lactic acidosis

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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.

lac·tic ac·i·do·sis

a type of metabolic acidosis caused by accumulation of lactic acid due to tissue hypoxia, drug effect, or unknown etiology.

lactic acidosis

Metabolism Metabolic acidosis due to ↑ lactic acid resulting from tissue hypoxia or ↓ conversion of lactate to pyruvate Etiology Exercise, endogenous or exogenous metabolic defects Lab ↓ Bicarbonate, ↓ pH, ↑ anion gap, ↑ PO4 Treatment Dichloro-acetate treatment of Pts with severe LA results in statistically significant but clinically unimportant changes in the pH and arterial blood lactate and does not alter the hemodyanimcs or survival

lac·tic ac·i·do·sis

(laktik asi-dōsis)
Metabolic form caused by accumulation of lactic acid due to tissue hypoxia, drug side effects, or unknown etiology.

Lactic acidosis

A serious condition caused by the build up of lactic acid in the blood, causing it to become excessively acidic. Lactic acid is a by-product of glucose metabolism.
Mentioned in: Diabetic Ketoacidosis

lac·tic ac·i·do·sis

(laktik asi-dōsis)
Metabolic acidosis caused by accumulation of lactic acid due to tissue hypoxia, drug effect, or unknown etiology.
References in periodicals archive ?
A high incidence of lactic acidosis and symptomatic hyperlactatemia in women receiving highly active antiretroviral therapy in Soweto, South Africa.
Our patient did not show hypotension and hypoxia (Sa[O.sub.2] on ambient air was 98%), factors responsible for type A lactic acidosis. In a case reported by Hulme ad Sherwood, severe lactic acidosis of 31 mmol/L was seen in a patient with alcohol-related generalized seizures.(r) Our patient did not experience seizures before admission.
Church, "Ruminal changes during the onset and recovery of induced lactic acidosis in sheep," Journal of Animal Science, vol.
Guidelines for the prevention, diagnosis and management of NRTI-associated symptomatic hyperlactataemia and lactic acidosis. Southern African Journal of HIV Medicine 2006;7(1):8-15.
I'll never forget what a brilliant medical doctor personally told me after a large study came out that dispelled the myth connecting metformin with lactic acidosis. This doctor knew how effective metformin was, but was terrified of creating lactic acidosis in any of his patients.
(6) The most common causes of high AG metabolic acidosis are: diabetic or alcoholic ketoacidosis, lactic acidosis, uraemic acidosis and intoxication with alcohol, methanol, ethylene glycol, salicylate, or carbon monoxide (Table 4).
Severe lactic acidosis complicating Metformin overdose successfully treated with high volume venovenous hemofiltration and aggressive alkalization.
The maleimide method of PEGylation demonstrated superior durability in lactic acidosis and should therefore be incorporated into the focus of further studies while the cyanuric method should be re-evaluated.
Asymptomatic lactic acidosis has been reported previously during acute severe asthma and attributed to fatiguing respiratory muscles, hypoxaemia and liver ischaemia.
In this case, the anion gap 24 mEq/L and suggests the accumulation of fixed acid consistent with lactic acidosis. The significantly elevated lactate level confirms this cause of primary metabolic acidosis.
(8.) Kezar WW, Church DC Ruminal changes during the onset and the recovery of induced lactic acidosis in sheep.