Acidosis
Acidosis is a process causing increased
Acidemia
The term acidemia describes the state of low blood pH, when arterial pH falls below 7.35 (except in the fetus – see below) while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction is relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal 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).
Signs and symptoms
Metabolic acidosis
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Metabolic acidosis may result from either increased production of metabolic acids, such as lactic acid, or disturbances in the ability to excrete acid via the kidneys, such as either renal tubular acidosis or the acidosis of kidney failure, which 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:
- severe (hypoxemiacausing a fall in the rate of oxygen diffusion from arterial blood to tissues.
- 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
Acid consumption from poisoning such as methanol ingestion, 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
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.
The
Treatment
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 or kidneys, neutralizing the acidosis with infusions of bicarbonate may be required.
Fetal metabolic acidemia
In the
Respiratory acidosis
Respiratory acidosis results from a build-up of carbon dioxide in the blood (
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 that 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 extraneous 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]
Fetal respiratory acidemia
In the fetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45; umbilical artery pH is normally 7.20 to 7.38).[2] In the fetus, the lungs are not used for ventilation. Instead, the placenta performs ventilatory functions (gas exchange). Fetal respiratory acidemia is defined as an umbilical vessel pH of less than 7.20 and an umbilical artery PCO2 of 66 or higher or umbilical vein PCO2 of 50 or higher.[3]
See also
- Acid–base homeostasis
- Acid–base imbalance
- Alkalinizing agent
- Alkaline diet
- Arterial blood gas
- Chemical equilibrium
- Lactic acidosis
- pCO2
- pKa
References
- ^ PMID 19932372.
- ^ PMID 3919587.
- ^ ISBN 978-0-9752621-0-8.
- ^ "MedlinePlus Medical Encyclopedia: Respiratory acidosis". Archived from the original on 11 December 2008. Retrieved 2008-12-06.
- ^ "eMedicine - Respiratory Acidosis : Article by Jackie A Hayes". Archived from the original on October 29, 2008. 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.
- Rose, BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed.[permanent dead link] (No content available.) 2000. New York: McGraw Hill Professional.
External links
The dictionary definition of acidosis at Wiktionary