Diseases & Conditions



Acidosis is excessive blood acidity caused by an overabundance of acid in the blood or a 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 slow breathing (respiratory acidosis). Blood acidity increases when people ingest substances that contain or produce acid or when the lungs do not expel enough carbon dioxide. People with metabolic acidosis have nausea, vomiting, and fatigue and may breathe faster and deeper than normal. People with respiratory acidosis have headache and confusion, and breathing may appear shallow, slow or both. Tests on blood samples show there is too much acid. Doctors treat the cause of the acidosis.

If an increase in acid overwhelms the body's pH buffering systems, the blood will become acidic. As blood pH drops, the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing. 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 coma.


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 Some Trade Names ECOTRIN ASPERGUM ( acetylsalicylic acid Some Trade Names See Aspirin ). 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. 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 and Metabolic Alkalosis

Metabolic acidosis Diabetic ketoacidosis (buildup of ketones) Drugs and substances such as acetazolamide Some Trade Names DIAMOX , alcohol, aspirin Some Trade Names ECOTRIN ASPERGUM , iron Lactic acidosis (buildup of lactic acid as occurs in shock) Loss of bases, such as bicarbonate, through the digestive tract from diarrhea, an ileostomy, or a colostomy Kidney failure Poisons such as carbon monoxide, cyanide, ethylene glycol, methanol, Renal tubular acidosis (a form of kidney malfunction) Metabolic alkalosis Loss of acid from vomiting or drainage of the stomach Overactive adrenal gland (Cushing's syndrome) Use of diuretics (thiazides, furosemide Some Trade Names LASIX , ethacrynic acid Some Trade Names EDECRIN )

Respiratory acidosis develops when the lungs do not expel carbon dioxide adequately, a problem that can occur in diseases that severely affect the lungs (such as emphysema, chronic bronchitis, severe pneumonia, pulmonary edema, and asthma). Respiratory acidosis can also develop when diseases of the brain or of the nerves or muscles of the chest impair breathing. In addition, people can develop respiratory acidosis when their breathing is slowed due to oversedation from opioids (narcotics) or strong drugs that induce sleep (sedatives).

Major Causes of Respiratory Acidosis and Alkalosis

Respiratory acidosis Lung disorders, such as emphysema, chronic bronchitis, severe asthma, pneumonia, or pulmonary edema Sleep-disordered breathing Diseases of the nerves or muscles of the chest that impair breathing, such as Guillain-Barré syndrome or amyotrophic lateral sclerosis Overdose of drugs such as alcohol, opioids, and strong sedatives Respiratory alkalosis Anxiety Aspirin Some Trade Names ECOTRIN ASPERGUM overdose (early stages) Fever Low levels of oxygen in the blood Pain


People with mild metabolic acidosis may have no symptoms but usually experience nausea, vomiting, and fatigue. Breathing becomes deeper and slightly faster (as the body tries to correct the acidosis by expelling more carbon dioxide). As the acidosis worsens, people begin to feel extremely weak and drowsy and may feel confused and increasingly nauseated. Eventually, blood pressure can fall, leading to shock, coma, and death.

The first symptoms of respiratory acidosis may be headache and drowsiness. Drowsiness may progress to stupor and coma. Stupor and coma can develop within moments if breathing stops or is severely impaired, or over hours if breathing is less dramatically impaired.


The diagnosis of acidosis generally requires the measurement of blood pH in a sample of arterial blood, usually taken from the radial artery in the wrist. Arterial blood is used because venous blood contains high levels of bicarbonate and thus is generally not as accurate a measure of the body's pH status.

To learn more about the cause of the acidosis, doctors also measure the levels of carbon dioxide and bicarbonate in the blood. Additional blood tests may be done to help determine the cause.


The treatment of metabolic acidosis depends primarily on the cause. For instance, treatment may be needed to control diabetes with insulin Some Trade Names HUMULIN NOVOLIN or to remove the toxic substance from the blood in cases of poisoning.

The treatment of respiratory acidosis aims at improving the function of the lungs. Drugs that open the airways (bronchodilators, such as albuterol Some Trade Names PROVENTIL VENTOLIN ) may help people who have lung diseases such as asthma and emphysema. People who have severely impaired breathing or lung function, for whatever reason, may need mechanical ventilation to aid breathing (see Respiratory Failure and Acute Respiratory Distress Syndrome: Acute Respiratory Distress Syndrome (ARDS) ).

Acidosis may also be treated directly. If the acidosis is mild, the administration of intravenous fluids may be all that is needed. Rarely, when acidosis is very severe, bicarbonate may be given intravenously. However, bicarbonate provides only temporary relief and may cause harm—for instance, by overloading the body with sodium and water.

Last full review/revision July 2008 by James L. Lewis, III, MD

Source: The Merck Manual Home Edition