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 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) as well as resulting from inhalation of CO2.
Inability of the lungs to clear carbon dioxide, or inhalation of elevated levels of CO2, leads to respiratory acidosis.
Specific symptoms attributable to early hypercapnia are dyspnea (breathlessness), headache, confusion and lethargy.
greater than 10 kPa or 75 mmHg), symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death.
[8][9] Carbon dioxide is a normal metabolic product but it accumulates in the body if it is produced faster than it is cleared.
[11] 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.
Lanphier's work at the US Navy Experimental Diving Unit answered the question, "Why don't divers breathe enough?
[19] 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.
[5] In closed-circuit 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.
[18] Hypercapnia normally triggers a reflex which increases breathing and access to oxygen (O2), such as arousal and turning the head during sleep.
[21] 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),[clarification needed] and a propensity toward cardiac arrhythmias.
EEG changes denoting minor narcotic effects can be detected for expired gas end tidal partial pressure of carbon dioxide (
Vasodilation is another effect, notably in the skin, where feelings of unpleasant heat are reported, and in the brain, where blood flow can increase by 50% at a
Hypercapnia is generally defined as an arterial blood carbon dioxide level over 45 mmHg (6 kPa).
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,
[citation needed] The blood pressure (BP) decreased transiently during the increased respiratory movement and then rose again and maintained the original level for a while.
After 30–90 min, the respiratory center was depressed, and hypotension occurred gradually or suddenly from reduced cardiac output, leading to an apnea and eventually to circulatory arrest.
These findings imply that the cause of death in breathing high concentrations of CO2 is not the hypoxia but the intoxication of carbon dioxide.
[12] 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,[24] and it does not feature in recent professional guidelines.
[25][26] Hypercapnia is the opposite of hypocapnia, the state of having abnormally reduced levels of carbon dioxide in the blood.