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Two studies that did not provide any bilateral-unilateral comparative data but that analyzed success predictors in children were identified (Van Deun et al. Two studies (total, n=70) could find no correlation between age at deafness onset and auditory testing results (speech perception in Cochlear Implants ­ Final Evidence Report Page 59 Health Technology Assessment April 17, 2013 noise and lateralization) (Steffens et al. Six studies (7 publications; total, n=247) evaluated age at first implant with variable findings (Steffens et al. Six analyses of the correlation between age at first implant and bilateral advantage in speech perception (quiet and noise) and lateralization were all negative (no correlation). Four analyses of this factor as an absolute success predictor had mixed results: younger age was related to better speech perception in noise (statistical testing not reported) and with better lateralization (significant after adjustment for other factors) in two studies but no association with speech perception in quiet or noise or with functional status was found in two other studies. Five studies (total, n=197) reported mixed results for age at second implant (Steffens et al. Two studies suggested that younger age may be associated with a greater bilateral advantage with respect to speech perception in noise or with sound localization, while another study found no correlation between bilateral advantage and either speech perception or localization. The remaining 2 studies reported conflicting results for an association between age and absolute lateralization outcomes. However, given the very poor quality of the available evidence, future findings could alter the conclusions that are possible at this time. The results were somewhat mixed with respect to both effect modification and success prediction, but the betterquality studies found no relationship with speech perception or lateralization. Effectiveness According to Hearing Aid Use A single noncomparative study reported a positive relationship between duration of prior hearing aid use and absolute lateralization scores, after adjustment for other factors (Van Deun et al. Two studies reported both types of comparisons in speech perception tests for the same patients. Effectiveness According to Other Factors Single studies reported no relationship between effectiveness and etiology of deafness (Steffens et al. However, these small studies provide insufficient data to allow any conclusion for these particular factors. Baseline data for these factors was not sufficient to allow any inferences from the overall body of 21 comparative studies. No data on Cochlear Implants ­ Final Evidence Report Page 60 Health Technology Assessment April 17, 2013 differential effectiveness according to device or provider were identified. There were also no data on effectiveness according to sex, ethnicity, race, or disability other than hearing loss. No analyses of differential safety according to device or provider were available. Masterson and colleagues did observe, however, a large difference in the rates of device failure between early models and new generation devices. The authors of one of the case series selected for safety data reported that a disproportionate number of children requiring reimplantation (12 of 345 procedures) had a structural deformity or had been affected by bacterial meningitis or a congenital infection, but no statistical analysis was performed (Masterson et al. For evaluating bodies of evidence, data pertaining to effect modification were considered of higher quality than the more indirect data pertaining to success predictors. The vast majority of analyses, whether they were designed to measure effect modifiers or success predictors, were some form of correlation analysis, which does not provide any information on the magnitude of differences in effect or differences in outcome. Among the few analyses where authors specified a cutoff value and treated the factor of interest as a binary variable. In patients with a substantial difference in performance between the two ears, no binaural advantage over the better ear was observed. However, the authors did not define a threshold of relative or absolute performance in the better ear at which no binaural advantage was observed. Furthermore, the relative performance of the two ears was determined after the second implant; thus, these findings do not help define patient selection criteria for a second implant. A single study found that a reduction in tinnitus annoyance occurred only in patients who were decompensated, i. Another study found no relationship between the effect of bilateral implantation on speech perception in quiet and time between implants, age at second implant, or deafness duration in either ear (Zeitler et al. However, the study showed a negative correlation between poorer sound location (greater deviation from correct location) and age at onset of deafness, as well as a positive correlation between poorer sound localization and duration of deafness as a fraction of age. The authors did find significant negative correlation between the interimplant interval and binaural speech perception in quiet. No studies explored the relationship between effectiveness and sex, ethnicity, race, concomitant disability, age at first implantation, prelingual versus postlingual deafness, choice of first-implanted ear, specific device, or provider characteristics. Masterson and colleagues did observe, Cochlear Implants ­ Final Evidence Report Page 62 Health Technology Assessment April 17, 2013 however, a large difference in the rates of device failure between early models and new generation devices.

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The 1994 TenWolde paper describes manual tools used to design building envelopes for moisture control. There is a discussion of limitations of manual design tools including their focus on condensation rather than moisture damage, their failure to address phenomena such as mold or paint failure that are not necessarily related to surface condensation, their ignoring of air leakage through the assemblies being modeled, their failure to address capillary transport or other transport mechanisms besides diffusion, their inability to model transient conditions, their failure to model latent heat, and their one-dimensional nature which rules out detailed analysis of thermal bridges, corners, holes, cracks, etc. It is recommended they be used only in relatively airtight structures, with monthly average (not design) temperature data (to avoid overly stringent conclusions), and that follow-up evaluation of any condensation indicated in the calculations be performed to assess whether it is potentially hazardous or benign. None of the numerical methods identified in this paper appear to have been further developed. All three methods compare vapor pressures at different points (based on vapor diffusion equations) with the saturation vapor pressures. This requires profiling temperature through the assembly (based on assumed indoor and outdoor conditions as well as the thermal resistances of different components) and comparing it to the local vapor pressure to determine whether condensation will occur. Once condensation occurs, subsequent steps along the flow path are not accurately modeled. A simplified method of incorporating airflow through the assembly is also described. Limitations in the methods, including limitation to vapor diffusion and failure to account for water absorption by materials or drying potential, are described. While these tools are simple enough to be used for design, and have been widely used for that purpose, the text cautions that "[r]esults obtained with any of these methods should therefore be considered as approximations and be used with extreme care. One substantive change is elimination of one of the "Recommendations for Use" in the earlier paper, which had suggested that under some conditions a construction might be acceptable for use even though one of the manual methods had identified the potential for condensation. Straube and Schumacher, "The Role of Hygrothermal Modeling in Practical Building Design - Case Studies" Presented at eSim 2002, Montreal Canada, September 2002. It begins with a summary of the results of an International Energy Agency review of the subject that identified 28 relevant models. The others were more sophisticated, all the way up to two models classified as "three dimensional heat, air and moisture transport models. The model is designed to focus on residential building walls of lightweight construction. These applications include (1) moisture accumulation due to air convection over a period of 31 days, (2) exfiltration of indoor air through different points of a wall over a period of 100 hours, and (3) air exfiltration and moisture accumulation in residential wall cavities over a 52-week period, in nine Canadian and three Finnish locations. Sensitivity of the results to rate of exfiltration, indoor relative humidity and point airflow vs. The concluding remarks emphasize the progress made in this field between 1984 and 1994, but caution that users must fully understand the assumptions and limitations, embedded in these modeling approaches. Like many other sources, they also argue that while absolute results of the model may not be correct, the primary value of the modeling is in assessing the relative performance of different constructions. Chapter 23 of the 2001 Handbook of Fundamentals includes a short section on mathematical models for moisture analysis. The focus is on transient models that solve for conditions on an hourly basis rather than steady-state models. This part of the text is written in general terms and specific models are not described. It emphasizes that transient models are essential for capturing short-term processes including driving rain absorption, condensation under rapidly varying summer conditions, and phase changes. A comprehensive list of "features of a complete moisture analysis model" is also presented. These features include various material properties and their dependence on humidity and temperature; detailed weather data including wind and rainfall; and many others. The text cautions that "[t]wo-dimensional and three-dimensional hygrothermal models are extremely complex and mostly require the direct expertise of the authors. It begins with a discussion of the relationship between the purpose of the analysis and the appropriate tool to use, distinguishing between applications for design of new buildings and assessments of existing buildings or research. Introductory sections present a general description of the modeling process and identify required choices faced by the model user. The first case study involves choosing a specific wall design for a multi-story apartment building in the Pacific Northwest. It involves evaluating the potential need for the walls to include (1) polyethylene sheeting as a vapor retarder and (2) insulating sheathing. The key concern was the effect of driving rain and rainwater absorption on moisture levels in the wall. The second case study involved heat loss through insulated and uninsulated basement floor slabs with embedded radiant heat pipes, but did not involve moisture analysis.

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Patients typically present with hyperkalemia and a mild hyperchloremic metabolic acidosis. The hyperkalemia is usually managed with a low potassium diet and use of loop or thiazide diuretics. The most common cause of acute respiratory acidosis in hospitalized patients is drug-induced respiratory depression with hypoventilation, due to narcotics, sedatives, or anesthesia. It can be a response to any disease that causes hypoxia, such as a pulmonary embolism, but is also often seen as a manifestation of an anxiety disorder with hyperventilation. Hypocapnia causes decreased cerebral blood flow, so symptoms manifest as lightheadedness or dizziness. With acute alkalosis, there is increased affinity between albumin and calcium, so more calcium becomes protein bound. Patients may then experience symptoms of hypocalcemia (perioral numbness, paresthesias). This alkalosis is termed "chloride resistant" or "saline resistant," meaning that it cannot be corrected by the administration of sodium chloride solution. He has edema of the optic disc, and his neurologic examination does not reveal any focal neurologic deficits. With alkaline urine and hypercalciuria, patients are predisposed to recurrent calcium phosphate stones. Urine chloride is useful for judging the volume status of patients with metabolic alkalosis, and is used to classify them as either volume depleted (low urine Cl) or volume repleted (high urine Cl). If low urine chloride, they are considered chloride responsive, and the alkalosis can be corrected with the infusion of saline. This toxic metabolite causes mental status depression, papilledema, optic neuritis, and metabolic acidosis. Patients with respiratory alkalosis may experience symptoms of cerebral vasoconstriction (dizziness) and transient hypocalcemia (perioral numbness and paresthesias). In metabolic alkalosis, low urine chloride can determine that the alkalosis can be corrected by saline infusion (chloride responsive). She has had this pain off and on for several years; however, for the past 2 days it is worse than it has ever been. It started after she vigorously vacuumed a rug, is primarily on the right lower side, radiates down her posterior right thigh to her knee, but is not associated with any numbness or tingling. It is relieved by laying flat on her back with her legs slightly elevated and lessened somewhat when she takes ibuprofen 400 mg. Except for moderate obesity and difficulty maneuvering onto the examination table because of pain, her examination is fairly normal. The only abnormalities you note are a positive straight leg raise test, with raising the right leg eliciting more pain than the left. Learn the history and physical examination findings that help to distinguish benign musculoskeletal low back pain from more serious causes of low back pain. Understand the variety of treatment options and their effectiveness in low back pain. Learn the judicious use of laboratory and imaging tests in evaluating low back pain. Considerations this young patient with chronic back pain has an acute exacerbation with pain radiating down her leg, which may indicate possible sciatic nerve compression. She has no other neurologic abnormalities, such as sensory deficits, motor weakness, or "red flag" symptoms of more serious etiologies of back pain, which if present would demand a more urgent evaluation. Thus, this individual has a good prognosis for recovery with conservative therapy, perhaps time being the most important factor. This condition can result from spondylolysis or from degenerative disk disease in the elderly. This complaint is most common in adults in their working years, usually affecting patients between 30 and 60 years of age. Although it is common in workers required to perform lifting and twisting, it is also a common complaint in those who sit or stand for prolonged periods.

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Signs Tender points, widely and symmetrically distributed, are the characteristic sign of the syndrome. Relief Relief may be provided by reassurance and explanation about the nature of the syndrome and possible mechanisms of pain: anxiety may thus be reduced, expensive and hazardous investigations and treatments limited, and use of medication reduced. Low dose amitriptyline, cyclobenzaprine, and aerobic exercise have been shown, in placebo controlled double blind studies, to improve symptoms. Blood flow during exercise is reduced, and decreased oxygen uptake in muscles has been noted. Two studies have found increased levels of substance P in the cerebrospinal fluid of patients. In general, these findings, some of which may be secondary phenomena, have been insufficient to explain the major signs and symptoms of the syndrome. It also is noted frequently following trauma, and has been known to develop after apparent viral illness. Thus the syndrome may be the final common pathway, perhaps as hyperalgesia, for a number of causative factors. Trauma or degenerative changes in the cervical or lumbar regions might precipitate the syndrome. An association with previous major depression in patients and families has suggested a genetic factor. Classification Criteria for Primary and Concomitant Fibromyalgia (from Wolfe et al. History of Widespread Pain Definition Pain is considered widespread when all of the following are present: pain in the left side of the body, pain in the right side of the body, pain above the waist and below the waist. In addition, axial skeletal pain (cervical spine or anterior chest or thoracic spine or low back) must be present. In this definition, shoulder and buttock pain is considered as pain for each involved side. Pain in 11 of 18 Tender Point Sites on Digital Palpation Definition Pain, on digital palpation, must be present in at least 11 of the following 18 tender point sites: Occiput: bilateral, at the suboccipital muscle insertions. Low Cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7. Supraspinatus: bilateral, at origins above the scapula spine near the medial border. Second Rib: bilateral, at the second costochondral junctions, just lateral to the junctions on upper surfaces. Gluteal: bilateral, in upper outer quadrants of buttocks in anterior fold of muscle. For a tender point to be considered "positive," the subject must state that the palpation was painful. Page 47 For classification purposes, patients will be said to have fibromyalgia if both criteria are satisfied. The presence of a second clinical disorder does not exclude the diagnosis of fibromyalgia. Main Features Diffuse aching, burning pain in joints, usually moderately severe; usually intermittent with exacerbations and remissions. Diagnostic criteria of the American Rheumatism Association describe and further define the illness. They are as follows: (1) morning stiffness, (2) pain on motion or tenderness at one joint or more, (3) swelling of one joint, (4) swelling of at least one other joint, and (5) symmetrical joint swelling. Further criteria include: (6) subcutaneous nodules, (7) typical radiographic changes, (8) positive test for rheumatoid factor in the serum, (9) a poor response in the mucin clot test in the synovial fluid, (10) synovial histopathology consistent with rheumatoid arthritis, and (11) characteristic nodule pathology. Definite rheumatoid arthritis may be diagnosed on five criteria, and probable rheumatoid arthritis on three criteria. Signs Tenderness, swelling, loss of range of motion of joints, ligaments, tendons. Relief Usually good relief of pain and stiffness can be obtained with nonsteroidal anti-inflammatory drugs, but some patients require therapy with gold or other agents. Morning stiffness in and around joints lasting at least Note: Specific Myofascial Pain Syndromes Synonyms: fibrositis (syndrome), myalgia, muscular rheumatism, nonarticular rheumatism. Specific myofascial syndromes may occur in any voluntary muscle with referred pain, local and referred tenderness, and a tense shortened muscle. Passive stretch or strong voluntary contraction in the shortened position of the muscle is painful.

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This article highlights the reality that walls with these features provide a continuum of different levels of performance with respect to each attribute. For example, claddings on some buildings may exhibit greater pressure equalization than others. In turn, pressure equalization effectiveness of the cladding also depends on the degree of airtightness (effectiveness of air barrier) on the wall system behind the cladding so that the structural wall system (which serves as an air barrier behind the cladding) experiences most of the wind load, rather than the cladding sharing a large portion of the wind load with the wall system. The more effective this equalization effect, the less water penetration will occur as a result of liquid water transport due to pressure differentials from the outside to the inside of the cavity. Also, there are different degrees of efficiency in handling and expelling water that penetrates the rainscreen cladding. This efficiency may be related to the amount of drainage space required to allow water to drain freely, and is dependent on the amount of water that penetrates the rainscreen cladding. The amount of ventilation area behind the rainscreen wall cladding also may affect the drying rate of wetted materials following a wetting event. The effectiveness of different variations of rainscreen systems depend on detailing and, more importantly, the ability of a particular wall system to moderate pressure differentials across the cladding that can greatly increase leakage rates. As a matter of jargon, as discussed by Rousseau, the distinction of whether the pressure differential is actually (or intentionally) designed to be moderated or whether it is not intentionally considered in the design of a wall cladding system is often the distinguishing factor in whether it may be called a "rainscreen" wall or just a "cavity" wall (regardless of what pressure equalization is actually achieved in either case). All of the foregoing studies of wood frame walls with various cladding systems rely on indexing of wall system performance based on a laboratory moisture loading condition. Future work will require better correlation of these relative test methods, loading conditions, and modeling studies to actual in-field performance and moisture loading variation and a wall systems ability to accommodate these conditions with reasonable serviceability over a reasonable service life with reasonable expectations for maintenance and repair. This is not a trivial task and stands as a significant challenge toward drawing practical applications from this type of information. It is likely that use of this type of information cannot be completely separated from judgment and experience. Therefore, better correlation of these test methods and moisture control design tools with actual experience is needed if practical applications are to be made with a reasonable level of confidence. The degree of applied wind pressure and the degree of pressure equalization across the cladding determine the amount of water penetration experienced in a given cladding system, with or without defects. Having complete pressure equalization will reduce, but not eliminate water intrusion through the rainscreen (cladding) and joints, because of other moisture drivers that exist. Better pressure equalization is achieved by having a relatively flexible rainscreen (cladding) and relatively rigid air-barrier (wall behind cladding). Depending on cladding type, an increase in air-barrier (wall behind cladding) air leakage results in increases in cladding pressure. The vent size in the rainscreen cladding relative to the volume of air behind the cladding served by the vent is important in moderating dynamic wind pressure differentials on the cladding. Air restriction along the flow path to a vent as well as distance from the vent to the farthest portion of the cavity served will tend to decrease pressure equalization. A tight air barrier behind the cladding is more important to static pressure equalization than dynamic pressure equalization. Pressure gradients on a building wall surface are largest at corner and eave regions and, therefore, smaller compartmentization of the air cavity behind the cladding is required in these areas than in more centrally located areas of a wall. All of the tested cladding types have exhibited some degree of pressure moderation, and all leaked water under the fairly stringent test conditions, sometimes also including intentional cladding defects. These reports describe two test houses monitored for cladding pressure where it was determined that the conventionally installed (no air cavity) hardboard siding generally experienced exfiltrative air-pressures which would tend to expel water and the pressures tended to be significantly moderated. The authors conclude that an air space is not necessarily required to provide substantial pressure equalization across the siding. However, the authors recommend that an air space should be considered for its other benefits (better drainage around windows and doors and reduced water load directly on the secondary weather barrier). In any case, there was no sign of moisture entry through the siding when it was removed from the building some two years after being installed. A small amount of moisture staining was found around windows and doors due to failed caulking. The reasons are fairly practical and are in reasonable agreement with the data covered above.

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It may also be one of the presenting symptoms of patients with primary movement disorders such as parkinsonism. These symptoms may be exacerbated by medications, particularly in the elderly; examples include antihypertensives, antidepressants, and anticholinergic agents that can cause orthostatic hypotension or dizziness as a side effect. Vertigo is the illusory sensation of movement or spinning, and usually arises from a disorder in the vestibular system. In the inner ear, the semicircular canals transduce angular acceleration, while the otolith organs sense linear acceleration. The vestibular ocular reflex maintains visual stability during head movements through these same cranial nerves, as well as projections through the medial longitudinal fasciculus. This integration of the inner ear, brain, and eyes explains why nystagmus is observed in patients during bouts of vertigo. It is asymmetry or discordance between the vestibular inputs from the two labyrinths or their central pathways that causes the sensation of vertigo. Physiologic vertigo includes motion sickness, or the sensation of movement that may occur when watching motion pictures. The first task in evaluating a patient with vertigo is to try to distinguish peripheral (labyrinthine apparatus or vestibular nerve) from central (brain stem or cerebellum) causes of vertigo. Central causes, such as cerebellar hemorrhage or infarction, can be immediately life-threatening or signify serious underlying disease and require urgent investigation. Peripheral causes typically signify less serious diseases and can be managed comfortably on an outpatient basis. Thus, the presence of other neurologic abnormalities, headache, or evidence of increased intracranial pressure is critical to address. Typically, this type of vertigo is precipitated by changes in head position, as in rolling over in bed, bending over, or looking upward. Patients may not have all of the typical symptoms at the same time; however, the first bout usually is abrupt in onset and associated with nausea. Patients turn their head toward the examiner and lay down quickly with their head hanging somewhat lower than the body. There is a lag of 5 to 10 seconds for the nystagmus to occur, and it is accompanied by the sensation of vertigo. Anticholinergic agents, such as meclizine or diphenhydramine, or benzodiazepines may help lessen symptoms. Alternatively one may attempt positional maneuvers in the office to displace the otolith from the semicircular canal back into the utricle or saccule, such as the Epley maneuver (Figure 60­2). Individuals with benign positional vertigo will demonstrate nystagmus after a delay of a few seconds. Treatment includes antihistamines or anticholinergics during acute attacks, and diuretics to reduce endolymphatic fluid. Because they are slow-growing, the subtle imbalances in vestibular input are often compensated, and patients may not experience significant vertigo, only vague imbalance. Finally, approximately 10% to 15% of patients have nonspecific dizziness, which cannot be classified as vertigo, presyncope, or dysequilibrium. Patients cannot clearly describe one of these syndromes, can report only that they feel "dizzy," have vague or unusual sensations, and have normal neurologic and vestibular examinations. The majority of these patients have some underlying psychiatric disorder, such as major depression, generalized anxiety, or panic disorder. Often the dizziness is associated with hyperventilation and can be reproduced in the office by purposeful hyperventilation. Treatment should be aimed at reassurance regarding the lack of pathologic causes of dizziness and at therapy for the underlying disorder with medication such as serotonin-specific reuptake inhibitors or benzodiazepines for anxiety disorders. When asked to describe the feeling, she gives a vague story of just feeling like "her head is too big. His medical history is notable for coronary artery disease and well-controlled hypertension. On examination he refuses to open his eyes or move his head, but when finally coaxed to sit up, he immediately starts to retch and vomit. Between episodes she generally feels normal but occasionally somewhat "off-balance. The word "dizzy" can mean several different things, so it is extremely important when obtaining the history to have the patient describe, as best he or she can, what is meant by "dizzy.

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If the occlusion is complete and remains for more than 30 minutes, infarction occurs. In contrast, the mechanism of chronic stable angina usually is a flow-limiting stenosis caused by atherosclerotic plaque that causes ischemia during exercise without acute thrombosis (Table 1­1). It is of the same character as angina pectoris-described as heavy, squeezing, or crushing-and is localized to the retrosternal area or epigastrium, sometimes with radiation to the arm, lower jaw, or neck. In contrast to stable angina, however, it persists for more than 30 minutes and is not relieved by rest. The pain often is accompanied by sweating, nausea, vomiting, and/or the sense of impending doom. Cardiac auscultation may reveal an S4 gallop, reflecting myocardial noncompliance because of ischemia; an S3 gallop, representing severe systolic dysfunction; or a new apical systolic murmur of mitral regurgitation caused by ischemic papillary muscle dysfunction. The earliest changes are tall, positive, hyperacute T waves in the ischemic vascular territory. Cardiac-specific troponin I (cTnI) and cardiac-specific troponin T (cTnT) are more specific to heart muscle and are the preferred markers of myocardial injury. Cardiacspecific troponin I levels may remain elevated for 7 to 10 days and cTnT levels for 10 to 14 days. They are very sensitive and fairly specific indicators of myocardial injury, and their levels may be elevated with even small amounts of myocardial necrosis. Aortic dissection often presents with unequal pulses or blood pressures in the arms, a new murmur of aortic insufficiency, or a widened mediastinum on chest x-ray film. Because the process is caused by acute thrombosis, antiplatelet agents such as aspirin and anticoagulation with heparin are used. To limit infarct size, beta-blockers are used to decrease myocardial oxygen demand, and nitrates are given to increase coronary blood flow. In addition, morphine may be given to reduce pain and the consequent tachycardia, and patients are placed on supplemental oxygen (Figure 1­3). Because myocardium can be salvaged only before it is irreversibly injured ("time is muscle"), patients benefit maximally when the drug is given early, for example, within 1 to 3 hours after the onset of chest pain, and the relative benefits decline with time. Because systemic coagulopathy may develop, the major risk of thrombolytics is bleeding, which can be potentially disastrous, for example, intracranial hemorrhage. The risk of hemorrhage is relatively constant, so the risk begins to outweigh the benefit by 12 hours, at which time most infarctions are completed, that is, the at-risk myocardium is dead. Sometimes intraluminal expandable stents are deployed, which may improve vessel patency. This has diminished in recent years with earlier and more aggressive treatment of ischemia and arrhythmias. Electrolyte deficiency, such as hypokalemia or hypomagnesemia, which can potentiate ventricular arrhythmias, should be corrected. One benign ventricular arrhythmia that is generally not suppressed by antiarrhythmics is the accelerated idioventricular rhythm. This is a wide-complex escape rhythm between 60 and 110 bpm that frequently accompanies reperfusion of the myocardium but causes no hemodynamic compromise. If the rate is slow enough to cause cardiac output and blood pressure to fall, intravenous atropine usually is administered. Ischemic reduction in ventricular diastolic compliance may lead to transient pulmonary congestion, associated with elevated left-sided filling pressures. Extensive myocardial necrosis and less contracting heart muscle may cause systolic failure and reduced cardiac output. Patients with hypotension frequently are evaluated by pulmonary artery (Swan-Ganz) catheterization to assess hemodynamic parameters. Cardiogenic shock is diagnosed when the patient has hypotension with systolic arterial pressure less than 80 mm Hg, markedly reduced cardiac index less than 1. Clinically, such patients appear hypotensive, with cold extremities because of peripheral vasoconstriction, pulmonary edema, and elevated jugular venous pressure, reflecting high left- and right-sided filling pressures.

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In multiple trials with the fields either on or not on, the subject experienced and reported temporal pain, feeling of usease, skipped heartbeats, muscle twitches and/or strong headache when the pulsed field (100 ms, duration at 10 Hz) was on, but no or mild symptoms when it was off. The authors conclude that electromagnetic hypersensitivity is a neurological syndrome, and statistically reliable somatic reactions could be provoked in this patient by exposure to 60-Hz electric fields at 300 volts per meter (V/m). Johansson et al (2010) studied symptoms, personality traits and stress in people with mobile phone-related symptoms and electromagnetic hypersensitivity. Johansson (2007, 2009) provide an extensive overview of the relevant literature on electrohypersensitivity. The need for new, biologically-based public exposure standards is recommended in both publications, in order to address electrohypersensitivity. Landgrebe et al (2007) reported that their study of electrosensitive patients showed participants had a reduced intracortical facilitation as compared to two control groups. The team of Sandstrom, Hansson Mild and Lyskov produced numerous papers between 1994 and 2003 involving people who are electrosensitive (Lyskov et al, 1995; Lyskov et al, 1998; Sandstrom et al, 1994; Sandstrom et al, 1995; Sandstrom et al, 1997; Sandstrom et al, 2003). Sandstrom et al (2003) presented evidence that heart rate variability is impaired in people with electrical hypersensitivity and showed a dysbalance of the autonomic nervous system. The reports referenced above provide evidence that persons who report being electrosensitive differ from others in having some abnormalities in the autonomic nervous system, reflected in measures such as heart rate variability. But given the relatively high percentage of persons reported to be electrosensitive (5% of the general population of Switzerland according to Schreier et al, 2006), with some being severely disabled as a consequence, it is critical that there be more study of this syndrome. The continuous detection of capillary blood flow is an important tool in analyzing the capacity of the autonomic nervous system. If the damage is ongoing (if cell and cordless phone use continues to occur over months and years), the potential for harmful effects increases. Volkow et al (2011a, b) reported increased glucose metabolism in the brain with cell phone use in humans. This important investigation of 47 human subjects used a randomized crossover design and labeled fluorodeoxyglucose to measure the metabolisms of the brain when the cell phone was activated but muted for 50 minutes as compared to not being activated. While the effect was small, the negative correlation of the effect with distance was statistically significant (R = -0. This study is particularly important in that it demonstrates definitively that an active cell phone, placed on the ear as one would normally be used, alters brain metabolic activity, but only in the region close to the cell phone. Their 2012 work concludes: "Based on epidemiological studies there is a consistent pattern of increased risk for glioma and acoustic neuroma associated with use of mobile phones and cordless phones. The evidence comes mainly from two study centres, the Hardell group in Sweden and the Interphone Study Group. A systematic bias in the studies that explains the results would also have been the case for meningioma. The different risk pattern for tumor type strengthens the findings regarding glioma and acoustic neuroma. Meta-analyses of the Hardell group and Interphone studies show an increased risk for glioma and acoustic neuroma. Supportive evidence comes also from anatomical localisation of the tumor to the most exposed area of the brain, cumulative exposure in hours and latency time that all add to the biological relevance of an increased risk. In addition risk calculations based on estimated absorbed dose give strength to the findings. Nervous System Damage: Factors that act directly or indirectly on the nervous system can cause morphological, chemical, or electrical changes in the nervous system that can lead to neurological effects. The Presidential Cancer Panel (2010) found that children `are at special risk due to their smaller body mass and rapid physical development, both of which magnify their vulnerability to known carcinogens, including radiation. It is essential that any new standards for cell phones or other wireless devices be based on protecting the youngest and most vulnerable populations to ensure thay are safeguarded through their lifetimes. However, in terms of threshold exposures that result in human disease, new research on male reproduction and neurobehavioral alterations provide evidence for harm at even lower exposure levels. Belyaev is helpful in identifying key factors which must be known and controlled for in experiments (biological variables and physical parameters include bandwidth, frequency, modulation, polarization, intermittence and coherence time of exposure, static magnetic field, electromagnetic stray fields, sex, age, individual traits, and cell density during exposure). This is consistent with established weak field effects on coupled biological oscillators in living tissues. Biological systems of the heart, brain and gut are dependent on the cooperative actions of cells that function according to principles of non-linear, coupled biological oscillations for their synchrony, and are dependent on exquisitely timed cues from the environment at vanishingly small levels (Buzsaki, 2006; Strogatz, 2003). The key to synchronization is the joint actions of cells that co-operate electrically - linking populations of biological oscillators that couple together in large arrays and synchronize spontaneously according to the mathematics described for Josephson junctions (Brian Josephson, the 1993 Nobel prize winner for this concept). This concept has been professionally presented in journal articles and also popularized in print by Prof.

References:

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