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Acidosis
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<h2 id="acidemia">Acidemia</h2> <p class="note">"Acidemia" redirects here; not to be confused with <a href="/facts/Academia/Q1cenQyr">Academia</a>.</p> <p>The term acidemia describes the state of low blood pH, when arterial <a href="/facts/PH/RnSv8D7y">pH</a> falls below 7.35 (except in the fetus – see below) while <i>acidosis</i> 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 and <a href="/facts/Alkalosis/SoUSH8No">alkalosis</a>, wherein the relative severity of both determines whether the result is a high, low, or normal pH. </p><p><a href="/facts/Alkalosis/SoUSH8No">Alkalemia</a> occurs at a pH over 7.45. <a href="/facts/Arterial_blood_gas/LGJ1peJh">Arterial blood gas</a> analysis and other tests are required to separate the main causes. In certain situations the main cause is clear. For instance, a diabetic with ketoacidosis is a recognizable case where the main cause of acidemia is essentially obvious. </p><p>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). </p> <h2 id="signs-and-symptoms">Signs and symptoms</h2> <p><a href="/facts/Central_nervous_system/k8I6To97">Nervous system</a> 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 include <a href="/facts/Headache/mdmmC9DP">headaches</a>, confusion, <a href="/facts/Fatigue_(medical)/C2oo4Hvg">feeling tired</a>, <a href="/facts/Tremor/rD6ogM7X">tremors</a>, <a href="/facts/Somnolence/mIlFhyf0">sleepiness</a>, <a href="/facts/Asterixis/hztzd0A4">flapping tremor</a>, and dysfunction of the <a href="/facts/Cerebrum/zjpAVDgA">cerebrum</a> of the brain which may progress to coma if there is no intervention.<a class="footnote-ref" id="fnref:1" href="#fn:1"><sup>1</sup></a> </p> <h2 id="metabolic-acidosis">Metabolic acidosis</h2> <p class="note">Main article: <a href="/facts/Metabolic_acidosis/sSKCKBHA">Metabolic acidosis</a></p> <p>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 <a href="/facts/Kidney/HBspPrv9">kidneys</a>, such as either <a href="/facts/Renal_tubular_acidosis/PcrVnYW5">renal tubular acidosis</a> or the acidosis of <a href="/facts/Kidney_failure/gsqb5nos">kidney failure</a>, which is associated with an accumulation of <a href="/facts/Urea/6j84AoCG">urea</a> and <a href="/facts/Creatinine/gkebqj2L">creatinine</a> as well as metabolic acid residues of protein <a href="/facts/Catabolism/CFWUdphX">catabolism</a>. </p><p><a href="/facts/Lactic_acidosis/PSDwP9lP">Lactic acidosis</a> 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, with <a href="/facts/Perfusion/EFVLNUTg">hypoperfusion</a> as occurs in hemorrhagic shock. </p><p>A rise in lactate out of proportion to the level of <a href="/facts/Pyruvate/qJTgl4J9">pyruvate</a>, e.g., in mixed venous blood, is termed "excess lactate", and is an indicator of <a href="/facts/Anaerobic_glycolysis/GwU4yYvo">anaerobic glycolysis</a> 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 <a href="/facts/Starvation/xXxdp2CM">starvation</a> and <a href="/facts/Diabetic_ketoacidosis/QhhbSbeM">diabetic ketoacidosis</a>. It is due to the accumulation of ketoacids (via excessive <a href="/facts/Ketosis/GIzSt3mL">ketosis</a>) and reflects a severe shift from <a href="/facts/Glycolysis/a5ApxLoG">glycolysis</a> to <a href="/facts/Lipolysis/wuQwM0nb">lipolysis</a> for energy needs. </p><p>Acid consumption from <a href="/facts/Poison/XIQjhpsw">poisoning</a> such as <a href="/facts/Methanol/EIfpoNCg">methanol</a> ingestion, elevated levels of <a href="/facts/Iron/QK1JYy8E">iron</a> in the blood, and chronically decreased production of <a href="/facts/Bicarbonate/zzSVVAl1">bicarbonate</a> may also produce metabolic acidosis. </p><p>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 <a href="/facts/Chemoreceptor/KC6IDxzf">chemoreceptors</a>, which increases <a href="/facts/Alveolar_ventilation/92Wov2gk">alveolar ventilation</a>, leading to respiratory compensation, otherwise known as <a href="/facts/Kussmaul_breathing/rSs9R8l3">Kussmaul breathing</a> (a specific type of <a href="/facts/Hyperventilation/ElocGGlI">hyperventilation</a>). Should this situation persist, the patient is at risk of exhaustion leading to <a href="/facts/Respiratory_failure/R3GcdkJ1">respiratory failure</a>. </p><p>Mutations to the <a href="/facts/V-ATPase/K1Lh2P3j">V-ATPase</a> 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural <a href="/facts/Deafness/PT2xcLaX">deafness</a>. </p><p><a href="/facts/Arterial_blood_gas/LGJ1peJh">Arterial blood gases</a> will indicate low <a href="/facts/PH/RnSv8D7y">pH</a>, low blood <a href="/facts/HCO3/zzSVVAl1">HCO3</a>, and normal or low PaCO2. In addition to arterial blood gas, an <a href="/facts/Anion_gap/Cn1UXy35">anion gap</a> can also differentiate between possible causes. </p><p>The <a href="/facts/Henderson-Hasselbalch_equation/LrduPhHB">Henderson-Hasselbalch equation</a> is useful for calculating blood pH, because blood is a <a href="/facts/Buffer_solution/zrLz9eaa">buffer solution</a>. In the clinical setting, this equation is usually used to calculate <a href="/facts/HCO3/zzSVVAl1">HCO3</a> from measurements of pH and PaCO2 in <a href="/facts/Arterial_blood_gas/LGJ1peJh">arterial blood gases</a>. 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 <a href="/facts/Lactic_acid/BsVRFx7s">lactic acid</a>, which disappears as blood flow and oxygen debt are corrected. </p> <h3>Treatment</h3> <p>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 <a href="/facts/Bicarbonate/zzSVVAl1">bicarbonate</a> may be required. </p> <h3>Fetal metabolic acidemia</h3> <p>In the <a href="/facts/Fetus/evocHd0Y">fetus</a>, the normal range differs based on which umbilical vessel is sampled (<a href="/facts/Umbilical_vein/DY9DgcMV">umbilical vein</a> pH is normally 7.25 to 7.45; <a href="/facts/Umbilical_artery/lIl0cl0z">umbilical artery</a> pH is normally 7.18 to 7.38).<a class="footnote-ref" id="fnref:2" href="#fn:2"><sup>2</sup></a> Fetal metabolic <a href="/facts/Acidemia/hmfAo1uR">acidemia</a> is defined as an umbilical vessel pH of less than 7.20 and a <a href="/facts/Base_excess/XeUog8Bf">base excess</a> of less than −8.<a class="footnote-ref" id="fnref:3" href="#fn:3"><sup>3</sup></a> </p> <h2 id="respiratory-acidosis">Respiratory acidosis</h2> <p class="note">Main article: <a href="/facts/Respiratory_acidosis/3IHb1Lc9">Respiratory acidosis</a></p> <p>Respiratory acidosis results from a build-up of carbon dioxide in the blood (<a href="/facts/Hypercapnia/wBArR1mW">hypercapnia</a>) due to <a href="/facts/Hypoventilation/ruqIr4oa">hypoventilation</a>. It is most often caused by <a href="/facts/Lung/gTWXI6Fj">pulmonary</a> problems, although <a href="/facts/Head_injury/KvqnqIbG">head injuries</a>, drugs (especially <a href="/facts/Anaesthetic/0xG7I2ou">anaesthetics</a> and <a href="/facts/Sedative/JWzvq66P">sedatives</a>), and <a href="/facts/Brain_tumor/avjI5Nhm">brain tumors</a> can cause this acidemia. <a href="/facts/Pneumothorax/oaCPSynh">Pneumothorax</a>, <a href="/facts/Emphysema/ud3oXGCr">emphysema</a>, chronic <a href="/facts/Bronchitis/IATP1XWJ">bronchitis</a>, <a href="/facts/Asthma/7GkJvxn3">asthma</a>, severe <a href="/facts/Pneumonia/Jw0KquTA">pneumonia</a>, and <a href="/facts/Aspiration_pneumonia/c92nqX66">aspiration</a> are among the most frequent causes. It can also occur as a compensatory response to chronic <a href="/facts/Metabolic_alkalosis/M4KlT5b7">metabolic alkalosis</a>. </p><p>One key to distinguish between respiratory and metabolic acidosis is that in respiratory acidosis, the CO2 is increased while the <a href="/facts/Bicarbonate/zzSVVAl1">bicarbonate</a> 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. </p><p>However, in cases where chronic illnesses that compromise pulmonary function persist, such as late-stage emphysema and certain types of <a href="/facts/Muscular_dystrophy/uU5xD0h8">muscular dystrophy</a>, 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, <a href="/facts/Mechanical_ventilation/XSQ84JX9">mechanical ventilation</a> will usually be applied.<a class="footnote-ref" id="fnref:4" href="#fn:4"><sup>4</sup></a><a class="footnote-ref" id="fnref:5" href="#fn:5"><sup>5</sup></a> </p> <h3>Fetal respiratory acidemia</h3> <p>In the <a href="/facts/Fetus/evocHd0Y">fetus</a>, the normal range differs based on which umbilical vessel is sampled (<a href="/facts/Umbilical_vein/DY9DgcMV">umbilical vein</a> pH is normally 7.25 to 7.45; <a href="/facts/Umbilical_artery/lIl0cl0z">umbilical artery</a> pH is normally 7.20 to 7.38).<a class="footnote-ref" id="fnref:6" href="#fn:6"><sup>6</sup></a> In the fetus, the lungs are not used for ventilation. Instead, the <a href="/facts/Placenta/7XUoks1b">placenta</a> performs ventilatory functions (<a href="/facts/Gas_exchange/3vUewPNH">gas exchange</a>). Fetal respiratory acidemia is defined as an umbilical vessel pH of less than 7.20 and an umbilical artery <a href="/facts/PCO2/3jPc7ToV">PCO2</a> of 66 or higher or umbilical vein PCO2 of 50 or higher.<a class="footnote-ref" id="fnref:7" href="#fn:7"><sup>7</sup></a> </p> <h2 id="see-also">See also</h2> <ul><li><a href="/facts/Acid%E2%80%93base_homeostasis/y4U6UENE">Acid–base homeostasis</a></li> <li><a href="/facts/Acid%E2%80%93base_imbalance/sGmJmvBq">Acid–base imbalance</a></li> <li><a href="/facts/Alkalinizing_agent/fYoUQr3V">Alkalinizing agent</a></li> <li><a href="/facts/Alkaline_diet/hIjnL1D3">Alkaline diet</a></li> <li><a href="/facts/Arterial_blood_gas/LGJ1peJh">Arterial blood gas</a></li> <li><a href="/facts/Chemical_equilibrium/y8ToYXHp">Chemical equilibrium</a></li> <li><a href="/facts/Lactic_acidosis/PSDwP9lP">Lactic acidosis</a></li> <li><a href="/facts/PCO2/3jPc7ToV">pCO2</a></li> <li><a href="/facts/PKa/t4YyRtKC">pKa</a></li></ul> Notes <ul><li>Hobler KE, Carey LC. Effect of acute progressive hypoxemia on cardiac output and plasma excess lactate. <i>Ann. Surg.</i> 1973 Feb;177(2):199-202.</li> <li>Hobler KE, Napodano RJ. Tolerance of swine to acute blood volume deficits. <i>J Trauma.</i> 1974 Aug;14(8):716-8.</li> <li>Rose, BD, Post TW. <i><a href="https://books.google.com/books?id=cQZsAAAAMAAJ">Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed.</a></i> (No content available.) 2000. New York: McGraw Hill Professional.</li></ul> <h2 id="external-links">External links</h2> <p> The dictionary definition of acidosis at Wiktionary </p> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>Yee AH, Rabinstein AA (February 2010). "Neurologic presentations of acid-base imbalance, electrolyte abnormalities, and endocrine emergencies". Neurol Clin. 28 (1): 1–16. doi:10.1016/j.ncl.2009.09.002. PMID 19932372. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>Yeomans, ER; Hauth, JC; Gilstrap, LC III; Strickland DM (1985). "Umbilical cord pH, PCO2, and bicarbonate following uncomplicated term vaginal deliveries (146 infants)". Am J Obstet Gynecol. 151 (6): 798–800. doi:10.1016/0002-9378(85)90523-x. PMID 3919587. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Pomerance, Jeffrey (2004). Interpreting Umbilical Cord Gases: For Clinicians Caring for the Fetus or Newborn. Pasadena, CA: BNMG. ISBN 978-0-9752621-0-8. <a href="978-0-9752621-0-8" target="_blank">978-0-9752621-0-8</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>"MedlinePlus Medical Encyclopedia: Respiratory acidosis". Archived from the original on 11 December 2008. Retrieved 2008-12-06. <a href="https://www.nlm.nih.gov/medlineplus/ency/article/000092.htm" target="_blank">https://www.nlm.nih.gov/medlineplus/ency/article/000092.htm</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>"eMedicine - Respiratory Acidosis : Article by Jackie A Hayes". Archived from the original on October 29, 2008. Retrieved 2008-12-06. <a href="http://www.emedicine.com/MED/topic2008.htm" target="_blank">http://www.emedicine.com/MED/topic2008.htm</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>Yeomans, ER; Hauth, JC; Gilstrap, LC III; Strickland DM (1985). "Umbilical cord pH, PCO2, and bicarbonate following uncomplicated term vaginal deliveries (146 infants)". Am J Obstet Gynecol. 151 (6): 798–800. doi:10.1016/0002-9378(85)90523-x. PMID 3919587. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>Pomerance, Jeffrey (2004). Interpreting Umbilical Cord Gases: For Clinicians Caring for the Fetus or Newborn. Pasadena, CA: BNMG. ISBN 978-0-9752621-0-8. <a href="978-0-9752621-0-8" target="_blank">978-0-9752621-0-8</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></p></li> </ol>