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العنوان
Neuromuscular Blockers In Acute Respiratory
Distress Syndrome\
المؤلف
Hassanin, Ebrahem Marei Zakarya.
هيئة الاعداد
باحث / Ebrahem Marei Zakarya Hassanin
مشرف / Amr Essam El-Din Abd El-Hameed El-Hennami
مشرف / Melad Ragae Zakri Bastta
مناقش / Ghada Mohamed Samir El-Saied
تاريخ النشر
2014.
عدد الصفحات
97p. :
اللغة
الإنجليزية
الدرجة
ماجستير
تاريخ الإجازة
1/1/2014
مكان الإجازة
اتحاد مكتبات الجامعات المصرية - الرعاية المركزة
الفهرس
Only 14 pages are availabe for public view

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Abstract

Summary
Acute Respiratory Distress Syndrome (ARDS) is an acute
condition characterized by bilateral pulmonary infiltrates and
severe hypoxemia in the absence of evidence for cardiogenic
pulmonary edema.The etiology of ARDS is either direct
injury like aspiration of gastric contents or indirect like
sepsis. Pathophysiology of ARDS includes injury to the
vascular endothelium or to alveolar epithelium there is a rule
to neutrophils,cytokines and positive pressure
ventilation.Pathophysiology has 3 stages Inflammatory,
Proliferative and Fibrotic. The Laboratory investigations of
importance are arterial blood gases, compelete blood count,
renal functions, liver functions, brain natriuretic peptide and
serum cytokines. Chest X ray is essential for
diagnosis,Computed tomography is more sensitive if the
patient condition is suitable. Echocardiography also has a
role in the diagnosis.
The neuromuscular junction is made up of a motor neurone
and a motor endplate with a synaptic cleft or junctional gap
dividing them. Acetylcholine (Ach) is the neurotransmitter in
these synapses. Acetylcholine is synthesised from choline
and acetylcoenzyme A in the axoplasm of the cholinergic
nerve terminals. The mechanisms of the four modes of
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release of Ach are Quantal, Subquantal, Giant and Molecular
leakage. Acetylcholine Nicotinic receptors are made up of
five protein subunits. Acetylcholine molecules that do not
react with a receptor or are released from the binding site are
destroyed almost immediately by the enzyme
Acetylcholinesterase. Many drugs enhance or block
transmission at the neuromuscular junction.
NMBAs interact with the acetylcholine receptor either by
depolarizing the endplate (depolarizing agents) or by
competing with acetylcholine for binding sites
(nondepolarizing agents). Succinylcholine is the only
depolarizing NMBA in clinical use. Non-depolarizing
NMBAs include Benzylisoquinolinium compounds
(atracurium, mivacurium, doxacurium and cisatracurium) and
Aminosteroid compounds (Pancuronium, Vecuronium,
Rocuronium and Rapacuronium). NMBAs may have a role
in ARDS by decrease the oxygen consumption of respiratory
and other muscles, reducing cardiac output, increasing the
mixed venous partial pressure of oxygen, increasing the
partial pressure of arterial oxygen and may indirectly
minimize various manifestations of ventilator-induced lung
injury.
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Methods to improve oxygenation in ARDS include
recruitment maneuvers like applying high level of PEEP,
permissive hypercapnia, prone position, high frequency
oscillatory ventilation, extracorporeal membrane
oxygenation, corticosteroids, early administration of
NMBAs,neutrophil elastase inhibitors like Sivelestat, β-
Adrenergic agonists and dietary oil supplementation due to
antiinflammatory effects resulting from modulation of
arachidonic acid metabolism.