Acidosis is abiological process producinghydrogen ions and increasing their concentration inblood or body fluids.pH is the negative log of hydrogen ion concentration and so it is decreased by a process of acidosis.
The term acidemia describes the state of low blood pH, when arterialpH falls below 7.35 (except in the fetus – see below) whileacidosis is used to describe the processes leading to these states. The use of acidosis for a low pH creates an ambiguity in its meaning. The difference is important where a patient has factors causing both acidosis andalkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH.[citation needed]
Alkalemia occurs at a pH of over 7.45.Arterial blood gas analysis and other tests are required to separate the main causes, which are clear in certain situations. For instance, a diabetic with ketoacidosis is a recognizable case where the main cause of acidemia is essentially obvious.[1]
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).[2]
Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen in acidosis includeheadaches, confusion,feeling tired,tremors,sleepiness,flapping tremor, and dysfunction of thecerebrum of the brain which may progress to coma if there is no intervention.[3]
In extreme cases symptoms can beanorexia,diabetes mellitus,chronic nephritis orpneumonia.[4]
 | This sectionneeds additional citations forverification. Please helpimprove this article byadding citations to reliable sources in this section. Unsourced material may be challenged and removed.(October 2014) (Learn how and when to remove this message) |
Metabolic acidosis may result from either increased production of metabolic acids, such as lactic acid, or disturbances in the ability to excrete acid via thekidneys, such as eitherrenal tubular acidosis or the acidosis ofkidney failure, which is associated with an accumulation ofurea andcreatinine as well as metabolic acid residues of proteincatabolism.
Lactic acidosis occurs whenever the demand for oxygen by tissues exceeds the supply and the more efficient aerobic metabolism is supplemented by anaerobic metabolism that produces lactate.Increased demand occurs, for example, with high intensity exercise such as sprinting.Inadequate supply occurs, for example, withhypoperfusion as occurs in hemorrhagic shock.
A rise in lactate out of proportion to the level ofpyruvate, e.g., in mixed venous blood, is termed "excess lactate", and is an indicator ofanaerobic glycolysis 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 instarvation anddiabetic ketoacidosis. It is due to the accumulation of ketoacids (via excessiveketosis) and reflects a severe shift fromglycolysis tolipolysis for energy needs.
Acid consumption frompoisoning such asmethanol ingestion, elevated levels ofiron in the blood, and chronically decreased production ofbicarbonate 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 tochemoreceptors, which increasesalveolar ventilation, leading to respiratory compensation, otherwise known asKussmaul breathing (a specific type ofhyperventilation). Should this situation persist, the patient is at risk of exhaustion leading torespiratory failure.
Mutations to theV-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineuraldeafness.
Arterial blood gases will indicate lowpH, low bloodHCO3, and normal or low PaCO2.In addition to arterial blood gas, ananion gap can also differentiate between possible causes.
TheHenderson-Hasselbalch equation is useful for calculating blood pH, because blood is abuffer solution. In the clinical setting, this equation is usually used to calculateHCO3 from measurements of pH and PaCO2 inarterial blood gases. 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 islactic acid, which disappears as blood flow and oxygen debt are corrected.[citation needed]
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 ofbicarbonate may be required.[citation needed]
In thefetus, 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 7.18 to 7.38).[5] Fetal metabolicacidemia is defined as an umbilical vessel pH of less than 7.20 and abase excess of less than −8.[6]
Respiratory acidosis results from a build-up of carbon dioxide in the blood (hypercapnia) due tohypoventilation. It is most often caused bypulmonary problems, althoughhead injuries, drugs (especiallyanaesthetics andsedatives), andbrain tumors can cause this acidemia.Pneumothorax,emphysema, chronicbronchitis,asthma, severepneumonia, andaspiration are among the most frequent causes. It can also occur as a compensatory response to chronicmetabolic alkalosis.[citation needed]
One key to distinguish between respiratory and metabolic acidosis is that in respiratory acidosis, the CO2 is increased while thebicarbonate 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.[citation needed]
However, in cases where chronic illnesses that compromise pulmonary function persist, such as late-stage emphysema and certain types ofmuscular 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.[7][8]
In thefetus, 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).[5] In the fetus, the lungs are not used for ventilation. Instead, theplacenta performs ventilatory functions (gas exchange). Fetal respiratory acidemia is defined as an umbilical vessel pH of less than 7.20 and an umbilical arteryPCO2 of 66 or higher or umbilical vein PCO2 of 50 or higher.[6]
{{cite book}}:ISBN / Date incompatibility (help)[page needed]{{cite book}}:ISBN / Date incompatibility (help)
The dictionary definition ofacidosis at Wiktionary
| International | |
|---|---|
| National | |
| Other | |
