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Can Copd Cause Lactic Acidosis?

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 | Definition Of Lactic Acidosis By Medical Dictionary

Lactic Acidosis | Definition Of Lactic Acidosis By Medical Dictionary

Lactic acidosis | definition of lactic acidosis by Medical dictionary 1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH. 2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidotic. Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma. In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to acidosis are patients with shock, hyperthyroidism, advanced circulatory failure, renal failure, 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 >>

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of 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 >>

Contractile Fatigue, Muscle Morphometry, And Blood Lactate In Chronic Obstructive Pulmonary Disease

Contractile Fatigue, Muscle Morphometry, And Blood Lactate In Chronic Obstructive Pulmonary Disease

American Journal of Respiratory and Critical Care Medicine Centre de recherche, Hpital Laval, Institut Universitaire de Cardiologie et de Pneumologie de l'Universit Laval; Centre de recherche du CHUQ pavillon CHUL, Universit Laval, Qubec, Canada; Laboratoire de Physiologie des Interactions, Hpital Arnaud de Villeneuve, Montpellier, France; and Pulmonary, Critical Care, and Sleep Medicine, State University of New York at Buffalo and the Buffalo VAMC, Buffalo, New York We hypothesized that patients with chronic obstructive pulmonary disease developing contractile fatigue of the quadriceps during cycle exercise may have characteristic metabolic and muscle features that could increase their susceptibility to fatigue, thus differentiating them from those who do not develop fatigue. We examined, in 32 patients, the fiber-type proportion, enzymatic activities, and capillary density in the vastus lateralis and the arterial blood lactate level during constant work-rate cycling exercise. Contractile fatigue was defined as a postexercise fall in quadriceps twitch force greater than 15% of resting values. Twenty-two patients developed contractile fatigue after exercise. No significant differences were found between fatiguers and nonfatiguers for the endurance time, fiber-type proportion, and oxidative enzyme activities. The lactate dehydrogenase activity was significantly higher (p < 0.05) and muscle capillarization significantly reduced in fatiguers (p < 0.05). Compared with nonfatiguers, the arterial lactate level during exercise was significantly higher in fatiguers (p < 0.001). A significant relationship was found between the fall in quadriceps twitch force and lactate dehydrogenase activity, capillary/fiber ratio, and blood lactate level. We conclude that changes in muscle en 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 >>

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 >>

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 >>

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 Production And Exercise-induced Metabolic Acidosis: Guilty Or Not Guilty?

Lactate Production And Exercise-induced Metabolic Acidosis: Guilty Or Not Guilty?

Lactate production and exercise-induced metabolic acidosis: guilty or not guilty? European Respiratory Journal 2005 26: 744; DOI: 10.1183/09031936.05.00059005 In the excellent and very interesting chapter concerning clinical exercise testing published in the European Respiratory Monograph on lung function testing, Roca and Rabinovitch 1 wrote the following. Increased lactate production is responsible for the fall in muscle pH, which in turn may play a role in determining exercise intolerance in these patients (COPD patients). Premature lactic acidosis during exercise in COPD patients has been associated with reduced oxidative enzyme concentrations in the lower limb muscles. We would like to emphasise that the widespread belief that lactic acid is produced in working muscles as a result of oxygen insufficiency, and that it directly causes exercise-induced metabolic acidosis, has been criticised. In addition, numerous findings on different species are discordant with the prevailing theory 2 . We all accept that when looking at the end result of metabolism during intense exercise, the observed metabolic acidosis coincides with an accumulation of lactate, but does it mean that lactate production is guilty? Recently, combining a large series of papers, Robergs et al. 3 have presented convincing empirical observations that lactate is a consequence rather than a cause of cellular events that cause acidosis. From the transformation of a glucose molecule to two pyruvate molecules, three reactions release four protons, one of which is driven by pyruvate kinase and consumes two protons. The conversion of two pyruvate molecules to two lactate molecules by lactate dehydrogenase (LDH) consumes two protons. Another source of protons is adenosine triphosphate (ATP) hydrolysis. During 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 >>

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 >>

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 >>

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 >>

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