|
|
| (56 intermediate revisions by 7 users not shown) |
| Line 1: |
Line 1: |
| | __NOTOC__ |
| | {| class="infobox" style="float:right;" |
| | |- |
| | | [[File:Siren.gif|30px|link=Respiratory acidosis resident survival guide]]|| <br> || <br> |
| | | [[Respiratory acidosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| | |} |
| | {{Respiratory acidosis}} |
| '''For patient information page, click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information page, click [[{{PAGENAME}} (patient information)|here]]''' |
|
| |
|
| {{Infobox_Disease | | | {{CMG}}; {{AE}} {{VKG}} |
| Name = {{PAGENAME}} |
| |
| Image = |
| |
| Caption = |
| |
| DiseasesDB = 95 |
| |
| ICD10 = {{ICD10|E|87|2|e|70}} |
| |
| ICD9 = {{ICD9|276.2}} |
| |
| ICDO = |
| |
| OMIM = |
| |
| MedlinePlus = |
| |
| MeshID = D000142 |
| |
| }} | |
| {{Search infobox}} | |
| {{CMG}}
| |
| ==Overview==
| |
|
| |
|
| '''Respiratory acidosis''' is [[acidosis]] (abnormal 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>).
| | {{SK}} Acidosis, respiratory; blood carbon dioxide raised; hypercapnia; hypercarbia |
|
| |
|
| 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> 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. | | ==[[Respiratory acidosis overview|Overview]]== |
| | ==[[Respiratory acidosis classification|Classification]]== |
| | ==[[Respiratory acidosis pathophysiology |Pathophysiology]]== |
| | ==[[Respiratory acidosis causes|Causes]]== |
| | ==[[Respiratory acidosis differential diagnosis|Differentiating Respiratory acidosis from other Diseases]]== |
| | ==[[Respiratory acidosis epidemiology and demographics|Epidemiology and Demographics]]== |
| | ==[[Respiratory acidosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| | ==Diagnosis== |
| | [[Respiratory acidosis history and symptoms|History and Symptoms]] | [[Respiratory acidosis physical examination|Physical Examination]] | [[Respiratory acidosis laboratory findings|Laboratory Findings]] | [[Respiratory acidosis chest x ray|Chest X Ray]] | [[Respiratory acidosis CT|CT]] | [[Respiratory acidosis other imaging findings|Other Imaging Findings]] | [[Respiratory acidosis other diagnostic studies|Other Diagnostic Studies]] |
|
| |
|
| == Classification == | | ==Treatment== |
| Respiratory acidosis can be acute or chronic.
| | [[Respiratory acidosis medical therapy|Medical Therapy]] | [[Respiratory acidosis surgery|Surgery]] | [[Respiratory acidosis primary prevention|Primary Prevention]] | [[Respiratory acidosis secondary prevention|Secondary Prevention]] | [[Respiratory acidosis future or investigational therapies|Future or Investigational Therapies]] |
| * 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).
| | ==Case Studies== |
| * 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).
| | :[[Respiratory acidosis case study one|Case #1]] |
| | |
| == 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.
| |
| | |
| ===Causes in Alphabetical Order===
| |
| | |
| Respiratory failure type 2]]
| |
| Respiratory distress syndrome (neonatal)
| |
| | |
| Trauma, mechanical and physical conditions
| |
| | |
| Obstructive sleep apnoea
| |
| | |
| Drugs, hormones and mediators
| |
| | |
| Alfentanil
| |
| Fentanyl
| |
| Oxygen
| |
| Remifentanil
| |
| Sufentanil
| |
| | |
| == Physiological response == | |
| ===Mechanism===
| |
| Metabolism rapidly generates a large quantity of volatile acid (CO<sub>2</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.
| |
| | |
| ===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]].
| |
|
| |
|
| | ==Related Chapters== |
| | * [[Metabolic alkalosis]] |
| | * [[Acid-base imbalance]] |
| | * [[Metabolic acidosis]] |
| | * [[Respiratory alkalosis]] |
| | * [[Anion gap]] |
| | * [[Hypocalcemia]] |
| | [[Category:Electrolyte disturbance]] |
| [[Category:Inborn errors of metabolism]] | | [[Category:Inborn errors of metabolism]] |
| [[Category:Signs and symptoms]] | | [[Category:Medical tests]] |
| [[Category:Pulmonology]] | | [[Category:Laboratory Test]] |
| [[Category:Electrolyte disturbance]]
| |
| [[Category:Nephrology]]
| |
| | |
| [[fr:Acidose respiratoire]]
| |
| | |
|
| |
|
| {{WikiDoc Help Menu}} | | {{WH}} |
| {{WikiDoc Sources}} | | {{WS}} |
