metabolic acidosis

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Metabolic Acidosis



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.


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, methanol, or ethylene glycol) also produce symptoms of metabolic acidosis.
In mild cases of metabolic acidosis, symptoms include headache, lack of energy, and sleepiness. Breathing may become fast and shallow. Nausea, vomiting, diarrhea, dehydration, and loss of appetite are also associated with metabolic acidosis. Diabetic patients with symptoms of metabolic acidosis may also have breath that smells fruity. The patient may lose consciousness or become disoriented. Severe cases can produce coma and death.


Metabolic acidosis is suspected based on symptoms, but is usually confirmed by laboratory tests on blood and urine samples. Blood pH below 7.35 confirms the condition. Levels of other blood components, including potassium, glucose, ketones, or lactic acid, may also be above normal ranges. The level of bicarbonate in the blood will be low, usually less than 22 mEq/L. Urine pH may fall below 4.5 in metabolic acidosis.


Treatment focuses first on correcting the acid imbalance. Usually, sodium bicarbonate and fluids will be injected into the blood through a vein. An intravenous line may be started to administer fluids and allow for the quick injection of other drugs that may be needed. If the patient is diabetic, insulin may be administered. Drugs to regulate blood pressure or heart rate, to prevent seizures, or to control nausea and vomiting might be given. Vital signs like pulse, respiration, blood pressure, and body temperature will be monitored. The underlying cause of the metabolic acidosis must also be diagnosed and corrected.


If the metabolic acidosis is recognized and treated promptly, the patient may have no long-term complications, however, the underlying condition that caused the acidosis needs to be corrected or managed. Severe metabolic acidosis that is left untreated will lead to coma and death.


Diabetic patients need to routinely test their urine for sugar and acetone, strictly follow their appropriate diet, and take any medications or insulin to prevent metabolic acidosis. Patients receiving tube feedings or intravenous feedings must be monitored to prevent dehydration or the accumulation of ketones or lactic acid.



"Fluid, Electrolyte, and Acid-Base Disorders." In Family Medicine Principles and Practices. 5th ed. New York: Springer-Verlag, 1998.

Key terms

Diabetic ketoacidosis — A condition caused by low insulin levels where the amount of sugar and ketones in the blood is high.
pH — A measurement of the acidity or alkalinity of a solution based on the amount of hydrogen ions available. 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 alkaline (basic) with a normal range of 7.36-7.44.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.


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 acidot´ic.

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, respiratory disorders, or liver disease.
compensated acidosis a condition in which the compensatory mechanisms have returned the pH toward normal.
diabetic acidosis a metabolic acidosis produced by accumulation of ketones in uncontrolled diabetes mellitus.
hypercapnic acidosis respiratory acidosis.
hyperchloremic acidosis renal tubular acidosis.
lactic acidosis a metabolic acidosis occurring as a result of excess lactic acid in the blood, due to conditions causing impaired cell respiration. It occurs most commonly in disorders in which oxygen is inadequately delivered to tissues, such as shock, septicemia, or extreme hypoxemia, but it can also result from exogenous or endogenous metabolic defects. Initially manifesting as hyperventilation, it progresses to mental confusion and coma.
metabolic acidosis any of the types of acidosis resulting from accumulation in the blood of keto acids (derived from fat metabolism) at the expense of bicarbonate; this diminishes the body's ability to neutralize acids. This type is contrasted with respiratory acidosis. It occurs when there is either an acid gain (as in diabetic ketoacidosis, lactic acidosis, poisoning, or failure of the renal tubules to reabsorb bicarbonate) or a bicarbonate loss (as in diarrhea or a gastrointestinal fistula).

The symptoms of metabolic acidosis include weakness, malaise, and headache. As the acid level goes up these symptoms progress to stupor, unconsciousness, coma, and death. The breath may have a fruity odor owing to the presence of acetone, and the patient may experience vomiting and diarrhea. Loss of fluids can deplete body fluid content and aggravate the acidosis. Hyperventilation may occur as a result of stimulation of the hypothalamus. blood gas analysis will reveal a lowered pH and an elevated PaCO2. (See accompanying table.)
Treatment and Patient Care. Treatment of metabolic acidosis is primarily concerned with control of the underlying causes. Diabetic ketoacidosis may be corrected by the administration of insulin and fluids. In acute renal failure the patient requires dialysis, and in chronic uremic acidosis the condition is controlled by restricting sodium intake and buffering with bicarbonate. The patient's vital signs should be checked frequently to assess the progress of compensation. A rising pulse rate and a drop in blood pressure frequently occur as a result of hypovolemia in the diabetic-acidotic patient, and cardiac arrhythmias can be caused by increased calcium levels in the blood. A careful recording of intake and output provides a means of determining the kidneys' ability to regulate the acid-base balance. Safety measures to avoid injury during involuntary muscular contractions should be carried out. (See also convulsions.) Nursing measures to relieve discomfort from vomiting and to avoid the hazards of aspiration of vomitus are required. Education of the patient and family in the prevention of acute episodes of metabolic acidosis, particularly diabetic ketoacidosis, is of primary importance.
renal tubular acidosis (RTA) a metabolic acidosis resulting from impairment of the reabsorption of bicarbonate by the renal tubules, characterized by low plasma bicarbonate and high plasma chloride; the urine is alkaline.
respiratory acidosis acidosis resulting from ventilatory impairment and subsequent retention of carbon dioxide, in contrast to metabolic acidosis. The respiratory system has an important role in maintaining acid-base balance. In response to an increase in the hydrogen ion concentration in body fluids, the respiratory rate increases, causing more carbon dioxide to be released from the lung. When either an acute obstruction of the airways or a chronic condition involving the organs of respiration causes interference with the exhalation of the carbon dioxide produced by metabolic activity, carbon dioxide accumulates in the blood and unites with water to form carbonic acid.

Acute respiratory acidosis occurs when there is a relatively sudden malfunction of respiratory activities, as in upper airway obstruction, acute infections and inflammation of the lung and bronchial tissues, and pulmonary edema. In acute respiratory acidosis the compensatory chemical buffer systems are of limited benefit in restoring the acid-base balance because they depend on normal blood circulation and tissue perfusion for optimal effect. The physiologic regulators, the lungs and kidneys, are of little help because the lungs are malfunctioning and the kidneys require more time to compensate than the acute condition permits.

Chronic respiratory acidosis results from gradual and irreversible loss of ventilatory function, as in chronic obstructive pulmonary disease (COPD). Although the patient in this condition does have an increased retention of CO2, there is time for the kidneys to compensate by retaining bicarbonate and thereby maintaining a pH within tolerable limits. If, however, even a minor respiratory infection develops, the patient is subject to a rapidly developing state of acute acidosis because the lungs cannot be depended upon to remove more than a minimal amount of CO2.
Treatment and Patient Care. The initial treatment for acute respiratory acidosis is to establish an airway immediately and maintain adequate ventilation and hydration. Acute cases may require the use of an endotracheal tube or tracheostomy tube. Some form of intermittent positive pressure breathing is applied through a machine-driven ventilator, essentially to force adequate O2 delivery and concomitant CO2 removal from the lungs, thereby avoiding further rises in CO2 levels to the point that CO2 narcosis will develop. Beyond a certain point the respiratory center may cease responding to the higher CO2 levels, and breathing will stop abruptly. Drugs that further depress the respiratory center (narcotics, hypnotics, and tranquilizers) must be avoided. Patients in the acute stage are watched for cessation of breathing and cardiac arrest. cardiopulmonary resuscitation may be required to revive the patient.

It is recommended that oxygen administration be limited in patients with chronic obstructive pulmonary disease (COPD). In COPD the stimulus to breathe is a hypoxic state, therefore administration of high concentrations of O2 will remove this needed stimulus. The rate of oxygen flow should be closely correlated with blood gas studies. In patients with acute lung diseases the stimulus to breathe is still dependent on CO2 concentrations, so that O2 can be supplied without fear of inhibiting the stimulus to breathe.

Measures that facilitate breathing are essential to patient care during respiratory acidosis. Frequent turning, coughing, and deep breathing exercises to encourage oxygen–carbon dioxide exchange are beneficial, as is suctioning when needed to remove secretions obstructing the airway. postural drainage, unless contraindicated by the patient's condition, may be effective in promoting adequate ventilation.
starvation acidosis a metabolic acidosis due to accumulation of ketones following a severe caloric deficit.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

met·a·bol·ic ac·i·do·sis

decreased pH and bicarbonate concentration in the body fluids caused either by the accumulation of acids or by abnormal losses of fixed base from the body, as in diarrhea or renal disease.
Farlex Partner Medical Dictionary © Farlex 2012

metabolic acidosis

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

metabolic acidosis

A condition in which there is a decreased pH due to either an increase in acids or loss of bicarbonate.
Clinical findings
Rapid, deep breathing, fruity breath, headache, lethargy, nausea, vomiting, coma.
pH < 7.35, HCO3– < 22 mEq/L; in “compensating” cases, PaCO2 < 35 mm Hg.
Bicarbonate (HCO3–) depletion due to renal disease, diarrhoea, fistulas of GI tract; increased production of organic acids due to liver disease, endocrinopathies (e.g., diabetes), hypoxia, shock, drug overdose; decreased excretion of acids due to renal disease.
A pH of under 7.1 is a medical emergency requiring IV bicarbonate.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.

metabolic acidosis

Physiology A condition in which there is a ↓ pH due to either an ↑ in acids or loss of bicarbonate Lab pH < 7.35, HCO3 < 22 mEq/L, and in 'compensating' cases PaCO2 < 35 mm Hg Etiology Bicarbonate–HCO3– depletion due to renal disease, diarrhea, fistulas of GI tract; ↑ production of organic acids due to liver disease, endocrinopathies–eg, DM, hypoxia, shock, drug overdose; ↓ excretion of acids due to renal disease Clinical Rapid, deep breathing, fruity breath, headache, lethargy, N&V, coma. See Metabolic alkalosis, Respiratory acidosis, Respiratory alkalosis.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

met·a·bol·ic ac·id·o·sis

(met'ă-bol'ik as'i-dō'sis)
Decreased pH and bicarbonate concentration in the body fluids caused either by the accumulation of acids or by abnormal losses of fixed base from the body, as in diarrhea or renal disease.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

met·a·bol·ic ac·id·o·sis

(met'ă-bol'ik as'i-dō'sis)
Decreased pH and bicarbonate concentration in body fluids caused either by accumulation of acids or abnormal losses of fixed base from the body.
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
The management of acute methanol toxicity includes gastric lavage, treating metabolic acidosis, administration of ethanol which leads to competitive inhibition of methanol oxidation and hemodialysis to remove both formate and methanol.
Finally, when trying to account for the persistence of low pC[O.sub.2] despite correction of the metabolic acidosis in hemodialysis, the issue of potential C[O.sub.2] loss through the dialyzer membrane needs to be addressed.
Inborn error of metabolism was considered in this patient because of lethargy, hepatomegaly, hypoglycemia, metabolic acidosis, elevated ALT and AST levels, and history of previous attack.
The heightened hormonal drive (cortisol, human placental lactogen and glucagon), insulin resistance, elevated resting serum ketone concentration and reduced ability to buffer hydrogen ions (chronic respiratory alkalosis and a compensatory metabolic acidosis) together with the state of accelerated starvation in pregnancy predispose the pregnant woman to rapid development of ketoacidosis compared with her non-pregnant counterpart.
High doses of INH may lead to metabolic acidosis, rhabdomyolysis, convulsions, lactic acidosis, coma, and eventually death (1).
THAM is a proton acceptor (11) that can bind both carbon dioxide and metabolic acid, and due to its favorable buffer properties, THAM has been propagated as an effective alkalinizing agent in either respiratory or metabolic acidosis (3, 5, 12).
Knowledge of the analytical interference of glycolate and glyoxylate leading to false lactate elevation on many POC blood gas analyzers is therefore crucial when seeing patients with severe metabolic acidosis and massive lactate elevation [6].
This differs from previous publications where chronic metabolic acidosis is most frequently due to the interdialytic accumulation of volatile acids [2, 6, 8].
Kurtzman, "Bicarbonate therapy in severe metabolic acidosis," Journal of the American Society of Nephrology, vol.
Kidney involvement in our reported case was responsible for the non-anion gap part of metabolic acidosis which mandates further search for the cause of acidosis.
However, the older age, the co-occurrence of malnutrition/inflammation, the bigger dialysis vintage, and the lower urine output may contribute to a higher metabolic acidosis state in intradialytic hypertension patients.
Its metabolites are responsible for metabolic acidosis, blindness, hemodynamic instability, and methanol intoxication that can cause death (3).