Approach to respiratory acidosis: Clinical sciences

Respiratory acidosis refers to an increase in partial pressure of carbon dioxide or pCO2, with or without a compensatory increase in bicarbonate resulting in increased hydrogen ion concentration in the blood. This is almost always caused by hypoventilation, usually from the central nervous system, pulmonary, or iatrogenic conditions.

Generally, respiratory acidosis is characterized by an arterial pH below 7.35 and a pCO2 above 45 millimeters of mercury. As a reference, the normal pCO2 range is between 35 and 45 millimeters of mercury.

If a patient presents with a chief concern suggesting respiratory acidosis, first perform an ABCDE assessment to determine if your patient is stable or unstable.

If your patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring. Finally, provide supplemental oxygen, if needed.

Here’s a clinical pearl! Respiratory acidosis can be acute or chronic.

The chronic form is asymptomatic. However, if it worsens, or if the patient has an acute case, they might present with headache, confusion, and altered mental status. Their exam might show tremors, myoclonic jerks, and asterixis. These patients may require adequate ventilation by either endotracheal intubation or noninvasive positive pressure ventilation.

Now that unstable patients are taken care of, let’s talk about stable ones.

Your next step here is to obtain a focused history and physical examination and order labs, including an arterial blood gas analysis or ABG, and BMP.

History findings depend on the specific cause, but most patients have shortness of breath. The physical exam might show abnormal breathing patterns, such as a decreased respiratory rate, and signs of hypoxemia, like cyanosis.

As for the labs, ABG typically reveals an arterial pH below 7.35, and a pCO2 above 45 millimeters of mercury. BMP usually reveals normal or increased serum bicarbonate depending on whether there is metabolic compensation; and possibly electrolyte imbalances, such as increased serum potassium. If you see these findings, that’s respiratory acidosis.

Here’s a clinical pearl to keep in mind! After diagnosing respiratory acidosis, remember to assess for metabolic compensation by checking the serum bicarbonate level. A compensated respiratory acidosis is characterized by a normal or slightly decreased arterial pH, increased pCO2, and increased serum bicarbonate level.

This occurs in chronic conditions where the kidneys have been able to reabsorb enough bicarbonate, restoring the acid-base balance. Examples include interstitial lung diseases, restrictive chest wall disorders, and obesity.

On the other hand, uncompensated respiratory acidosis will have a decreased arterial pH, increased pCO2, and normal serum bicarbonate level.

A simple way to know if there is metabolic compensation in respiratory acidosis and alkalosis is to use the 1-2-3-4-5 rule. In the case of acidosis, for every 10 millimeters of mercury rise of pCO2 from the baseline of 40 millimeters of mercury, bicarbonates or HCO3 should increase by 1 in the acute, or by 4 in the chronic respiratory acidosis from their baseline of 24 mmol/L.

When it comes to alkalosis, for every 10 millimeters of mercury decrease of pCO2 from the baseline, bicarbonate should decrease by 2 for the acute, or 5 for the chronic respiratory alkalosis from the baseline.

Alright, let’s talk about underlying causes, starting with iatrogenic ones.

This is usually seen with hospitalized patients on respiratory support such as mechanical ventilation, so you'll need to check the ventilator settings. If either the respiratory rate or tidal volume is too low, or if there’s any evidence of equipment failure, your patient might not be exhaling enough carbon dioxide. In this case, diagnose iatrogenic hypoventilation.

Here’s another clinical pearl! Other major causes of iatrogenic respiratory acidosis include medications that primarily work by depressing the CNS activity. Examples include anesthetic agents like propofol, sedatives like benzodiazepines, and opioids such as morphine.

Let’s move on to the central nervous system, or CNS-related causes.

These can lead to a decrease in the activity of the respiratory centers in the brainstem.

Examples include intracranial pathologies, such as brainstem stroke or trauma, substance abuse, and alcohol intoxication.

First up are intracranial pathologies. The history might reveal an acute onset of headache, and risk factors for stroke such as high blood pressure, smoking, or atrial fibrillation. Also, don’t forget to ask about any recent head trauma.

The physical exam reveals a decreased respiratory rate, and possibly altered mental status, or focal neurological deficits like slurred speech. With these findings, consider intracranial pathology, and order a head CT scan or MRI.