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. However, hypercarbia can be caused by different factors and conditions. Generally, there are 5 different “worlds” or situations, with different meaning 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
1. Causes of hypercarbia related to emergency medicine and critical care
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
various respiratory
conditions that
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
hypercapnia include:
- 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
pulmonary),
- 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
- coma
- 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 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 medical 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.
3. Hypercapnia during treatment with carbogen and physiological tests
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 treatment 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 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.)
4. Hypercarbia due to chronic diseases
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.
Minute ventilation rates (chronic diseases)
| Condition | Minute ventilation |
Number of people |
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 |
| COPD | 14 (±2) l/min | 12 | Palange et al, 2001 |
| COPD | 12 (±2) l/min | 10 | Sinderby et al, 2001 |
| COPD | 14 l/min | 3 | Stulbarg et al, 2001 |
| Asthma | 13 (±2) l/min | 16 | Chalupa et al, 2004 |
| Asthma | 15 l/min | 8 | Johnson et al, 1995 |
| Asthma | 14 (±6) l/min | 39 | Bowler et al, 1998 |
| Asthma | 13 (±4) l/min | 17 | Kassabian et al, 1982 |
| Asthma | 12 l/min | 101 | McFadden & Lyons, 1968 |
| 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 (±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 destroy lung tissue in
these groups of patients and worsen oxygen delivery to body cells.
There are additional effects of hyperventilation that cause: cell hypoxia, the 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.
5. Hypercapnia during breathing exercises
Numerous breathing exercises and techniques
naturally cause
increased CO2. Thus, hypercapnia is a normal outcome of Pranayama,
Buteyko reduced breathing exercise (the main breathing exercise in the
Buteyko breathing technique), Frolov breathing device therapy and
application of many other breathing devices due to increased
respiratory dead volume (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 Yoga Breathing web page.
6. Treatment of hypercapnia or hypercarbia
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 that provides also treatment for hypoxemia.
References: CO2 Effects Web Pages
Vasodilation: CO2 expands arteries and arterioles facilitating perfusion
(or blood
supply) to all vital organs
The Bohr effect
How and why oxygen is released by red blood cells in tissues
Cell Oxygen Levels and oxygen transport are controlled by
alveolar CO2 and breathing
Oxygen Transport depends on
breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr
effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2
content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes
place due to anaerobic cell respiration caused by cell hypoxia. Hence,
antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by
breathing since hypoxia leads to or intensifies chronic inflammation through over-expression
of the hypoxia-inducible factor 1, while normal
breathing reduces these processes
Nerve stabilization takes place due to calmative or
sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells
is normal at high CO2, while hypocapnia causes muscular tension, poor posture
and, sometimes, aggression and violence
Brochodilation - dilation of
airways (bronchi and bronchioles) by carbon dioxide, and their constriction due
to hypocapnia
CO2: Best Natural Cough Suppressant
and "home remedy" since it calms urge-to-cough nerve receptors located in the
tracheobronchial tree and larynx
Blood
pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon
dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine
in the Brain, CO2 fixation, and other chemical reactions
CO2 myth
"CO2 is a toxic waste gas" myth
Breathing control
How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic?
References
- 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.
| Disclaimer | Copyright © 2011 Artour Rakhimov | About Artour | Contributions | Contact details | Promote this site |
