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1. |
PrefacePathophysiology |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 157-157
Dennis Cheek,
Iain Buxton,
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ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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2. |
Hemodynamic and Sympathetic Nervous System Responses to Stress During the Menstrual Cycle |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 158-167331
Judith McFetridge,
Andrew Sherwood,
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摘要:
In this study, the impact of menstrual cycle phase on hemodynamic and sympathetic nervous system responses was examined during exposure to a battery of laboratory stressors. Participants were 40 healthy premenopausal women, aged 26 to 51. Impedance cardiography was used to measure stroke volume, heart rate, and cardiac output. Systemic vascular resistance was derived on the basis of concurrently recorded blood pressure and cardiac output. The menstrual cycle's effect on the sympathetic nervous system response was explored by evaluating plasma catecholamine responses during stress. In luteal compared with follicular subjects, systemic vascular resistance was significantly lower during all stress tasks (P< 0.03). Catecholamine responses were also significantly lower in luteal subjects (P< 0.004). The results suggest that the sympathetic nervous system may respond to stress differently during different phases of the menstrual cycle. This finding has implications for understanding "whitecoat hypertension" in women, and highlights the need to measure blood pressure during several office visits. Perhaps high blood pressure readings recorded during the follicular phase should be reexamined during the luteal phase before considering pharmacologic intervention.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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3. |
Pain: Neuroanatomy, Chemical Mediators, and Clinical Implications |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 168-178
Jeannette McHugh,
William McHugh,
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摘要:
Most pain information begins at simple, naked nerve endings called nociceptors that form a functional pain unit with nearby tissue capillaries and mast cells. Tissue injury causes these nerve terminals to depolarize, an event that is propagated along the entire afferent fiber eventuating in sensory impulses reaching the spinal cord. This firing of primary afferent fibers at the site of tissue injury causes axonal release of vesicles containing neuropeptides such as substance P, which acts in an autocrine and paracrine manner to sensitize the nociceptor and increase its rate of firing. Cellular damage and inflammation increase concentrations of other chemical mediators such as histamine, bradykinin, and prostaglandins in the area surrounding functional pain units. These additional mediators act synergistically to augment the transmission of nociceptive impulses along sensory afferent fibers. Primary fibers travel from the periphery to the dorsal horn where they synapse on secondary neurons and interneurons. When activated, interneurons exert inhibitory influences on further pain signal trafficking. Efferent supraspinal influences, in turn, determine the activity of interneurons by releasing a variety of neurotransmitter substances, thus resulting in a high degree of modulation of nociception within the dorsal horn. Events occurring in the periphery and in the dorsal horn can cause a dissociation of pain perception from the presence or degree of actual tissue injury. These phenomena involve many chemical mediators and receptor systems, and can increase pain experience qualitatively, quantitatively, temporally, and spatially. The complexity and plasticity of the nociceptive system can make clinical management of pain difficult. Understanding the structure and chemical signals associated with this system can improve the use of existing analgesics and provide targets for development of newer and more specific pain-fighting drugs.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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4. |
Pathophysiology and Implications for Treatment of Acute Respiratory Distress Syndrome |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 179-197333
Mary van Soeren,
William Diehl-Jones,
Robert Maykut,
Wael Haddara,
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摘要:
Acute respiratory distress syndrome is a complex group of signs and symptoms caused by direct or indirect lung injury. In spite of decades of research, it is still associated with a high mortality rate. Pathogenesis of this disease is related to alveolar endothelial and epithelial cell injury and associated release and sequestration of inflammatory mediators and cells, including cytokines and neutrophils, respectively. Pharmacologic interventions have been largely unsuccessful, and ventilation strategies to support oxygenation while limiting ventilator associated lung injury have not demonstrated any significant reductions in the mortality rate. However, novel therapies are in development, based on the knowledge of the pathologic processes of acute respiratory distress syndrome. In this article an overview of the disease process and mediator involvement is presented, followed by a review of pharmacologic and ventilation treatments currently in use or under study.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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5. |
Risk Factors for Nosocomial Pneumonia in Critically Ill Trauma Patients |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 198-231
Janet Harris,
Manjari Joshi,
Patricia Morton,
Karen Soeken,
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摘要:
Nosocomial pneumonia is the most common pulmonary complication in trauma patients and the leading cause of death in nosocomial infections. A comprehensive review of pneumonia studies is provided. The Centers for Disease Control's nosocomial pneumonia pathogenesis model is reviewed and was used to guide the selection of risk factors evaluated in this study. The purposes of this research were to identify underlying dimensions (factors) of variables that increase the risk of nosocomial pneumonia and to identify predictors of nosocomial pneumonia in critically ill trauma patients.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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6. |
Biologic Markers of Airway Inflammation in Asthma |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 232-240
Susan Janson,
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摘要:
Asthma is a serious chronic disease of the airways that affects approximately 14% of the population in the United States. The fundamental pathophysiologic component of asthma is airway narrowing, which causes airflow obstruction. Both inflammation and bronchoconstriction contribute to airway narrowing. The pathogenesis of airway inflammation in asthma and the natural history of the disease are the subject of intense research and study in many countries of the world. The mechanisms of airway inflammation are only partially understood but are the basis for the devastating symptoms that affect the quality of life of millions of people. Treatment of asthma is directed at decreasing airway inflammation to gain long-term control of the disease.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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7. |
Role of Nucleotides and Nucleosides in the Regulation of Cardiac Blood Flow |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 241-251
Brian Oxhorn,
Dennis Cheek,
Iain Buxton,
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摘要:
The regulation of blood flow in the heart on a moment-to-moment basis is essential to meet changes in the oxygen demands of cardiac muscle. The signals that subserve this regulation are not all firmly established. Although the formation and release of adenosine by cardiac muscle during periods of hypoxia or regional ischemia in the heart are well known to produce regional vasodilation and salvage of at-risk myocardium, these extracellular actions of adenosine are believed to occur abluminally and thus do not explain the origin or predict the potent actions of intravascular adenosine. The notion that purines such as adenosine and adenosine 5′-triphosphate (ATP) might be available to act in the lumen of the blood vessel has been proposed by the authors and others to help explain the regulation of blood flow in the heart in nonpathologic states. This article details the background and current understanding of the vascular actions of adenosine and ATP, defines the Nucleotide Axis Hypothesis, and reviews clinical studies in which its likely importance in the maintenance of blood flow in the heart has been investigated.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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8. |
Reperfusion Injury of Cardiac Myocytes: Mechanisms, Treatment, and Implications for Advanced Practice Nursing |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 252-260
Jason Brennan,
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摘要:
Reperfusion injury is a major complication associated with the restoration of blood flow to previously ischemic myocardium. The deleterious effects associated with reperfusion injury result from several complex pathologic mechanisms. The complexity of these mechanisms makes development of treatment protocols difficult. The purpose of this article is to review the pathophysiology of reperfusion injury and currently indicated therapies. Implications for advanced practice nursing and areas for further research are presented.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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9. |
Channelopathies: Potassium-Related Periodic Paralyses and Similar Disorders |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 261-270
Eleanor Bond,
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摘要:
Channelopathy is a term used to describe clinical problems caused by disorders of membrane ion channels. Included in this disease category are certain types of periodic paralyses, ataxia, myotonia, migraine headache, epilepsy, nephrolithiasis, and long QT syndrome. This article briefly summarizes membrane ion channel structure and function and details several relatively common channelopathies. In hyperkalemic periodic paralysis, mutant skeletal muscle sodium channels fail to close completely after an action potential. This evokes two apparently opposite symptoms: myotonia (caused by a small depolarization and repetitive excitation) or paralysis (caused by larger depolarization and inexcitability). In hypokalemic periodic paralysis, mutation affects the closing of skeletal muscle calcium channels, causing transient paresis or paralysis. The task of the advanced practice nurse is to recognize these disorders, institute appropriate prophylactic measures and treatments, monitor symptom progression, and avoid complications. Understanding of channelopathies is advancing rapidly. On the horizon are therapies tailored to counter specific membrane ion channel defects.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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10. |
Regulation of Uterine Contraction: Mechanisms in Preterm Labor |
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AACN Clinical Issues: Advanced Practice in Acute and Critical Care,
Volume 11,
Issue 2,
2000,
Page 271-282
Iain Buxton,
Windee Crow,
Shaji Mathew,
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摘要:
Preterm labor (PTL) is defined as uterine irritability accompanied by cervical dilation and/or effacement that occurs before 37 weeks gestation. In most cases, PTL becomes preterm delivery (PTD), accounting for 8% to 10% of births in the United States. Fetuses born before 37 weeks' gestation are at risk for a multitude of health and developmental problems. Most perinatal morbidity and mortality in the United States are caused by PTL. It is a costly problem, in both monetary and human terms. Although some risk factors have been identified, they by no means identify, in advance, every case of PTL and PTD. Despite the understandable emphasis on attempts to find and test risk factors that predict PTL, the ultimate benefit-preventing PTD-will come only from an understanding of the physiologic mechanisms of parturition and how to halt those processes when they occur too early. This article reviews current approaches to preventing PTD, describes the biology of myometrial contraction, and discusses recent progress from several laboratories including the authors' that may shed light on approaches to inhibit uterine contractility in the setting of PTL.
ISSN:1079-0713
出版商:OVID
年代:2000
数据来源: OVID
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