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Metabolic Acidosis: Pathophysiology, Diagnosis And Management. Pdf

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Vetfolio

Vetfolio

This article discusses the pathophysiology, causes, diagnosis, treatment, and prognosis of renal tubular acidosis (RTA) in veterinary patients. RTA is classified as a non-anion-gap metabolic acidosis in the presence of a normal glomerular filtration rate. Proximal RTA occurs because of a deficiency in bicarbonate resorption in the proximal tubule, whereas distal RTA occurs because of decreased production of bicarbonate in the distal tubule. RTA can be transient or permanent and can occur secondary to other diseases. Therapy includes bicarbonate supplementation with careful acid-base and electrolyte monitoring and treatment of underlying causes. There are few published discussions of renal tubular acidosis (RTA) in the veterinary literature despite the abundance of reports of such disorders in humans. Although it is possible that the incidence of such conditions in small animals is less than that in humans, it is also plausible that tubular disorders are overlooked in veterinary patients (Table 1). RTA typically causes metabolic acidosis with both a normal anion gap and normal glomerular filtration rate (GFR). In contrast, renal failure is often associated with an increased anion gap due to the presence of phosphates, sulfates, and organic anions as well as a reduced GFR. Traditionally, RTA has been classified into four types in human medicine: type 1 (i.e., distal tubular acidosis), type 2 (i.e., proximal tubular acidosis), type 3 (i.e., an ill-defined combination of proximal and distal tubular acidosis), and type 4 (i.e., hyperkalemic RTA). Type 3 RTA is an obsolete term because it is no longer considered a distinct form of RTA. Type 4 RTA is associated with hyperkalemia and decreased renin and aldosterone concentrations. In humans, this is most commonly recognized in Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Abstract | Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3 concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of ~1 mmHg for concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum ] + [Cl]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for the treatment of chronic metabolic acidosis is associated with improved cellular Kraut, J. A. & Madias, N. E. Nat. Rev. Nephrol. 6, 274285 (2010); publshed online 23 March 2010; doi:10.1038/nrneph.2010.33 Metabolic acidosis is characterized by a primary reduc- tion in the serum concentration of bicarbonate (HCO3 a secon dary decrease in the arterial partial pre Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Chapter 47. Acidosis And Alkalosis

Chapter 47. Acidosis And Alkalosis

Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent derangements of neural respiratory control or are due to compensatory changes in response to a primary alteration in the plasma [HCO3−]. The kidneys regulate plasma [HCO3−] through three main processes: (1) “reabsorption” of filtered HCO3−, (2) formation of titratable acid, and (3) excretion of NH4+ in the urine. The kidney filters ∼4000 mmol of HCO3− per day. To reabsorb the filtered load of HCO3−, the renal tubules must therefore secrete 4000 mmol of hydrogen ions. Between 80 and 90% of HCO3− is reabsorbed in the proximal tubule. The distal nephron reabsorbs the remainder and secretes H+ to defend systemic pH. While this quantity of protons, 40–60 mmol/d, is small, it must be sec Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Jeffrey A. Kraut, MD is Chief of Dialysis in the Division of Nephrology at the Greater Los Angeles Veterans Administration Healthcare System, Professor of Medicine at the David Geffen School of Medicine at UCLA, and an investigator at the UCLA Membrane Biology Laboratory, Los Angeles, CA, USA. He completed his nephrology training at the TuftsNew England Medical Center where he performed basic research examining the mechanisms regulating acid excretion by the kidney. His present research is focused on delineating the mechanisms contributing to cellular damage with various acidbase disturbances, including metabolic acidosis, with the goal of developing newer treatment strategies. Nicolaos E. Madias, MD is Chairman of the Department of Medicine at St. Elizabeth's Medical Center in Boston, and Maurice S. Segal, MD Professor of Medicine at Tufts University School of Medicine, Boston, MA, USA. He completed his nephrology training at TuftsNew England Medical Center. He has previously served as Chief of the Division of Nephrology at TuftsNew England Medical Center, Established Investigator of the American Heart Association, member of the Internal Medicine and Nephrology Boards of the American Board of Internal Medicine, and Executive Academic Dean and Dean ad interim of Tufts University School of Medicine. His research interests are focused on acidbase and electrolyte physiology and pathophysiology. Nature Reviews Nephrology volume 6, pages 274285 (2010) Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of 1 mmHg for every 1 mmol/l fall in serum HCO3 concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chro Continue reading >>

Details And Download Full Text Pdf: Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Details And Download Full Text Pdf: Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol 2010 May 23;6(5):274-85. Epub 2010 Mar 23. Division of Nephrology, Veterans Administration Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO(3)(-)) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO(2)) of approximately 1 mmHg for every 1 mmol/l fall in serum HCO(3)(-) concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum anion gap, calculated as [Na(+)] - ([HCO(3)(-)] + [Cl(-)]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for th Continue reading >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

1 A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2 The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a β- hydroxybutyrate dominated ketoacidosis. 3 Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4 The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5 The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6 The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7 It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recom mended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication. Continue reading >>

Metabolic Acidosis: Causes, Symptoms, And Treatment

Metabolic Acidosis: Causes, Symptoms, And Treatment

The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>

Pathophysiology And Management Of Rhabdomyolysis : Oxford Textbook Of Critical Care

Pathophysiology And Management Of Rhabdomyolysis : Oxford Textbook Of Critical Care

Rhabdomyolysis is a potentially life-threatening syndrome characterized by the breakdown of skeletal muscle. It is associated with myalgia, muscle tenderness, swelling, and/or stiffness, accompanied by weakness and raised levels of creatine kinase (CK), myoglobin, phosphate and potassium, sometimes with acute kidney injury (AKI). There are multiple causes of this syndrome, traumatisms and myotoxic effect of drugs being the most frequent in developed countries. The pathophysiology involves direct trauma, as well as energy (ATP) depletion with disruption of sarcolemma integrity and muscle destruction. The sequestration of plasma water leads to hypovolaemic shock, while the release of muscle content, mainly myoglobin and potassium lead to the most severe complications of this syndrome, acute kidney injury/hyperkalaemia. The kidney injury is driven both by renal ischaemia due to vasoconstriction and to the toxic effects of myoglobin. The local oedema produced by the release of muscle content remains trapped within the fascia and can lead to compartment syndrome. Volume repletion with saline is essential to avoid hypovolaemic shock and acute kidney injury (AKI). With respect to compartment syndrome, close monitoring of clinical signs and compartment pressures is essential, since it can evolve to a surgical emergency. The prognosis of rhabdomyolysis is determined by age, baseline conditions and, most importantly, whether or not severe AKI develops. Continue reading >>

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

University of Gondar, Ethopia *Corresponding Author: Habtamu Wondifraw Baynes Lecturer Clinical Chemistry University of Gondar, Gondar Amhara 196, Ethiopia Tel: +251910818289 E-mail: [email protected] Citation: Baynes HW (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541 Copyright: © 2015 Baynes HW. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia either immune-mediated (Type 1 diabetes), insulin resistance (Type 2), gestational or others (environment, genetic defects, infections, and certain drugs). According to International Diabetes Federation Report of 2011 an estimated 366 million people had DM, by 2030 this number is estimated to almost around 552 million. There are different approaches to diagnose diabetes among individuals, The 1997 ADA recommendations for diagnosis of DM focus on fasting Plasma Glucose (FPG), while WHO focuses on Oral Glucose Tolerance Test (OGTT). This is importance for regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications. Keywords Diabetes mellitus; Epidemiology; Diagnosis; Glycemic management Abbreviations DM: Diabetes Mellitus; FPG: Fasting Plasma Glucose; GAD: Glutamic Acid Decarboxylase; GDM: Gestational Diabetes Mellitus; HDL-cholesterol: High Density Lipoprotein cholesterol; HLA: Human Leucoid Antigen; IDD Continue reading >>

Phenformin-associated Lactic Acidosis: Pathogenesis And Treatment

Phenformin-associated Lactic Acidosis: Pathogenesis And Treatment

Phenformin-Associated Lactic Acidosis: Pathogenesis and Treatment Article, Author, and Disclosure Information Author, Article, and Disclosure Information Requests for reprints should be addressed to Robert I. Misbin, M.D.; Division of Endocrinology and Metabolism, Box J-226, JHM Health Center, University of Florida; Gainesville, FL 32610. Since phenformin's introduction into clinical medicine, a total of 552 cases of lactic acidosis have been reported in patients taking this hypoglycemic agent. In 306 cases, sufficient documentation was available to establish the diagnosis with reasonable certainty (blood lactate, 6 meq/litre or greater, and blood pH, 7.33 or less). The mortality rate among insulin-treated patients (15%) was considerably less than the mortality rate in the group as a whole (42%). Taken together with results from animal studies, these data suggest that insulin is the treatment of choice for phenformin-associated lactic acidosis. Sodium bicarbonate should be administered to patients with severe acidosis, but should be withheld from patients with mild acidosis. Overly aggressive administration of sodium bicarbonate can be deleterious and should be avoided. Although dialysis has been suggested by some authors for the treatment of phenformin-associated lactic acidosis, the mortality rate among dialyzed patients (48%) was roughly the same as for the group as a whole (42%). Continue reading >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Nonanion Gap Metabolic Acidosis In A Patient With A Pancreaticopleural Fistula | The Journal Of The American Osteopathic Association

Nonanion Gap Metabolic Acidosis In A Patient With A Pancreaticopleural Fistula | The Journal Of The American Osteopathic Association

NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula Benjamin Eovaldi, OMS IV ; Claude Zanetti, MD From the Department of Medicine at Midwestern University/Chicago College of Osteopathic Medicine in Downers Grove, Illinois, and the Department of Pulmonary Medicine at Swedish Covenant Hospital in Chicago, Illinois. Address correspondence to Benjamin Eovaldi, OMS IV, 555 31st Street, Downers Grove, IL 60615-1235.E-mail: [email protected] . NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula The Journal of the American Osteopathic Association, May 2011, Vol. 111, 344-345. doi:10.7556/jaoa.2011.111.5.344 The Journal of the American Osteopathic Association, May 2011, Vol. 111, 344-345. doi:10.7556/jaoa.2011.111.5.344 Eovaldi B, Zanetti C. NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula. J Am Osteopath Assoc 2011;111(5):344345. doi: 10.7556/jaoa.2011.111.5.344. NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account While acid-base disturbances are known to occur with chronic pancreatitis, few cases have been reported in which nonanion gap metabolic acidosis is caused by pancreaticopleural fistula, a known complication of chronic pancreatitis. The current report describes the case of a 49-year-old African American woman who presented with severe pleuritic chest pain and dyspnea at rest. The patient had a history of alcohol-induced chronic pancreatitis. Her chest radiograph was positive for a large left-sided pleural effusion. Magnetic resonance cholangiopancreatography revealed a small connection between the pancreas a 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 >>

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