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Pressors And Lactic Acidosis

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 >>

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 >>

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 >>

Emdocs.net Emergency Medicine Educationan Evidence-based Approach To Pressors In Shock: Part I - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationan Evidence-based Approach To Pressors In Shock: Part I - Emdocs.net - Emergency Medicine Education

An Evidence-Based Approach to Pressors in Shock: Part I Author: Sarah Brubaker, MD (EM Resident, San Antonio TX) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit) An 86-year-old man with a history of COPD, CHF, CAD, and ESRD presents to your emergency department via EMS for decreased mental status. When he arrives, he is alert but confused, with a rectal temperature of 102.4F, heart rate of 113, and blood pressure of 75/55. You immediately treat for sepsis, administering a fluid bolus, antipyretics, and broad-spectrum antibiotics. However, you think to yourself, What if this patients blood pressure doesnt respond to fluids? When should I give pressors? Which pressors should I use? The evaluation and treatment of patients with cardiovascular shock is a cornerstone of emergency care. Unfortunately, the literature behind the use of vasoactive medications in cardiovascular shock is inconsistent. A Cochrane review in 2004 declared the current available evidence is not suited to inform clinical practice (1). Since 2004, there has been an impressive amount of research to investigate the use and safety of pressors, including several large, multi-center clinical trials. However, the results continue to be inconsistent and conflicting. An updated Cochrane review in 2016 concluded that, with the exception of an increased risk for arrhythmia associated with dopamine, there is no significant difference in mortality between vasopressors and evidence of any other differences between any of the six vasopressors examined is insufficient (2). These findings reflect the underlying complexity of vasopressor use. With that in mind, lets delve into the literature behind each pressor, so that we can make informed decisions about which pressors are appropriate for pati 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 >>

Inotropes & Vasopressors In Intensive Care

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 >>

Inotropes, Vasopressors And Other Vasoactive Agents

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 >>

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 >>

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 >>

Lactic Acidosis - Now@nejm Now@nejm

Lactic Acidosis - [email protected] [email protected]

Posted by Carla Rothaus December 11th, 2014 When lactic acidosis accompanies low-flow states or sepsis, mortality rates increase sharply. A new review summarizes our current understanding of the pathophysiological aspects of lactic acidosis, as well as the approaches to its diagnosis andmanagement. Lactic acidosis results from the accumulation of lactate and protons in the body fluids and is often associated with poor clinical outcomes. The effect of lactic acidosis is governed by its severity and the clinical context. Mortality is increased by a factor of nearly three when lactic acidosis accompanies low-flow states or sepsis, and the higher the lactate level, the worse theoutcome. Hyperlactatemia occurs when lactate production exceeds lactate consumption. In tissue hypoxia, whether global or localized, lactate is overproduced and underutilized as a result of impaired mitochondrial oxidation. Even if systemic oxygen delivery is not low enough to cause generalized hypoxia, microcirculatory dysfunction can cause regional tissue hypoxia and hyperlactatemia. Hyperlactatemia can also result from aerobic glycolysis, a term denoting stimulated glycolysis that depends on factors other than tissue hypoxia. Activated in response to stress, aerobic glycolysis is an effective, albeit inefficient, mechanism for rapid generation of ATP. In the hyperdynamic stage of sepsis, epinephrine-dependent stimulation of the (beta)2-adrenoceptor augments the glycolytic flux both directly and through enhancement of the sarcolemmal Na+,K+-ATPase (which consumes large quantities of ATP). Other disorders associated with elevated epinephrine levels, such as severe asthma (especially with overuse of beta2-adrenergic agonists), extensive trauma, cardiogenic or hemorrhagic shock, and pheochromocytoma, 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 >>

What Is Septic Shock?

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 >>

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 >>

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 >>

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