Causes Of Lactic Acidosis
INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis . Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>
Congestive Heart Failure & Lactic Acidosis: Causes & Diagnoses | Symptoma.com
 real justification in the treatment of lactic acidosis: severe pulmonary hypertension and right heart failure to optimized right ventricular function severe IHD where [lifeinthefastlane.com] acidosis a condition in which the compensatory mechanisms have returned the pH toward normal. lactic acidosis a metabolic acidosis occurring as a result of excess lactic acid [medical-dictionary.thefreedictionary.com] Dialysis may also be useful when severe lactic acidosis exists with chronic kidney disease or congestive heart failure, or with metformin intoxication. [ 7 ] Complications [patient.info]  renally filtered (180mmol/day) is fully reabsorbed PATHOPHYSIOLOGY lactic acidosis can occur due to: (i) excessive tissue lactate production (ii) impaired hepatic metabolism [lifeinthefastlane.com] acidosis Metabolism Metabolic acidosis due to lactic acid resulting from tissue hypoxia or conversion of lactate to pyruvate Etiology Exercise, endogenous or exogenous metabolic [medical-dictionary.thefreedictionary.com] Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. [patient.info] This animation helps explain how congestive heart failure develops. [sharecare.com] Congestive heart failure. [medical-dictionary.thefreedictionary.com] What is Congestive Heart Failure? [acls.net] Congestive heart failure can also impair the funciton of the kidneys. [sharecare.com] Clinical portrait of congestive heart failure. [medical-dictionary.thefreedictionary.com] Thus the name, congestive heart failure. [acls.net] Congenital lactic acidosis Mitochondrial dna mutations cause this condition [ edit on Wikidata ] Congenital lactic acidosis (CLA) is a rare disease caused by mutations in [en.wikipedia.org] Congenital lactic acidos Continue reading >>
Lactic Acidosis In Pulmonary Edema Due To Left Ventricular Failure
Lactic Acidosis in Pulmonary Edema due to Left Ventricular Failure MILFORD FULOP; MICHAEL HOROWITZ, M.D.; ARNOLD ABERMAN, M.D.; ERNST R. JAFF, M.D. Author, Article, and Disclosure Information Grant support: Grant AM 13698, National Institutes of Health. Requests for reprints should be addressed to Milford Fulop, M.D., Department of Medicine, Bronx Municipal Hospital Center, Pelham Parkway South and Eastchester Road, Bronx, NY 10461. Acidemia is common in severe pulmonary edema due to acute heart failure and is caused by metabolic and respiratory acidosis, in various combinations in different patients. The findings in our study show that the metabolic acidosis is a lactic acidosis. Among 18 patients with acute pulmonary edema due to left ventricular failure, 14 had a blood pH of less than 7.36, and blood lactate concentrations were elevated in most cases (mean, 4.5 millimol/litre 2.9 SD). Both the severity of the acidemia and the lowering of the plasma bicarbonate concentration were closely related to the plasma lactate concentration. As pulmonary edema regressed, the lactic acidosis largely abated, within a few hours in most patients, and the blood pH and plasma bicarbonate concentration returned toward normal without the administration of sodium bicarbonate. Continue reading >>
Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus
Introduction A 49-year-old man presented to the emergency department complaining of dyspnea for 2 days. He had a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and a severe dilated cardiomyopathy. He had been hospitalized several times in the previous year for decompensated congestive heart failure (most recently, 1 month earlier). The plasma creatinine concentration was 1.13 mg/dl on discharge. Outpatient medications included insulin, digoxin, warfarin, spironolactone, metoprolol succinate, furosemide (80 mg two times per day; increased from 40 mg daily 1 month earlier), metolazone (2.5 mg daily; added 1 month earlier), and metformin (2500 mg in three divided doses; increased from 1000 mg 1 month earlier). Physical examination revealed an obese man in moderate respiratory distress. The temperature was 36.8°C, BP was 119/83 mmHg, and heart rate was 96 per minute. Peripheral hemoglobin oxygen saturation was 97% on room air, with a respiratory rate of 26 per minute. The heart rhythm was irregularly irregular; there was no S3 or murmur. Jugular venous pressure was about 8 cm. There was 1+ edema at the ankles. A chest radiograph showed cardiomegaly and central venous prominence. The N-terminal pro-B-type natriuretic peptide level was 5137 pg/ml (reference range = 1–138 pg/ml). The peripheral hemoglobin concentration was 12.5 g/dl, the white blood cell count was 12,500/µl (76% granulocytes), and the platelet count was 332,000/µL. Initial plasma chemistries are shown in Table 1. The impression was decompensated congestive heart failure. After administration of furosemide (160 mg intravenously), the urine output increased to 320 ml over the next 1 hour. There was no improvement in the dyspnea. Within 2 hours, the patient’s BP fell to 100/64 mmHg Continue reading >>
Metformin, Heart Failure, And Lactic Acidosis: Is Metformin Absolutely Contraindicated?
Many patients with type 2 diabetes are denied treatment with metformin because of “contraindications” such as cardiac failure, which may not be absolute contraindications Summary points Treatment with metformin is not associated with an increased risk of lactic acidosis among patients with type 2 diabetes mellitus who have no cardiac, renal, or liver failure Despite increasing disregard of contraindications to metformin by physicians, the incidence of lactic acidosis has not increased, so metformin may be safe even in patients with “contraindications” The vast majority of case reports relating metformin to lactic acidosis report at least one other disease/illness that could result in lactic acidosis Use of metformin in patients with heart failure might be associated with lower mortality and morbidity, with no increase in hospital admissions and no documented increased risk of lactic acidosis Further studies are needed to assess the risk of lactic acidosis in patients with type 2 diabetes and traditional contraindications to metformin Metformin first became available in the United Kingdom in 1957 but was first prescribed in the United States only in 1995.w1 The mechanism of action has been extensively reviewed.w2 w3 The UK prospective diabetes study showed that metformin was associated with a lower mortality from cardiovascular disease than sulphonylureas or insulin in obese patients with type 2 diabetes mellitus.1 It was also associated with reduced all cause mortality, which was not seen in patients with equally well controlled blood glucose treated with sulphonylureas or insulin.1 Despite the evidence base for the benefits of metformin, concerns remain about its side effects and especially the perceived risk of lactic acidosis in the presence of renal, hepatic Continue reading >>
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: 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. 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. Causes of lactic acid Continue reading >>
Lactate And Acute Heart Failure Syndrome
This chapter discusses the different pathways of lactate metabolism and the mechanisms by which hyperlactatemia could appear during acute heart failure. The clinical practical interpretation of hyperlactatemia requires repeated lactate measurement. In all cases, it must be compared with the clinical situation and other biologic parameters. Hyperlactatemia entails a poor prognosis, especially if it is persistent. But even though it has been considered deleterious for a long time, recent data show that lactate is probably a key metabolic intermediate substrate during acute energetic crisis. Thus, hyperlactatemia, and more precisely a high lactate turnover, may be viewed as an adaptive or protective response to acute illness. Neither low pH nor hyperlactatemia requires a specific treatment ( 1 ). Cardiogenic ShockLactic AcidosisAcute Heart FailureTissue HypoxiaBlood Lactate Level These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Cohen RD, Woods HF. Lactic acidosis revisited. Diabetes 1983;32:18191. PubMed Google Scholar Gutierrez G, Wulf M. Lactic acidosis in sepsis: a commentary. Intensive Care Med 1996;22:616. PubMed CrossRef Google Scholar Vincent JL. Lactate levels in critically ill patients. Acta Anaesth Scand 1995;107(suppl):2616. CrossRef Google Scholar Leverve X. Lactic acidosis. A new insight. Minerva Anesthesiol 1999;65:2059. Google Scholar Pagano C, Granzotto M, Giaccari A, et al. Lactate infusion to normal rats during hyperglycemia enhances in vivo muscle glycogen synthesis. Am J Physiol 1997;273:R20729. PubMed Google Scholar Schurr A, Payne Continue reading >>
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Lactic Acidosis: What You Need To Know
Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>
What Causes Heart Attacks?
The story of how I came to understand the cause, and therefore the appropriate treatment, of acute coronary syndrome involves fascinating elements of surprise and serendipity. I thought it best, therefore, to describe how this tale unfolded for me. Acute Coronary Syndrome (ACS) describes a constellation of illnesses that include angina (chest pain), unstable angina (basically bad chest pain) and myocardial infarction (otherwise known as heart attack or MI). These three illnesses form a continuum, with angina as the mildest symptom and heart attackwhen there is actual death of the heart cellsas the most severe. The history of thought about this group of illnesses is both fascinating and controversial. It seems that heart attacks were rare in this country until about the 1930s. The incidence of fatal MIs quickly increased from about 3,000 per year during that decade to almost half a million per year during the 1950s. In fact, mid century, this formerly rare disease had become the leading cause of death in the US. The incidence has risen continually since then until just recently, when it seems that the tide may be turning a bit and the incidence lessening, or at least leveling off. Nevertheless, after decades of reckless fiddling with the American diet as a way to prevent heart disease, almost a million Americans still die from heart disease each year. As you can imagine, when it became clear that we were suffering from an epidemic of this disease, physicians and cardiologists developed an intense interest in the cause and possible treatment of the disease. Around the late 1940s, the medical establishment proposed a simple and plausible explanation for MI, and this explanation soon became universally accepted. The current thinking about heart attacks focuses on the blood Continue reading >>
Lactic Acid - The Truth Myheart
Surprisingly the truth is that lactic acid actually protects against the acidosis it was accused of causing and as such is a helpful product that can actually allow muscles to contract for longer. When we look back at the literature it becomes evident that scientists have been questioning the misconception of lactic acid for decades ( Wilkie 1979 ) so it is amazing how this myth still perpetuates. To understand why lactic acid isnt the enemy we must deconstruct the lactic acid myth . As explained the belief is that lactic acid is produced by the cell when there is not enough oxygen or the energy requirements are more than the cell can produce using the oxidative phosphorylation system. It is then thought that the acid environment caused by the lactic acid decreases the functionality of the muscle to contract. lactic acid does not make the cell acidic The fact is that lactic acid is not the source of acidosis in the cell. When we look at the full reaction of the conversion of glucose to pyruvate ( glycolysis ) and then lactic acid what we see is that there is no net production of hydrogen ions (acid). Even more interesting than this is the fact that if we feed glycogen and not glucose into the glycolysis reaction it actually results in consumption of a hydrogen ion and is thus reducing the acid within the cell! Also as explained earlier, if we look at the conversion of pyruvate to lactate we see that the conversion of pyruvate to lactate not only consumes a hydrogen ion (acid) but also produces NAD+ which allows the whole glycolysis cycle to continue Glucose + 2 NAD+ + 2 ADP + 2 Pi 2 Pyruvate + 2 NADH + 2 H+ + 2 ATP + 2 H2O So lactic acid is actually produced to buffer the cell against acidosis and helps to keep going the reactions that the cells need to produce energy Continue reading >>
What Is A Lactic Acid Blood Test?
It’s a test that measures the amount of lactic acid (also called “lactate”) in your blood. This acid is made in muscle cells and red blood cells. It forms when your body turns food into energy. Your body relies on this energy when its oxygen levels are low. Oxygen levels might drop during an intense workout or when you have an infection or disease. Once you finish your workout or recover from the illness, your lactic acid level tends to go back to normal. But sometimes, it doesn't. Higher-than-normal lactic acid levels can lead to a condition called lactic acidosis. If it’s severe enough, it can upset your body’s pH balance, which indicates the level of acid in your blood. Lactic acidosis can lead to these symptoms: It’s a simple blood test. Your doctor will draw blood from a vein or artery using a needle. In rare cases, he may take a sample of cerebrospinal fluid from your spinal column during a procedure called a spinal tap. Normally, you don’t have to adjust your routine to prepare for the test. If your lactic acid level is normal, you don’t have lactic acidosis. Your cells are making enough oxygen. It also tells your doctor that something other than lactic acidosis is causing your symptoms. He’ll likely order other tests to find out what it is. If your lactic acid level is high, it could be caused by a number of things. Most often, it’s because you have a condition that makes it hard for you to breathe in enough oxygen. Some of these conditions could include: Severe lung disease or respiratory failure Fluid build-up in your lungs Very low red blood cell count (severe anemia) A higher-than-normal lactic acid level in your blood can also be a sign of problems with your metabolism. And, your body might need more oxygen than normal because you have o Continue reading >>
Metformin Use In Patients With Diabetes And Heart Failure: Cause For Concern?
Patients with type 2 diabetes are 2.5 times more likely to develop heart failure than those without diabetes,1 and > 30% of patients with heart failure have concurrent diabetes.2 Biguanides, namely phenformin and metformin, have been used for the treatment of diabetes for decades. In certain clinical situations, however, the use of biguanides can result in an accumulation of lactic acid, which may result in a rare condition known as acute lactic acidosis (ALA), which is fatal in ∼ 50% of cases.3,4 In most instances, the development of ALA arises secondary to conditions predisposing patients to hemodynamic compromise and overt tissue hypoxia, such as acute myocardial infarction (MI), acute uncompromised heart failure, or sepsis.5,6 Phenformin was removed from the market in 1976 because of reports of both fatal and nonfatal phenformin-associated lactic acidosis (PALA).7 The incidence of PALA at the time was estimated to be between 40 and 64 cases per 100,000 patient-years, or four to six times that seen in patients with diabetes who were not on phenformin.8,9 Unlike phenformin, which is metabolized through the liver via hydroxylation, metformin is excreted unchanged in the urine.10 Therefore, metformin is less likely to inhibit hepatic lactate clearance and lead to ALA. The estimated incidence of metformin-associated lactic acidosis (MALA) in patients with diabetes is between 3 and 9 cases per 100,000 patient-years, roughly the same as that reported in patients with diabetes who are not taking a biguanide.4,7,11–13 Epidemiological data reveal that metformin is often used in patients with heart failure. Prospective and retrospective cohort studies have evaluated health care databases of hospitalized and outpatient diabetic populations to determine metformin usage in pa Continue reading >>
Background In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [1, 2] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection.  By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac Continue reading >>
Metformin And Heart Failure
Innocent until proven guilty Throughout the world and for many years, metformin has been a mainstay of therapy for patients with type 2 diabetes. This highly effective and usually well-tolerated oral agent is, to date, the only one demonstrated to reduce cardiovascular disease (CVD) complications in newly diagnosed type 2 diabetic patients (1). It's precise mechanism of action remains enigmatic, although it clearly results in a reduction of endogenous glucose production, primarily hepatic gluconeogenesis, most likely involving the stimulation of AMP-activated protein kinase activity (2). A peripheral insulin-sensitizing effect in skeletal muscle has also been demonstrated by some, but not all, investigators (3). In small studies, metformin appears to exert benefit on various other fundamental biological processes that influence atherogenesis, such as lipid metabolism, inflammation, and vascular endothelial function (4). Another insulin sensitizer category, the thiazolidinediones (TZDs), has also been proposed to reduce CVD risk, but that class carries with it concerns of weight gain and fluid retention. As a result, TZDs remain more popular in combination therapy regimens. Perhaps of greatest import to clinicians is the recognition that metformin is the only oral antidiabetic agent associated with weight loss. Accordingly, metformin remains, in the eyes of many authorities, the optimal initial drug choice in most type 2 diabetic patients if diet and exercise have not succeeded in adequately reducing blood glucose levels (5). Approval of metformin in the U.S. was delayed because of previous experience with phenformin, which was associated with lactic acidosis. Although the risk of such metabolic decompensation with metformin was known to be significantly lower than with Continue reading >>
Review Article Metformin In Heart Failure Patients
Summary The use of metformin was considered a contraindication in heart failure patients because of the potential risk of lactic acidosis; however, more recent evidence has shown that this should no longer be the case. We reviewed the current literature and the recent guideline to correct the misconception. Continue reading >>