Respiratory acidosis is a medical emergency in which decreased ventilation causes increased
blood carbon dioxide concentration and decreased pH.
Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will
accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar
hypoventilation thus leads to an increased PaCO2. The increase in PaCO2 in turn decreases
the HCO3−/PaCO2 ratio and decreases pH.
Terminology Acidosis refers to disorders that lower cell/tissue
pH to < 7.35. Acidemia refers to an arterial pH < 7.36.
Types of respiratory acidosis Respiratory acidosis can be acute or chronic.
In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference
range with an accompanying acidemia. In chronic respiratory acidosis, the PaCO2
is elevated above the upper limit of the reference range, with a normal blood pH or near-normal
pH secondary to renal compensation and an elevated serum bicarbonate.
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, or airway obstruction
related to asthma or chronic obstructive pulmonary disease 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, 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 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. The lungs normally 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 PaCO2 is maintained within a range of
35–45 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 PaCO2, 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 PaCO2.
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 only slightly, approximately 1 mEq/L for each 10-mm
Hg increase in PaCO2. 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−. Estimated changes
In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm
Hg in PaCO2. 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 PaCO2. Chronic respiratory acidosis: HCO3− rises
3.5 mEq/L for each 10 mm Hg rise in PaCO2. The expected change in pH with respiratory
acidosis can be estimated with the following equations:
Acute respiratory acidosis: Change in pH = 0.008 X
Chronic respiratory acidosis: Change in pH = 0.003 X
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.
See also respiratory alkalosis
metabolic acidosis metabolic alkalosis
References
External links Physiology at MCG 77ch12p43