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Metabolic Acidosis Definition

Causes And Consequences Of Fetal Acidosis

Causes And Consequences Of Fetal Acidosis

The causes and consequences ofacute (minutes or hours) andchronic (days or weeks) fetal acidosis are different In the past much attention has been paid to acute acidosis during labour, but in previously normal fetuses this israrely associated with subsequent damage In contrast, chronic acidosis, which is often not detected antenatally, is associated with a significant increase in neurodevelopmental delay The identification of small for gestational age fetuses by ultrasound scans and the use of Doppler waveforms to detect which of these have placental dysfunction mean that these fetuses can be monitored antenatally Delivery before hypoxia has produced chronic acidosis, may prevent subsequent damage and good timing of delivery remains the only management option at present. What is acidosis? Acidosis means a high hydrogen ion concentration in the tissues. Acidaemia refers to a high hydrogen ion concentration in the blood and is the most easily measured indication of tissue acidosis. The unit most commonly used is pH, which is log to base 10 of the reciprocal of the hydrogen ion concentration. Whereas blood pH can change quickly, tissue pH is more stable. The cut off taken to define acidaemia in adults is a pH of less than 7.36, but after labour and normal delivery much lower values commonly occur in the fetus (pH 7.00), often with no subsequent ill effects. Studies looking at the pH of fetuses from cord blood samples taken antenatally and at delivery have established reference ranges. Other indices sometimes used to assess acidosis are the base excess or bicarbonate. Neither of these is measured by conventional blood gas machines but is calculated from the measured pH and pCO2. The major sources of hydrogen ions in the fetus are carbonic and lactic acids from aerobic and a Continue reading >>

Late Metabolic Acidosis: A Reassessment Of The Definition*

Late Metabolic Acidosis: A Reassessment Of The Definition*

The term “late metabolic acidosis” is generally used to define a population of apparently health LBW infants who fail to grow and have a base deficit in excess of 5 mEq/l (CO2TOT<21 mM). A relationship between hypobasemia and the lack of appropriate growth was postulated. This conclusion was reached, however, in the absence of adequate information regarding the distribution of acid-base variables in healthy LBW infants. The results of this study demonstrate that the CO2TOT of LBW infants (n=114) rises between birth and three weeks of life from a mean of 18.6 to 20.3 mM. The frequency distribution of CO2TOT values did not show any significant deviations from normality, and 2 SD included values as low as 14.5 mM. No difference in the rate of growth was detected between “hypobasemic” infants given a solution of bicarbonate calculated to bring their blood CO2TOT to >21 mM and those given similar amounts of isotonic saline solution. The ability of the LBW infants to excrete an ammonium chloride load was not related to their acid-base status and was comparable to that of term infants. It is apparent that the definition of late metabolic acidosis needs to be reconsidered. To access this article, please choose from the options below 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 >>

Late Metabolic Acidosis (lma): A Reassessment

Late Metabolic Acidosis (lma): A Reassessment

There is substantial controversy regarding the definition and the clinical consequences of LMA. Well, low birth weight (LBW) infants fed standard formula were screened for blood tCO2 q. 3-4 days, (n=114). Values for the entire group were normally distributed (19.1 ± 2.6 (SD) mmol/l). From 1-21 days of age the mean rose linearly from 18.2 to 19.7 mmol/l and then plateaued. 16/74 infants had “acidosis” arbitrarily defined as tCO2 <18 mmol/l. Eight of them were matched for maturity and weight and randomly allocated to treatment either with 5% NaHCO3 p.o. to raise tCO2 to >21 mmol/l (E) or 0.9% NaCl (1 ml/feed) (C). The weight gain was 16.0±3.8(SE)g/kg/day in E, 17.2 ± 1.4 in C, (p>.7), and 14.4±1.21 in non-acidotic babies. Values for titratable acidity, ammonium excretion, net acid excretion (NAE) or minimum urinary pH attained during ammonium chloride loading were not different in E or C and were similar to those previously reported for non-acidotic infants. Thus: a) values of tCO2 as low as 14 mmol/l during the first month of life fall within 2 SD for age and cannot be considered abnormal; b) the appropriate NAE for age suggests that blood tCO2 in LBW infants reflects their HCO3 threshold; c) LMA did not result in an increased capacity to excrete H+; d) since no association was found between weight gain and tCO2, the failure to thrive of LBW infants might be spuriously attributed to low tCO2. Continue reading >>

5.1 - Metabolic Acidosis : Definition

5.1 - Metabolic Acidosis : Definition

Acid-Base Physiology A metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood. This causes the arterial plasma bicarbonate to fall to a level lower than expected. The fall in plasma bicarbonate is due to titration of HCO3- by H+. Secondary or compensatory processes which cause a fall in plasma bicarbonate should not be confused with primary processes. A fall in bicarbonate occurring in response to a chronic respiratory alkalosis should be referred to as a compensatory response and never as a �secondary metabolic acidosis�. This distinction between a primary process and a secondary one has been discussed previously in section 3.1.2 when discussing terminology of acid-base disorders. It is of course possible for a patient to have a mixed acid-base disorder with both a metabolic acidosis and a respiratory alkalosis. An example would be an adult presenting following a salicylate overdose. In this situation, direct stimulation of the respiratory centre occurs resulting in a respiratory alkalosis as well as the salicylate-related metabolic acidosis. 'Acid-base pHysiology' by Kerry Brandis -from Acid-Base Physiology 5.2.1 Classification by Patho-physiological Mechanism A decrease in plasma bicarbonate can be caused by two mechanisms: A gain of strong acid A loss of base All causes of a metabolic acidosis must work by these mechanisms. The gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion). Bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis). An alternative to the above, is to classify the causes of metabolic acidosis into two groups depending on whether the anion ga Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

The low HCO3- in metabolic acidosis results from the addition of acids (organic or inorganic) or from a loss of HCO3-; causes of metabolic acidosis are classically categorized by presence or absence of an increase in the anion gap (Table 1-6). Increased anion-gap acidosis (>12 mmol/L) is due to addition of acid (other than HCl) and unmeasured anions to the body. Common causes include ketoacidosis (diabetes mellitus [DKA], starvation, alcohol), lactic acidosis, poisoning (salicylates, ethylene glycol, and methanol), and renal failure. TABLE 1-6: METABOLIC ACIDOSIS Non-Anion-Gap Acidosis Anion-Gap Acidosis Cause Clue Cause Clue Diarrhea enterostomy RF RTA Proximal Distal—hypokalemic Distal—hyperkalemic Distal—hyporeninemic hypoaldosteronism Dilutional Ureterosigmoidostomy Hyperalimentation Acetazolamide, NH4Cl, lysine HCl, arginine HCl, sevelamer-HCl Hx; ↑ K+ drainage Early chronic kidney disease ↓ K+, presence of other proximal tubular defects (Fanconi syndrome) ↓ K+; hypercalciuria; UpH >5.5 ↑ K+; nl PRA/aldo; UpH >5.5 ↑ K+; ↓ PRA/aldo; UpH <5.5 Massive volume expansion with saline Obstructed ileal loop Amino acid infusion Hx of administration of these agents DKA RF Lactic acidosis (L-lactate) Alcoholic ketoacidosis Starvation Salicylates Methanol Ethylene glycol D-lactic acidosis Propylene glycol Pyroglutamic aciduria, 5-oxoprolinuria Hyperglycemia, ketones Late chronic kidney disease Clinical setting + ↑ serum lactate Hx; weak + ketones; + osm gap Hx; mild acidosis; + ketones Hx; tinnitus; high serum level; + ketones; + lactate Large AG; concomitant respiratory alkalosis; retinitis; + toxic screen; + osm gap RF; CNS symptoms; + toxic screen; crystalluria; + osm gap Small-bowel disease; prominent neuro symptoms IV infusions, e.g., lorazepam; + osm g Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

acidosis and bicarbonate concentration in the body fluids resulting either from the accumulation of acids or the abnormal loss of bases from the body (as in diarrhea or renal disease) In medicine, metabolic acidosis is a condition that occurs when the body produces too much acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low due to increased production of hydrogen by the body or the inability of the body to form bicarbonate in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. The numerical value of metabolic acidosis in Pythagorean Numerology is: 6 Use the citation below to add this definition to your bibliography: 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 >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>

Metabolic Acidosis And The Progression Of Chronic Kidney Disease

Metabolic Acidosis And The Progression Of Chronic Kidney Disease

Abstract Metabolic acidosis is a common complication of chronic kidney disease. Accumulating evidence identifies acidosis not only as a consequence of, but as a contributor to, kidney disease progression. Several mechanistic pathways have been identified in this regard. The dietary acid load, even in the absence of overt acidosis, may have deleterious effects. Several small trials now suggest that the treatment of acidosis with oral alkali can slow the progression of kidney disease. Keywords BicarbonateDietary acidNet endogenous acid productionSodium bicarbonateAlkaliAmmoniaComplementEndothelinAldosterone Review Metabolic acidosis is a common complication of chronic kidney disease (CKD). Based on a cross-sectional analysis of the National Health and Nutrition Examination Survey, an estimated 26 million adults in the United States have CKD, and approximately 700,000 individuals have an estimated glomerular filtration rate (eGFR) less than 30 mL/min/1.73 m2[1]. As 30-50% of those with eGFR <30 mL/min/1.73 m2 have metabolic acidosis [2–4], approximately 200,000 to 350,000 individuals with CKD stage 4 and 5 have chronic metabolic acidosis in the United States. Chronic metabolic acidosis may have various adverse effects in patients with CKD, including altered skeletal metabolism [5], insulin resistance [6], protein-energy wasting [7–9], and accelerated progression of kidney disease. In epidemiologic studies, low serum bicarbonate levels have been associated with high mortality (Table 1). In a study of 1,240 male patients with non-dialysis dependent CKD, the lowest mortality was observed among those with baseline serum bicarbonate levels of 26–29 mEq/L, whereas patients with levels <22 mEq/L had a 43% higher risk of mortality [10]. Using data from the African American S Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

7â© Springer International Publishing Switzerland 2017 D. Ayres-de-campos, Obstetric Emergencies, Doi 10.1007/978-3-319-41656-4_2

7â© Springer International Publishing Switzerland 2017 D. Ayres-de-campos, Obstetric Emergencies, Doi 10.1007/978-3-319-41656-4_2

2Acute Fetal Hypoxia/Acidosis 2.1 Definition, Incidence and Main Risk Factors Fetal hypoxia refers to the condition in which there is decreased oxygen concentra- tion in fetal tissues, and this is insufficient to maintain normal cell energy produc- tion by way of aerobic metabolism. Oxygen is supplied to fetal tissues via a long pathway that involves the maternal respiratory system, maternal circulation, gas exchange at the placenta and finally the umbilical and fetal circulations (Fig. 2.1). Problems occurring at any of these levels may result in decreased oxygen concen- tration in the fetal circulation (hypoxaemia) and ultimately in fetal tissues (hypoxia). Acute fetal hypoxia refers to the condition in which there is a rapid reduction in oxygen levels, i.e. occurring over the course of a few minutes. Its main causes are considered in Table 2.1. In the absence of oxygen, fetal cells may continue to produce the energy required for maintenance of basic homeostatic functions during a few more minutes, by resorting to anaerobic metabolism. However, the latter yields much less energy than aerobic metabolism and results in the production of lactic acid. The intra- and extracellular accumulation of hydrogen ions, due to increased lactic acid produc- tion, results in the development of metabolic acidosis (decreased pH caused by acids of intracellular origin) and, because these ions are taken away by the fetal circulation, metabolic acidaemia. The whole process of decreased oxygen concen- tration in tissues is therefore known as hypoxia/acidosis. Some constituents of fetal blood are capable of neutralising (buffering) hydrogen ions. These are called bases, and they include bicarbonate, haemoglobin and plasma proteins. However, their availability is limited, and their depletion Continue reading >>

Defining Metabolic Acidosis

Defining Metabolic Acidosis

Metabolic acidosis is common in ill and injured animals. In humans, metabolic acidosis has diagnostic, therapeutic, and prognostic value; this may also be true in animals. Metabolic acidosis occurs when the accumulation of nonvolatile acids or loss of bicarbonate exceeds the body’s buffering capability. Acid base parameters, electrolytes, and lactate concentrations were reviewed from dogs and cats admitted to a veterinary medical teaching hospital over 13 months. Values were measured from heparinized blood samples immediately after collection on a point-of-care machine. Metabolic acidosis was defined as a standardized base excess of <-4 mmol/L (dogs) and <-5mmol/L (cats). Of the 1805 dogs and cats having ≥1 blood sample analyzed, 887 (49%) had metabolic acidosis (753 dogs, 134 cats). Metabolic acidosis was associated with various underlying diseases; neoplasia was most common in dogs and renal disease most common in cats. The most common acid–base abnormality was primary metabolic acidosis. Mixed acid–base disorders were more common in both dogs and cats than were simple disorders; primary respiratory alkalosis was the least common abnormality. Hyperchloremic metabolic acidosis was more common than high anion gap (AG) metabolic acidosis. Twenty-five percent of dogs and 34% of cats with metabolic acidosis could not be classified as having either hyperchloremia or high AG. Routine categorization of metabolic acidosis based on high AG or hyperchloremia alone may be misleading. Commentary AG, bicarbonate/TCO2, and chloride levels are all means by which acid–base status can be evaluated in practice. Even without a blood gas analyzer, a potential metabolic imbalance can be gleaned via serum biochemistry panel and evaluation. Metabolic acidosis results from either a Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

What keeps your blood from becoming too acidic or basic? How does the body control this? Read this lesson to learn about what happens when this balance is overthrown and the blood becomes too acidic, in a scenario called metabolic acidosis. Your body needs to stay approximately around a given equilibrium to function normally. There is a little bit of wiggle room, but not much, and when things go awry, the body begins to suffer. Our blood is literally our life source - it carries oxygen to the body and helps remove waste materials so we can function properly. Under normal conditions, our blood pH is around 7.4, but sometimes this balance is thrown off and the blood becomes more acidic. This condition is called metabolic acidosis. In this scenario, the body is either producing too much acid, not getting rid of enough acid, or fails to make enough base to neutralize the acid. (A neutral pH value is 7.0; higher numbers are more basic or alkaline and lower numbers are more acidic.) Causes of Metabolic Acidosis Metabolic acidosis sounds like something out of a horror movie - acidic blood?! What would cause the body to do this? Well, there are a few known causes, some of which we'll discuss below. Ketoacidosis: The body creates ketones when it burns fats instead of carbohydrates for energy, and ketones make the blood acidic. When you are fasting, causing your body to switch to fats for fuel, or when you drink too much alcohol, you risk the build up of ketones in the blood. Diabetics are also at risk of this condition when the body fails to produce enough insulin. Lactic acidosis: Notice an acidosis trend here? The body's cells create lactic acid when they are deprived of oxygen. You may experience bouts of lactic acidosis during intense exercise or due to heart conditions. Ren Continue reading >>

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