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Vasopressors For Lactic Acidosis

1148: A Puzzling Case Of Altered Mental Status And Severe Lactic Acidosis In A Pediatric Patient

1148: A Puzzling Case Of Altered Mental Status And Severe Lactic Acidosis In A Pediatric Patient

Introduction: Lactic acidosis is divided into 2 categories. Type A, an issue of tissue hypoxia and Type B, a biochemical defect leading to increased lactate production or decreased clearance. We present a case of severe Type B lactic acidosis. Case Presentation: 10 y/o with mixed phenotypic leukemia was noted to have altered mental status on day +21 post-stem cell transplant. On presentation, he was listless but arousable, tachycardic and normotensive. Head CT was negative and labs were notable for: lactate > 20 meq/L, ammonia 229 mcg/dL, amylase 217 U/L, lipase 223 U/L and tacrolimus (TAC) 28.9 ng/ml. Fluid resuscitation, NaHCO3 drip and CVVH were employed without improvement. On day 2, hypotension and worsening mental status ensued requiring intubation and 3 vasopressors. Medications suspicious for causing lactic acidosis or hyperammonemia were held. On day 3, aminophylline was given to increase clearance of TAC. It was also noted that the patient (Pt) had multivitamin removed from total parenteral nutrition 3 weeks prior for a possible allergic reaction. Thus, Pt was given IV Thiamine (50mg). In the following 5 hours, lactate dropped from 26 to 3.14 meq/L and Pt was weaned off all vasopressors. Discussion: The differential for Type B lactic acidosis in our Pt is broad and may be multifactorial. Possible contenders include: TAC toxicity, thiamine deficiency, malignancy and critical illness. We theorize thiamine deficiency was a key player. Thiamine is a cofactor for pyruvate dehydrogenase, the enzyme that converts pyruvate to acetyl-CoA, following the path of aerobic metabolism via the Krebs cycle. Without thiamine, the body shifts towards anaerobic metabolism and pyruvate is converted to lactate. Thiamine is also a cofactor in branched amino acid (AA) metabolism. Ou Continue reading >>

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

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 >>

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 | 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 >>

Use Of Bicarbonate In Lacticacidosis

Use Of Bicarbonate In Lacticacidosis

Five days post emergency colorectal surgery, an elderlywoman, following a brief period of chest pain a few hours earlier, developed progressive hypotension and tachycardia on the ward. She had a background of hypertension, type 2 diabetes and a chronic left foot ulcer. On examination she was found to be clammy, mottled and peripherally vasoconstricted with a GCS of 15/15. Her abdomen was soft and non-tender. Her initial ECG had showed no ischaemic changes and subsequent ECGs showed only a sinus tachycardia. Initial blood gas analysis showed a metabolic acidosis (pH 7.21 Lactate 2.8mmol/l, HCO3 11.1mmol/l with a pCO2 of 2.7kPa). A starting differential diagnosis of a cardiac event, a pulmonary embolism, critical ischaemia or sepsis related to a hip or foot ulcer were made. Urgent orthopaedic and vascular review were obtained, and it was deemed that neither the hip, ulcer or vascular insufficiency were a likely source for the deterioration. Initially it was planned to transfer her for a CTPA, however she became progressively unstable, was no longer fluid responsive, and was intubated on the ward and transferred to the intensive care unit (ICU) for stabilisation. On arrival on ICU she continued to deteriorate, and in addition to fluid resuscitation required a high dose noradrenaline infusion to maintain her blood pressure. Broad spectrum antibiotics were started, a bedside echocardiogram and blood tests performed and hydrocortisone started. Her metabolic acidosis continued to deteriorate, subsequent arterial blood gas showed a pH 6.91, Lactate of 13.7mmol/l, HCO3 7.7mmol/l, base excess -25mmol/l with a pCO2 of 5.4kPa. It was decided to correct this acidosis with a bicarbonate infusion and initially 200ml of 8.4% was given over an hour, based on correcting half the calcula Continue reading >>

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

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 >>

Understanding Lactate In Sepsis & Using It To Our Advantage

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 >>

Sodium Bicarb For Treatment Of Acidosis?

Sodium Bicarb For Treatment Of Acidosis?

SDN members see fewer ads and full resolution images. Join our non-profit community! Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? except, when a sudden intolerable decrease in pH is expected (ie release of a clamp or tourniquet), or when all else is failing (ie during a code when i want the pressors to work long enough to gain a foothold - little evidence for this). Agreed. Bicarb is only masking the acidosis and it is better to treat the cause rather than correct the pH. However, if things are beginning to go south in a hurry and you can't correct the problem rapidly enough then bicarb can be a benefit. Mostly by increasing the effectiveness of your inotropes, as Slavin said. Remember, some of the criticism of bicarb came from codes where removal of CO2 was impaired. We don't usually have that issue so some say it won't harm anything to give bicarb. I disagree, CO2 will Continue reading >>

Vasopressor Agentsinfluence Of Acidosis On Cardiac And Vascular Responsiveness

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 >>

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

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 >>

Lactic Acidosis: Clinical Implications And Management Strategies

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 >>

Cardiac Pressors - Anesthesia General

Cardiac Pressors - Anesthesia General

Critically ill patients often require cardiac inotrope and/or cardiac pressors support to maintain adequate cardiac output and adequate blood pressure to sustain end-organ perfusion. Because end-organ perfusion has already likely been compromised and may continue to be problematic despite use of these agents, anaerobic metabolism rather than aerobic metabolism is likely to be generating a limited amount adenosine triphosphate (ATP) in the hypoperfused tissues. The consequence is lactic acid production and acidosis. Additionally, critically ill patients may have other causes of acidosis contributing to the overall acidotic state including renal failure, hyperchloremia, or ketoacidosis. The acidosis may be severe with pH values well below 7.0. Binding of the cardiac inotropes or cardiac pressors agents to their receptors is influenced by pH, along with other factors such as temperature and concentration. Presumably, the greater the deviation in either direction from the optimal pH for the drug-ligand interaction, the less binding that will occur and hence, the less the effect of the drug. This has led to the widely held opinion that cardiac inotropes and cardiac pressors dont work at the acidic pH values often encountered in critically ill patients. The actual relationship is much more complex since the target of the cardiac inotropes and cardiac pressors, the alpha and beta adrenergic receptors, includes several subtypes whose individual responsiveness to these agents is quite variable under acidic conditions. The variability in responsiveness stems from not only changes in affinity for binding to the receptors but also because acidic conditions have been shown to change receptor numbers on cell surfaces as well as alter the downstream regulation mediated by G-coupled p Continue reading >>

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

Volume 147, Issue 5 , May 2014, Pages 1698-1705 Acidosis is a very common pathologic process in perioperative management. However, how to correct severe acidosis to improve the efficacy of vasoconstrictors in hemodynamically unstable patients is still debated. The present study investigated whether severe extracellular acidosis influences the vasoactive properties of vasoconstrictors on human isolated arteries. Segments of intact distal internal mammary arteries were removed from 41 patients undergoing artery bypass grafting. The arterial rings were washed in Krebs-Henseleit solution and suspended in an organ bath. The rings were set at a pretension equivalent of 100 mm Hg, and the relaxation response to 10 M acetylcholine was verified. Concentrationresponse curves for epinephrine, norepinephrine, methoxamine (1A/D-adrenoceptor agonist), phenylephrine (equipotent agonist of 1A/B-adrenoceptors), and clonidine (2-adrenoceptor agonist) were achieved under control conditions (pH 7.40) and under acidic conditions by substitution of the Krebs-Henseleit solution with a modified solution. Decreasing the pH from 7.40 to 7.20, 7.0, or 6.80 did not significantly alter the potency and efficacy of epinephrine and norepinephrine, although the standardized effect size was sometimes large. Severe acidosis (pH6.80) did not significantly change the potency and efficacy of phenylephrine and clonidine, although it increased the efficacy and potency of methoxamine (P<.001 and P=.04 vs paired control conditions, respectively). Extracellular acidosis did not impair the vasoactive properties of epinephrine and norepinephrine in human medium-size arteries until pH 6.80. The results of the present study also suggest that acidosis might potentiate arterial responsiveness to vasoconstrictors, mos Continue reading >>

Review: Lactate & Sepsis

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 >>

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

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 >>

Levo And Ph | Allnurses

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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