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Which Metabolic Rate Resulted In Metabolic Acidosis?

The Effects Of Acute Total Asphyxia And Metabolic Acidosis On Cerebrospinal Fluid

The Effects Of Acute Total Asphyxia And Metabolic Acidosis On Cerebrospinal Fluid

Pediatr. Res., 14: 286-290 (1980) acid-base balance cerebrospinal fluid asphyxia metabolic acidosis Bicarbonate Regulation in Newborn Puppies EUGENE E. NATTIE"'' AND WILLIAM H. EDWARDS Departments of Maternal and Child Health and Physiology, Dartmouth Medical School, Hanover, New Ifampshire, USA Summary We evaluated CSF [HCO;] regulation in lightly anesthetized newborn puppies following: (1) acute total asphyxiq (2) metabolic acidosis; and (3) metabolic acidosis induced after acute asphyxia. Five and one-half min of total asphyxia resulted in a 4.4 mM/liter decrease in mean CSF [HCO;]. During 65 min of recovery with mechanical ventilation mean CSF [HCOJ] increased 1.7 mM/ liter. Mean plasma [HCO;] decreased 7 mM/liter and recovered 4.5 mM/liter in the same period. We produced a stable metabolic acidosic for 4 hr using a peritoneal dialysis technique with PaCOs maintained at the normal value. With acidosis in nonaspbyxiated control puppies, CSF [HCOSl decreased steadily. At 4 hr, the ratio, ACSF [HCOSl/Aplasma [HCO;], was 0.43, a value close to that observed in adults of many species with metabolic acid- base disturbances, 0.41. With acidosis in asphyxiated puppies allowed 1 hr of recovery, the time course and mean values of plasma and CSF [HCO;] were indistinguishable from those of the nonasphyxiated acidotic controls. Newborn puppies appear to regulate CSF [HCOJl in response to acute asphyxia or metabolic acidosis, and acute asphyxia does not impair the puppy's ability to regulate CSF [HCOsl in metabolic acidosis. two wk before the estimated date of delivery. The dogs were fed Purina dog chow and water ad libitum. Following normal spon- taneous birth, puppies were at least one hr and no more than 4 days of age at the time of experiment. The general design included 4 gr Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Practice Essentials Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide.[1][3] This condition is one of the four basic categories of disruption of acid–base homeostasis.[medical citation needed] Signs and symptoms[edit] Signs and symptoms of respiratory alkalosis are as follows:[4] Palpitation Tetany Convulsion Sweating Causes[edit] Respiratory alkalosis may be produced as a result of the following causes: Stress[1] Pulmonary disorder[2] Thermal insult[5] High altitude areas[6] Salicylate poisoning (aspirin overdose) [6] Fever[1] Hyperventilation (due to heart disorder or other, including improper mechanical ventilation)[1][7] Vocal cord paralysis (compensation for loss of vocal volume results in over-breathing/breathlessness).[8] Liver disease[6] Mechanism[edit] Carbonic-acid The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system. Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase according to the following reaction: This causes decreased circulating hydrogen ion concentration, and increased pH (alkalosis).[9][10] Diagnosis[edit] The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual.[1] The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentr Continue reading >>

Exam 4: Lab #10

Exam 4: Lab #10

Sort B Compensation of metabolic alkalosis includes which of the following? A) conserving bicarbonate ion in the renal system B) excreting bicarbonate ion in the renal system and retaining carbon dioxide through the respiratory system C) conserving bicarbonate ion in the renal system and retaining carbon dioxide through the respiratory system D) retaining carbon dioxide through the respiratory system E) excreting bicarbonate ion in the renal system Continue reading >>

Exercise 47: Acid-base Balance: Computer Simulation

Exercise 47: Acid-base Balance: Computer Simulation

4. ACTIVITY 2: HYPERVENTILATION WHAT ACID-BASE IMBALANCE OCCURRED WITH HYPERVENTILATION? THE pH VALUE BEGAN TO EXCEED THE NORMAL RANGE BETWEEN 10 AND 20 SECONDS - AS SOON AS IT ROSE ABOVE 7.45, THIS INDICATED THE CONDITION OF ALKALOSIS. 8. ACTIVITY 3: REBREATHING DID REBREATHING RESULT IN ACIDOSIS OT ALKALOSIS? WHY? HINT: SPECIFICALLY RELATE THIS TO THE LEVEL OF CO2. REBREATHING RESULTED IN ACIDOSIS BECAUSE THE pH VALUE BEGAN TO DIP BELOW THE NORMAL RANGE BETWEEN 20 AND 30 SECONDS - SOON AS IT WENT BELOW 7.35. ACIDOSIS IS THE RESULT OF IMPAIRED RESPIRATION (HYPOVENTILATION) THAT LEADS TO THE ACCUMULATION OF TOO MUCH CARBON DIOXIDE IN THE BLOOD. Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic Acidosis Definition Metabolic acidosis is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid. Description Metabolic acidosis, as a disruption of the body's acid/base balance, can be a mild symptom brought on by a lack of insulin, a starvation diet, or a gastrointestinal disorder like vomiting and diarrhea. Metabolic acidosis can indicate a more serious problem with a major organ like the liver, heart, or kidneys. It can also be one of the first signs of drug overdose or poisoning. Causes and symptoms Metabolic acidosis occurs when the body has more acid than base in it. Chemists use the term "pH" to describe how acidic or basic a substance is. Based on a scale of 14, a pH of 7.0 is neutral. A pH below 7.0 is an acid; the lower the number, the stronger the acid. A pH above 7.0 is a base; the higher the number, the stronger the base. Blood pH is slightly basic (alkaline), with a normal range of 7.36-7.44. Acid is a natural by-product of the breakdown of fats and other processes in the body; however, in some conditions, the body does not have enough bicarbonate, an acid neutralizer, to balance the acids produced. This can occur when the body uses fats for energy instead of carbohydrates. Conditions where metabolic acidosis can occur include chronic alcoholism, malnutrition, and diabetic ketoacidosis. Consuming a diet low in carbohydrates and high in fats can also produce metabolic acidosis. The disorder may also be a symptom of another condition like kidney failure, liver failure, or severe diarrhea. The build up of lactic acid in the blood due to such conditions as heart failure, shock, or cancer, induces metabolic acidosis. Some poisonings and overdoses (aspirin, Continue reading >>

Merck And The Merck Manuals

Merck And The Merck Manuals

Acidosis is caused by an overproduction of acid in the blood or an excessive loss of bicarbonate from the blood (metabolic acidosis) or by a buildup of carbon dioxide in the blood that results from poor lung function or depressed breathing (respiratory acidosis). If an increase in acid overwhelms the body's acid-base control systems, the blood will become acidic. As blood pH drops (becomes more acidic), the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing (respiratory compensation). Breathing faster and deeper increases the amount of carbon dioxide exhaled. The kidneys also try to compensate by excreting more acid in the urine. However, both mechanisms can be overwhelmed if the body continues to produce too much acid, leading to severe acidosis and eventually heart problems and coma. The acidity or alkalinity of any solution, including blood, is indicated on the pH scale. Metabolic acidosis develops when the amount of acid in the body is increased through ingestion of a substance that is, or can be broken down (metabolized) to, an acid—such as wood alcohol (methanol), antifreeze (ethylene glycol), or large doses of aspirin (acetylsalicylic acid). Metabolic acidosis can also occur as a result of abnormal metabolism. The body produces excess acid in the advanced stages of shock and in poorly controlled type 1 diabetes mellitus (diabetic ketoacidosis). Even the production of normal amounts of acid may lead to acidosis when the kidneys are not functioning normally and are therefore not able to excrete sufficient amounts of acid in the urine. Major Causes of Metabolic Acidosis Diabetic ketoacidosis (buildup of ketoacids) Drugs and substances such as acetazolamide, alcohols, and aspirin Lactic acidosis (buildup of lactic acid Continue reading >>

Interpretation Of Arterial Blood Gas

Interpretation Of Arterial Blood Gas

Go to: Introduction Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygenation status and acid–base balance. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results. Disorders of acid–base balance can create complications in many disease states, and occasionally the abnormality may be so severe so as to become a life-threatening risk factor. A thorough understanding of acid–base balance is mandatory for any physician, and intensivist, and the anesthesiologist is no exception. The three widely used approaches to acid–base physiology are the HCO3- (in the context of pCO2), standard base excess (SBE), and strong ion difference (SID). It has been more than 20 years since the Stewart’s concept of SID was introduced, which is defined as the absolute difference between completely dissociated anions and cations. According to the principle of electrical neutrality, this difference is balanced by the weak acids and CO2. The SID is defined in terms of weak acids and CO2 subsequently has been re-designated as effective SID (SIDe) which is identical to “buffer base.” Similarly, Stewart’s original term for total weak acid concentration (ATOT) is now defined as the dissociated (A-) plus undissociated (AH) weak acid forms. This is familiarly known as anion gap (AG), when normal concentration is actually caused by A-. Thus all the three methods yield virtually identical results when they are used to quantify acid–base status of a given blood sample.[1] Continue reading >>

Glutamine Metabolism: Role In Acid-base Balance*

Glutamine Metabolism: Role In Acid-base Balance*

Abstract The intent of this review is to provide a broad overview of the interorgan metabolism of glutamine and to discuss in more detail its role in acid-base balance. Muscle, adipose tissue, and the lungs are the primary sites of glutamine synthesis and release. During normal acid-base balance, the small intestine and the liver are the major sites of glutamine utilization. The periportal hepatocytes catabolize glutamine and convert ammonium and bicarbonate ions to urea. In contrast, the perivenous hepatocytes are capable of synthesizing glutamine. During metabolic acidosis, the kidney becomes the major site of glutamine extraction and catabolism. This process generates ammonium ions that are excreted in the urine to facilitate the excretion of acids and bicarbonate ions that are transported to the blood to partially compensate the acidosis. The increased renal extraction of glutamine is balanced by an increased release from muscle and liver and by a decreased utilization in the intestine. During chronic acidosis, this adaptation is sustained, in part, by increased renal expression of genes that encode various transport proteins and key enzymes of glutamine metabolism. The increased levels of phosphoenolpyruvate carboxykinase result from increased transcription, while the increase in glutaminase and glutamate dehydrogenase activities result from stabilization of their respective mRNAs. Where feasible, this review draws upon data obtained from studies in humans. Studies conducted in model animals are discussed where available data from humans is either lacking or not firmly established. Because there are quantitative differences in tissue utilization and synthesis of glutamine in different mammals, the review will focus more on common principles than on quantification. Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Abstract: Steady state blood CO2 levels remain relatively constant in compensated respiratory acidosis and alkalosis (i.e., CO2 in = CO2 out). Uncompensated respiratory alkalosis is associated with an increased blood pH, and a modestly decreased HCO3 – concentration. Renal compensation for respiratory alkalosis involves a decrease in HCO3 – reabsorption. The blood pH may be within the normal range in some mixed acid-base disorders. A mixed acid-base disturbance is indicated when the Pco2 and blood HCO3 – concentration are moving in opposite directions. Mixed acid-base distrubances can be additive, or subtractive. The bicarbonate buffer equation is shifted to the left in metabolic acidosis and respiratory alkalosis. Respiratory alkalosis can be due to either direct or reflex hypoxemic stimulation of the respiratory center, to pulmonary disease, or to excessive mechanical ventilation. Respiratory Alkalosis Respiratory alkalosis results from excessive ventilation (hyperventilation). In respiratory alkalosis, Pco2 falls, leading to an increase in pH (alkalosis). If the alkalosis persists for more than 12 hours, the alkalosis may be partially compensated by decreased renal H+ excretion. During respiratory alkalosis, HCO3− may fall acutely owing to equilibration with depleted CO2. There is a 2 mEq/L decrease in HCO3− per 10 mm Hg decrease Pco2 that is chemical and not part of the renal compensation. Common causes of respiratory alkalosis include hyperventilation from voluntary effort (anxiety) or stimulation of central respiratory centers secondary to meningitis or a fever. 2 Respiratory Alkalosis Respiratory alkalosis is associated with an increase in pH and a decrease in pCO2. a Causes of Respiratory Alkalosis Respiratory alkalosis is due to hyperventilation, whic Continue reading >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus Continue reading >>

Disorders Of Acid-base Balance

Disorders Of Acid-base Balance

Metabolic Acidosis: Primary Bicarbonate Deficiency Metabolic acidosis occurs when the blood is too acidic (pH below 7.35) due to too little bicarbonate, a condition called primary bicarbonate deficiency. At the normal pH of 7.40, the ratio of bicarbonate to carbonic acid buffer is 20:1. If a person’s blood pH drops below 7.35, then he or she is in metabolic acidosis. The most common cause of metabolic acidosis is the presence of organic acids or excessive ketones in the blood. [link] lists some other causes of metabolic acidosis. *Acid metabolites from ingested chemical. Common Causes of Metabolic Acidosis and Blood Metabolites Cause Metabolite Diarrhea Bicarbonate Uremia Phosphoric, sulfuric, and lactic acids Diabetic ketoacidosis Increased ketones Strenuous exercise Lactic acid Methanol Formic acid* Paraldehyde β-Hydroxybutyric acid* Isopropanol Propionic acid* Ethylene glycol Glycolic acid, and some oxalic and formic acids* Salicylate/aspirin Sulfasalicylic acid (SSA)* The first three of the eight causes of metabolic acidosis listed are medical (or unusual physiological) conditions. Strenuous exercise can cause temporary metabolic acidosis due to the production of lactic acid. The last five causes result from the ingestion of specific substances. The active form of aspirin is its metabolite, sulfasalicylic acid. An overdose of aspirin causes acidosis due to the acidity of this metabolite. Metabolic acidosis can also result from uremia, which is the retention of urea and uric acid. Metabolic acidosis can also arise from diabetic ketoacidosis, wherein an excess of ketones is present in the blood. Other causes of metabolic acidosis are a decrease in the excretion of hydrogen ions, which inhibits the conservation of bicarbonate ions, and excessive loss of bicarbonate Continue reading >>

Acidosis

Acidosis

The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis. Respiratory acidosis develops when there is too much carbon dioxide (an acid) in the body. This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include: Chest deformities, such as kyphosis Chest injuries Chest muscle weakness Chronic lung disease Overuse of sedative drugs Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis: Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by: Cancer Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar (hypoglycemia) Medications, such as salicylates MELAS (a very rare genetic mitochondrial disorder that affects energy production) Prolonged lack of oxygen from shock, heart failure, or seve Continue reading >>

Metabolic Alkalosis In Patients With Renal Failure

Metabolic Alkalosis In Patients With Renal Failure

Introduction Alkalosis is most unusual in patients with advanced renal failure. When patients are also hyponatraemic, hypochloraemic and hypokalaemic, management can be a considerable challenge. The purpose of this report is to illustrate by means of three patients the potential for diagnostic uncertainty and therapeutic error in these metabolic settings and to outline some simple principles in diagnosis and management. Cases Patient 1 A 38-year-old man presented to the A&E department giving a history of vomiting and intermittent diarrhoea for 2 weeks. He could keep nothing down other than cider and water, and his urine output had fallen. His alcohol intake was excessive and he smoked heavily but he denied taking recreational drugs. His only medication was ranitidine. A known epileptic he had had a seizure 1 week previously. On several occasions in the past he had been admitted with drug overdoses. On examination his breath smelt of alcohol. He was restless but orientated with a Glasgow Coma Score (GCS) of 15/15. His blood pressure (BP) was 140/80 mmHg with a pulse of 90 beats/min in sinus rhythm. His jugular venous pressure (JVP) was visible 1 cm above the level of the manubrio–sternal joint. His respiratory and abdominal systems were unremarkable and neurological examination revealed only truncal ataxia. Blood results are shown in Table 1. In addition, his liver enzymes, amylase and thyroid hormones were within the normal range; calcium 2.33 mmol/l, phosphate 2.12 mmol/l, magnesium 0.77 mmol/l, creatine kinase 1111 U/l, random cortisol 1207 U/l, total cholesterol 3.4 mmol/l. Arterial blood revealed: pH 7.59, pO2 12.06 kPa (on air), pCO2 5.2 kPa, HCO3– 38.4 mmol/l and lactate 0.7 mmol/l. Serum was negative for opiates, benzodiazepines, cocaine, cannabinoids, salicy Continue reading >>

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2018 UpToDate, Inc. All topics are updated as new evidence becomes available and our peer review process is complete. INTRODUCTION — Most individuals produce approximately 15,000 mmol (considerably more with exercise) of carbon dioxide and 50 to 100 meq of nonvolatile acid each day. Acid-base balance is maintained by normal elimination of carbon dioxide by the lungs (which affects the partial pressure of carbon dioxide [PCO2]) and normal excretion of nonvolatile acid by the kidneys (which affects the plasma bicarbonate concentration). The hydrogen ion concentration of the blood is determined by the ratio of the PCO2 and plasma bicarbonate concentration. (See "Simple and mixed acid-base disorders", section on 'Introduction'.) Acidosis associated with chronic kidney disease (CKD) will be discussed in this topic. An overview of simple acid-base disorders and renal tubular acidosis, as well as the approach to patients with metabolic acidosis, are presented elsewhere. (See "Simple and mixed acid-base disorders" and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance" and "Approach to the adult with metabolic acidosis" and "Approach to the child with metabolic acidosis".) ACID-BASE BALANCE IN CHRONIC KIDNEY DISEASE — Acid-base balance is normally maintained by the renal excretion of the daily acid load (about 1 meq/kg per day, derived mostly from the generation of sulfuric acid during the metabolism of sulf Continue reading >>

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