Respiratory acidosisis a state in which decreased ventilation (hypoventilation) increases the concentration ofcarbon dioxidein the blood and decreases the blood'spH(a condition generally calledacidosis).
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| Specialty | Intensive care medicine,pulmonology,internal medicine |
Carbon dioxide is produced continuously as the body's cells respire, and this CO2will accumulate rapidly if the lungs do not adequately expel it throughalveolarventilation. Alveolar hypoventilation thus leads to an increasedPaCO2(a condition calledhypercapnia). The increase inPaCO2in turn decreases the HCO3−/PaCO2ratio and decreases pH.
Types
editRespiratory acidosis can be acute or chronic.
- Inacute respiratory acidosis,thePaCO2is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.35).
- Inchronic respiratory acidosis,thePaCO2is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary torenal compensationand an elevated serumbicarbonate(HCO3−>30 mEq/L).
Causes
editAcute
editAcute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of thecentral respiratory centerby cerebral disease or drugs, inability to ventilate adequately due toneuromuscular disease(e.g.,myasthenia gravis,amyotrophic lateral sclerosis,Guillain–Barré syndrome,muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.
Chronic
editChronic respiratory acidosis may be secondary to many disorders, includingCOPD.Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness tohypoxiaandhypercapnia,increasedventilation-perfusion mismatchleading to increaseddead space ventilation,and decreaseddiaphragmfunction secondary to fatigue and hyperinflation.
Chronic respiratory acidosis also may be secondary toobesity hypoventilation syndrome(i.e.,Pickwickian syndrome), neuromuscular disorders such asamyotrophic lateral sclerosis,and severe restrictive ventilatory defects as observed ininterstitial lung diseaseandthoracicdeformities.
Lung diseases that primarily cause abnormality inalveolar gas exchangeusually 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
editMechanism
editMetabolism rapidly generates a large quantity ofvolatile acid(H2CO3) andnonvolatile acid.The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2.The CO2combines with H2O to formcarbonic acid(H2CO3). The lungs normally excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO2can cause a respiratory acid-base disorder. ThePaCO2is maintained within a range of 35–45 mm Hg in normal states.
Alveolar ventilation is under the control of therespiratory center,which is located in theponsand themedulla.Ventilation is influenced and regulated bychemoreceptorsforPaCO2,PaO2,and pH located in the brainstem, and in theaortic and carotid bodiesas well as by neural impulses from lungstretch receptorsand impulses from thecerebral cortex.Failure of ventilation quickly increases thePaCO2.
In acute respiratory acidosis, compensation occurs in 2 steps.
- The initial response is cellular buffering (plasma protein buffers) that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO3−) only slightly, approximately 1 mEq/L for each 10-mm Hg increase inPaCO2.
- The second step isrenalcompensation that occurs over 3–5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased. For instance,PEPCKis upregulated inrenal proximal tubule brush border cells,in order to secrete moreNH3and thus to produce moreHCO3−.[1]
Estimated changes
editIn renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg inPaCO2.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 inPaCO2.
- Chronic respiratory acidosis: HCO3−rises 3.5 mEq/L for each 10 mm Hg rise inPaCO2.
The expected change in pH with respiratory acidosis can be estimated with the following equations:
- Acute respiratory acidosis: Change in pH = 0.08 X ((40 −PaCO2)/10)
- Chronic respiratory acidosis: Change in pH = 0.03 X ((40 −PaCO2)/10)
Respiratory acidosis does not have a great effect onelectrolytelevels. 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 significanthyperkalemia.
Diagnosis
editDiagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH <7.35 and a PaCO2 >45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH.
Terminology
edit- Acidosisrefers to disorders that lower cell/tissue pH to < 7.35.
- Acidemiarefers to an arterial pH < 7.36.[2]
See also
editReferences
edit- ^Boron, Walter F. (2005).Medical Physiology: A Cellular And Molecular Approaoch.Elsevier/Saunders. p. 858.ISBN1-4160-2328-3.
- ^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.PMID19932372.
External links
edit- Nosek, Thomas M."Section 7/7ch12/7ch12p43".Essentials of Human Physiology.Archived fromthe originalon 2016-03-24.