diabetestalk.net

Lactic Acidosis Chf

Metformin, Heart Failure, And Lactic Acidosis: Is Metformin Absolutely Contraindicated?

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 >>

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

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 >>

Congestive Heart Failure & Lactic Acidosis: Causes & Diagnoses | Symptoma.com

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 >>

Causes Of Lactic Acidosis

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 [1]. 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 >>

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Abstract Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin, along with other drugs in the biguanide class, increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e.g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment since its FDA approval in patients with normal renal function or mild renal insufficiency to minimize the potential for toxic metformin levels and MALA. However, the reported incidence of lactic acidosis in clinical practice has proved to be very low (< 10 cases per 100,000 patient-years). Several groups have suggested that current renal function cutoffs for metformin are too conservative, thus depriving a substantial number of type 2 diabetes patients from the potential benefit of metformin therapy. On the other hand, the success of metformin as the first-line diabetes therapy may be a direct consequence of conservative labeling, the absence of which could have led to excess patient risk and eventual withdrawal from the market, as happened with earlier biguanide therapies. An investigational delayed-release metformin currently under development could potentially provide a treatment option for patients with renal impairment pending the resu Continue reading >>

Acute Lactic Acidosis

Acute Lactic Acidosis

Author: Bret A Nicks, MD, MHA; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Metabolic acidosis is defined as a state of decreased systemic pH resulting from either a primary increase in hydrogen ion (H+) or a reduction in bicarbonate (HCO3-) concentrations. In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in PaCO2. Chronically, renal compensation occurs by means of reabsorption of HCO3. [ 1 , 2 ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may result from numerous conditions. [ 2 , 3 , 4 ] It remains the most common cause of metabolic acidosis in hospitalized patients. The normal blood lactate concentration in unstressed patients is0.5-1 mmol/L. Patients with critical illness can be considered to have normal lactate concentrations of less than 2 mmol/L. Hyperlactatemia is defined as a mild to moderate persistent increase in blood lactate concentration (2-4 mmol/L) without metabolic acidosis, whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually >4-5 mmol/L) in association with metabolic acidosis. [ 1 , 5 ] Elevated lactate levels, while typically thought of as a marker of inadequate tissue perfusion with concurrent shift toward increased anaerobic metabolism, can be present in patients in whom systemic hypoperfusion is not present and therefore should be considered wit Continue reading >>

Lactic Acidosis - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i Continue reading >>

Lactate And Acute Heart Failure Syndrome

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 >>

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 >>

Lactate

Lactate

To detect high levels of lactate in the blood, which may be an indication of lack of oxygen ( hypoxia ) or the presence of other conditions that cause excess production or insufficient clearing of lactate from the blood; this test is not meant to be used for screening for health status. When you have symptoms such as rapid breathing, nausea, and sweating that suggest a lack of oxygen or an abnormal blood pH (acid/base imbalance); when a health practitioner suspects that you may be experiencing sepsis , shock, heart attack , severe congestive heart failure , kidney failure , or inadequately treated (uncontrolled) diabetes ; when a health practitioner suspects that you have inherited a rare metabolic or mitochondrial disorder A blood sample drawn from a vein in your arm; sometimes a blood sample collected from an artery and, rarely, a sample of cerebrospinal fluid collected from the spine You may be told to rest prior to sample collection. Rarely, fasting may be required. You may be able to find your test results on your laboratory's website or patient portal. However, you are currently at Lab Tests Online. You may have been directed here by your lab's website in order to provide you with background information about the test(s) you had performed.You will need to return to your lab's website or portal, or contact your healthcare practitionerin order to obtainyour test results. Lab Tests Online is an award-winning patient education website offering information on laboratory tests. The content on the site, which has been reviewed by laboratory scientists and other medical professionals,provides general explanations of what results might mean for each test listed on the site, such as what a high or low value might suggest to your healthcare practitionerabout your health or Continue reading >>

What To Know About Lactic Acidosis

What To Know About Lactic Acidosis

Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. shallow, rapid, or other breathing problems Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some peoples bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus, especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acid Continue reading >>

Lactic Acidosis In Acute Congestive Heart Failure

Lactic Acidosis In Acute Congestive Heart Failure

@article{cceb1ca8c7cc4a0fb40c047ae4527bfc, title = "Lactic acidosis in acute congestive heart failure", abstract = "Lactic acidosis appears to be a common complication of acute congestive heart failure. Like other metabolic acidoses that complicate various illnesses, it must be corrected in order to treat the underlying disease successfully. Routine determinations of the lactic acid level of the blood may have value in both diagnosis and treatment of acute congestive failure. Lactic acid and bicarbonate values are inversely correlated, but oxygen and carbon dioxide tensions are poorly correlated with the lactic acid level and with the clinical course. However, both the initial level and changes in lactic acid are of value in assessing treatment response and prognosis.", T1 - Lactic acidosis in acute congestive heart failure N2 - Lactic acidosis appears to be a common complication of acute congestive heart failure. Like other metabolic acidoses that complicate various illnesses, it must be corrected in order to treat the underlying disease successfully. Routine determinations of the lactic acid level of the blood may have value in both diagnosis and treatment of acute congestive failure. Lactic acid and bicarbonate values are inversely correlated, but oxygen and carbon dioxide tensions are poorly correlated with the lactic acid level and with the clinical course. However, both the initial level and changes in lactic acid are of value in assessing treatment response and prognosis. AB - Lactic acidosis appears to be a common complication of acute congestive heart failure. Like other metabolic acidoses that complicate various illnesses, it must be corrected in order to treat the underlying disease successfully. Routine determinations of the lactic acid level of the blood m Continue reading >>

Lactate And Lactate Clearance In Acute Cardiac Care Patients

Lactate And Lactate Clearance In Acute Cardiac Care Patients

Lactate and lactate clearance in acute cardiac care patients Azienda Ospedaliero-Universitaria Careggi, Florence, Italy Paola Attan, Intensive Cardiac Care Unit, Heart and Vessel Department, Viale Morgagni 85, 50134 Florence, Italy. Email: [email protected]_aloap Received 2012 Feb 16; Accepted 2012 May 19. Copyright The European Society of Cardiology 2012 This article has been cited by other articles in PMC. Hyperlactataemia is commonly used as a diagnostic and prognostic tool in intensive care settings. Recent studies documented that serial lactate measurements over time (or lactate clearance), may be clinically more reliable than lactate absolute value for risk stratification in different pathological conditions. While the negative prognostic role of hyperlactataemia in several critical ill diseases (such as sepsis and trauma) is well established, data in patients with acute cardiac conditions (i.e. acute coronary syndromes) are scarce and controversial. The present paper provides an overview of the current available evidence on the clinical role of lactic acid levels and lactate clearance in acute cardiac settings (acute coronary syndromes, cardiogenic shock, cardiac surgery), focusing on its prognostic role. Keywords: Acute cardiac setting, lactate, lactate clearance First isolated in 1780 by Carl Wilhelm Scheele, 1 lactic acid (LA) is still recognized as a gauge of metabolic function and has a diagnostic and/or prognostic role in different clinical settings. 2 While the negative prognostic role of hyperlactataemia in several critical ill diseases (such as sepsis and trauma) is well established, 3 5 data in patients with acute cardiac conditions (i.e. acute myocardial ischaemia) are scarce and controversial. 6 , 7 The present manuscript is aimed at summarizing availab Continue reading >>

Lactic Acidosis | Md Nexus

Lactic Acidosis | Md Nexus

Cohen-Woods Classification of Lactic Acidosis Type A: due to decreased perfusion or oxygenation However, these may cause type A lactic acidosis in some cases Type B2: due to medication or intoxication Type B3: due to inborn error of metabolism Mitochondrial Encephalomyopathy + Lactic Acidosis + Stroke-Like Episodes (MELAS) Tumors May Benefit from Acidosis: acidic microenvironment is critical for tumorigenesis, angiogenesis, and metastasis Physiology: decreased lactate clearance (with severe liver metastases)+ increased glycolytic activity of tumor (Warburg Effect) + tissue tumor hypoxia Treatment: bicarbonate administration may increase lactic acid production Tumor Lysis Syndrome (see Tumor Lysis Syndrome , [[Tumor Lysis Syndrome]]) Anaphylaxis (see Anaphylaxis , [[Anaphylaxis]]) Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Congestive Heart Failure (CHF)/Cardiogenic Shock (see Congestive Heart Failure , [[Congestive Heart Failure]] and Cardiogenic Shock , [[Cardiogenic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hemorrhagic Shock (see Hemorrhagic Shock , [[Hemorrhagic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hypovolemic Shock (see Hypovolemic Shock , [[Hypovolemic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Sepsis (see Sepsis , [[Sepsis]]): common etiology of lactic acidosis Physiology: decreased lactate clearance (likely due to inhibition of pyruvate dehydrogenase + epinephrine-induced 2-adrene Continue reading >>

What Is A Lactic Acid Blood Test?

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 >>

More in ketosis