Bicarbonate loss Proximal RTA,diarrhoea,Carbonic anhydrase inhibitorsPrimary hyperparathyroidism.
Failure of Bicarbonate Regeneration Hypereninemic Hyperaldosteronism Potassium sparing diuretics. Accumulaiton of Organic acid, Lactic Acidosis, Keto-acidosis diabetic, alcoholic, starvation, infection, salicylates, ethylenglycol, Methanol. Symptoms are not specific,Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain and joint pain. Extreme acidemia leads to  (1)Neurological complications: lethargy, stupor, coma, seizures.
Other tests that are relevant in this context are electrolytes (including chloride), glucose, renal function and a full blood count. To distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions.


When there is a hyperkalemia with acidosis diarrhoea, diabetic ketoacidosis, Renal Tubular Acidosis and acetazolamide toxicity are to be excluded. Tufts OCW material is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License. In chronic renal failure acidosis primarily due to inability of the kidneys to form ammonia. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Urinalysis can reveal acidity (salicylate poisoning) or alkalinity (renal tubular acidosis type I). It is also important to differentiate between acidosis-induced hyperventilation and asthma; otherwise, treatment could lead to inappropriate bronchodilation. Together with respiratory acidosis, it is one of the two general causes of acidemia.Acidosis refers to a process that causes a low pH in blood and tissues. Some compensation is achieved by buffering of acid anions by phosphates released from bones.


Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Due to respiratory compensation (hyperventilation), carbon dioxide is decreased and conversely oxygen is increased. In RTA (Renal Tubular Acidosis) complete correction with oral bicarbonate is required as it then reduces nephrocalcinosis, hypercalciuria and osteomalacia. Acidosis developing in patients on ventilators is fatal as the compensatory hyperventilation is lacking. Rapid alkalization in harmful because it may precipitate tetany, cardiac arrhythmia and convulsion due to paradoxical CSF acidosis.



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