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:
Hypercarbia in emergency medicine and critical care
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
Hypercarbia due to chronic diseases
Hypercapnia during breathing exercises
Treatment of hypercapnia
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
In this setting hypercarbia is a life-threatening condition
requires professional medical attention.
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
(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
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.
“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
an air with higher-CO2 content. (Furthermore, such CO2-rich air may
trigger panic attacks and some subjects may even lower their already
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
|| Medical textbooks
|| Results of 14 studies
||13 (+-2) L/min
|| Chalupa et al, 2004
|| Johnson et al, 1995
||14 (+-6) L/min
|| Bowler et al, 1998
||13 (+-4) L/min
|| Kassabian et al, 1982
|| McFadden, Lyons, 1968
||14 (+-2) L/min
|| Palange et al, 2001
||12 (+-2) L/min
|| Sinderby et al, 2001
|| Stulbarg et al, 2001
||Fauroux et al, 2006
||Browning et al, 1990
||Ward et al, 1999
|CF and diabetes*
||Ward et al, 1999
||Dodd et al, 2006
||McKone et al, 2005
||13 (+-2) L/min
|| Bell et al, 1996
|| Tepper et al, 1983
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
Numerous breathing exercises and techniques
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 studies measured various respiratory parameters in meditating Buddhist monks. It was discovered that these people meditate in the state of severe hypoventilation. Experience of Russian doctors and ancient yoga Sanskrit texts also suggest that, with very slow and reduced breathing, people can achieve numerous amazing health effects. More information (specific effects on health) and exact numbers (which CO2 levels, breathing rates, maximum breath holding times, etc.) are provided on another web page. The link to this web page is provided below as your bonus content.
Yoga masters also have very slow and light breathing at rest. For quotes from ancient yoga books and their 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;
- 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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