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Lactic Acidosis In Copd Exacerbation

Lactic Acidosis: Lactic Acidosis Associated With Metformin Use In Treatment Of Type 2 Diabetes Mellitus

Lactic Acidosis: Lactic Acidosis Associated With Metformin Use In Treatment Of Type 2 Diabetes Mellitus

Lactic acidosis: Lactic acidosis associated with metformin use in treatment of type 2 diabetes mellitus Metformin was stopped on admission. The patient was started on antibiotics and methylprednisolone for a COPD exacerbation. The patient's lactate level was 7.8 mmol/L, creatinine level was 2.1 mg/dL, and glucose was 340 mg/dL. Her treatment included blood transfusion, a 3-hour session of hemodialysis, 29 PD sessions, and a bicarbonate infusion. Her respiratory system was unable to compensate for the acid-base derangement. The patient did not want endotracheal intubation, so non-invasive positive pressure mechanical ventilation (NPPV) was initiated. Glucose was difficult to control, she required a continuous insulin infusion. On the 4th day, acid-base status and glucose level had improved. PD and the bicarbonate and insulin infusions were discontinued. Although the lactic acidosis cleared with treatment (lactate level 1.7 mmol/L, anion gap 2, and pH 7.33), the renal failure worsened. She continued on NPPV. On the 7th day, she became hypotensive and died. The lactic acid level was 1.8 mmol/L; the creatinine level was 2.6 mg/dL; the anion gap was 9. An 80-year-old man was admitted with fever, cough, and weakness. He was tachypneic, oxyhemoglobin saturation was 89% to 90%, and breath sounds were decreased at the right lung base. Chest radiograph confirmed a right lower lobe infiltrate. Medical history included type 2 diabetes, MI, femoral-popliteal bypass graft, emphysema, and pulmonary fibrosis not requiring corticosteroids or supplemental oxygen. His medications included metformin, enalapril, sertraline hydrochloride, and glipizide. Metformin was discontinued on admission. The patient was started on ciprofloxacin, methylprednisolone, ipratropium bromide and albuterol, a 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 Acid Levels In Patients With Chronic Obstructive Pulmonary Disease Accomplishing Unsupported Arm Exercises

Lactic Acid Levels In Patients With Chronic Obstructive Pulmonary Disease Accomplishing Unsupported Arm Exercises

Patients with chronic obstructive pulmonary disease (COPD) may suffer dyspnea when performing unsupported arm exercises (UAE). However, some factors related to the tolerance of the upper limbs during these exercises are not well understood. Our investigation was to determine if an unsupported arm exercise test in patients with COPD accomplishing diagonal movements increases lactic acid levels; also, we assessed the metabolic, ventilatory and cardiovascular responses obtained from the unsupported arm exercise test. The study used results of maximal symptom limited tests with unsupported arms and legs performed on 16 patients with COPD. In order to do the test, some metabolic, respiratory and cardiovascular parameters such as ), respiratory rate (RR), pulmonary ventilation (VE), heart rate (HR) and blood pressure (BP) were measured during the exercise tests. Furthermore, blood lactate concentration was measured during the arm test. We detected a significant increase in the mean blood lactate , VE and RR from the resting to the peak phase of the UAE test. The mean values of and VE obtained at the peak of the UAE test corresponded to 52.5%, 50.0% and 61.2%, respectively, of the maximal values obtained at the peak of the leg exercise test. In comparison, the mean heart rate and systolic arterial blood pressure were significantly lower at the peak of the UAE test than at the peak leg exercise test and corresponded to 76.2% and 83.0%, respectively. Unsupported incremental arm exercises in patients with COPD increases blood lactic acid levels. unsupported arm exercise test, COPD, lactate concentration Patients with chronic obstructive pulmonary disease (COPD) may develop high ventilatory and metabolic output when accomplishing simple activities of daily especially when perform Continue reading >>

Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Received 29 September 2011; Accepted 26 October 2011 Copyright 2012 Cosimo Marcello Bruno and Maria Valenti. 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. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. Chronic obstructive pulmonary disease (COPD) is a major public health problem. Its prevalence varies according to country, age, and sex. On the basis of epidemiologic data, the projection for 2020 indicates that COPD will be the third leading cause of death worldwide and the fifth leading cause of disability [ 1 ]. About 15% of COPD patients need admission to general hospital or intensive respiratory care unit for acute exacerbation, leading to greater use of medical resources and increased costs [ 2 5 ]. Even though the overall prognosis of COPD patients is lately improved, the mortality rate remains high, and, among others, acid-base disorders occurring in these subjects can affect the outcome. The aim of this pa Continue reading >>

Exercise And The Lungs

Exercise And The Lungs

The amount of air you need to breathe in depends on how active you are. When you are sitting down you only take in about 15 breaths a minute, giving you around 12 litres of air (a litre is one and three-quarter pints). From this your lungs will extract just one fifth of a litre of oxygen. During exercise your breathing and heart rate increase. Exercising flat out, a top-class athlete can expect to increase his/her breathing rate to around 40 to 60 breaths a minute. This means they take in an incredible 100 to 150 litres of air, extracting around five litres of oxygen every single minute. Even those of us with more modest goals need to double our lung intake when we exercise. Our lungs must be able to respond to our bodys increased demands for oxygen. As you start to move about, the muscles in your body send messages to your brain that they need more oxygen. Your brain then sends signals to the muscles that control breathing your diaphragm and the muscles between your ribs so that they shorten and relax more often. This causes you to take more breaths. More oxygen will be absorbed from your lungs and carried to the muscles you are using to exercise mainly your arms and legs. For you to become more active your muscles will need to produce more energy. They do this by breaking down glucose from your food, but to do this they need oxygen. If there is too little oxygen they will try to produce energy in a different way. But this can lead to a build-up of a chemical called lactic acid, which causes cramp something that many athletes are all too familiar with. Athletes train so that their lungs and muscles become more efficient and it takes longer for lactic acid to build up. This means that their muscles can work harder. In fact, everyone can benefit from exercise to strengt Continue reading >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co Continue reading >>

Contribution Of The Respiratory Muscles To The Lactic Acidosis Of Heavy Exercise In Copd.

Contribution Of The Respiratory Muscles To The Lactic Acidosis Of Heavy Exercise In Copd.

Contribution of the respiratory muscles to the lactic acidosis of heavy exercise in COPD. Department of Medicine, Harbor-UCLA Medical Center, Torrance 90509, USA. Patients with COPD usually are limited in their exercise tolerance by a limited ventilatory capacity. Lactic acidosis induced by exercise increases the stress on the ventilatory system due to CO2 generated by bicarbonate buffering and hydrogen ion stimulation. Patients with COPD are often observed to increase blood lactate levels at low levels of exercise. We wished to determine whether patients with COPD who experience lactic acidosis do so because of respiratory muscle production of lactate. Eight patients with moderate to severe COPD (FEV1 = 43.5 +/- 11.6% predicted) and 5 healthy subjects performed 10 min of moderate constant work rate exercise either breathing spontaneously or volitionally increasing their ventilation for 5 min to approximate the peak minute ventilation seen during incremental exercise. During volitional increased ventilation, 3% CO2 was added to the inspirate to prevent alkalosis and hypocapnia. In neither the healthy subjects nor the COPD group was the end-exercise lactate level significantly higher during volitional ventilation increase than during spontaneous ventilation. Further, in the COPD patients, the blood lactate levels during volitional ventilation increase were much lower than during maximal exercise (averaging 2.4 vs 5.3 mmol/L) despite similar ventilation levels (averaging 50 and 53 L/min). We conclude that it is unlikely that the respiratory muscles have an important influence on the blood lactate level elevation seen during maximal exercise in COPD patients. Continue reading >>

Case Report: Inhaled -agonist Therapy And Respiratory Muscle Fatigue As Under-recognised Causes Of Lactic Acidosis

Case Report: Inhaled -agonist Therapy And Respiratory Muscle Fatigue As Under-recognised Causes Of Lactic Acidosis

Inhaled -agonist therapy and respiratory muscle fatigue as under-recognised causes of lactic acidosis We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Inhaled -agonist therapy and respiratory muscle fatigue as under-recognised causes of lactic acidosis Emily Lau, Jeffrey Mazer, and Gerardo Carino A 49-year-old man with chronic obstructive pulmonary disease (COPD) presented with significant tachypnoea, fevers, productive cough and increased work of breathing for the previous 4 days. Laboratory data showed elevated lactate of 3.2 mEq/L. Continuous inhaled ipratropium and albuterol nebuliser treatments were administered. Lactate levels increased to 5.5 and 3.9 mEq/L, at 6 and 12 h, respectively. No infectious source was found and the lactic acidosis cleared as the patient improved. The lactic acidosis was determined to be secondary to respiratory muscle fatigue and inhaled -agonist therapy, two under-recognised causes of lactic acidosis in patients presenting with respiratory distress. Lactic acidosis is commonly used as a clinical marker for sepsis and shock, but in the absence of tissue hypoperfusion and severe hypoxia, alternative aetiologies for elevated levels should be sought to avoid unnecessary and potentially harmful medical interventions. Lactic acidosis is a common marker of tissue hypoperfusion and hypoxia, most frequently associated with sepsis and systemic shock. 1 Two commonly overlooked aetiologies of lactic acidosis 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 >>

Lactic Acid Levels In Patients With Chronic Obstructive Pulmonary Disease Accomplishing Unsupported Arm Exercises.

Lactic Acid Levels In Patients With Chronic Obstructive Pulmonary Disease Accomplishing Unsupported Arm Exercises.

Lactic acid levels in patients with chronic obstructive pulmonary disease accomplishing unsupported arm exercises. de Souza GF, et al. Chron Respir Dis. 2010. Pulmonary Rehabilitation Center, Federal University of So Paulo, Unifesp, Brazil. Chron Respir Dis. 2010;7(2):75-82. doi: 10.1177/1479972310361833. Epub 2010 Mar 26. Patients with chronic obstructive pulmonary disease (COPD) may suffer dyspnea when performing unsupported arm exercises (UAE). However, some factors related to the tolerance of the upper limbs during these exercises are not well understood. Our investigation was to determine if an unsupported arm exercise test in patients with COPD accomplishing diagonal movements increases lactic acid levels; also, we assessed the metabolic, ventilatory and cardiovascular responses obtained from the unsupported arm exercise test. The study used results of maximal symptom limited tests with unsupported arms and legs performed on 16 patients with COPD. In order to do the test, some metabolic, respiratory and cardiovascular parameters such as oxygen uptake (VO(2)), carbon dioxide production (VCO(2)), respiratory rate (RR), pulmonary ventilation (VE), heart rate (HR) and blood pressure (BP) were measured during the exercise tests. Furthermore, blood lactate concentration was measured during the arm test. We detected a significant increase in the mean blood lactate concentration, VO(2), VCO(2), VE and RR from the resting to the peak phase of the UAE test. The mean values of VO(2), VCO(2) and VE obtained at the peak of the UAE test corresponded to 52.5%, 50.0% and 61.2%, respectively, of the maximal values obtained at the peak of the leg exercise test. In comparison, the mean heart rate and systolic arterial blood pressure were significantly lower at the peak of the UAE t Continue reading >>

Lactic Acidosis, Copd

Lactic Acidosis, Copd

CAUTION! Be sure & check with your Dr. about any advice given by Forum Members! Post by al on Aug 26, 2012 23:48:35 GMT -5 Lactic acidosis is a type of acidosis that occurs when the blood becomes too acidic due to the presence of excess lactic acid in the body. Blood pH is tightly controlled because even slight changes in your pH can have severe effects on many organs. Normally, your blood is slightly basic, or alkaline. Acidosis occurs when the blood becomes more acidic than normal. Lactic acid is created when structures in the cells called mitochondria respond to high-energy demands in cases of relatively low oxygen levels. Lactic acid commonly increases with exercises designed to increase speed, strength, and muscle mass, such as sprinting and lifting weights, but is typically cleared quickly during rest periods, mostly by the liver. Conditions that decrease blood oxygen levels, interfere with the mitochondria, or decrease the clearance of lactic acid can allow lactic acid to increase to harmful levels. As lactic acid builds up, symptoms such as nausea and vomiting, abdominal pain, weakness, rapid breathing, rapid heart rate or irregular heart rhythm, and mental status changes can occur. Medical conditions that can cause lactic acidosis include severe infections, kidney or liver disease, respiratory disease, heart disease, seizures, shock, cancer, severe anemia, and diabetes. Although rare, lactic acidosis can occasionally occur with metformin, a diabetes medication, and nucleoside reverse transcriptase inhibitors (NRTIs), medications used to treat HIV and AIDS. In order to correct lactic acidosis, the underlying problem needs to be addressed. Additional treatment of lactic acidosis may include intravenous fluids, supplemental oxygen or mechanical ventilation, and v Continue reading >>

Mixed Acid-base Disorders, Hydroelectrolyte Imbalance And Lactate Production In Hypercapnic Respiratory Failure: The Role Of Noninvasive Ventilation

Mixed Acid-base Disorders, Hydroelectrolyte Imbalance And Lactate Production In Hypercapnic Respiratory Failure: The Role Of Noninvasive Ventilation

Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Laboratory of Biostatistics, Department of Biomedical Science, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosismetabolic alkalosis, 10/36 (27.8%) respiratory acidosis 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 >>

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 Levels - British Lung Foundation | Healthunlocked

Lactate Levels - British Lung Foundation | Healthunlocked

could anybody,in laymans term,try and explain to me,lactate levels combined with COPD? joedimagio , so far as I know has it something to do with exercise where the lactate levels are been measured.It would be some how a benefit, but here is a link for a article I found. Hope it will explain a bit My understanding is that when we have normal levels of oxygen in our blood then it is used to turn blood sugar into carbon dioxide an water (respiration in our cells). If our oxygen levels are reduced, either because we are using it up quickly when exercising or when our breathing is poor, as in COPD, then instead of sugar being turned into carbon dioxide and water it becomes lactate (or lactic acid) ... called anaerobic respiration. So high levels of lactate would I think be connected with low blood oxygen .... athletes have to develop lactate tolerance when competing, I think high levels for long periods can be dangerous, undiagnosed diabetics can also have high lactate levels as low insulin levels stops oxygen being used in cells. postscript has summed it up pretty well, but while researching the subject I came across the following, which I thought interesting . . . [Quote] Perhaps the single most important benefit of exercise training in COPD is its effect on dyspnea. Shortness of breath plagues almost all pulmonary patients, and the fear of dyspnea often inhibits exertion and severely compromises the ability to perform such day-to-day activities as shopping or housecleaning. There is ample evidence that an exercise program can delay the appearance of dyspnea to higher levels of exertion. In one study, 20 patients were randomly assigned to either a control group or a group following a schedule of light, biweekly exercise. The exercise group showed declines in dyspnea at a Continue reading >>

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