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Copd Lactic Acidosis

Respiratory Acidosis: Causes, Symptoms, And Treatment

Respiratory Acidosis: Causes, Symptoms, And Treatment

Respiratory acidosis develops when air exhaled out of the lungs does not adequately exchange the carbon dioxide formed in the body for the inhaled oxygen in air. There are many conditions or situations that may lead to this. One of the conditions that can reduce the ability to adequately exhale carbon dioxide (CO2) is chronic obstructive pulmonary disease or COPD. CO2 that is not exhaled can shift the normal balance of acids and bases in the body toward acidic. The CO2 mixes with water in the body to form carbonic acid. With chronic respiratory acidosis, the body partially makes up for the retained CO2 and maintains acid-base balance near normal. The body's main response is an increase in excretion of carbonic acid and retention of bicarbonate base in the kidneys. Medical treatment for chronic respiratory acidosis is mainly treatment of the underlying illness which has hindered breathing. Treatment may also be applied to improve breathing directly. Respiratory acidosis can also be acute rather than chronic, developing suddenly from respiratory failure. Emergency medical treatment is required for acute respiratory acidosis to: Regain healthful respiration Restore acid-base balance Treat the causes of the respiratory failure Here are some key points about respiratory acidosis. More detail and supporting information is in the main article. Respiratory acidosis develops when decreased breathing fails to get rid of CO2 formed in the body adequately The pH of blood, as a measure of acid-base balance, is maintained near normal in chronic respiratory acidosis by compensating responses in the body mainly in the kidney Acute respiratory acidosis requires emergency treatment Tipping acid-base balance to acidosis When acid levels in the body are in balance with the base levels in t 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 | 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

Review: Lactate & Sepsis

Review: Lactate & Sepsis

On this snowy, Stockholm Sunday, I look out from my quarters on the Mlardrottningen across the still, icy waters and I think about a cirrhotic patient for whom I recently cared. She presented with significant dyspnea as she had stopped taking her diuretics. Instead, she was using excessivedoses of her friends albuterol inhaler to treat her shortness of breath. Additionally, she had been drinking alcohol heavily for seven days prior to admission. Her venous pH was 7.38, and her lactate concentration was over 7.0 mmol/L a sepsis alert was called. In a very recent and fantastic review by Suetrong and Walley , the mechanisms of lactate formation are revisited. Notably, a distinction is made between hyperlactatemia an elevated concentration of lactate in the blood and lactic acidosis, which is comprised of both hyperlactatemia and systemic acidosis. The authors discuss the mechanisms by which lactate is formed and aptly detail that many of these processes do not result in acid formation. Notably, while the generation of pyruvate from glucose does generate [H+], the conversion of pyruvate to lactate consumes an equimolar amount of [H+] such that the production of lactate does not result in a net gain of protons [i.e. acidosis]. So where does the acidosis with which we are so familiar come from? The excess protons are the result of an impaired Krebs Cycle. In states of true tissue oxygen debt, intracellular protons can no longer be consumed during the Krebs Cycle; consequently, intracellular acidosis and acidemia ensue. It is this latter means of hyperlactatemia to which we attach the label type A or lactic acidosis with clinical evidence of tissue hypoxia. However, as described 40 years ago , excessive lactate may come from clinical states where there is no evidence of tissu 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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