Page 16 - 麻醉与监护论坛2015年第7期

Review and CME Lecture
are two independent risk factors which contribute to the
spontaneous circulation unable to restore[13]. Sufficient
oxygen for the organs post-resuscitation will improve
and maintain the function of cells, but the amount of
oxygen level is still controversial. Animal experimental data
indicate that the high level of arterial oxygen may produce
ischemic free radicals to aggravate reperfusion injury so
as to affect the prognosis of the nervous system. Another
animal experiments show that 95% of the pulse oxygen
saturation level could significantly improve the prognosis
of nervous system in a short time comparing with 100%
level .[14-16] In addition, patients should get rid of the
respirator as soon as their basic respiratory status achieves
the standard in order to prevent the complications brought
about by continued mechanical ventilation.
The meaning of sustaining high capacity CRRT
In the SIRS period of PRS, as ischemic reperfusion
injury is the basis, a variety of cytokines and inflammatory
mediators uncontrolled release, inducing cell damage by
hypoxic metabolites, and then uncontrolled SIRS process
transfers to MODS, and finally changed to MOF. The initial
CRRT after resuscitation is not only renal replacement
therapy, but a support of the recovery of multiple organs
for more. The main advantage of the high capacity CRRT
is to remove inflammatory factors efficiently. Small-sized
molecular solutes such as serum creatinine, urea and
electrolytes are eliminated by convection and diffusion, and
medium-sized or large molecular solutes such as TNF-ɑ,
IL-1, IL -6, IL-8, PAF and myocardial inhibitor are cleaned
up by convection and adsorption in order to block waterfall
effect of inflammatory cytokines, and to relieve organ
damage of them. Second, the CRRT is able to maintain the
acid-base balance, and to stabilize the ions and osmotic
pressure between intra- and extra- in cells and blood
vessels, which is the basic condition for the maintenance of
cell membrane activities, and is also an effective method to
modify internal environmental disorders in PRS patients.
Furthermore, the CRRT achieve capacity regulation better,
which is benefit for the hemodynamic stability, the relief of on the basis of understanding the pathophysiology of the
tissue edema for advanced stage, providing the possibility
for the implementation of the mild hypothermia treatment.
The preliminary result of an ongoing study in Australia
and Europe shows that utilizing the CRRT to adjust the
patient's temperature, mild hypothermia for 24h at the
LaboratoryRaenvdieCwlinaincdalCInMvEesLteigcatutiroen 26
123
initial stage of post-resuscitation can improve the survival
rate .[17]
Early initiate enteral nutrition
Ischemia, hypoxia and permeability in intestinal
tract post-resuscitation will be invaded by sepsis
easily, stimulating the large production and release of
inflammatory cytokines, promoting the occurrence of
MODS, especially those with liver and renal dysfunction.
Therefore, enteral nutrition should be initiated timely
and rationally. Combining mucosal protective agents and
acid-suppressing agents can effectively reduce the risk of
stress ulcers, gastrointestinal bleeding and intestinal-borne
infections. In this case, enteral nutrition was initiated at
the third day after the patient’s resuscitation when her
hemodynamics was stable, which prevented the occurrence
of enteritis and dysbacteriosis and protected the intestinal
mucosa well.
According to the clinical data review of the case, we
recognize that the treatment of PRS is systemic, which
calls for clinicians to establish a global clinical thinking
disease, to promote the significance in brain protection
and the initial hemodynamic stabilization and utilize a
comprehensive treatment. Only in that way will we truly
increase the survival rate of patients after CRP and improve
the prognosis of PRS.
REFERENCES
[1] Stiell IG, Wells GA, Field B, et al. Advanced cardiac life support in out-of-hospital cardiac arrest [J]. N Engl J
Med, 2004, 351:647-656.
[2] Ma MH, Chiang WC, Ko PC, et al. Outcomes from out-of-hospital cardiac arrest in Metropolitan Taipei: does
an advanced life support service make a difference [J]? Resuscitation, 2007, 74:461-469.
[3] Werling M, Thoren AB, Axelsson C, et al. Treatment and outcome in postresuscitation care after out-of-
hospital cardiac arrest when a modern therapeutic approach was introduced [J]. Resuscitation, 2007, 73:40-45.
[4] Fairbanks RJ, Shah MN, Lerner EB, et al. Epidemiology and outcomes of out of-hospital cardiac arrest in
Rochester, New York [J]. Resuscitation, 2007, 72: 415-424.
[5] Seelig M. Cardiovascular consequences of magnesium deficiency and loss: pathogenesis, prevalence and
manifestations—magnesium and chloride loss in refractory potassium repletion [J]. Am J Cardiol, 1989,
63:4G- 21G.
[6] Altura BM, Altura BT. New perspective on the role of Mg in the pathophysiology of the cardiovascular system.
I. Clinical aspects [J]. Magnesium, 1985, 4:226-244.
[7] Dubey A, Solomon R. Magnesium, myocardial ischaemia and arrhythmias: the role of magnesium in myocardial
infarction [J]. Drugs, 1989, 37:1-7.
[8] Kotamraju S, Chitambar CR, Kalivendi SV, et al. Transferrin receptor-dependent iron uptake is responsible
for doxorubicin-mediated apoptosis in endothelial cells: role of oxidant-induced iron signaling in apoptosis [J].
J Biol Chem, 2002, 277:179-187.
[9] Kramer JH, Spurney C, Iantorno M, et al. Neurogenic inflammation and cardiac dysfunction due to
hypomagnesemia [J]. Am J Med Sci, 2009, 338(1):22-27.
[10] Laver S, Farrow C, Turner D, et al. Mode of death after admission to an intensive care unit following cardiac
arrest [J]. Intensive Care Med, 2004, 30:2126-2128.
[11] Takeda Y, Hashimoto H, Fumoto K, et al. Effects of pharyngeal cooling on brain temperature in primates and
humans: a study for proof of principle [J]. Anesthesiology, 2012, 117(1):117-125.
[12] Losert H, Sterz F, Roine RO, et al. Strict normoglycaemic blood glucose levels in the therapeutic management
of patients within 2 h after cardiac arrest might not be necessary [J] . Resuscitation, 2008, 76:214-220.
[13] Song ZF, Guo XH, Pan ZP, et al. The evaluation of effective artificial ventilation in cardiac pulmonary cerebral
resuscitation. [J]. Chinese Critical Care Medicine, 2002, 14(4): 213-215.
[14] Liu Y, Rosenthal RE, Haywood Y, et al. Normoxic ventilation after cardiac arrest reduces oxidation of brain
lipids and improves neurological outcome [J]. Stroke 1998; 29:1679-1686.
[15] Zwemer CF, Whitesall SE, D’Alecy LG. Cardiopulmonary-cerebral resuscitation with 100% oxygen
exacerbates neurological dysfunction following nine minutes of normothermic cardiac arrest in dogs [J].
Resuscitation, 1994, 27:159-170.
[16] Balan IS, FiskumG, Hazelton J, et al. Oximetry-guided reoxygenation improves neurological outcome after
experimental cardiac arrest [J]. Stroke, 2006, 37:3008-3013.
[17] Nolan JP. Optimizing outcome after cardiac arrest [J]. Curr Opin Crit Care, 2011, 17:520-526.
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