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|Main symptoms of carbon dioxide toxicity, by increasing volume percent in air.|
|Specialty||Pulmonology, critical care medicine|
Hypercapnia (from the Greek hyper = "above" or "too much" and kapnos = "smoke"), also known as hypercarbia and CO2 retention, is a condition of abnormally elevated carbon dioxide (CO2) levels in the blood. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs. Carbon dioxide may accumulate in any condition that causes hypoventilation, a reduction of alveolar ventilation (the clearance of air from the small sacs of the lung where gas exchange takes place). Inability of the lungs to clear carbon dioxide leads to respiratory acidosis. Eventually the body compensates for the raised acidity by retaining alkali in the kidneys, a process known as "metabolic compensation".
Acute hypercapnia is called acute hypercapnic respiratory failure (AHRF) and is a medical emergency as it generally occurs in the context of acute illness. Chronic hypercapnia, where metabolic compensation is usually present, may cause symptoms but is not generally an emergency. Depending on the scenario both forms of hypercapnia may be treated with medication, with mask-based non-invasive ventilation or with mechanical ventilation.
Hypercapnia usually happens in the context of an underlying health condition, and symptoms may relate to this condition or directly to the hypercapnia. Specific symptoms attributable to early hypercapnia are dyspnea (breathlessness), headache, confusion and lethargy. Clinical signs include flushed skin, full pulse (bounding pulse), rapid breathing, premature heart beats, muscle twitches, and hand flaps (asterixis). The risk of dangerous irregularities of the heart beat is increased.
Hypercapnia is generally caused by hypoventilation, lung disease, or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide, such as from volcanic or geothermal activity, or by rebreathing exhaled carbon dioxide. In this situation the hypercapnia can also be accompanied by respiratory acidosis.
Acute hypercapnic respiratory failure may occur in acute illness caused by chronic obstructive pulmonary disease (COPD), chest wall deformity, some forms of neuromuscular disease (such as myasthenia gravis, and obesity hypoventilation syndrome. AHRF may also develop in any form of respiratory failure where the breathing muscles become exhausted, such as severe pneumonia and acute severe asthma. It can also be a consequence of profound suppression of consciousness such as opioid overdose.
Normal respiration in divers results in alveolar hypoventilation resulting in inadequate CO2 elimination or hypercapnia. Lanphier's work at the US Navy Experimental Diving Unit answered the question, "Why don't divers breathe enough?":
A variety of reasons exists for carbon dioxide not being expelled completely when the diver exhales:
Skip breathing is a controversial technique to conserve breathing gas when using open-circuit scuba, which consists of briefly holding one's breath between inhalation and exhalation (i.e., "skipping" a breath). It leads to CO2 not being exhaled efficiently. The risk of burst lung (pulmonary barotrauma of ascent) is increased if the breath is held while ascending. It is particularly counterproductive with a rebreather, where the act of breathing pumps the gas around the "loop", pushing carbon dioxide through the scrubber and mixing freshly injected oxygen.
In closed-circuit SCUBA (rebreather) diving, exhaled carbon dioxide must be removed from the breathing system, usually by a scrubber containing a solid chemical compound with a high affinity for CO2, such as soda lime. If not removed from the system, it may be reinhaled, causing an increase in the inhaled concentration.
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Hypercapnia normally triggers a reflex which increases breathing and access to oxygen (O2), such as arousal and turning the head during sleep. A failure of this reflex can be fatal, for example as a contributory factor in sudden infant death syndrome.
Hypercapnia can induce increased cardiac output, an elevation in arterial blood pressure (higher levels of carbon dioxide stimulate aortic and carotid chemoreceptors with afferents -CN IX and X- to medulla oblongata with following chrono- and ino- tropic effects), and a propensity toward cardiac arrhythmias. Hypercapnia may increase pulmonary capillary resistance.
Blood gas tests may be performed, typically by radial artery puncture, in the setting of acute breathing problems or other acute medical illness. Hypercapnia is generally defined as a arterial blood carbon dioxide level over 45 mmHg (6 kPa). Since carbon dioxide is in equilibrium with carbonic acid in the blood, hypercapnia drives serum pH down, resulting in respiratory acidosis. Clinically, the effect of hypercapnia on pH is estimated using the ratio of the arterial pressure of carbon dioxide to the concentration of bicarbonate ion, PaCO2/[HCO3-].
|Expected tolerance for useful activity on continued exposure to elevated CO2|
|0.5||lifetime||no detectable limitations (Note: refer to modern research in Carbon dioxide#Below 1% which shows measurable effects below 1%.)|
|1.5||> 1 month||mild respiratory stimulation|
|2.0||> 1 month|
|2.5||> 1 month|
|3.0||> 1 month||moderate respiratory stimulation|
|3.5||> 1 week|
|4.0||> 1 week||moderate respiratory stimulation, exaggerated respiratory response to exercise|
|4.5||> 8 hours|
|5.0||> 4 hours||prominent respiratory stimulus, exaggerated respiratory response to exercise|
|5.5||> 1 hours|
|6.0||> 0.5 hours||prominent respiratory stimulus, exaggerated respiratory response to exercise, beginnings of mental confusion|
|6.5||> 0.25 hours|
|7.0||> 0.1 hours||limitation by dyspnea and mental confusion|
The treatment for acute hypercapnic respiratory failure depends on the underlying cause, but may include medications and mechanical respiratory support. In those without contraindications, non-invasive ventilation (NIV) is often used in preference to invasive mechanical ventilation. In the past, the drug doxapram (a respiratory stimulant), was used for hypercapnia in acute exacerbation of chronic obstructive pulmonary disease but there is little evidence to support its use compared to NIV, and it does not feature in recent professional guidelines.
Very severe respiratory failure, in which hypercapnia may also be present, is often treated with extracorporeal membrane oxygenation (ECMO), in which oxygen is added to and carbon dioxide removed directly from the blood.
A relatively novel modality is extracorporeal carbon dioxide removal (ECCO2R). This technique removes CO2 from the bloodstream and may reduce the time mechanical ventilation is required for those with AHRF; it requires smaller volumes of blood flow compared to ECMO.
Hypercapnia is the opposite of hypocapnia, the state of having abnormally reduced levels of carbon dioxide in the blood.
Carbon dioxide can accumulate insidiously in the diver who intentionally holds the breath intermittently (skip breathing) in a mistaken attempt to conserve air