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Báo cáo y học: " Vasopressor stays vasopressor and inotrope stays inotrope"

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Available online http://ccforum.com/content/12/2/415 Letter Vasopressor stays vasopressor and inotrope stays inotrope! Günter Luckner1, Walter R Hasibeder2 and Martin W Dünser1 1Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse, 6020 Innsbruck, Austria 2Department of Anesthesiology and Critical Care Medicine, Krankenhaus der Barmherzigen Schwestern, Ried im Innkreis, Austria Corresponding author: Martin W Dünser, Martin.Duenser@i-med.ac.at Published: 14 April 2008 Critical Care 2008, 12:415 (doi:10.1186/cc6850) This article is online at http://ccforum.com/content/12/2/415 © 2008 BioMed Central Ltd See related research by Müller et al., http://ccforum.com/content/12/1/R20 We should like to comment on the interesting work reported shock will subsequently develop an additional vasodilatory by Müller and colleagues [1]. We feel that the results of their component [2]. Although they require an inotrope at early experiment were predictable and that arginine vasopressin stages, a vasopressor may be useful to restore a (sub)normal (AVP) was not indicated in that setting. Infusing a vascular tone at later stages. vasoconstrictor without relevant inotropic potential in an acute low flow state with maintained or increased vascular We therefore believe that this experiment does not tone must further augment organ vascular resistance and appropriately reflect the clinical situation and does not thereby reduce cardiac output. In the critical care setting, a support the conclusion that AVP, as a rule, should not be vasopressor can only be beneficial in patients with applied in patients with myocardial infarction and cardiogenic pathological vasodilatation, whereas patients with low shock. Indeed, preliminary clinical experience suggests that systemic blood flow and maintained vascular tone require when overwhelming systemic inflammation translates into either fluids and/or an inotrope. In their report Müller and vasodilatation in some patients with cardiogenic shock, the colleagues indiscriminately interchange vasodilatory and addition of AVP (attaining plasma levels as observed after cardiogenic shock. However, these forms of shock must be AVP withdrawal by Müller and coworkers [1]) can decrease strictly separated when considering the use of a strong high catecholamine dosages, thus attenuating adrenergic vasopressor such as AVP. Some patients with cardiogenic stress and myocardial oxygen demand [3]. Authors’ response Ole-Jakob How, Stig Müller and Truls Myrmel It was not our intention to ‘indiscriminately interchange contribution to our understanding of this agent’s effect in a vasodilatory and cardiogenic shock’, and we do not think that circulation supported by a postischaemic and failing heart. the report in fact can be interpreted in that way. On the Our observations raise serious concerns, particularly because contrary, our experimental design was aimed at testing the the drug appeared to override the metabolic regulation of the ‘clean’ effect of vasopressin in the setting of postischaemic coronary circulation. We therefore agree with the comment left ventricular dysfunction. The reason for conducting these by Parillo [7] in a recent editorial included in the New experiments was prompted by a series of reports questioning England Journal of Medicine on the effect of vasopressin in the vasoconstrictive effect of vasopressin in the coronary, sepsis; ‘… the equivalence in the rate of adverse events seen pulmonary and cerebral circulations [4], and the inclusion of in the two groups probably resulted, in part, from ensuring the drug among the treatment options for cardiogenic shock that patients with underlying heart disease were not entered [5,6]. Our limited clinical experience with the drug in this in the trial. Without these exclusions, it is possible that clinical setting mandates great caution. vasopressin might have increased the mortality rate.’ Competing interests An assessment of the effect of vasopressin as monotherapy in an experimental setting, in our opinion, makes an important The authors declare that they have no competing interests. Page 1 of 2 (page number not for citation purposes)
Critical Care Vol 12 No 2 Luckner et al. References 1. Müller S, How OJ, Hermansen SE, Stenberg TA, Sager G, Myrmel T: Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia. Crit Care 2008, 12:R20. 2. Landry DW, Oliver JA: The pathogenesis of vasodilatory shock. N Engl J Med 2001, 345:588-595. 3. Mayr VD, Luckner G, Jochberger S, Wenzel V, Hasibeder WR, Dünser MW: Vasopressin as a rescue vasopressor agent. Treatment of selected cardiogenic shock states. Anaesthesist 2007, 56:1017-1020. 4. Holmes CL, Patel BM, Russell JA, and Walley KR: Physiology of vasopressin relevant to management of septic shock. Chest 2001, 120:989-1002. 5. Jolly S, Newton G, Horlick E, Seidelin PH, Ross HJ, Husain M, Dzavik V: Effect of vasopressin on hemodynamics in patients with refractory cardiogenic shock complicating acute myocar- dial infarction. Am J Cardiol 2005, 96:1617-1620. 6. Luckner G, Dünser MW, Jochberger S, Mayr VD, Wenzel V, Ulmer H, Schmid S, Knotzer H, Pajk W, Hasibeder W, Mayr AJ, Friese- necker B: Arginine vasopressin in 316 patients with advanced vasodilatory shock. Crit Care Med 2005, 33:2659-2666. 7. Parrillo JE: Septic shock: vasopressin, norepinephrine, and urgency. N Engl J Med 2008, 358:954-956. Page 2 of 2 (page number not for citation purposes)

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