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Why Don't Vasopressors Work In Acidosis

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 >>

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 >>

Levo And Ph | The Health Science - Medical News, Wiki And Forum For Doctors, Nurses And Other Healthcare Professionals

Levo And Ph | The Health Science - Medical News, Wiki And Forum For Doctors, Nurses And Other Healthcare Professionals

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!!! Permalink Submitted by Guest (not verified) on Wed, 11/20/2013 - 22:44 Sounds like she needed emergent VAD or ECMO. Epi would not be a good idea in this situation if the patient is already acidotic, it's just going to worsen that. At 10% EF and frank cardiogenic shock, she needed LV pump assistance. Even IABP is not going to do much in that situation, she needs more than 1-2 l of CO. Permalink Submitted by Guest (not verified) on Wed, 11/20/2013 - 22:44 Think like a cell. If your body reverts to anaerobic respiration you are producing alot of lactic acid. This causes vasodilation and the levophed cannot overcome this even with boluses of sodium bicarb. As a neurotransmitter levophed facilitates communication betwee 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 >>

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 >>

Remember That Cardiac Pressors Do Not Work In A Low-ph Environment

Remember That Cardiac Pressors Do Not Work In A Low-ph Environment

Remember that Cardiac Pressors do not Work in a Low-pH Environment Remember that Cardiac Pressors do not Work in a Low-pH Environment Critically ill patients often require inotropic and/or pressor 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 inotropic or pressor 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 inotropes and vasopressors 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 inotropes and vasopressors, the alpha and beta adrenergic receptors, includes several subtypes whose individual responsiveness to these agents is quite variable under acidic conditions. Only gold members can continue reading. Log In or Register to continue 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 >>

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 >>

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 >>

Acid-base Balance Understanding Is Critical To Treat Patients

Acid-base Balance Understanding Is Critical To Treat Patients

Acid-Base Balance Understanding is Critical to Treat Patients By James Tanis, MD, NRP dvxxtrvscafftzcatwdtzeytyyc , Joseph E. DiCorpo, BSC, MMSc, PA , Daniel Friedman, DO, EMT-P , Mark Merlin, DO, EMT-P, FACEP Every critically ill patient we encounter in the field will have an acid-base derangement; therefore, an understanding of acid-base balance is critical to properly treat patients. First, its important you appreciate that every chemical reaction that occurs in the human body is regulated or substantially influenced by the hydrogen ion (H+) concentration in the surrounding tissue, from the way hemoglobin picks up and delivers oxygen to the tissues to the way that sugar, protein and fat are metabolized by the body. The regulation of hydrogen ions, which we measure as pH, is what acid-base balance refers to. The bodys concentration of hydrogen ions must be maintained within a strict range for optimal cellular function, and even a small deviation can significantly affect a patient.1Its a complex balancing act that you can affect based upon your assessment of the patients vital signs. An acid has a pH below 7.0 and an increased concentration of hydrogen ions, while an alkaline has a pH above 7.0 and a decreased concentration of hydrogen ions. The body maintains a slightly alkaline pH range of 7.35 to 7.45. Therefore, a pH higher than this range is in a state of alkalosis and a pH below this range is considered to be acidosis. A pH of 6.9 on the acid side and 7.8 on the alkaline side are considered non-compatible with life.1(See Table 1, above) An excess of acid is usually produced during the normal process of metabolism, so the body must rid itself of this excess acid to maintain the acid-base balance and keep a normal hydrogen ion concentration. Three defense mechanis Continue reading >>

Acid-base Disorder? Mind The Gaps

Acid-base Disorder? Mind The Gaps

You are at: Home Current Features Acid-Base Disorder? Mind the Gaps A 56 year old Russian speaking male (limited English capability) presents to the emergency department via EMS with the chief complaint of generalized abdominal pain. In triage he is noted to be rubbing his stomach and touching his lower back. He indicates that this has been bothering him for the past two hours. He is noted to be verbal in triage but appears confused and is moaning in discomfort. A step-wise emergency approach to acid-base disorders including the Rule of 15 and the Delta Gap formulas can help uncover processes that are hidden in the labs. A 56 year old Russian speaking male (limited English capability) presents to the emergency department via EMS with the chief complaint of generalized abdominal pain. In triage he is noted to be rubbing his stomach and touching his lower back. He indicates that this has been bothering him for the past two hours. He is noted to be verbal in triage but appears confused and is moaning in discomfort. A prior ED visit record indicates that the patient has some sort of liver disease and EtOH abuse history (with no prior reported home medications). His initial triage vitals are recorded as: The patient is placed in a treatment room to await physician evaluation. Approximately 50 minutes later, the patient is found by nursing to be unresponsive on the stretcher with agonal respirations and a questionable thready pulse. The patient is emergently intubated and ACLS protocol is initiated (two minutes of chest compressions and 1 round of epinephrine with return of a perfusing pulse). His post-event EKG shows a bifasicular block and T wave inversions in the precordial leads, raising concerns for an ischemic event. The patient has emergent imaging, including a CXR (n Continue reading >>

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild metabolic acidosis impairs the -adrenergic response in isolated human failing myocardium Schotola et al.; licensee BioMed Central Ltd.2012 Pronounced extracellular acidosis reduces both cardiac contractility and the -adrenergic response. In the past, this was shown in some studies using animal models. However, few data exist regarding how the human end-stage failing myocardium, in which compensatory mechanisms are exhausted, reacts to acute mild metabolic acidosis. The aim of this study was to investigate the effect of mild metabolic acidosis on contractility and the -adrenergic response of isolated trabeculae from human end-stage failing hearts. Intact isometrically twitching trabeculae isolated from patients with end-stage heart failure were exposed to mild metabolic acidosis (pH 7.20). Trabeculae were stimulated at increasing frequencies and finally exposed to increasing concentrations of isoproterenol (0 to 1 10-6 M). A mild metabolic acidosis caused a depression in twitch-force amplitude of 26% (12.1 1.9 to 9.0 1.5 mN/mm2; n = 12; P < 0.01) as compared with pH 7.40. Force-frequency relation measurements yielded no further significant differences of twitch force. At the maximal isoproterenol concentration, the force amplitude was comparable in each of the two groups (pH 7.40 versus pH 7.20). However, the half-maximal effective concentration (EC50) was significantly increased in the acidosis group, with an EC50 of 5.834 10-8 M (confidence interval (CI), 3.48 10-8 to 9.779 10-8; n = 9), compared with the control group, which had an EC50 of 1.056 10-8 M (CI, 2.626 10-9 to 4.243 10-8; n = 10; P < 0.05), indicating an impaired -adrenergic force response. Our data show that mild metabolic acidosis reduces cardiac contractility and significantly impairs the -adrenerg Continue reading >>

Your Patient In Extremis: Tham To The Rescue?

Your Patient In Extremis: Tham To The Rescue?

Your Patient In Extremis: THAM To The Rescue? By: Prathap Sooriyakumaran, MD and Curtis Geier, PharmD One of the final common denominators dictating the success or failure of any resuscitative effort, be it a trauma or medical code, is the patients acid-base status. In the presence of acidosis, many of the tools at your disposal, including vasopressors, become impotent and the patients ability to strike a balance between bleeding and clotting or mounting an appropriate inflammatory response become deranged.16 So what are the options to tilt the acid-base status in our favor? One thing is clear, sodium bicarbonate is not the hero we have been searching for. Unfortunately, the buffer we all know and want to love is ineffective in producing any significant change that will alter outcomes in the setting of the acutely acidemic patient.7,8 Why? Well to understand this, well have to do a brief dive (a wade) into the relevant human biochemistry. So if you give sodium bicarbonate in an attempt to scavenge your troublemaking protons, youll get carbonic acid which dissociates into carbon dioxide and water, which can freely diffuse across the cell membrane creating an intracellular acidosis.9 If you can get rid of carbon dioxide (blow it off), you will force the equation to the right and get rid of your protons. However, patients in extremis may not be able to compensate for the increased carbon dioxide with increased respiratory drive further exacerbating intracellular acidemia. THAM (trometanol; tris-hydroxymethyl aminomethane) is an inert amino alcohol which is theoretically amore effective buffer than bicarbonate in the physiological range of blood pH because it has a pKa of 7.8 at normal body temperatures (compared to a pKa of 6.1 for sodium bicarbonate). Why may it be more 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 >>

Noradrenaline - Deranged Physiology

Noradrenaline - Deranged Physiology

Noradrenaline is an endogenous catecholamine, a sympathomimetic drug with a strong alpha-1 receptor selectivity. This chapter is a tribute to it, as it is the true workhorse of intensive care, and a drug with which one ought to become intimately familiar. It is the gateway drug to understanding the effects of catecholamines. Chemical structure and chemical properties of noradrenaline Noradrenaline is the prototypical alpha-agonist. The relationship of its structure to its function is discussed elsewhere. The hydroxyl group on its beta-carbon increases its overall potency, and the absence of alkyl substitutes on the amine group gives it a degree of alpha-1 selectivity, but takes away beta-activity. The Australian variety (Levophed) arrives in your hands as a 2ml ampoule, containing 2mg of noradrenaline. It has a pH of about 3.5-4.0. In order to make it isotonic, Hospira thoughtfully provides 8mg of sodium chloride per ml, which equates to a concentration of about 136 mmol/L. Additionally, sodium metabisulfite (0.2mg/ml) is added as an antioxidant; as far as I can tell it plays no real role in the ensuing discussion. The importance of acidic pH for noradrenaline preservation Why does it have to be so acidic? Because noradrenaline (and adrenaline for that matter) are degraded by an alkaline environment, particularly at above room temperature. This is one of the reasons the ICU nurses never run sodium bicarbonate into the same CVC lumen as the noradrenaline. The importance of dilution of noradrenaline in dextrose rather than saline Why do we always seem to prepare it in a bag of 100ml dextrose? It doesnt matter whether you put it in dextrose or saline, right? Certainly, it seems to be equally stable in either solution. However, the prescribing guidelines for the Levophed p Continue reading >>

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