Chapter 23: Use Of Vasopressors
1) Which of the following conditions can result in a lowering of blood pressure in critically ill patients? B.Decreased pulmonary capillary wedge pressure 2) The central venous pressure (CVP) catheter is a device that is used to effectively perform what function in critically ill patients? B.Administer drugs directly into the central circulation 3) Which of the following statements about central venous oxygen saturation is correct? A.It indirectly measures oxygen extraction by tissues. B.It may be low in inadequately volume-resuscitated patients with septic shock. C.It measures adequacy of volume resuscitation more accurately than does blood pressure measurement. D.It should be targeted to a value in excess of 70%. 4) Which of the following parameters is a measurement of regional perfusion? A.Arterial blood lactate concentration 5) Stimulation of the beta adrenergic receptor by agonists results in a physiologic response mediated by which of the following? 7) Which of the following outcomes is a goal that should be achieved within THREE hours of presentation in a patient with septic shock? 8) Which of the following explains the development of lactic acidosis by a catecholamine? A.Enhanced vasoconstriction in peripheral arteries C.Mobilization of lactate from peripheral tissues 9) Which of the following catecholamines is associated with a fall in intramucosal pHi and rise in blood lactate concentration during treatment? 12) Which of the following statements is true regarding the use of corticosteroid therapy for the treatment of sepsis? A.It should be used in all patients with sepsis. B.It should be started within 48 hours of the diagnosis of severe sepsis. C.It should be used when hemodynamic goals are not achieved despite fluid resuscitation and vasopressor therapy. D. Continue reading >>
What Is Septic Shock?
In my medical ICU, many of the patients are in septic shock because of some type of infection. Have you ever had a patient's family ask you about sepsis? "Why is my family member's blood pressure so low?" Is there any easy way to explain this to them or do you just say, "their body is reacting abnormally to a widespread infection?" So this is how I like to explain it. Say that you have a splinter in your finger--what happens to it? It becomes red, hot and infected. Why is it red and hot? The body has opened up the veins around the splinter to let white blood cells out and fight the infection. Just like this, when someone is septic, all of the patient's vessels open up (decreasing the blood pressure) to try and fight the infection. The only problem is that the body is fighting the infection systemically.So what causes this widespread response? The Mayo Clinic states that "sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammatory responses throughout the body. This inflammation can trigger a cascade of changes that can damage multiple organ systems, causing them to fail." Common causes are pneumonia, urinary tract infections, cellulitis, and abdominal infections. Sepsis can be caused by bacteria, viruses, or fungal infections. The usual presentation for sepsis is tachypnea (increased respiratory rate), tachycardia (increased heart rate), fever, and hypotension (low blood pressures). Patients can also exhibit organ dysfunction if the sepsis becomes severe. Symptoms would show decreased urine output, lactic acidosis, hypoxemia (low oxygen levels), elevated liver enzymes, and an increased white blood cell count. Renal failure causes the decreased urine output as well as electrolyte imbalances. Respiratory failure causes the hypox Continue reading >>
Vasopressor Agentsinfluence Of Acidosis On Cardiac And Vascular Responsiveness
VASOPRESSOR AGENTSInfluence of Acidosis on Cardiac and Vascular Responsiveness This article has been cited by other articles in PMC. Clinical observations have indicated that patients who are in shock and who have coexisting acidosis respond relatively poorly to sympathomimetic amines. In experiments with dogs, it was found that, in the presence of acidosis, the pressor action of epinephrine, norepinephrine and metaraminol was considerably reduced. The effect on cardiac rhythm was also considerably lessened after the pH value of the blood had been lowered. In view of these observations in animals, six human patients with profound shock and acidosis were studied. All had a considerably lessened pressor response to vasopressor agents; then, after elevation of the blood pH by intravenous infusion of a 1-molar solution of sodium lactate, responsiveness was restored. These observations emphasize the desirability of close observation of the acid-base status, and early treatment of acidosis, as an important aspect in the management of patients with shock. Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (662K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . Continue reading >>
Inotropes & Vasopressors In Intensive Care
- effect more pronounced at low heart rates - slower onset and longer duration than beta1 receptor mediated response presynaptic alpha2 receptors in heart and vasculature appear to be activated by norepinephrine released by sympathetic nerve itself and mediate negative feedback inhibition of further norepinephrine release post synaptic alpha1 and alpha2 receptors in peripheral vessels mediate vasoconstriction post synaptic beta1 receptors are predominant adrenergic receptors in heart. Stimulation causes increased rate and force of cardiac contraction. Mediated by cAMP post synaptic beta2 receptors in vasculature mediate vasodilatation peripheral DA1 receptors mediate renal, coronary and mesenteric arterial vasodilatation and a natriuretic response DA2 receptors: presynaptic receptors found on nerve endings, inhibit norepinephrine release from sympathetic nerve endings, inhibit prolactin release and may reduce vomiting stimulation of either DA1 or DA2 receptors suppresses peristalsis and may precipitate ileus Immediate precursor of norepinephrine and epinephrine <5 mcg/kg/min predominantly stimulates DA1 and DA2 receptors in renal, mesenteric and coronary beds causing vasodilatation 5-10 mcg/kg/min: beta2 effects predominate. Increases cardiac contractility and HR >10 mcg/kg/min: alpha effects predominate causing arterial vasoconstriction and increased BP Marked variability in clearance in the critically ill. As a result plasmaconcentrations cannot be predicted from infusion rates variable effects due to variable clearance increases cardiac output (mainly due to increased stroke volume) with minimal effect on SVR in patients with septic shock Synthetic catecholamine structurally related to dopamine Distribution: extensive tissue distribution. Drug acts as a substrate fo Continue reading >>
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Lactic Acidosis: Clinical Implications And Management Strategies
Lactic acidosis: Clinical implications and management strategies Cleveland Clinic Journal of Medicine. 2015 September;82(9):615-624 Quality Officer, Medical Intensive Care Unit, Departments of Pulmonary Medicine and Critical Care Medicine, Respiratory Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Department of Pharmacy, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Medical ICU Clinical Specialist, Department of Pharmacy, Cleveland Clinic Director, Medical Intensive Care Unit, Department of Critical Care Medicine, Respiratory Institute, Cleveland Clinic Address: Anita J. Reddy, MD, Department of Critical Care Medicine, Respiratory Institute, A90, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: [email protected] Andersen LW, Mackenhauer J, Roberts JC, Berg KM, Cocchi MN, Donnino MW. Etiology and therapeutic approach to elevated lactate levels. Mayo Clin Proc 2013; 88:11271140. Fuller BM, Dellinger RP. Lactate as a hemodynamic marker in the critically ill. Curr Opin Crit Care 2012; 18:267272. Fall PJ, Szerlip HM. Lactic acidosis: from sour milk to septic shock. J Intensive Care Med 2005; 20:255271. Kruse O, Grunnet N, Barfod C. Blood lactate as a predictor for in-hospital mortality in patients admitted acutely to hospital: a systematic review. Scand J Trauma Resusc Emerg Med 2011;19:74. Howell MD, Donnino M, Clardy P, Talmor D, Shapiro NI. Occult hypoperfusion and mortality in patients with suspected infection. Intensive Care Med 2007; 33:18921899. Puskarich MA, Trzeciak S, Shapiro NI, et al. Outcomes of patients undergoing early sepsis resuscitation for cryptic shock compa Continue reading >>
Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside
Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Antoine Kimmoun , Emmanuel Novy , Thomas Auchet , Nicolas Ducrocq , and Bruno Levy CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France Antoine Kimmoun, Email: [email protected] . Author information Copyright and License information Disclaimer Copyright Kimmoun et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution Continue reading >>
Approach To Hemodynamic Shock And Vasopressors
Approach to Hemodynamic Shock and Vasopressors Departments of *Nephrology and General, Visceral and Transplant Surgery, University Hospital, University Duisburg-Essen, Essen, Germany; and Critical Care Medicine and Nephrology, George Washington University Medical Center, Washington, DC Dr. Stefan Herget-Rosenthal, Klinik fr Nieren- und Hochdruckkrankheiten, Universittsklinikum Essen, Universitt Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany. Phone: +49-201-723-2552; Fax: +49-201-723-5633; E-mail: stefan.herget-rosenthal{at}uni-due.de Hemodynamic shock (HS) is a clinical syndrome that is commonly observed in hospitalized patients. Prompt recognition and intervention are the cornerstones of mitigating the dire consequences of HS. Untreated HS usually leads to death. Unlike other types of clinical syndromes (e.g., chest pain), for which a clinical diagnosis is made before treatment is initiated in earnest, the treatment of shock often occurs concurrently or ahead of the diagnostic process. The maintenance of end-organ perfusion is critical to prevent irreversible organ injury and failure, and this frequently requires the use of fluid resuscitation and vasopressors. A complete review of all of the signs and symptoms, diagnosis, and treatment of HS has been reviewed in detail elsewhere ( 1 ). This article provides a concise summary of how to approach the patient in HS, diagnostic and therapeutic decision making, and the use of vasopressors. In addition, the effects of vasopressors on end organs with particular focus on renal hemodynamics is reviewed. Clinical Manifestations and Recognition of Hemodynamic Shock HS is classically described as an acute clinical syndrome initiated by ineffective perfusion, resulting in severe dysfunction of organs vital to survival Continue reading >>
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The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate
Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and Continue reading >>
Inotropes, Vasopressors And Other Vasoactive Agents
Bangash MN, Kong ML, Pearse RM. Use of inotropes and vasopressor agents in critically ill patients. Br J Pharmacol. 2012 Apr;165(7):2015-33. doi: 10.1111/j.1476-5381.2011.01588.x. Review. PubMed PMID: 21740415 ; PubMed Central PMCID: PMC3413841 . Evans N. Which inotrope for which baby? Arch Dis Child Fetal Neonatal Ed. 2006 May;91(3):F213-20. Review. PubMed PMID: 16632650 ; PubMed Central PMCID: PMC2672709 . Gillies M, Bellomo R, Doolan L, Buxton B. Bench-to-bedside review: Inotropic drug therapy after adult cardiac surgery a systematic literature review. Crit Care. 2005 Jun;9(3):266-79. Epub 2004 Dec 16. Review. PubMed PMID: 15987381 ; PubMed Central PMCID: PMC1175868 . Hollenberg SM. Vasoactive drugs in circulatory shock. American journal of respiratory and critical care medicine. 183(7):847-55. 2011. [ pubmed ] Hollenberg SM. Inotrope and vasopressor therapy of septic shock. Critical care clinics. 25(4):781-802, ix. 2009. [ pubmed ] Jentzer JC, Coons JC, Link CB, Schmidhofer M. Pharmacotherapy update on the use of vasopressors and inotropes in the intensive care unit. Journal of cardiovascular pharmacology and therapeutics. 20(3):249-60. 2015. [ pubmed ] Overgaard CB, Dzavk V. Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. Circulation. 2008 Sep 2;118(10):1047-56. doi: 10.1161/CIRCULATIONAHA.107.728840. Review. PubMed PMID: 18765387 .[ Free Full Text ] Senz A, Nunnink L. Review article: inotrope and vasopressor use in the emergency department. Emerg Med Australas. 2009 Oct;21(5):342-51. doi: 10.1111/j.1742-6723.2009.01210.x. Epub 2008 Aug 18. Review. PubMed PMID: 19694785 . [ Free Full Text ] Vasu TS, Cavallazzi R, Hirani A, Kaplan G, Leiby B, Marik PE. Norepinephrine or dopamine for septic shock: systematic review of ran Continue reading >>
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Understanding Lactate In Sepsis & Using It To Our Advantage
You are here: Home / PULMCrit / Understanding lactate in sepsis & Using it to our advantage Understanding lactate in sepsis & Using it to our advantage Once upon a time a 60-year-old man was transferred from the oncology ward to the ICU for treatment of neutropenic septic shock. Over the course of the morning he started rigoring and dropped his blood pressure from 140/70 to 70/40 within a few hours, refractory to four liters of crystalloid. In the ICU his blood pressure didn't improve with vasopressin and norepinephrine titrated to 40 mcg/min. His MAP remained in the high 40s, he was mottled up to the knees, and he wasn't making any urine. Echocardiography suggested a moderately reduced left ventricle ejection fraction, not terrible but perhaps inadequate for his current condition. Dobutamine has usually been our choice of inotrope in septic shock. However, this patient was so unstable that we chose epinephrine instead. On an epinephrine infusion titrated to 10 mcg/min his blood pressure improved immediately, his mottling disappeared, and he started having excellent urine output. However, his lactate level began to rise. He was improving clinically, so we suspected that the lactate was due to the epinephrine infusion. We continued the epinephrine, he continued to improve, and his lactate continued to rise. His lactate level increased as high as 15 mM, at which point the epinephrine infusion was being titrated off anyway. Once the epinephrine was stopped his lactate rapidly normalized. He continued to improve briskly. By the next morning he was off vasopressors and ready for transfer back to the ward. This was eye-opening. It seemed that the epinephrine infusion was the pivotal intervention which helped him stabilize. However, while clinically improving him, the epineph Continue reading >>
Review: Lactate & Sepsis
On this snowy, Stockholm Sunday, I look out from my quarters on the Mlardrottningen across the still, icy waters and I think about a cirrhotic patient for whom I recently cared. She presented with significant dyspnea as she had stopped taking her diuretics. Instead, she was using excessivedoses of her friends albuterol inhaler to treat her shortness of breath. Additionally, she had been drinking alcohol heavily for seven days prior to admission. Her venous pH was 7.38, and her lactate concentration was over 7.0 mmol/L a sepsis alert was called. In a very recent and fantastic review by Suetrong and Walley , the mechanisms of lactate formation are revisited. Notably, a distinction is made between hyperlactatemia an elevated concentration of lactate in the blood and lactic acidosis, which is comprised of both hyperlactatemia and systemic acidosis. The authors discuss the mechanisms by which lactate is formed and aptly detail that many of these processes do not result in acid formation. Notably, while the generation of pyruvate from glucose does generate [H+], the conversion of pyruvate to lactate consumes an equimolar amount of [H+] such that the production of lactate does not result in a net gain of protons [i.e. acidosis]. So where does the acidosis with which we are so familiar come from? The excess protons are the result of an impaired Krebs Cycle. In states of true tissue oxygen debt, intracellular protons can no longer be consumed during the Krebs Cycle; consequently, intracellular acidosis and acidemia ensue. It is this latter means of hyperlactatemia to which we attach the label type A or lactic acidosis with clinical evidence of tissue hypoxia. However, as described 40 years ago , excessive lactate may come from clinical states where there is no evidence of tissu Continue reading >>
Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine
Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery. The former is addressed by various therapies, including administration of appropriate antibiotics, surgical drainage and debridement of a septic focus, chemotherapy of malignant disorders, discontinuation of causative drugs, and dietary modification in certain types of congenital lactate acidosis. Cardiovascular collapse secondary to hypovolemia or sepsis should be treated with fluid replacement. Both crystalloids and colloids can restore intravascular volume, but hydroxyethyl starch solutions should be avoided owing to increased mortality. [ 21 ] Excessive normal saline administration can cause a nongap metabolic acidosis due to hyperchloremia, which has been associated with increased acute kidney injury. [ 32 ] Balanced salt solutions such as Ringer lactate and Plasma-Lyte will not cause a nongap metabolic acidosis and may reduce the need for renal replacement therapy; however, these can cause a metabolic alkalosis. [ 33 ] No randomized, controlled trial has yet established the safest and most effective crystalloid. If a colloid is indicated, albumin should be used. Despite appropriate fluid management, vasopressors or inotropes may still be required to augment oxygen delivery. Acidemia decreases the response to catecholamines, and higher doses may be needed. Conversely, high doses may exacerbate ischemia in critical tissue beds. Careful dose titration is needed to maximize benefit and reduce harm. Lactic acidosis causes a compensatory increase in minute ventilation. Patients may be tachypneic initially, but respiratory muscle fatigue can ensue rapidly a Continue reading >>
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Levo And Ph | Allnurses
we had the most awful night last night starting at the beginning of the shift (1945). got a "code blue to c-section #2" page overhead so the sc and myself (the float/resource nurse) ran there and they're doing compressions on a lady who's not even closed up from her c-s yet! baby was good, but the mom ended up coming to us and it was basically an all night medical code with another official "code blue" called on her at around 0200. first time i've cried on the way home from work anyways, my question was about the levo not working for her bp. her ph was in the 7.2 range on the first abg and she got an amp of hco3. then on the next abg (maybe an hour later) it was down to 7.19. then, since the bp was dropping so fast, the pma in the unit said to just run it wide open, but it wasn't working. the primary nurse (who's very experienced, whereas i've barely been in the icu for 2 years) said that the levo wouldn't do anything for the bp while the ph was so low. can someone explain this? god, every night i work i seem to be overwhelmed with everything i don't know!!! Continue reading >>
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Lactate Clearance And Vasopressor Seem To Be Predictors For Mortality In Severe Sepsis Patients With Lactic Acidosis Supplementing Sodium Bicarbonate: A Retrospective Analysis
Lactate Clearance and Vasopressor Seem to Be Predictors for Mortality in Severe Sepsis Patients with Lactic Acidosis Supplementing Sodium Bicarbonate: A Retrospective Analysis Contributed equally to this work with: Su Mi Lee, Seong Eun Kim Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Contributed equally to this work with: Su Mi Lee, Seong Eun Kim Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliations: Department of Internal Medicine, Dong-A University, Busan, Korea, Institute of Medical Science, Dong-A University College of Medicine, Busan, Korea Initial lactate level, lactate clearance, C-reactive protein, and procalcitonin in critically ill patients with sepsis are associated with hospital mortality. However, no study has yet discovered which factor is most important for mortality in severe sepsis patients with lactic acidosis. We sought to clarify this issue in patients with lactic acidosis who were supplementing with sodium bicarbonate. Data were collected from a single center between May 2011 and April 2014. One hundred nine patients with severe sepsis and lactic acidosis who were supplementing with sodium bicarbonate were included. The 7-day mortality rate was 71.6%. The survivors had higher albumin levels and lower SOFA, APACHE II scores, vasopressor use, and follow-up lactate levels at an elapsed time after their initial lactate levels were checked. In particular, a decrement in lactate clearance of at least 10% for the first 6 hours, 24 hours, and 48 hours of tre Continue reading >>
Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications
Efficient Extra- and Intracellular Alkalinization Improves Cardiovascular Functions in Severe Lactic Acidosis Induced by Hemorrhagic Shock From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Bra Continue reading >>
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