Respiratory Acidosis ?>

Respiratory Acidosis

Respiratory Acidosis


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 partial arterial pressure of carbon dioxide (PaCO2). The reference range for PaCO2 is 36-44. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2 in turn decreases the HCO3 -/PaCO2 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.

Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH <7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (ie, HCO3 – >30 mm Hg).

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 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.

Metabolism rapidly generates a large quantity of volatile acid (CO2) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2. The CO2 combines with H2 O to form carbonic acid (H2 CO3). 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 PaCO2 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 PaCO2, PaO2, and pH located in the brainstem, 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 (HCO3 -) 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. 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 (40 – PaCO2)
Chronic respiratory acidosis: Change in pH = 0.003 X (40 – PaCO2)

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.

The morbidity and mortality of respiratory acidosis depends on the underlying cause of the respiratory acidosis, associated conditions, the patient’s compensatory mechanisms, and ease of access to medical care.

The clinical manifestations of respiratory acidosis often are those of the underlying disorder. Manifestations vary depending on the severity of the disorder and on the rate of development of hypercapnia. Mild-to-moderate hypercapnia that develops slowly usually has minimal symptoms.

Patients may be anxious and may complain of dyspnea. Some patients may have disturbed sleep and daytime hypersomnolence. As the PaCO2 increases, the anxiety may progress to delirium, and patients become progressively more confused, somnolent, and obtunded. This condition sometimes is referred to as CO2 narcosis.

The findings on physical examination in patients with respiratory acidosis usually are nonspecific and related to the underlying illness or the cause of the respiratory acidosis.
During thoracic examination, patients with obstructive lung disease may have diffuse wheezing, hyperinflation (ie, barrel chest), decreased breath sounds, hyperresonance on percussion, and prolonged expiration. Rhonchi also may be heard.
Cyanosis may be noted if accompanying hypoxemia is present, and the finding of clubbing may indicate the presence of a chronic respiratory disease.
Mental status may be depressed in severe elevations of PaCO2. Patients may have asterixis, myoclonus, and seizures.
Papilledema may be found during the examination. Conjunctival and superficial facial blood vessels also may be dilated.

Respiratory acidosis may have numerous etiologies, including the following:
Chronic obstructive pulmonary disease
Severe asthma
Chronic bronchitis
Neuromuscular diseases
Amyotrophic lateral sclerosis
Diaphragm paralysis
Severe kyphoscoliosis
Guillain-Barré syndrome
Myasthenia gravis
Muscular dystrophy
Obesity hypoventilation syndrome
CNS depression
Drugs – Narcotics, barbiturates, benzodiazepines, other CNS depressants
Neurologic disorders – Encephalitis, brainstem disease, trauma
Primary alveolar hypoventilation

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