Page 14 - 麻醉与监护论坛2015年第7期

Review and CME Lecture
treated by infusing plasma and prothrombin complex.
With the hemodynamic gradually stabilized, urine output
increased to an average of 2000 ml/d. Liver enzymes and
bilirubin were changed to normal level three weeks post-
resuscitation, as well as clotting function and magnesium
in the blood. The patient was discharged from hospital
after salvage therapy in the ICU for 46 days with the Ⅲ
level muscle strength of upper limbs and the Ⅱ+ level of
lower limbs. After 3 months of follow-up, muscle strength
completely recovered, and the patient resumed normal
work and life.
Discuss
The clinical thinking of PRS
Clinicians should establish the clinical thinking of
PRS treatment on the basis of pathophysiology. The major
pathophysiology of PRS is the hypoperfusion of tissues
and organs, the reperfusion injury after the successful
resuscitation and subsequent SIRS, involving every organ
and system of the whole body. It requires clinicians must
have a strong overall view in the treatment process, operate
to the point in different pathophysiological stages, and
strengthen the support and protection of key organs as
well. The starting mechanism of PRS is the cessation of
respiratory cycle so as to interrupt oxygen supply for
organs and cause the injury, thus, it is vitally important
to regain oxygen supplement quickly, and to shorten the
organ hypoxia time. Because the capability of hypoxia
toleration of various organs differs greatly, effective blood
perfusion should be restored as soon as possible within
the ischemic threshold time of tissues. At the stage of
ischemia and reperfusion, microcirculatory dysfunction
Figure 1b 4 hours later, V1-3 leads displayed as QS, and
pathological Q waves appeared in V4-6 leads, suggesting that the AVL, Ⅱ, Ⅲ, AVF leads were upside down severely, suggesting
evolution of acute anterior myocardial infarction was underway.
LaboratoryRaenvdieCwlinaincdalCInMvEesLteigcatutiroen 24
123
caused by multifocal hypoxia leads the release of harmful
enzymes and free radicals rapidly into the cerebrospinal
fluid and blood, causing secondary damage. With the
further development of metabolic disorders, organ damage
continues to aggravate, and then levels of cytokines
and adhesion molecules elevate in the cycle, inducing
dysfunction of producing cytokines in the leukocyte, then
triggering SIRS, and finally resulting in MODS. Heart and
brain 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 stress-
antagonistic, to reduce the release of inflammatory factors,
as well as the elimination of harmful factors by CRRT and
other means to protect organ function.
PRS treatment strategies
Judge the reason of cardiac arrest precisely and
administer the treatment in time
The major incentives of cardiac arrest are vagal reflex
and electrolyte disorder caused by cardiovascular diseases,
non-cardiovascular diseases, surgery and other technical
operations in diagnosis and treatment. We should diagnose
the primary disease accurately and administer the treatment
in the process of resuscitation and post-resuscitation to
reduce the occurrence of MODS. During the course of
disease in this case, the patient was always accompanied by
hypomagnesemia. In the human body, magnesium mainly
exists in intracellular mitochondria and microsomes,
only 1% of which can be found in the extracellular fluid.
Magnesium is one of the most important coenzyme among
Figure 1c Low voltage was in limb leads. Q waves appeared
in Ⅱ, Ⅲ, AVF, V4-6 leads, and V1-3 leads displayed as QS,
amplitude of R waves in V4-6 leads significantly decreased
compared with that of the admission time. T waves of Ⅰ,
extensive anterior myocardial infarction.
FAM 2013 Jan/Feb Vol.20 Issue 1