Review and CME Lecturetreated by infusing plasma and prothrombin complex.With the hemodynamic gradually stabilized, urine outputincreased to an average of 2000 ml/d. Liver enzymes andbilirubin were changed to normal level three weeks postresuscitation,as well as clotting function and magnesiumin the blood. The patient was discharged from hospitalafter salvage therapy in the ICU for 46 days with the Ⅲlevel muscle strength of upper limbs and the Ⅱ + level oflower limbs. After 3 months of follow-up, muscle strengthcompletely recovered, and the patient resumed normalwork and life.DiscussThe clinical thinking of PRSClinicians should establish the clinical thinking ofPRS treatment on the basis of pathophysiology. The majorpathophysiology of PRS is the hypoperfusion of tissuesand organs, the reperfusion injury after the successfulresuscitation and subsequent SIRS, involving every organand system of the whole body. It requires clinicians musthave a strong overall view in the treatment process, operateto the point in different pathophysiological stages, andstrengthen the support and protection of key organs aswell. The starting mechanism of PRS is the cessation ofrespiratory cycle so as to interrupt oxygen supply fororgans and cause the injury, thus, it is vitally importantto regain oxygen supplement quickly, and to shorten theorgan hypoxia time. Because the capability of hypoxiatoleration of various organs differs greatly, effective bloodperfusion should be restored as soon as possible withinthe ischemic threshold time of tissues. At the stage ofischemia and reperfusion, microcirculatory dysfunctionFigure 1b 4 hours later, V1-3 leads displayed as QS, andpathological Q waves appeared in V4-6 leads, suggesting that theevolution of acute anterior myocardial infarction was underway.caused by multifocal hypoxia leads the release of harmfulenzymes and free radicals rapidly into the cerebrospinalfluid and blood, causing secondary damage. With thefurther development of metabolic disorders, organ damagecontinues to aggravate, and then levels of cytokinesand adhesion molecules elevate in the cycle, inducingdysfunction of producing cytokines in the leukocyte, thentriggering SIRS, and finally resulting in MODS. Heart andbrain are the most important target organs; therefore,it is particularly significant to protect these two organs.Thus, the core of treatment in this stage should be stressantagonistic,to reduce the release of inflammatory factors,as well as the elimination of harmful factors by CRRT andother means to protect organ function.PRS treatment strategiesJudge the reason of cardiac arrest precisely andadminister the treatment in timeThe major incentives of cardiac arrest are vagal reflexand electrolyte disorder caused by cardiovascular diseases,non-cardiovascular diseases, surgery and other technicaloperations in diagnosis and treatment. We should diagnosethe primary disease accurately and administer the treatmentin the process of resuscitation and post-resuscitation toreduce the occurrence of MODS. During the course ofdisease in this case, the patient was always accompanied byhypomagnesemia. In the human body, magnesium mainlyexists in intracellular mitochondria and microsomes,only 1% of which can be found in the extracellular fluid.Magnesium is one of the most important coenzyme amongFigure 1c Low voltage was in limb leads. Q waves appearedin Ⅱ, Ⅲ, AVF, V4-6 leads, and V1-3 leads displayed as QS,amplitude of R waves in V4-6 leads significantly decreasedcompared with that of the admission time. T waves of Ⅰ,AVL, Ⅱ, Ⅲ, AVF leads were upside down severely, suggestingextensive anterior myocardial infarction.Laboratory Review and Clinical and CME Investigation Lecture 24 FAM 2013 Jan/Feb Vol.20 Issue 1123
Review and CME Lecturemetabolic enzymes in the body, playing an important rolein the contraction and conduction of neuromuscular andmyocardial cells and the adjustment of smooth muscles inblood vessels, tracheas and bronchia. Studies have shownthat hypomagnesemia (serum magnesium
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