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Acidosis is an increased acidity (i.e. hydrogen ion concentration) of blood plasma. Generally 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.
Strictly speaking, the term acidemia would be more appropriate to describe the state of low blood pH, reserving acidosis to describe the processes leading to these states. Nevertheless, most physicians 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 (Needham, 2004).
Respiratory acidosis
Respiratory acidosis results from a build-up of carbon dioxide in the blood due to hypoventilation. It is most often caused by pulmonary problems, although head injuries, drugs (especially anaesthetics and sedatives), and brain tumors can also bring it on. Emphysema, chronic bronchitis, asthma, severe pneumonia, and aspiration are among the most frequent causes. It can also occur as a response to chronic metabolic alkalosis.
Blood gases show pH below 7.35 as above mentioned, and PaCO2 will be high (>45 mmHg / 6 kPa).
The key to distinguish between respiratory and metabolic acidosis is that in respiratory acidosis, the CO2 is increased while the bicarb is either normal (uncompensated) or increased (compensated). Compensation occurs if respiratory acidosis persists for days or longer and a chronic phase is entered with partial buffering of the acidosis through renal bicarbonate retension.
Metabolic acidosis
Metabolic acidosis may result 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 metabolic 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 is the best indicator of an inadequate flow of oxygen into the body's mitochondria from either cause. Oxygen debt (and muscle excess lactate)is also seen in strenuous exercise. Once oxgenation 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 fuel needs.
Acidic poisons, iron etc., and decreased production of bicarbonate may also produce metabolic acidosis.
Metabolic acidosis can result in stimulation of chemoreceptors and so increase alveolar ventilation, leading to respiratory compensation, otherwise known as 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.
In blood gas tests, it is characterised by a low pH, low blood HCO3, and normal or low PaCO2. In addition to arterial blood gas one can use the anion gap to 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 derivitive 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 it corrected.
Treatment of any of the varieties of metabolic acidosis is focused upon correction of the underlying problem. However, neutralizing the acidosis with infusions of bases like sodium bicarbinate may be temporarily helpful in some critical emergencies.
References
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
Electrolyte disturbance | Emergency medicine | Intensive care medicine
"Acidosis"