «head-of-bed» situation 30° and 60° the first and third day and 30° for the second and fifth day. Thus even short stay in horizontal position (0°) leads to the expressed growth of intracranial pressure and critical decrease in cerebral perfusion.

Cerebral vascular effects of loading dose of dexmedetomidine: A Transcranial Color Doppler study.

Background:Dexmedetomidine has been widely used in critical care settings because of its property of maintaining stable hemodynamics and inducing conscious sedation. The use of dexmedetomidine is in increasing trend particularly in patients with neurological disorders. Very few studies have focused on the cerebral hemodynamic effects of dexmedetomidine. This study is aimed to address this issue.Methods:Thirty patients without any intracranial pathology were included in this study. Middle cerebral artery flow velocity obtained from transcranial color Doppler was used to assess the cerebral hemodynamic indices. Mean flow velocity (mFV), pulsatility index (PI), cerebral vascular resistant index (CVRi), estimated cerebral perfusion pressure (eCPP), and zero flow pressure (ZFP) were calculated bilaterally at baseline and after infusion of injection Dexmedetomidine 1 mcg/Kg over 10 min.Results:Twenty-six patients completed the study protocol. After administration of loading dose of dexmedetomidine, mFV and eCPP values were significantly decreased in both hemispheres (P < 0.05); PI, CVRi, and ZFP values showed significant increase (P < 0.05) after dexmedetomidine infusion.Conclusion:Increase in PI, CVRi, and ZFP suggests that there is a possibility of an increase in distal cerebral vascular resistance (CVR) with loading dose of dexmedetomidine. Decrease in mFV and eCPP along with an increase in CVR may lead to a decrease in cerebral perfusion. This effect can be exaggerated in patients with preexisting neurological illness. Further studies are needed to evaluate the effect of dexmedetomidine on various other pathological conditions involving brain like traumatic brain injury and vascular malformations.

Malignant Cerebral Venous Sinus Thrombosis in Polycythemia.

Malignant Cerebral Venous Sinus Thrombosis in Polycythemia.

Vascular change and opposing effects of the angiotensin type 2 receptor in a mouse model of vascular cognitive impairment.

Our aims were to assess the spatiotemporal development of brain pathology in a mouse model of chronic hypoperfusion using magnetic resonance imaging (MRI), and to test whether the renin-angiotensin system (RAS) can offer therapeutic benefit. For the first time, different patterns of cerebral blood flow alterations were observed in hypoperfused mice that ranged from an immediate and dramatic to a delayed decrease in cerebral perfusion. Diffusion tensor imaging revealed increases in several quantitative parameters in different brain regions that are indicative of white-matter degeneration; this began around 3 weeks after induction of hypoperfusion. While this model may be more variable than previously reported, neuroimaging tools represent a promising way to identify surrogate markers of pathology. Vascular remodelling was observed in hypoperfused mice, particularly in the anterior part of the Circle of Willis. While the angiotensin II receptor type 2 agonist, Compound 21 (C21), did not influence this response, it did promote expansion of the basilar artery in microcoil animals. Furthermore, C21-treated animals exhibited increased brain lymphocyte infiltration, and importantly, C21 had opposing effects on spatial reference memory in hypoperfused and sham mice. These results suggest that the RAS may have a role in vascular cognitive impairment.

Обморок у детей и подростков как внезапная, проходная, краткосрочная и самостоятельно уступающая потеря сознания из-за снижения перфузии головного мозга

Обморок у детей и подростков как внезапная, проходная, краткосрочная и самостоятельно уступающая потеря сознания из-за снижения перфузии головного мозга

Omdlenia u dzieci i młodzieży jako nagła, przemijająca, krótkotrwała i samoistnie ustępująca utrata świadomości spowodowana zmniejszeniem perfuzji mózgu

Omdlenia u dzieci i młodzieży jako nagła, przemijająca, krótkotrwała i samoistnie ustępująca utrata świadomości spowodowana zmniejszeniem perfuzji mózgu

Lack of dystrophin results in abnormal cerebral diffusion and perfusion in vivo

Dystrophin, the main component of the dystrophin–glycoprotein complex, plays an important role in maintaining the structural integrity of cells. It is also involved in the formation of the blood–brain barrier (BBB). To elucidate the impact of dystrophin disruption in vivo, we characterized changes in cerebral perfusion and diffusion in dystrophin-deficient mice (mdx) by magnetic resonance imaging (MRI). Arterial spin labeling (ASL) and diffusion-weighted MRI (DWI) studies were performed on 2-month-old and 10-month-old mdx mice and their age-matched wild-type controls (WT). The imaging results were correlated with Evan's blue extravasation and vascular density studies. The results show that dystrophin disruption significantly decreased the mean cerebral diffusivity in both 2-month-old (7.38±0.30×10-4mm2/s) and 10-month-old (6.93±0.53×10-4mm2/s) mdx mice as compared to WT (8.49±0.24×10-4, 8.24±0.25×10-4mm2/s, respectively). There was also an 18% decrease in cerebral perfusion in 10-month-old mdx mice as compared to WT, which was associated with enhanced arteriogenesis. The reduction in water diffusivity in mdx mice is likely due to an increase in cerebral edema or the existence of large molecules in the extracellular space from a leaky BBB. The observation of decreased perfusion in the setting of enhanced arteriogenesis may be caused by an increase of intracranial pressure from cerebral edema. This study demonstrates the defects in water handling at the BBB and consequently, abnormal perfusion associated with the absence of dystrophin.

Abstract 064: Toll-like Receptor 2 Signaling Contributes To Cerebrovascular Dysfunction And Decreased Cerebral Blood Flow In Type-1 And Type-2 Diabetes.

We have shown that type 2 diabetic Goto-Kakizaki (GK) rats develop cerebrovascular endothelial dysfunction, impaired cerebral blood flow (CBF) and mild cognitive deficits. It is increasingly recognized that vascular cognitive impairment may be a new complication of the disease in both type 1 and type 2 diabetes. Toll-like receptor-2 (TLR2) plays a role in cardiovascular complications of diabetes but its involvement in diabetic cerebrovascular disease is unknown. Since brain function heavily depends on constant perfusion, and decreased CBF precedes development of inflammation and cognitive deficits, we hypothesized that enhanced TLR2 signaling in both type 1 and 2 diabetes would contribute to cerebrovascular dysfunction and decreased CBF. Endothelium-dependent relaxation was assessed by measuring acetylcholine (ACh, 10-9 -10-4 M) induced dilatory response in basilar arteries from GK rats in the presence and absence of an anti-TLR2 (1μg) antibody. Vascular contractility to serotonin (10-9 -10-5 M) stimulation was also assessed. Area under the curve (AUC) and maximal effective concentration (Emax as % of max KCl response) were calculated as indices of total relaxation and total contraction, respectively. Basilar artery relaxation was significantly improved in the vessels preincubated (30’) with antiTLR2 (184.8± 24.0 vs. 87.7± 4, p =0.007). The EMax in response to serotonin stimulation in the anti-TLR2 treated vessels was not significantly different than the vessels from the untreated diabetic GK rats (110.6± 4.9% vs 99.4.±4.5%). To further assess the in vivo functional effects of TLR2 signaling, CBF (relative intensity) was measured using laser speckle imaging in wild type and TLR2-knockout (KO) mice using an STZ induced diabetes model. Six weeks after induction of diabetes, wild-type diabetic mice exhibited a significant decrease in CBF vs. control (210±22.5 vs. 300.3±18.4, p&lt;0.05). This decrease in cerebral perfusion was attenuated in the TLR2-KO diabetic mice compared to TLR2 KO control (322.6±10.1 vs. 344. 5±11. 04). These findings suggest that TLR2 signaling leads to vascular dysfunction through decreased endothelium dependent relaxation, and could contribute to decreased CBF in diabetes predisposing to vascular cognitive impairment.

Abstract 33: Cerebral Blood Flow in Leukoaraiosis Regions is Unaffected by Acute Lowering of Blood Pressure in Intracerebral Hemorrhage Patients.

Introduction: Leukoariosis(LA) is associated with poor prognosis in intracerebral hemorrhage (ICH) patients. Patients with chronic small vessel ischemic changes may be more vulnerable to decreases in cerebral perfusion, in both LA and perihematoma(PH) regions. We tested the hypotheses that acute blood pressure reduction (BP) in ICH patients is associated with decreased cerebral blood flow (CBF) in areas of LA and the PH region. Methods: In the ICH Acutely Decreasing Arterial Pressure Trial (ICH ADAPT), patients with ICH &lt;24 hours duration were randomized to two systolic BP (SBP) target groups (&lt;150 mmHg vs. &lt;180 mmHg). Computed tomography (CT) perfusion imaging was performed 2 h post-randomization. LA tissue volume was planimetrically measured on the acute non-contrast CT, using Hounsfield Unit thresholds of 15-25. CBF, cerebral blood volume (CBV), and Tmax were measured in the LA regions. Results: Seventy-one patients were included with a mean age of 69.3±11.5 years and median (IQR) baseline NIHSS score of 10(11). LA was present in 74.6% (53/71) and the median volume was 8.5(20.6) ml. LA was associated with older age (70.9± 11.2 vs. 64.8 ±11.6, p=0.05) and larger ICH volumes (19.52(29.78) vs. 9.52(16.02) ml, p=0.007). Mean CBF in LA regions (32.5±13.5) was similar to that in normal appearing white matter (35.6±12.1, p=0.3). Despite a significant drop in SBP between aggressive (36.25(40) mmHg) and conservative (18.5(29) mmHg, p=0.01) treatment groups, relative CBF (rCBF) in LA regions was unaffected (0.88±0.1 vs. 0.89±0.09, p=0.6). Similarly, aggressive BP treatment did not affect relative CBV (0.83±0.16 vs. 0.82± 0.15, p=0.8) or Tmax (7.3±3.2 s vs. 6.5 ±2.4 s, p=0.3). The rCBF in the PH regions in patients’ with/without LA was similar (0.88±0.09 vs. 0.86±0.1, p=0.5). There was a trend to worse functional outcome at 90 days, measured with the modified Rankin Scale in patients with LA (4(4) vs. 2(1), p=0.06). Conclusion: LA is associated with larger baseline ICH volumes, but no differences in perihematoma CBF or the response to BP reduction. CBF in LA tissue is also unaffected by BP reduction. These data do not support a less aggressive approach to BP reduction in elderly patients with imaging evidence of chronic small vessel ischemia.

Early Diagnosis of Alzheimer's Disease and Parkinson's Disease Associated with Dementia Using Cerebral Perfusion SPECT

Background: Since patterns of cognitive dysfunction in mild Parkinson's disease associated with dementia (PDD) are similar to those in mild Alzheimer's disease (AD), it is difficult to accurately differentiate between these two types of dementia in their early phases using neuropsychological tests. The purpose of the current study was to investigate differences in cerebral perfusion patterns of patients with AD and PDD at the earliest stages using single photon emission computed tomography (SPECT). Methods: We consecutively recruited 31 patients with mild PDD, 32 patients with mild probable AD and 33 age-matched healthy subjects. All subjects underwent ^99mTc-hexamethylpropyleneamine oxime perfusion SPECT and completed general neuropsychological tests. Results: We found that both mild PDD and AD patients showed distinct hypoperfusion in frontal, parietal and temporal regions, compared with healthy subjects. More importantly, hypoperfusion in occipital and cerebellar regions was observed only in mild PDD. Conclusion: The observation of a significant decrease in cerebral perfusion in occipital and cerebellar regions in patients with mild PDD is likely useful to differentiate between PDD and AD at the earliest stages.

Hypercapnia-induced increases in cerebral blood flow do not improve lower body negative pressure tolerance during hyperthermia

Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapnia-induced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 ± 7 yr; 75 ± 12 kg) underwent passive heat stress (increased intestinal temperature ∼1.3°C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAvmean,) and end-tidal CO2 (PetCO2) were also measured. CO2 inhalation of 5% increased PetCO2 at ∼40 mmHg LBNP (by 16 ± 4 mmHg) and at LBNP tolerance (by 18 ± 5 mmHg) compared with SHAM (P < 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during ∼40 mmHg LBNP (by 21 ± 12 cm/s, ∼31%) and at LBNP tolerance (by 18 ± 10 cm/s, ∼25%) relative to the SHAM (P < 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 ± 155 mmHg × min; SHAM CSI: 273 ± 158 mmHg × min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic.

Syncope: A practical approach to diagnosis

Syncope is commonly encountered clinical problem by practicing clinicians. This is defined as a transient loss of consciousness resulting from decrease in cerebral perfusion. The importance of evaluation of this condition cannot be undermined as it has been said that syncope and death differ from each other in that in the former the patient wakes up while in the latter he does not. Occurrence of this event on one hand results in psychological duress to the patient and their relatives while on the other hand, it can be sometimes be a challenge to the treating physician to be able to confidently classify this as benign. Patient with syncope may present to different medical specialists - Physician, cardiologist, Neurologist, Emergency room physician or to a psychiatrist. Unless there is clarity in the mind of the clinician of the diagnostic plan, what will result is large number of expensive and non-contributory diagnostic tests, prolonged hospital stay leading to financial burden to the patient and frustration to the doctor. In the following paragraphs I will try to summarize the approach to the diagnosis of common conditions causing syncope. One should nevertheless be aware that in a significant number of cases, the cause of syncope cannot be exactly pinpointed. A physician should however be able to definitively exclude life threatening causes of syncope. This is a more achievable and important objective to achieve. Keywords: Syncope; pre-syncope

Cerebral Amyloid Angiopathy: Perspectives on Cerebrovascular Dysfunction

Cerebral amyloid angiopathy (CAA) occurs sporadically in elderly populations or in familial forms of Alzheimer’s disease (AD) and is characterized by insoluble deposition of amyloid-beta peptides (Aβ), within arterial vessels of the central nervous system. Amyloid precursor protein is processed by β- and γ-secretases generating Aβ1-40 and Aβ1-42 species that exist as soluble monomers, soluble oligomers (toxic intermediate species), and insoluble fibrils (principle component of CAA) [1]. Of interest, the co-morbidity and relationship between vascular compromise and neurodegenerative processes are not fully understood. CAA is an associated risk factor for intracerebral hemorrhage and ischemic stroke and also may contribute to the cognitive decline observed in aging, AD, or both [1]. Most AD cases feature early decreases in cerebral perfusion that may arise as a consequence of peripheral vascular disease (e.g., type II diabetes, hypertension) and/or loss of basalocortical cholinergic innervation that regulates cerebral blood flow (CBF) among other neurological functions [2]. Much remains to be understood concerning CAA-induced vasomotor impairment and its impact toward the occurrence and/or progression of impaired cognitive function within neurodegenerative disease.

Vascular aspects of multiple sclerosis: myth or reality?

The article contains recent literature data concerning vascular aspects of multiple sclerosis (MS). The review provides a summary of three vascular abnormalities described in MS which include increased risk of developing ischaemic stroke, widespread decrease in cerebral perfusion and chronic cerebral venouse insufficiency with the assessment of the endovascular interventions efficacy.

Cerebral Perfusion in Patients With Chronic Neck and Upper Back Pain: Preliminary Observations

ObjectiveThe purpose of this study was to determine the correlation between cerebral perfusion levels, Neck Disability Index (NDI) scores, and spinal joint fixations in patients with neck pain. MethodsForty-five adult patients (29 were female) with chronic neck/upper thoracic pain during exacerbation were studied. The subjects were grouped according to NDI scores: mild, moderate, and severe. The number of painful/blocked segments in the cervical and upper thoracic spine and costovertebral joints, pain intensity using the visual analog scale, and regional cerebral blood flow of the brain using single-photon emission computed tomography (SPECT) were obtained. The SPECT was analyzed semiquantitatively. Analysis of variance tests were conducted on total SPECT scores in each of the NDI groups (P < .05). Univariate correlations were obtained between blockage, pain, and SPECT scores, as well as age and duration. A multivariate analysis was then conducted. ResultsGroup 1 (mild) consisted of 14 patients. Cerebral perfusion measured by SPECT was normal in all 8 brain regions. Group 2 (moderate) consisted of 16 patients. In this group, a decrease in cerebral perfusion was observed (range, 20%-35%), predominantly in the parietal and frontal zones. Group 3 (severe) consisted of 15 patients. In this group, the decrease in cerebral perfusion observed was from 30% to 45%, again predominantly in the parietal and frontal zones. A significant difference was found between NDI groups (“moderate” and “severe” showed significantly greater hypoperfusion than “mild”). Total blockage score correlated with SPECT scores at r = 0.47, P = .001. In a multivariate analysis, NDI scores contributed 39% of the variance of SPECT scores. ConclusionIn this group of patients with neck and/or upper back pain, NDI scores strongly predicted cerebral hypoperfusion. Spinal joint dysfunction may be involved via hyperactivity in the regional sympathetic nervous system.

Abstract 8: Elevated Intrathoracic Pressure Is Common During Prehospital Ventilation of Patients with Traumatic Brain Injury

Background: Inadvertent hyperventilation is associated with poor outcomes from traumatic brain injury (TBI). Hypocapneic cerebral vasoconstriction is well described and causes an immediate and profound decrease in cerebral perfusion. The hemodynamic effects of positive-pressure ventilation (PPV) remain incompletely understood but may be equally important, particularly in the hypovolemic patient with TBI. Objective: To apply a previously described mathematical model of perfusion and ventilation to prehospital ventilation data to predict intrathoracic pressure. Methods: Ventilation data from 108 TBI patients (76 ground transported, 32 helicopter transported) were used for this analysis. Ventilation rate (VR) and end-tidal carbon dioxide (PetCO2) values were used to estimate tidal volume (VT). The values for VR and estimated VT were then applied to a previously described mathematical model of perfusion and ventilation. This model allows various lung parameters to be defined to create a pressure-volume relationship, then derives mean intrathoracic pressure (MITP) for various VT and VR values. For this analysis, normal lung parameters were assumed. Separate analyses were performed assuming fixed and variable PaCO2-PetCO2 differences. Data regarding VR, PetCO2, estimated VT, and estimated MITP were presented descriptively. Results: A total of 10,647 measurements were included from the 108 TBI patients, representing about 13 minutes of ventilation per patient. Mean VR values were higher for ground patients (21.6 breaths/min) than for air patients (19.7 breaths/min). Estimated VT values were similar for ground and air patients (399 mL vs. 392 mL, respectively). Mean PetCO2 values were lower for ground patients (30.6 mmHg) than for air patients (33.8 mmHg). MITP values were higher for ground versus air patients, assuming either fixed (9.0 vs. 8.1 mmHg) and variable (10.9 vs 9.7 mmHg) PaCO2-PetCO2 differences. Conclusions: Hyperventilation is common in prehospital TBI patients as reflected by both hypocapnia as well as rapid VR values. MITP values are elevated and would likely result in detrimental hemodynamic effects, particularly in hypovolemic patients.

Changes in Hemodynamic Parameters and Cerebral Saturation During Supraventricular Tachycardia

Induced supraventricular tachycardia (SVT) during electrophysiology studies (EPS) can be associated with hemodynamic changes. Traditionally, invasive arterial blood pressure has been used for continuous monitoring of these changes. This prospective study evaluated the efficacy of near-infrared spectroscopy (NIRS) monitoring during SVT. The use of NIRS has expanded with evidence of its accuracy and benefit in detecting cerebral hypoperfusion. This study aimed first to determine the hemodynamic changes associated with electrophysiology testing for SVT and second to determine whether the hemodynamic changes are associated with similar changes in the cerebral saturation as determined by NIRS. The study enrolled 30 patients 5-20 years of age with a history of SVT who underwent an EPS. The demographic data included age, gender, weight, height, and type of SVT. Hemodynamic data (invasive blood pressure and heart rate), NIRS, bispectral index (BIS), end-tidal carbon dioxide, and pulse oximetry were collected before and during three episodes of induced SVT. The linear correlation coefficient (r) was measured to calculate the relationship of the changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) to the changes in NIRS values during the SVT episodes. Data from 22 patients were collected. The induction of SVT was associated mainly with a change in SBP and a less prominent change in DBP and MAP from baseline. The changes in hemodynamic status were associated with minimal changes in cerebral saturations, as evidenced by an average absolute change in NIRS of <1 from baseline value. The changes in hemodynamics were correlated linearly with cerebral saturation. Changes in SBP, DBP, and MAP were correlated positively with changes in NIRS, as denoted by (r) values of 0.52, 0.57, and 0.67 respectively, and a P value less than 0.05 for all three association tests. Induction of SVT during electrophysiology testing is associated with hemodynamic changes, mainly in SBP. In this study, these hemodynamic changes resulted in a minimal decrease in cerebral perfusion, as evidenced by minimal changes in the cerebral saturation measured by NIRS (0.7% from baseline). Although the changes in the cerebral saturation were minimal, these changes were linearly correlated with the changes in the hemodynamics. This study is the first to demonstrate the possible application of NIRS monitoring during EPS and to document that despite changes in the hemodynamic status, the changes in cerebral oxygenation are minimal, thereby confirming the safety of EPS for SVT.

Index of Suspicion in the Nursery

Twins are born at 37-5/7 weeks gestation to a 41-year-old G4P2 woman who had unremarkable serology results. The delivery is via cesarean section because of a nonreassuring fetal heart rate. Twin B appears to be acrocyanotic and initially requires positive-pressure ventilation for 30 seconds before being able to maintain her oxygen saturation on her own. Apgar scores are 7 and 8 at 1 and 5 minutes, respectively. She also appears to be “jittery,” and her screening glucose concentration is 24 mg/dL (1.3 mmol/L). She consumes 20 mL of infant formula and a 10% dextrose (D10) infusion is begun at a rate of 60 mL/kg per day. Three hours after birth, a follow-up glucose evaluation measures 30 mg/dL (1.7 mmol/L), prompting administration of a 4-mL/kg bolus of D10 over 20 minutes and increase of the maintenance infusion rate to 100 mL/kg per day. Six hours after birth, glucose measures 80 mg/dL (4.4 mmol/L), and the infusion rate is decreased to 60 mL/kg per day. She is transferred to a hospital that has a neonatal intensive care unit (NICU) for close monitoring. On transfer, the oxygen saturation dips into the upper 80s/lower 90s, and nasal cannula administration of oxygen is initiated. Furthermore, during transfer (8 to 9 hours after birth), the blood glucose value is 44 mg/dL (2.4 mmol/l), so the D10 infusion rate is increased back to 100 mL/kg per day. On arrival at the second hospital, her oxygen saturation is about 85% and glucose is 50 mg/dL (2.8 mmol/L). In the NICU, she receives noninvasive respiratory support as well as 15% dextrose (D15) at a rate of 70 mL/kg per day. Twin A remains stable and continues to receive routine newborn care in the newborn nursery of the first hospital. Two days after birth, twin B continues to have glucose …