1. Description of the problem

Respiratory acidosis is caused by relative hypoventilation. Major risk is associated hypoxemia. Clinical importance depends on context and severity, and rate of change. pH effect is important. Respiratory acidosis is an expected part of planned mechanical hypoventilation in ICU (permissive hypercapnia).

Clinical features

Often combination of hypercapnia and hypoxia

Most effects are neurologic, ranging from anxiety and confusion to stupor to coma.

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Key management points

Management depends on the severity of hypoxemia, acidemia and patient’s physiological reserve.

Treat hypoxemia – oxygen +/- ventilation

Where possible reverse causes of altered mental state, particularly narcotics.

Ventilation – non-invasive or invasive

2. Emergency Management

Cardiopulmonary resuscitation

If pCO2 > 80 mmHg, particularly if pH < 7.10, immediate mechanical ventilation

Treat other medical or surgical emergencies, particularly intracranial.

Management points not to be missed

Do not miss hypoxemia.

Do not miss the cause for hypoventilation, particularly in a drowsy or unconscious patient:

  • drugs, especially narcotics

  • intracranial event

3. Diagnosis

Diagnostic tests

Key diagnostic test is partial pressure of carbon dioxide (pCO2) from arterial blood gasses.

Note that venous CO2 will often be only 5 mmHg greater than arterial.

Normal lab values

Arterial PCO2 reference range: 35 to 45 mmHg

Arterial pH reference range: 7.35 to 745

How do I know this is what the patient has?

pH < 7.35, CO2 > 45 mmHg, Standard base excess (SBE )> 0 mmol/L, bicarbonate >24 mmol/L

Differential diagnosis

Acidemia with a mixed disorder

Acidemia due to primary metabolic acidosis

Confirmatory tests

Check blood gas results for compensation or second disorder. Metabolic compensation will never be complete (pH > 7.40), and will take hours. Therefore early respiratory acidosis may appear uncompensated.

Compensation: metabolic side compensates for respiratory acidosis by increasing renal chloride excretion (retaining bicarbonate) leading to increased strong ion difference.

Metabolic side measured with corrected bicarbonate or standard base excess (SBE).

In acute respiratory acidosis: expected SBE + 0 mmol/L; expected bicarbonate mmol/L = 24 + 0.1 x (PCO2 – 40).

For both bicarbonate and base-excess range for this estimate is about +/- 2 mmol/L.

Underlying change will be chloride excretion leading to increased strong-ion difference.

In chronic respiratory acidosis there is adaptation (increase of compensatory effect), increased chloride excretion.

Measured by bicarbonate or standard base excess (SBE).

In acute respiratory acidosis: Expected SBE = 0.4 x (PCO2 – 40) mmol/L

Expected bicarbonate mmol/L = 24 + 0.35 x (PCO2 – 40)

4. Specific Treatment

Respiratory support
  • Oxygen

  • Ventilation

Non-invasive CPAP, BPAP

Endotracheal intubation – ventilation

Refractory cases

In refractory cases, consider:

Long-term ventilation including tracheotomy

After appropriate discussion, consider end-of-life care

5. Disease monitoring, follow-up and disposition

Expected response to treatment

If altered mental state is due to CO2 narcosis, expect improved mental state and pH with ventilation.

Key diagnostic test is arterial blood gasses. Increased ventilation with increased inspired oxygen should improve CO2, PO2, and pH.

Incorrect diagnosis

Patient fails to rouse with improved pH.

Consider respiratory compensation for metabolic alkalosis, Expected PaCO2 = 1.5 s (Bicarbonate + 8), or expected PaCO2 = 40 + SBE.


Medication review, especially pain relief and narcotics

Follow-up of underlying conditions


Respiratory acidosis is secondary to relative hypoventilation. The alveolar partial pressure of carbon dioxide, and arterial pCO2, is related to three factors: 1. inspired CO2 (usually zero but can increase in closed environments); 2. body CO2 production; and 3. (inversely) alvolar ventilation.

PCO2 = inspired CO2 + CO2 production / ventilation.

If inspired CO2 is zero this is simplified to PCO2 = CO2 production/ventilation.

The most common cause of increased PCO2 is an absolute decrease in ventilation. Increased CO2 production without increased ventilation, such as a patient with sepsis, can also cause respiratory acidosis. Patients who have increased physiological dead space (eg, emphysema) will have decreased effective ventilation.

Increased partial pressure of carbon dioxide will lead to increased acidity.

Underlying causes

CNS depression


Central sleep apnea

Intracranial lesion

Neuromuscular disorders

Myasthenia gravis


Motor neurone disease

Spinal cord injury

Muscular dystrophy

Multiple sclerosis

Chest wall, including diaphragm




Abdominal distention

Airway obstruction

Foreign body

Obstructive sleep apnea


Lung disease

Chronic obstructive airways disease

Severe asthma or pneumonia


Mechanical ventilation: inadvertent or planned hypercapnia

Increased CO2 production with fixed alveolar ventilation – sepsis

Dead space: Relative alveolar hypoventilation secondary to chronic obstructive airways disease.


Mild to moderate respiratory acidosis is very common in surgical patients. Chronic hypercapnia without other signs of respiratory or neuromuscular diasease is unusual.


Depends on underlying cause (eg, excess narcotics vs. intracranial hemorrhage).

Special considerations for nursing and allied health professionals.


What's the evidence?

Abelow, B. Understanding Acid-Base. 1998. (An easy-to-read but comprehensive text that covers both physiology and treatment of acid-base disorders using a bicarbonate-centered view of the non-respiratory side. No mention of base -excess.)

Gennari, FJ, Adrogue, HJ, Galla, JH, Madias, NE. “Acid-Base Disorders and Their Treatment”. 2005. (A more detailed text that highlights some of the clinical chemistry associations of respiratory acid-base changes. Again bicarbonate-centered.)

Kellum, JA, Elbers, PWG. Stewart's Textbook of Acid-Base. 2009. (A re-issue and extended edition of Stewart's landmark text. Detailed explanation of the Stewart and base-excess approaches.)

Swenson, E. “Sepsis and therapeutic hypercapnia: sailing too close to the wind?”. Anesthesiology. vol. 112. 2010. pp. 462-472.