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RESPIRATORY ACIDOSIS

Category: Medical

Topic: Acid-Base Balance

Level: AEMT

Next Unit: Respiratory Alkalosis

6 minute read

Respiratory Acidosis

Hypoventilation is impaired respiration (exchange of CO2 for O2).

Hypercapnia and respiratory acidosis: when ventilation is impaired and removal of CO2 is less than the CO2 production in the tissues.

Alveolar hypoventilation leads to an increased PaCO2 (i.e., hypercapnia). This increase in PaCO2 will decrease the ratio balance between bicarbonate and carbon dioxide toward CO2 (more carbonic acid), which will decrease the pH.

 

Hypercapnia

Hypercapnia can be either acute or chronic in nature:

  • Acute hypercapnia is always accompanied by a respiratory acidosis (pH <7.35), whereas
  • chronic hypercapnia is associated with a low-normal or near-normal pH (assuming the patient has normal renal function and the ability to excrete acid by the kidney).

Excretion of acid by the kidney is effective but slow, so the chronic nature of chronic hypercapnia gives the kidneys enough time to slowly compensate.

  • The combined acute-on-chronic hypercapnia lies in between these parameters.

Acute respiratory acidosis occurs with an abrupt failure of ventilation, such as in:

  • central nervous system disease or drug-induced respiratory depression,
  • severe acute airway disease, or
  • when an acute process worsens alveolar ventilation in a patient with limited pulmonary reserve (e.g., pneumonia in a patient with COPD).

Chronic respiratory acidosis develops over days to weeks such that bicarbonate rises as an indication that renal compensation, i.e., secretion of acid, has occurred (usually after 3-5 days), such as in:

  • COPD or
  • chronic neuromuscular disorders.

It is important to note that the metabolic compensation for respiratory acidosis is the secretion of acid by the kidney.

 

Signs and Symptoms

Mild: anxiety, dyspnea, daytime sluggishness, headaches, and sleepiness.

Moderate: alterations in sensorium--delirium, paranoia, depression, confusion--which can progress to the coma of CO2 narcosis. This usually does not develop until the PaCO2 is greater than 75-80 mm Hg.

Severe: asterixis (involuntary hand-flapping), myoclonus, seizures, papilledema, dilated superficial veins.

 

Diagnosis

Common etiologies may include a

  • drug history,
  • past history of chronic lung disease,
  • sleep apnea, or a
  • neuromuscular disorder, a smoking and travel history, as well as a history of recent trauma.

 

Management

Treatment is by addressing the underlying cause:

  • clearing the airway,
  • assisting ventilation,
  • bronchodilators,
  • corticosteroids, and
  • diuretics.

In the field, management includes increasing the rate and depth of ventilation: bag them to get rid of some CO2 for them.

Also, support for the ABC (airway, breathing, circulation), possible oxygen administration, and transport with comfort and reassurance.