Respiratory acidosis 1334036 223938670 2008-07-06T16:37:36Z 89.246.207.1 interwiki {{context}} {{Infobox_Disease | Name = {{PAGENAME}} | Image = Davenport Fig 11.jpg | Caption = [[Davenport diagram]] | DiseasesDB = 95 | ICD10 = {{ICD10|E|87|2|e|70}} | ICD9 = {{ICD9|276.2}} | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = med | eMedicineTopic = 2008 | MeshID = D000142 | }} '''Respiratory acidosis''' is [[acidosis]] (abnormally increased acidity of the blood) due to decreased [[Ventilation (physiology)|ventilation]] of the [[lung|pulmonary]] [[alveoli]], leading to elevated [[artery|arterial]] [[carbon dioxide]] concentration (''Pa''CO<sub>2</sub>). Respiratory acidosis is a clinical disturbance that is due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the level of ''Pa''CO<sub>2</sub>. Alveolar hypoventilation leads to an increased ''Pa''CO<sub>2</sub> (ie, [[hypercapnia]]). The increase in ''Pa''CO<sub>2</sub> in turn decreases the HCO<sub>3</sub><sup>-</sup>/''Pa''CO<sub>2</sub> ratio and decreases [[pH]]. [[Hypercapnia]] and respiratory acidosis occur when impairment in ventilation occurs and the removal of CO<sub>2</sub> by the lungs is less than the production of CO<sub>2</sub> in the tissues. == Types of respiratory acidosis == Respiratory acidosis can be acute or chronic. * In ''acute respiratory acidosis'', the ''Pa''CO<sub>2</sub> is elevated above the upper limit of the reference range (over 6.3 kPa or 47 mm Hg) with an accompanying acidemia (pH <7.35). * In ''chronic respiratory acidosis'', the ''Pa''CO<sub>2</sub> is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to [[renal compensation]] and an elevated serum bicarbonate (HCO<sub>3</sub><sup>-</sup> >30 mm Hg). == Causes == ===Acute=== Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the [[central respiratory center]] by cerebral disease or drugs, inability to ventilate adequately due to [[neuromuscular disease]] (eg, [[myasthenia gravis]], [[amyotrophic lateral sclerosis]], [[Guillain-Barré syndrome]], [[muscular dystrophy]]), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. ===Chronic=== Chronic respiratory acidosis may be secondary to many disorders, including [[COPD]]. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to [[Hypoxia (medical)|hypoxia]] and [[hypercapnia]], increased [[ventilation-perfusion mismatch]] leading to increased [[dead space]] ventilation, and decreased [[diaphragm (anatomy)|diaphragm]] function secondary to fatigue and hyperinflation. Chronic respiratory acidosis also may be secondary to [[obesity hypoventilation syndrome]] (ie, [[Pickwickian syndrome]]), neuromuscular disorders such as [[amyotrophic lateral sclerosis]], and severe restrictive ventilatory defects as observed in [[interstitial fibrosis]] and [[thoracic]] deformities. Lung diseases that primarily cause abnormality in [[alveolar gas exchange]] usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occurs. == Physiological response == ===Mechanism=== Metabolism rapidly generates a large quantity of volatile acid (H<sub>2</sub>CO<sub>3</sub>) and [[nonvolatile acid]]. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO<sub>2</sub>. The CO<sub>2</sub> combines with H<sub>2</sub>O to form [[carbonic acid]] (H<sub>2</sub>CO<sub>3</sub>). The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO<sub>2</sub> can cause a respiratory acid-base disorder. The ''Pa''CO<sub>2</sub> is maintained within a range of 39-41 mm Hg in normal states. Alveolar ventilation is under the control of the central respiratory centers, which are located in the [[pons]] and the [[medulla]]. Ventilation is influenced and regulated by [[chemoreceptors]] for ''Pa''CO<sub>2</sub>, PaO<sub>2</sub>, and pH located in the brainstem,and in the [[aortic and carotid bodies]] as well as by neural impulses from lung [[stretch receptors]] and impulses from the [[cerebral cortex]]. Failure of ventilation quickly increases the ''Pa''CO<sub>2</sub>. In acute respiratory acidosis, compensation occurs in 2 steps. * The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO<sub>3</sub><sup>-</sup>) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in ''Pa''CO<sub>2</sub>. * The second step is renal compensation that occurs over 3-5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased. For instance, [[PEPCK]] is upregulated in [[renal proximal tubule brush border cell]]s, in order to secrete more [[ammonia|NH<sub>3</sub>]] and thus to produce more [[bicarbonate|HCO<sub>3</sub><sup>-</sup>]].<ref name=boron858> {{cite book |author=Walter F., PhD. Boron |title=Medical Physiology: A Cellular And Molecular Approaoch |publisher=Elsevier/Saunders |location= |year= |pages= |isbn=1-4160-2328-3 |oclc= |doi=}} Page 858 </ref> ===Estimated changes=== In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in ''Pa''CO<sub>2</sub>. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: * Acute respiratory acidosis: HCO<sub>3</sub><sup>-</sup> increases 1 mEq/L for each 10-mm Hg rise in ''Pa''CO<sub>2</sub>. * Chronic respiratory acidosis: HCO<sub>3</sub><sup>-</sup> rises 3.5 mEq/L for each 10-mm Hg rise in ''Pa''CO<sub>2</sub>. The expected change in pH with respiratory acidosis can be estimated with the following equations: * Acute respiratory acidosis: Change in pH = 0.008 X (40 - ''Pa''CO<sub>2</sub>) * Chronic respiratory acidosis: Change in pH = 0.003 X (40 - ''Pa''CO<sub>2</sub>) Respiratory acidosis does not have a great effect on [[electrolyte]] levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant [[hyperkalemia]]. ==References== <references /> ==External links== * {{GeorgiaPhysiology|7/7ch12/7ch12p43}} {{Fluid, electrolyte, acid base metabolic pathology}} [[Category:Pulmonology]] [[Category:Electrolyte disturbances]] [[de:Respiratorische Azidose]] [[fr:Acidose respiratoire]] [[it:Acidosi respiratoria]]