Hypercapnia (Hypercarbia): Causes and Treatment
Definition of hypercapnia
Hypercapnia (or hypercarbia) is generally defined as an abnormally-high level of carbon dioxide (e.g., more than 45 mm Hg) in the arterial blood. Hypercarbia is a medical term that was more common many decades ago, but it is still popular in some areas of the world and among some medical professionals. We are going to use both terms ("hypercapnia" and "hypercarbia") interchangeably. The word "hypercapnia" is currently most-commonly used in emergency medicine and critical care.
Hypercarbia can be caused by different factors and conditions. Generally, there are 5 different “worlds” or situations, with different meanings of hypercarbia. They are all described below.
Content of this web page:
1. Hypercarbia in emergency medicine and critical care
2. Hypercapnia related to manipulation of artificial ventilation due to beneficial CO2 effects (e.g., permissive hypercapnia)
3. Hypercapnia during treatment with carbogen and physiological tests
4. Hypercarbia due to chronic diseases
5. Hypercapnia during breathing exercises
6. Treatment of hypercapnia
Severe hypercapnia can be a very serious concern for respiratory specialists, emergency and critical-care workers. It can be divided into chronic and acute.
Chronic hypercarbia can often accompany
compromise gas exchange in the lungs leading to inability of CO2 to
diffuse from the venous blood in the alveoli and/or inability of the
airways to provide normal ventilation of all alveoli. Common causes of
- respiratory diseases (e.g., asthma, bronchitis, emphysema, chronic lung disease - COPD)
- infectious diseases (bacterial pneumonia, bronchopneumonia, SARS or severe acute respiratory syndrome, botulism and pulmonary tuberculosis),
- inflammatory disorders (pulmonary sarcoidosis)
- cystic fibrosis (mucoviscidosis)
- neoplastic disorders (metastatic lung disease)
- pulmonary edema
- poisoning non-bacterial agents (asbestosis, berylliosis, coal workers lung or anthracosis, silicosis, and silicotuberculosis)
- metabolic disorders (obesity)
- sleep apnea syndrome
- primary hypoventilation
- Pickwick's syndrome.
Acute hypercapnia causes include
- status epilepticus
- congestive heart failure
- respiratory failure or pulmonary insufficiency
- asphyxia or suffocation
- respiratory dead space excess
- breathing pure oxygen
- ventilator malfunction
- presence of foreign bodies in airways
- respiratory arrest
- overdose of medical drugs or respiratory suppressants (e.g., sedative drugs, salicylate intoxication/overdose, curare, morphine and other opiates).
In this setting hypercarbia is a life-threatening condition that requires professional medical attention.
2. Hypercapnia caused by manipulation of artificial ventilation due to beneficial CO2 effects (e.g., permissive hypercapnia)
The fathers of respiratory physiology and the authors of the first medical textbooks on respiration definitely had a more objective view on the properties of CO2 (Haldane & Priestley, 1935; Henderson 1940). Later, the dangerous and unwise practice of indiscriminate use of pure (100%) oxygen became a norm in emergency care. However, since the 1990’s many respiratory professionals regained sanity. As a result, hundreds of clinical studies have been published in relation to permissive hypercapnia. (The term “permissive hypercapnia” defines a ventilatory strategy used for acute respiratory failure in which the lungs are ventilated with a low-inspiratory volume and pressure.)
Permissive hypercarbia is currently used for:
- preterm infants (Miller & Carlo, 2007)
- neonates (Toms & Ambalavanan, 2004; Varughese et al, 2002)
- pediatric acute lung injury (Rotta & Steinhorn, 2006)
- prevention of lung injuries (Lafgey et al, 2004)
- ARDS or acute respiratory distress syndrome (Lewandowski, 1996; Hickling & Joyce, 1995) and some other situations.
The terms “hypercapnia” and “hypercapnic” are also used in situations when CO2 gas is added to inspired air for treatment or testing various physiological effects. Gas mixtures (with 1%, 2%, 2.5%, or 5% CO2 and various O2 contents ranging from 20% to maximum) are used for testing patients with asthma, panic attacks, and for treating of cancer patients with carbogen mixtures for better oxygenation of tumors (carbogen gas, by definition, has only CO2 and O2). Note that during these studies the subjects usually do not have an elevated-CO2 level in the arterial blood. In fact, many of them have less than 40 mm Hg which is the normal-arterial-CO2 value. Thus, many researchers apply the term “hypercarbia” to a relative increase in arterial blood CO2 due to breathing an air with higher-CO2 content. (Furthermore, such CO2-rich air may trigger panic attacks and some subjects may even lower their already low-arterial-blood-CO2 values.)
Which health problems are routinely characterized by too-high-arterial-CO2 levels? This generally relates to severe forms of asthma, cystic fibrosis, COPD (emphysema and bronchitis included) and some other conditions with reduced-ventilation/perfusion ratio and hypoxemia (reduced oxygenation of the arterial blood). What is the mechanism or pathophysiology of these changes? Consider medical studies related to breathing rates in people with these conditions.
Ventilation rates (chronic diseases)
| All references or
click below for abstracts
|Normal breathing||6 L/min||-||Medical textbooks|
|Healthy Subjects||6-7 L/min||>400||Results of 14 studies|
|Asthma||13 (~+mn~2) L/min||16||Chalupa et al, 2004|
|Asthma||15 L/min||8||Johnson et al, 1995|
|Asthma||14 (~+mn~6) L/min||39||Bowler et al, 1998|
|Asthma||13 (~+mn~4) L/min||17||Kassabian et al, 1982|
|Asthma||12 L/min||101||McFadden, Lyons, 1968|
|COPD||14 (~+mn~2) L/min||12||Palange et al, 2001|
|COPD||12 (~+mn~2) L/min||10||Sinderby et al, 2001|
|COPD||14 L/min||3||Stulbarg et al, 2001|
|Cystic fibrosis||15 L/min||15||Fauroux et al, 2006|
|Cystic fibrosis||10 L/min||11||Browning et al, 1990|
|Cystic fibrosis*||10 L/min||10||Ward et al, 1999|
|CF and diabetes*||10 L/min||7||Ward et al, 1999|
|Cystic fibrosis||16 L/min||7||Dodd et al, 2006|
|Cystic fibrosis||18 L/min||9||McKone et al, 2005|
|Cystic fibrosis*||13 (~+mn~2) L/min||10||Bell et al, 1996|
|Cystic fibrosis||11-14 L/min||6||Tepper et al, 1983|
We see elevated minute ventilation (up to about 2-2.5 times more than the norm). This leads to low-alveolar-carbon-dioxide-levels. CO2 is a potent dilator of airways (bronchodilator) and is crucial for repair of alveoli (see references for hypocapnic-lung-injury effects below). As a result, overbreathing, is the main factor that destroys lung tissue in these groups of patients and worsens oxygen delivery to body cells.
There are additional effects of hyperventilation that cause: cell hypoxia; a suppressed immune system (hence, frequent respiratory infections); reduced efficiency of ion pumps in mucosal layers due to tissue hypoxia causing more viscous mucus (with devastating health effects in cystic fibrosis), overcooling and drying of airways, irritation of cough receptors located in the larynx and many other negative effects.
Numerous breathing exercises and techniques naturally cause increased CO2. Thus, hypercapnia is a normal outcome of Pranayama, the Buteyko- reduced-breathing exercise (the main breathing exercise in the Buteyko breathing technique), the Frolov breathing device therapy and the application of many other breathing devices due to increased-respiratory-dead volume (Samozdrav, Karbonic, Cosmic Breath, and many others).
Furthermore, clinical experience of Russian doctors suggests that people in super health with diaphragmatic breathing and only 3-8 breaths/minute for their automatic respiratory frequency at rest and about 2-4 L/min for minute ventilation have abnormally high arterial CO2 (e.g., more than 45 mm Hg), as it is clear from the Buteyko Table of Health Zones. Yoga masters also have very slow and light breathing at rest. For Dr. Buteyko quotes about yoga secret of super health, which is based on hypercapnia, visit the Yoga Breathing web page.
Treatment of hypercapnia generally relates to chronic conditions, such as severe asthma, chronic bronchitis, emphysema, and other disorders. For all these conditions, hypercapnia is accompanied by abnormally-low-oxygen saturation (hypoxemia) due to hyperventilation (see the Table above). The detailed information about treatment of hypercarbia can be found on the page Treatment of Hyperventilation, which also provides treatment for hypoxemia.
- Haldane JS and Priestley JG, Respiration, 2nd Edition,
Oxford University Press, 1935.
- Hasselbalch: Bioch. Zeitsch., 1912, xlvi (46), 416.
- Henderson Y, Professor, MD, PhD, Carbon Dioxide, from the: Cyclopedia of Medicine, 1940.
- Hickling KG, Joyce C. Permissive hypercapnia in ARDS and its effect on tissue oxygenation. Acta Anaesthesiol Scand Suppl. 1995; 107: 201-8.
- Laffey JG, O'Croinin D, McLoughlin P, Kavanagh BP. Permissive hypercapnia--role in protective lung ventilatory strategies. Intensive Care Med. 2004 Mar; 30(3): 347-56.
- Lewandowski K. Permissive hypercapnia in ARDS: just do it? Intensive Care Med. 1996 Mar;22(3):179-81.
- Miller JD, Carlo WA. Safety and effectiveness of permissive hypercapnia in the preterm infant. Curr Opin Pediatr. 2007 Apr; 19(2): 142-4.
- Rotta AT, Steinhorn DM. Is permissive hypercapnia a beneficial strategy for pediatric acute lung injury? Respir Care Clin N Am. 2006 Sep; 12(3): 371-87.
- Toms R, Ambalavanan N. Permissive hypercapnia during mechanical ventilation of neonates. Indian Pediatr. 2004 Aug; 41(8): 775-8.
- Varughese M, Patole S, Shama A, Whitehall J. Permissive hypercapnia in neonates: the case of the good, the bad, and the ugly. Pediatr Pulmonol. 2002 Jan; 33(1): 56-64.
- Woodgate PG, Davies MW. Permissive hypercapnia for the prevention of morbidity and mortality in mechanically ventilated newborn infants. Cochrane Database Syst Rev. 2001;(2):CD002061.
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