Assessment of respiratory acidosis

Last reviewed: June 2019

Last updated: March 2019

Summary

Respiratory acidosis occurs when acute or chronic derangements of the respiratory system lead to inefficient clearance of carbon dioxide. These derangements may involve:

Primary disease of the lung parenchyma
Problems with the chest wall
Neuromuscular failure
A disorder of central control of ventilation.

When alveolar gas exchange units are unable to sufficiently excrete carbon dioxide, this leads to an increase in the arterial carbon dioxide levels above the normal range of 35 to 45 mmHg (4.7-6.0 kPa). With the increase in carbon dioxide, hydrogen ions accumulate, causing the arterial pH to fall below the normal range (i.e., <7.35). [1]

Respiratory acidosis may be acute or chronic. Acute respiratory acidosis is usually secondary to acute respiratory failure.

In acute respiratory failure, there is insufficient buffering capacity to handle the dramatic increase in arterial and venous carbon dioxide. Over time, more and more carbon dioxide is processed by carbonic anhydrase to bicarbonate (the Hamburger shift). This leads to chloride excretion by the kidney with ammonium, and the pH gradually rises. [2]

The consequences of failing to recognise acute respiratory failure include marked hypoxaemia, hyperkalaemia, cardiovascular instability, and cardiac arrest.

Differentials

Common

COPD
Multilobar pneumonia
Foreign body aspiration
Drug use (narcotics, alcohol, sedatives, anaesthetics)
Oxygen therapy in COPD
CNS infarct or haemorrhage
Head trauma
CNS infection
Hypoventilation syndrome in obesity
Pleural effusion
Pneumothorax
Obesity
Kyphoscoliosis
Hypokalaemia
Hypophosphataemia
Inadequate mechanical ventilation

Full details

Uncommon

Cardiogenic pulmonary oedema
Acute lung injury/acute respiratory distress syndrome
Pulmonary fibrosis
Status asthmaticus
Laryngospasm
Angio-oedema
Primary alveolar hypoventilation
Empyema
Haemothorax
Flail chest
Scleroderma
Ankylosing spondylitis
Fibrothorax
Hypothyroidism
Paralytic agents and organophosphates
High cord trauma/lesions (above C4)
Guillain-Barre syndrome
Multiple sclerosis
Myasthenia gravis
Muscular dystrophy
Amyotrophic lateral sclerosis
Polymyositis and dermatomyositis
Phrenic nerve trauma
Tetanus
Botulism
Poliomyelitis
Sepsis
Fever/malignant hyperthermia
Insufflation of CO₂ into body cavity (e.g., laparoscopic surgery)

Full details

Contributors

Authors VIEW ALL 

M. Bradley Drummond, MD

Associate Professor

Pulmonary and Critical Care Medicine

University of North Carolina at Chapel Hill

Chapel Hill

Disclosures

MBD declares that he has no competing interests.

Eddy Fan, MD, PhD

Associate Professor of Medicine

Interdepartmental Division of Critical Care Medicine

University of Toronto

Toronto General Hospital

Toronto

Canada

Disclosures

EF has received fees from MC3 Cardiopulmonary and ALung Technologies.

Peer reviewers VIEW ALL 

Guy Soo Hoo, MD, MPH

Director

Intensive Care Unit

West Los Angeles VA Healthcare Center

Clinical Professor of Medicine

Geffen School of Medicine

UCLA

Los Angeles

Disclosures

GSH declares that he has no competing interests.

Harman Paintal, MBBS

Division of Pulmonary and Critical Care Medicine

Veterans Affairs Palo Alto Health Care System (VAPAHCS)

Palo Alto

Disclosures

HP declares that he has no competing interests.

Patrick J. Neligan, MA, MB BcH, FCARCSI, FJFICM

Consultant in Anaesthesia and Intensive Care

Galway University Hospitals

Senior Lecturer in Anaesthesia

National University of Ireland

Galway Department of Anaesthesia and Intensive Care

University College Hospitals

Galway

Ireland

Disclosures

Not disclosed.

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Assessment of respiratory acidosis

Summary

Differentials

Common

Uncommon

Contributors

Authors VIEW ALL 

M. Bradley Drummond, MD

Disclosures

Eddy Fan, MD, PhD

Disclosures

Peer reviewers VIEW ALL 

Guy Soo Hoo, MD, MPH

Disclosures

Harman Paintal, MBBS

Disclosures

Patrick J. Neligan, MA, MB BcH, FCARCSI, FJFICM

Disclosures

Guidelines

Patient leaflets

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