Respiratory acidosis

Infobox_Disease
Name = PAGENAME

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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 of the pulmonary alveoli, leading to elevated arterial carbon dioxide concentration ("Pa"CO₂).

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"CO₂. Alveolar hypoventilation leads to an increased "Pa"CO₂ (ie, hypercapnia). The increase in "Pa"CO₂ in turn decreases the HCO₃^-/"Pa"CO₂ ratio and decreases pH. Hypercapnia and respiratory acidosis occur when impairment in ventilation occurs and the removal of CO₂ by the lungs is less than the production of CO₂ in the tissues.

Types of respiratory acidosis

Respiratory acidosis can be acute or chronic.
* In "acute respiratory acidosis", the "Pa"CO₂ 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"CO₂ 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 (HCO₃^- >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 and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased 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 (H₂CO₃) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO₂. The CO₂ combines with H₂O to form carbonic acid (H₂CO₃). The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO₂ can cause a respiratory acid-base disorder. The "Pa"CO₂ 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"CO₂, PaO₂, 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"CO₂.

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 (HCO₃^-) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in "Pa"CO₂.
* 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 cells, in order to secrete more NH₃ and thus to produce more HCO₃^-. 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 ]

Estimated changes

In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in "Pa"CO₂. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:

* Acute respiratory acidosis: HCO₃^- increases 1 mEq/L for each 10-mm Hg rise in "Pa"CO₂.

* Chronic respiratory acidosis: HCO₃^- rises 3.5 mEq/L for each 10-mm Hg rise in "Pa"CO₂.

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"CO₂)

* Chronic respiratory acidosis: Change in pH = 0.003 X (40 - "Pa"CO₂)

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

External links

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