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
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).
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.
The consequences of failing to recognise acute respiratory failure include marked hypoxaemia, hyperkalaemia, cardiovascular instability, and cardiac arrest.
- 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
- Inadequate mechanical ventilation
- Cardiogenic pulmonary oedema
- Acute lung injury/acute respiratory distress syndrome
- Pulmonary fibrosis
- Status asthmaticus
- Primary alveolar hypoventilation
- Flail chest
- Ankylosing spondylitis
- 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
- Fever/malignant hyperthermia
- Insufflation of CO₂ into body cavity (e.g., laparoscopic surgery)
M. Bradley Drummond, MD
Pulmonary and Critical Care Medicine
University of North Carolina at Chapel Hill
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
EF has received fees from MC3 Cardiopulmonary and ALung Technologies.
Guy Soo Hoo, MD, MPH
Intensive Care Unit
West Los Angeles VA Healthcare Center
Clinical Professor of Medicine
Geffen School of Medicine
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)
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
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