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Norepinephrine Acidosis

Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass

Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass

Objective To determine if lactic acidosis occurring after cardiopulmonary bypass could be attributed to the metabolic or other effects of epinephrine administration. Setting Postsurgical cardiothoracic intensive therapy unit. Patients Thirty-six adult patients, without acidosis, requiring vasoconstrictors for the management of hypotension after cardiopulmonary bypass. Interventions Randomized administration of either epinephrine or norepinephrine by infusion. Measurements and Main Results Hemodynamic and metabolic data were collected before commencement of vasoconstrictor therapy (time 0) and then 1 hr (time 1), 6 to 10 hrs (time 2), and 22 to 30 hrs (time 3) later. Six of the 19 patients who received epinephrine developed lactic acidosis. None of the 17 patients receiving norepinephrine developed lactic acidosis. In the epinephrine group, but not in the norepinephrine group, lactate concentration increased significantly at times 1 and 2 (p = .01), while pH and base excess decreased (p Continue reading >>

Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine

Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine

Montagnani and Nardi: Lactic Acidosis, Hyperlactatemia and Sepsis Lactic Acidosis, Hyperlactatemia and Sepsis [1] Division of Internal Medicine, Misericordia Hospital, Grosseto [2] Division of Internal Medicine, Maggiore Hospital, Bologna, Italy Correspondence to: Ospedale Misericordia di Grosseto, via Senese, 58100 Grosseto, Italy. +39.0564.485330. [email protected] Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic a 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 >>

Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass

Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass

The normal blood lactate level is 0-2 mmol/L, and a value above 3-5 mmol/L is variably used to define hyperlactatemia. In cardiac surgical patients, hyperlactatemia can arise from both hypoxic and non-hypoxic mechanisms. The major non-hypoxic mechanism is likely stress-induced accelerated aerobic metabolism, in which elevated lactate results from a mass effect on the lactate/pyruvate equilibrium. The lactate/pyruvate ratio is normal ( < 20) in this circumstance. Hyperlactatemia can also result from impaired global or regional oxygen delivery, in which case the lactate/pyruvate ratio is typically elevated ( > 20). Lactate is a strong anion that is virtually fully dissociated at physiological pH. As such, increased lactate concentration reduces the strong ion difference and exerts an acidifying effect on the blood. Hyperlactatemia in cardiac surgery patients has been categorized as either early or late onset. Early-onset hyperlactatemia is that which develops in the operating room or very early following intensive care unit (ICU) admission. Early-onset hyperlactatemia is strongly associated with adverse outcome and probably arises as a consequence of both hypoxic (e.g., microcirculatory shock) and nonhypoxic (accelerated aerobic metabolism) mechanisms. By contrast, late-onset hyperlactatemia is a benign, self-limiting condition that typically arises within 6-12 hours of ICU admission and spontaneously resolves within 24 hours. Late onset hyperlactatemia occurs in the absence of any evidence of global or regional tissue hypoxia. The mechanism of late onset hyperlactatemia is not understood. Hyperlactatemia is a common accompaniment to treatment with 2-agonists such as epinephrine. Epinephrine-induced hyperlactatemia is thought to be due to accelerated aerobic metabolism a Continue reading >>

Intravenous Sodium Bicarbonate

Intravenous Sodium Bicarbonate

Intravenous sodium bicarbonate, also known as sodium hydrogen carbonate, is a medication primarily used to treat severe metabolic acidosis . [1] For this purpose it is generally only used when the pH is less than 7.1 and when the underlying cause is either diarrhea , vomiting , or the kidneys . [2] Other uses include high blood potassium , tricyclic antidepressant overdose , and cocaine toxicity as well as a number of other poisonings . [1] [3] [4] It is given by injection into a vein . [2] Side effects may include low blood potassium , high blood sodium , and swelling . [1] [4] It is not recommended in people with low blood calcium . [5] Sodium bicarbonate is in the alkalinizing family of medication. [5] It works by increasing blood bicarbonate , which buffers excess hydrogen ion and raises blood pH . [5] Commercial production of sodium bicarbonate began between 1791 and 1823. [6] Intravenous medical use began around the 1950s. [4] It is on the World Health Organization's List of Essential Medicines , the most effective and safe medicines needed in a health system . [7] Sodium bicarbonate is available as a generic medication . [5] The wholesale cost in the developing world is about 0.09 to 2.58 USD per 10 ml of 8.4% solution. [8] In the United Kingdom this amount costs the NHS about 11.10 pounds. [2] Intravenous sodium bicarbonate is indicated in the treatment of metabolic acidosis , such as can occur in severe kidney disease , diabetic ketoacidosis , circulatory insufficiency , extracorporeal circulation of blood, in hemolysis requiring alkalinization of the urine to avoid nephrotoxicity of blood pigments, and certain drug intoxications , such as by barbiturate overdose , salicylate poisoning , tricyclic antidepressant overdose or methanol poisoning . [9] In addition Continue reading >>

Prime Pubmed | Influence Of Respiratory Acidosis On Ecg And Pressor Responses To Epinephrine, Norepinephrine And Metaramino

Prime Pubmed | Influence Of Respiratory Acidosis On Ecg And Pressor Responses To Epinephrine, Norepinephrine And Metaramino

HOULE, D B., et al. "Influence of Respiratory Acidosis On ECG and Pressor Responses to Epinephrine, Norepinephrine and Metaraminol." Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), vol. 94, no. 3, 1957, pp. 561-4. HOULE DB, WEIL MH, BROWN EB, et al. Influence of respiratory acidosis on ECG and pressor responses to epinephrine, norepinephrine and metaraminol. Proc Soc Exp Biol Med. 1957;94(3):561-4. HOULE, D. B., WEIL, M. H., BROWN, E. B., & CAMPBELL, G. S. (1957). Influence of respiratory acidosis on ECG and pressor responses to epinephrine, norepinephrine and metaraminol. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 94(3), pp. 561-4. HOULE DB, et al. Influence of Respiratory Acidosis On ECG and Pressor Responses to Epinephrine, Norepinephrine and Metaraminol. Proc Soc Exp Biol Med. 1957;94(3):561-4. PubMed PMID: 13408326. * Article titles in AMA citation format should be in sentence-case TY - JOURT1 - Influence of respiratory acidosis on ECG and pressor responses to epinephrine, norepinephrine and metaraminol.AU - HOULE,D B,AU - WEIL,M H,AU - BROWN,E B,JrAU - CAMPBELL,G S,PY - 1957/3/1/pubmedPY - 1957/3/1/medlinePY - 1957/3/1/entrezKW - ACIDOSIS/experimentalKW - ARTERENOL/effectsKW - ELECTROCARDIOGRAPHY/effect of drugs onKW - EPINEPHRINE/effectsKW - SYMPATHOMIMETICS/effectsSP - 561EP - 4JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)JO - Proc. Soc. Exp. Biol. Med.VL - 94IS - 3SN - 0037-9727UR - - PRIMEDP - Unbound MedicineER - 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 >>

Norepinephrine A Tangled Web

Norepinephrine A Tangled Web

Levophed, also known as norepinephrine, is another stress hormone, and the topic for today. Weve mentioned norepinephrine in the posts on dopamine and epinephrine , but now were going a little deeper. Levophed will leave em dead, I was taught as a new nurse in the ICU, and definitely it can. Norepinephrine is a powerful alpha-1-agonist, producing intense vascular vasoconstriction. High doses of this medication will clamp the vascular system, both arterial and venous, to the extent no perfusion occurs in the capillary beds. In other words, it increases afterload. In fact, it can increase afterload so much that it causes metabolic acidosis. Because of its venous activity it diminishes preload. At the same time, cardiac output drops as the heart rate falls.This mechanism makes it a poor choice as an inotrope. Lets look at this. Norepinephrine has beta-1 agonist activity comparable to epinephrine, but it has NO effect on beta-2 receptor sites. But didnt I say that beta-1 agonists increase contractility and heart rate ? Yes, I did. The increase in mean arterial pressure levophed induces will cause baroreceptor-mediated drop in heart rate, which the beta-1 stimulation of norepinephrine is often too weak to overcome. Not always, though. We use levophed as a first-line vasoactive agent, directly behind or in conjunction with crystalloid, for hypotensive patients in the presence of infection. This state is what we refer to as septic shock, and Im not going into SIRS criteria in this post. In these patients its unlikely to see the drop in heart rate, as the pathophysiology of sepsis results in tachycardia. Norepinephrine doesnt affect the alpha-2 receptor sites, which are found in the cerebral circulation. Since it lacks beta-2 activity, it also will not dilate the bronchioles, 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 >>

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 >>

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 >>

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 >>

Vasopressin

Vasopressin

endogenously produced by the magnocellular neurone cell bodies of the paraventricular and supraoptic nuclei of the posterior hypothalamus Vasopressin on multiple receptors (GPCRs = g protein coupled) vascular smooth muscle of the systemic, splanchnic, renal, and coronary circulations -> potent vasoconstriction renal efferent arterioles -> increased GFR renal collecting ducts -> anti-diuresis hemostatic system -> induces the release of Von Willebrand Factor (VWF) and Factor VIII:coagulant (FVIII:c) from endothelial cells -> increased platelet aggregation pituitary -> stimulates release of ACTH and hence increased cortisol secretion oxytocin receptor subtypes -> myometrium and vascular smooth muscle Effects are preserved during hypoxia and severe acidosis and catecholamine resistant states 0.01-0.1U/min (onset: fast, offset: fast for vascular, long for kidneys) refractory hypotension (potentiates the actions of over vasoconstrictors) haemostasis in bleeding oesophageal varicies Metabolism peptidases in the liver and kidney Factorial (22) multicenter, double blind, randomised controlled trial Vasopressin (titrated up to 0.06 U/min) +/-Hydrocortisone (50mg q6h and then weaned) versus noradrenaline (titrated up to 12 g/min +/-Hydrocortisone (50mg q6h and then weaned) If the patient was still hypotensive after the first dose of study drug 2 then additional open-label catecholamine vasopressors could be administered no difference in number of days alive and free of kidney failure (defined by AKIN group stage 3) no difference with the addition of steroids Vasopressin decreased norepinephrine requirement all patients: reduced mortality (relative risk (RR), 0.87 (0.77 to 0.99); P = 0.04). in adults: decreased mortality (RR, 0.87 (0.76 to 1.00); P = 0.05) in patients with septic Continue reading >>

Comparison Of Norepinephrine And Dobutamine To Epinephrine For Hemodynamics, Lactate Metabolism, And Gastric Tonometric Variables In Septic Shock: A Prospective, Randomized Study

Comparison Of Norepinephrine And Dobutamine To Epinephrine For Hemodynamics, Lactate Metabolism, And Gastric Tonometric Variables In Septic Shock: A Prospective, Randomized Study

Objectives: To compare the effects of norepinephrine and dobutamine to epinephrine on hemodynamics, lactate metabolism, and gastric tonometric variables in hyperdynamic dopamine-resistant septic shock. Design: A prospective, intervention, randomized clinical trial. Setting: Adult medical/surgical intensive care unit in a university hospital. Patients: 30 patients with a cardiac index (CI) > 3.5 l min1 m2 and a mean arterial pressure (MAP) 60 mmHg after volume loading and dopamine 20 g/kg per min and either oliguria or hyperlactatemia. Interventions: Patients were randomized to receive an infusion of either norepinephrine-dobutamine or epinephrine titrated to obtain an MAP greater than 80 mmHg with a stable or increased CI. Measurements and main results: Baseline measurements included: hemodynamic and tonometric parameters, arterial and mixed venous gases, and lactate and pyruvate blood levels. These measurements were repeated after 1, 6, 12, and 24 h. All the patients fulfilled the therapeutic goals. No statistical difference was found between epinephrine and norepinephrine-dobutamine for systemic hemodynamic measurements. Considering metabolic and tonometric measurements and compared to baseline values, after 6 h, epinephrine infusion was associated with an increase in lactate levels (from 3.1 1.5 to 5.9 1.0 mmol/l; p < 0.01), while lactate levels decreased in the norepinephrine-dobutamine group (from 3.1 1.5 to 2.7 1.0 mmol/l). The lactate/pyruvate ratio increased in the epinephrine group (from 15.5 5.4 to 21 5.8; p < 0.01) and did not change in the norepinephrine-dobutamine group (13.8 5 to 14 5.0). Gastric mucosal pH (pHi) decreased (from 7.29 0.11 to 7.16 0.07; p < 0.01) and the partial pressure of carbon dioxide (PCO2) gap (tonometer PCO2 arterial PCO2) increased Continue reading >>

Lactic Acidosis

Lactic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>

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