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Psychogenic Chest pain secondary to psychogenic etiology is a diagnosis of exclusion order albuterol on line amex, requiring a full evaluation for potential life-threatening causes buy 100mcg albuterol with visa. There often is a trigger for the onset of the pain purchase albuterol no prescription, including recent psychologic and emotional stress, or recent diagnosis of another organic disease. Psychogenic chest pain is more common in patients with a family history of cardiac disease (30). Treatment is difficult, and includes extensive reassurance and treatment/counseling for their underlying psychiatric concerns. Physiologically, this occurs secondary to respiratory alkalosis and subsequent coronary artery vasoconstriction (31). Treatment involves referral to a physiotherapist, who can help the patient learn specific breathing techniques to prevent the dysfunctional breathing patterns. Cardiac Causes of Chest Pain In a population of children and adolescents with chest pain, the proportion with a cardiac origin for the chest pain is extremely low. These include obstructive hypertrophic cardiomyopathy, aortic valve stenosis, pericarditis, arrhythmias, coronary artery insufficiency, aortic dissection (especially in patients with Marfan syndrome), and mitral valve prolapse. Causes of coronary artery insufficiency in children include Kawasaki disease, Williams syndrome, anomalous origin of the coronary arteries, and coronary arteriovenous and coronary cameral fistulae. Additionally, it is critical to obtain an accurate history of recent medication and drug intake, particularly substances that may induce coronary vasospasm. It is important to identify patients who are at high risk for these conditions by history and characteristics of the pain so that appropriate diagnostic and therapeutic steps can be taken. From 2000 to 2009, more than 3,700 children and adolescents were evaluated for chest pain. During this time period, only 41 patients with an initial presentation of chest pain were ultimately determined to have a cardiac cause (32). Patients with coronary artery anomalies and chest pain were far more likely to present to an outpatient clinic. Patients with chest pain secondary to myocarditis, pericarditis, or pulmonary embolism are more likely to present to an emergency department or inpatient setting (32). Among patients discharged from the outpatient setting with a diagnosis of noncardiac chest pain, no patients died over a median follow-up of 4. However, it has been shown to be associated with male gender, tobacco smoking, and substance abuse (34). Coronary thrombosis in the setting of nephrotic syndrome has been reported (35,36). Fortunately, hospital mortality for adolescents admitted for acute myocardial infarction is <1% (34). Medical Evaluation The evaluation of chest pain requires a thorough history and careful physical examination (1,15). The family history should be explored for premature forms of heart or lung disease and instances of premature death. In addition, it may be helpful to know whether other family members have chest pain, such as a parent or grandparent who experiences angina. In the majority of cases, the cause of the pain will be apparent after the history and physical examination. A thorough and thoughtful history and physical examination are important in reassuring the patient and family that there is no serious problem. The examination should include a complete heart, lung, neck, extremity, and abdominal examination. It is important to palpate the costochondral joints and other areas of the chest to try to elicit localized tenderness. A history of chest pain associated with presyncope, syncope, sweating, nausea, palpitations, cyanosis, or dyspnea should raise suspicion of a potentially serious underlying cause of the chest pain. A strong family history of sudden death, aortic dissection or cardiomyopathy also may prompt further evaluation despite an equivocal personal history. In the vast majority of cases of chest pain in children, only a history and physical examination are necessary and additional tests are not particularly helpful (1,2,32). In the unusual circumstance where cardiac disease is strongly suspected, several investigations may be performed. An echocardiogram can be performed to assess structural heart disease, cardiomyopathy, and coronary anomalies. Appropriate use criteria for initial transthoracic echocardiography in pediatric patients were recently endorsed by multiple cardiology societies (37). The specific criteria related to pediatric patients presenting with chest pain are shown in Table 70. For most patients with musculoskeletal causes of chest pain, an explanation of the cause of the pain and its benign nature frequently is enough to reassure the patient and their family. The goal in these discussions is to reduce the anxiety associated with the pain, allowing the patient to tolerate the pain with less fear. Children with noncardiac chest pain have been reported to have more symptoms of anxiety as compared to children with cardiac causes of chest pain (38). The use of medication usually is unnecessary for the majority of causes of chest-wall pain. If the history and physical examination suggest a cardiac cause, appropriate consultation and evaluation should be sought. In certain situations for patients with recurrent severe pain, consultation with a pain specialist may be useful to discuss potential options. They noted that the initial diagnosis was changed in 34% of the patients during follow-up, typically indicating a nonorganic cause of the chest pain. Therefore, patients should be counseled about the potential for recurrence of noncardiac chest pain. Characteristics of children presenting with chest pain to a pediatric emergency department. Chest pain in otherwise healthy children and adolescents is frequently caused by exercise-induced asthma. Slipping rib syndrome: an infrequently recognized entity in children: a report of three cases and review of the literature. Incidence of venous thromboembolism in infants and children: data from the National Hospital Discharge Survey. Pulmonary atresia with ventricular septal defect and persistent airway hyperresponsiveness. Needles in hay: chest pain as the presenting symptom in children with serious underlying cardiac pathology. Management of pediatric chest pain using a standardized assessment and management plan. Acute myocardial infarction in a young boy with nephrotic syndrome: a case report and review of the literature. Anxiety and depressive symptoms and anxiety sensitivity in youngsters with noncardiac chest pain and benign heart murmurs. Daniels Atherosclerosis Coronary artery disease and stroke are the most common causes of morbidity and mortality in developed countries.

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The pathology of hypertensive pulmonary vascular disease generic 100mcg albuterol; a description of six grades of structural changes in the pulmonary arteries with special reference to congenital cardiac septal defects order albuterol with american express. Early pulmonary vascular changes in congenital heart disease studied in biopsy tissue order genuine albuterol online. Illustration of the additional value of real-time 3-dimensional echocardiography to conventional transthoracic and transesophageal 2-dimensional echocardiography in imaging muscular ventricular septal defects: Does this have any impact on individual patient treatment? Importance of (perimembranous) ventricular septal aneurysm in the natural history of isolated perimembranous ventricular septal defect. Long follow-up (to 43 years) of ventricular septal defect with audible aortic regurgitation. The fate of raised pulmonary vascular resistance after surgery in ventricular septal defect. Pulmonary stenosis, aortic stenosis, ventricular septal defect: Clinical course and indirect assessment - Report from the Joint Study on the Natural History of Congenital Heart Defects. Captopril in infants for congestive heart failure secondary to a large ventricular left-to-right shunt. Effect of digoxin on contractility and symptoms in infants with a large ventricular septal defect. Spontaneous regression of left ventricular dilation in children with restrictive ventricular septal defects. Variation in outcomes for benchmark operations: an analysis of the Society of Thoracic Surgeons Congenital Heart Surgery Database. Permanent pacemaker for atrioventricular conduction block after operative repair of perimembranous ventricular septal defect. Incidence and risk factors of complete atrioventricular block after operative ventricular septal defect repair. Transcatheter closure of perimembranous ventricular septal defects: early and long-term results. Atrioventricular block after transcatheter closure of perimembranous ventricular septal defects. Transcatheter versus surgical closure of perimembranous ventricular septal defects in children: a randomized controlled trial. Reduced long-term exercise capacity in young adults operated for ventricular septal defect. Long-term behavior and quality of life after corrective cardiac surgery in infancy for tetralogy of Fallot or ventricular septal defect. Long-term follow-up and quality of life after closure of ventricular septal defect in adults. A functional understanding of moderate to complex congenital heart disease and the impact of pregnancy. The ductus arteriosus is an obligatory part of normal fetal circulation that allows blood returning to the heart to bypass the lungs, and instead flow directly into the descending aorta. Epidemiology Because the ductus arteriosus is a necessary part of normal fetal circulation, the presence of a patent ductus arteriosus immediately after birth can be assumed to be nearly universal. In most cases, the ductus constricts in response to increased blood oxygen content and other factors described below. While ductal constriction usually leads to functional and anatomic closure, in some cases the ductus may close only partially or not at all. With the advent of color Doppler echocardiography, the incidental recognition of asymptomatic “silent” ductus has become more common. Patency of the ductus in this scenario is influenced to a varying degree by a number of factors, including blood oxygen content and circulating prostaglandins. Oxygen One significant factor contributing to ductal patency in the fetus is the low dissolved oxygen concentration (pO2) supplied to the ductus. By contrast, the aortic dissolved oxygen concentration shortly after birth is near 100 mm Hg. Higher pO2 levels promote smooth muscle constriction within the wall of the ductus, probably by triggering calcium influx into the cell (6,7,8). Conversely, the low pO2 in fetal blood prevents such calcium influx and smooth muscle contraction, and helps to maintain ductal patency. Prostaglandins act to relax ductal smooth muscle resulting in vasodilation and patency of the ductus. Other Factors Other factors have been shown to affect vasodilation and vasoconstriction of the ductus arteriosus. Studies in lambs have shown that the concentration of adenosine is much higher in the fetus than in the neonate (19). These findings have led some to speculate about a potential role of adenosine in regulating patency of the ductus arteriosus (20). In addition, removal of the low resistance placenta from systemic circulation decreases the ratio of pulmonary vascular resistance (Rp) to systemic vascular resistance (Rs). At this point in the transition to postnatal life, the ductus arteriosus is exposed to systemic arterial pO2, which in room air at sea level is near 100 mm Hg. This high systemic arterial pO2 causes vasoconstriction of the ductus arteriosus through mechanisms that have not been completely elucidated. Smooth muscle contraction may be promoted by oxygen-sensitive potassium channels that in turn activate voltage-sensitive calcium channels that allow calcium influx into smooth muscle cells, resulting in smooth muscle contraction (6,21). Initial, “functional” closure of the ductus arteriosus is caused by smooth muscle contraction resulting from increased blood pO2 and decreased concentration of circulating prostaglandins. Functional closure occurs within the first 24 hours of life in about half of all healthy, term neonates and is nearly universal by 72 hours of life (22). The aortic end of the ductus is usually wider in diameter and is often referred to as the ductal ampulla. Following functional closure of the ductus arteriosus, lower pO2 and thickening of the ductal walls due to smooth muscle contraction produce hypoxia of the inner layers of the ductus. This hypoxia leads to cell destruction and fibrosis, and ultimately, anatomic (permanent) obliteration of the ductal lumen (23,24,25). The fibrous strand that remains in place of the ductus arteriosus is known as the ligamentum arteriosum. This low pO2 may result from poor alveolar-capillary oxygen diffusion due to immature lungs. It may also be compounded by persistently elevated pulmonary vascular resistance leading to right-to-left shunting across the ductus. Animal studies have suggested that the premature ductus may be less responsive to the vasoconstrictive effects of O2 (8). At extremely high altitude, the incidence may be 30 times greater than at sea level. This increased risk has been attributed to lower blood pO2 due to decreased ambient oxygen concentration (27,28).

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Controlling birth defects: reducing the hidden toll of dying and disabled children in low-income countries buy cheap albuterol 100mcg line. The improvement of care for paediatric and congenital cardiac disease across the World: a challenge for the World Society for Pediatric and Congenital Heart Surgery order albuterol 100mcg without prescription. The challenge of congenital heart disease worldwide: epidemiologic and demographic facts generic albuterol 100mcg with visa. Congenital heart surgery databases around the world: do we need a global database? Improving pediatric cardiac surgical care in developing countries: matching resources to needs. Determinants of early outcome after neonatal cardiac surgery in a developing country. The global burden of disease study 2010: interpretation and implications for the neglected tropical diseases. Innovation for the ‘bottom 100 million’: eliminating neglected tropical diseases in the Americas. Chagas Disease, from discovery to control—and beyond: history, myths and lessons to take home. The neglected tropical diseases of Latin America and the Caribbean: a review of disease burden and distribution and a roadmap for control and elimination. Accelerating the development of a therapeutic vaccine for human Chagas disease: rationale and prospects. McCrindle What is Evidence-Based Medicine and why are Clinical Trials so Relevant to that Practice? As a result, the practice is not based solely on research evidence, and should not be viewed as a directive or “cook book” approach. The sequence of steps in the practice of evidence-based clinical decision making is outlined in Table 81. Both Absence and Proliferation of Evidence The important necessary first step includes a search for applicable research evidence to inform the clinical question at hand and a critical appraisal of that evidence and subsequent synthesis. The task often seems very daunting, and so one may resort to expert opinion or review articles (often just another form of expert opinion) or to the claims of industry. This is actually largely what many patients are doing, making their own decisions on the basis of what they are exposed to in the media or what they are told by other laypeople. The popular “news” media are fraught with errors in both reporting the facts and their interpretation, are prone to sensationalism, and in the obligation to provide balanced viewpoints often resort to inclusion of dissenting unsupported opinions from the fringes of reason. An unregulated claim extolling the curative wonders of an alternative or complementary health product of unproven effectiveness or safety may carry more weight than the best evidence-based recommendation from their healthcare provider. Together with rising healthcare costs and stories regarding conflicts of interest and sometimes conflicting study results, many patients have become suspicious of the healthcare system and abandon therapies that are of proven benefit based on best evidence, sometimes to the detriment of their own health or that of others. Begin the process with a clinical scenario of immediate relevance, and specify the need for information as a well- thought-out and answerable question. Obtain the best available research evidence, usually by executing an informed and efficient search strategy of the published literature. Filter the results of the search by critically appraising the most relevant articles through assessment of methods and results in terms of their validity, the magnitude, and reliability of the reported effect, and their applicability and relevance to the clinical scenario at hand. From this integration and synthesis of the appraised evidence, together with the unique aspects of the clinical scenario, make the best-informed clinical decision. Assess the process itself, and strive for greater efficiency and benefit when applying it to future clinical scenarios. Evidence and Clinical Trials In order to provide the best possible care to their patients and to expertly and convincingly counsel them about that care, clinicians need to be expert users and appraisers of research evidence. One needs to be able to efficiently sift through the evidence and then be able to appraise the quality of that evidence before deciding how much weight to give it in P. One is looking to find evidence that is applicable to the clinical scenario and answerable question at hand, but of sufficient quality such that one can be confident that the findings are valid and reliable or as close to the truth as one can get. Clinical trials, by the nature of their design, execution, and systematic approach to appraisal, provide the greatest potential for freedom from biases that result in deviations from the truth and, thus, represent or contribute to the highest levels of evidence. This is why clinical trials have a greater impact within systems for developing and reporting clinical practice guidelines or recommendations. Clinical trials are assigned the highest grades in terms of quality of evidence and have the greatest influence in informing the strength of recommendations, as noted in Table 81. In some clearly defined circumstances, strong rationale for an alternative recommendations may be made on the basis of lesser approach is present. Recommendation The reporter(s) feel that the benefits exceed the harms but Clinicians should generally the quality of the evidence is not as strong (grade B or C). In follow a recommendation but some clearly defined circumstances, strong remain alert to new information recommendations may be made on the basis of lesser and sensitive to patient evidence when high-quality evidence is impossible to obtain preferences. Option Either the quality of the evidence that exists is suspect Clinicians should be flexible in (grade D) or well-performed studies (grade A, B or C) show their decision making little clear advantage to one approach versus another. No There is both a lack of pertinent evidence (grade D) and an Clinicians should feel little recommendation unclear balance between benefits and harms. Adapted from American Academy of Pediatrics, Steering Committee on Quality Improvement and Management. Well-designed and well-executed randomized clinical trials achieve a high grade of evidence for several reasons, as noted in Table 81. Causality Clinical trials provide the best evidence that any differences in the comparison of outcomes being assessed are a direct result of differences in the interventions being compared (or comparison to P. Clinical trials provide strong evidence for defining causality and can determine the efficacy (how well it works in a research or controlled setting), effectiveness (how well it works in clinical practice), and safety of an intervention. Many of these criteria are explicitly satisfied by clinical trials, and hence clinical trials provide the best evidence that an intervention either directly or indirectly (through reduction or elimination of intermediate causal factors) is the cause of observed differences in outcomes. The design and execution of clinical trials attempt to minimize confounding factors that may influence the outcomes of interest, with the observed effects then being confidently attributable to the interventions being compared. This is achieved by random allocation of study subjects, blinding of study assignment as far as possible, standardization of interventions and tracking of any cointerventions or crossovers, continuous accounting for all study subjects, and standardization of all assessments and interpretations of outcomes. Bias can be further detected and minimized during the data analysis, with statistical adjustment for any unbalances in potentially confounding factors. The prospective and concurrent nature of the data collection allows further minimization of bias through blinding, standardization, and quality control of measurements. The design, execution, and reporting for clinical trials allow standardization and more detailed and accurate critical appraisal than observational study designs. Is the relationship consistent across variations in study populations, settings and investigators, and design? If an intervention is successful in reducing or eliminating a particular risk factor or causal mechanism for an outcome, does this then alter the outcome in a consistent and predicted manner? Randomization The process of randomization, or random assignment of subjects to the study interventions, is a key feature of clinical trials that minimizes bias.

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