acidosis

An abnormal increase in the acidity of the body's fluids, caused either by accumulation of acids or by depletion of bicarbonates.

An increase in the acidity of blood plasma to below the normal range of pH 7.3-7.45, resulting from a loss of the buffering capacity of the plasma, alteration in the excretion of carbon dioxide, excessive loss of base from the body, or metabolic overproduction of acids.

The human body functions best when blood and tissue fluids are neither too alkaline nor too acidic. An abnormally high acidity of blood and tissue fluids is called acidosis. It results in chemical reactions taking place less efficiently and can impair muscular contractions which may lead to fatigue.

There are two main types of acidosis: metabolic acidosis and respiratory acidosis. Metabolic acidosis may be caused by loss of bases (chemicals which readily accept hydrogen ions and decrease acidity), ingestion of highly acidic foods, or the production of excessive amounts of acid in the body. Respiratory acidosis results from a failure to exhale carbon dioxide from the lungs as quickly as it forms in respiring tissues. Carbon dioxide accumulates in the blood and tissues where it forms carbonic acids. Heavy or severe exercise may also cause temporary acidosis by producing large amounts of both lactic acid and carbon dioxide. Persistent acidosis is rare and usually associated with disease.

We usually respond to acidosis by breathing very heavily in order to flush out excess carbon dioxide from the body and eliminate excess acids (a process called compensatory hyperventilation). Some athletes use sodium hydrogen carbonate (sodium bicarbonate or baking soda) as a performance enhancer in the belief that it decreases acidity and reduces the risk of acidosis. Research evidence suggests that ingestion of 300 mg of bicarbonate per kilogram of body weight can enhance the performance of all-out, maximal aerobic activities lasting from 1 to 7 minutes.

A pathologic disturbance of the acid-base balance of the body characterized by an excess of acid or inadequate base. Causes include acid ingestion, increased acid production such as that seen in diabetes or starvation, or loss of base through the kidneys or intestine.

An abnormally high acidity of the blood and tissue fluids. Acidosis can reduce the efficiency of metabolic reactions, interfere with muscle actions, and may lead to fatigue. There are two main types of acidosis: metabolic acidosis and respiratory acidosis. Metabolic acidosis may be caused by loss of bases, ingestion of highly acidic foods, or the production of excessive amounts of acids in the body (e.g. during severe exercise when large amounts of both lactic acid and carbon dioxide are produced). Respiratory acidosis results from a failure to exhale carbon dioxide from the lungs as quickly as it forms in respiring tissues. Carbon dioxide accumulates in the blood and tissues, where it forms carbonic acids. Sufferers of acidosis usually breathe very heavily in order to flush out excess carbon dioxide from the body and eliminate excess acids (a process called compensatory hyperventilation). Some athletes use sodium hydrogen carbonate (baking soda) as a performance enhancer in the expectation that it decreases acidity and reduces the risk of acidosis. Compare alkalosis.

A pathological condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by increase in hydrogen ion concentration (decrease in pH).
The optimal acid–base balance is maintained by chemical buffers, biological activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis.
It is rare that acidosis occurs in the absence of some underlying disease process. The more obvious signs of severe acidosis are muscle twitching, involuntary movement, cardiac arrhythmias, disorientation and coma.

• compensated a. — a condition in which the compensatory mechanisms have returned the pH toward normal.
• diabetic a. — a metabolic acidosis produced by accumulation of ketones in uncontrolled diabetes mellitus.
• hypercapnic a. — respiratory acidosis.
• iatrogenic a. — may result from administration of drugs, such as urinary acidifiers, or anesthetic agents which depress respiration.
• lactic a. — the accumulation of lactate in the rumen in ruminants and the stomach of horses, and hence in the blood, as a result of overfeeding with readily fermentable carbohydrate. See also carbohydrate engorgement.
• metabolic a. — acidosis resulting from accumulation in the blood of keto acids (derived from fat metabolism) at the expense of bicarbonate, thus diminishing the body's ability to neutralize acids. This type of acidosis can occur when there is an acid gain, as in diabetic ketoacidosis, lactic acidosis, poisoning and failure of the renal tubules to reabsorb bicarbonate. It can also result from bicarbonate loss due to diarrhea or a gastrointestinal fistula.
• mixed alkalosis and a. — characterized by low serum chloride, normal or slightly elevated plasma bicarbonate and a very high anion gap.
• organic a. — accumulation of organic anions occurs in uremia, diabetic acidosis and lactic acidosis, and ingestion of salicylates, ethylene glycol or methanol.
• renal tubular a. — renal tubular malfunction leads to faulty resorption of bicarbonate or excretion of acid and the production of alkaline urine; types I (distal tubular acidosis) and II (proximal tubular acidosis) are identified.
• respiratory a. — acidosis resulting from ventilatory impairment and subsequent retention of carbon dioxide.
• ruminal a. — acidosis caused by an altered metabolic state, usually lactic acidosis, in the rumen.
• starvation a. — a metabolic acidosis due to accumulation of ketones following a severe caloric deficit.
• uncompensated a. — a condition in which the compensatory mechanisms have not been applied sufficiently to return the pH of the blood to normal.
• uremic a. — see metabolic acidosis (above).

For acidosis referring to acidity of the urine, see renal tubular acidosis.

Acidosis
Classification and external resources
ICD-10	E87.2
ICD-9	276.2
DiseasesDB	87
MeSH	D000138

Acidosis is an increased acidity (i.e. an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma.

Acidosis is said to occur when arterial pH falls below 7.35, while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes.

The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, physicians sometimes use the terms interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, where the relative severity of both determines whether the result is a high or a low pH.

The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g. healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.^[1]

General symptoms of acidosis.^{[2] [3]} These usually accompany symptoms of another primary defect (respiratory or metabolic).

Contents 1 Metabolic acidosis 2 Respiratory acidosis 3 See also 4 References 5 External links

Metabolic acidosis

Metabolic acidosis is an increased production of metabolic acids, usually resulting from disturbances in the ability to excrete acid via the kidneys. Renal acidosis is associated with an accumulation of urea and creatinine as well as metabolic acid residues of protein catabolism.

An increase in the production of other acids may also produce metabolic acidosis. For example, lactic acidosis may occur from 1) severe (PaO₂ <36mm Hg) hypoxemia causing a fall in the rate of oxygen diffusion from arterial blood to tissues, or 2) hypoperfusion (e.g. hypovolemic shock) causing an inadequate blood delivery of oxygen to tissues. A rise in lactate out of proportion to the level of pyruvate, e.g. in mixed venous blood, is termed "excess lactate", and may also be an indicator of fermention due to anaerobic metabolism occurring in muscle cells, as seen during strenuous exercise. Once oxygenation is restored, the acidosis clears quickly. Another example of increased production of acids occurs in starvation and diabetic acidosis. It is due to the accumulation of ketoacids (ketosis) and reflects a severe shift from glycolysis to lipolysis for energy needs.

Acid consumption from poisoning, elevated levels of iron in the blood, and chronically decreased production of bicarbonate may also produce metabolic acidosis.

Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid. This is a result of stimulation to chemoreceptors which increases alveolar ventilation, leading to respiratory compensation, otherwise known as Kussmaul breathing (a specific type of hyperventilation). Should this situation persist the patient is at risk for exhaustion leading to respiratory failure.

Mutations to the V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural deafness.

Arterial blood gases will indicate low pH, low blood HCO₃, and normal or low PaCO₂. In addition to arterial blood gas, an anion gap can also differentiate between possible causes.

The Henderson-Hasselbalch equation is useful for calculating blood pH, because blood is a buffer solution. The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is lactic acid, which disappears as blood flow and oxygen debt are corrected.

Treatment of uncompensated metabolic acidosis is focused upon correcting the underlying problem. When metabolic acidosis is severe and can no longer be compensated for adequately by the lungs, neutralizing the acidosis with infusions of bicarbonate may be required.

Respiratory acidosis

Respiratory acidosis results from a build-up of carbon dioxide in the blood (hypercapnia) due to hypoventilation. It is most often caused by pulmonary problems, although head injuries, drugs (especially anaesthetics and sedatives), and brain tumors can cause this acidemia. Pneumothorax, emphysema, chronic bronchitis, asthma, severe pneumonia, and aspiration are among the most frequent causes. It can also occur as a compensatory response to chronic metabolic alkalosis.

One key to distinguish between respiratory and metabolic acidosis is that in respiratory acidosis, the CO₂ is increased while the bicarbonate is either normal (uncompensated) or increased (compensated). Compensation occurs if respiratory acidosis is present, and a chronic phase is entered with partial buffering of the acidosis through renal bicarbonate retention.

However, in cases where chronic illnesses which compromise pulmonary function persist, such as late-stage emphysema and certain types of muscular dystrophy, compensatory mechanisms will be unable to reverse this acidotic condition. As metabolic bicarbonate production becomes exhausted, and extraeneous bicarbonate infusion can no longer reverse the extreme buildup of carbon dioxide associated with uncompensated respiratory acidosis, mechanical ventilation will usually be applied.^[4][5]

See also

• Alkalosis
• Acid-base physiology
• Acid-base homeostasis
• Mixed disorder of acid-base balance

References

1. ^ Needham, A. 2004. Comparative and Environmental Physiology. Acidosis and Alkalosis.
2. ^ Answers.com Medical Encyclopedia: Metabolic Acidosis: Causes and symptoms By Altha Roberts Edgren. Retrieved on April 13, 2009
3. ^ Symptoms mentioned in both metabolic and respiratory acidosis from the following two references:
   - Wrongdiagnosis.com > Symptoms of Metabolic Acidosis Retrieved on April 13, 2009
   - Wrongdiagnosis.com > Symptoms of Respiratory acidosis Retrieved on April 13, 2009
4. ^ "MedlinePlus Medical Encyclopedia: Respiratory acidosis". http://www.nlm.nih.gov/medlineplus/ency/article/000092.htm. Retrieved 2008-12-06. 
5. ^ "eMedicine - Respiratory Acidosis : Article by Jackie A Hayes". http://www.emedicine.com/MED/topic2008.htm. Retrieved 2008-12-06. 

Notes

• Hobler KE, Carey LC. Effect of acute progressive hypoxemia on cardiac output and plasma excess lactate. Ann Surg. 1973 Feb;177(2):199-202.
• Hobler KE, Napodano RJ, Tolerance of swine to acute blood volume deficits.
• J Trauma. 1974 Aug;14(8):716-8.
• Clinical Physiology of Acid-Base and Electrolyte Disorders by Rose, Post
• Intensive Care Medicine by Irwin and Rippe
• The ICU Book by Marino

External links

Look up acidosis in Wiktionary, the free dictionary.

• The Importance of ph Balance

• National Kidney and Urologic Diseases Information Clearinghouse

v • d • e Water-electrolyte imbalance and acid-base imbalance (E86-E87, 276) Volume status Volume contraction (Dehydration/Hypovolemia)  · Hypervolemia Electrolyte Na+ Hypernatremia · Hyponatremia (Hypotonic, Isotonic) K+ Hyperkalemia · Hypokalemia Cl− Hyperchloremia · Hypochloremia Acid-base Acidosis Metabolic: High anion gap (Ketoacidosis/Diabetic ketoacidosis, Lactic) · Normal anion gap (Hyperchloremic, Renal tubular) Respiratory Alkalosis Metabolic: Contraction alkalosis Respiratory Both Mixed disorder of acid-base balance urinary system navs: anat/physio/dev, noncongen/acid+base/congen/neoplasia, symptoms+signs/eponymous, proc

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