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| Hypercapnia | |
|---|---|
| Other names | Hypercarbia, CO2 retention, carbon dioxide poisoning |
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| Main symptoms of carbon dioxide toxicity, by increasingvolume percent in air.[1][2] | |
| Specialty | Pulmonology,critical care medicine |
Hypercapnia (from theGreekhyper, "above" or "too much" andkapnos, "smoke"), also known ashypercarbia andCO2 retention, is a condition of abnormally elevatedcarbon dioxide (CO2) levels in the blood. Carbon dioxide is agaseous product of thebody'smetabolism and is normally expelled through thelungs. Carbon dioxide may accumulate in any condition that causeshypoventilation, a reduction ofalveolar ventilation (the clearance of air from the small sacs of the lung wheregas 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 torespiratory acidosis. Eventually the body compensates for the raised acidity by retaining alkali in the kidneys, a process known as "metabolic compensation".
Acute hypercapnia is calledacute 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-basednon-invasive ventilation or withmechanical ventilation.
Hypercapnia is a hazard of underwater diving associated with breath-hold diving, scuba diving, particularly on rebreathers, and deep diving where it is associated with highwork of breathing caused by increased breathing gas density due to the high ambient pressure.[3][4][5]
Hypercapnia may happen 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 aredyspnea (breathlessness), headache, confusion and lethargy. Clinical signs include flushed skin, fullpulse (bounding pulse),rapid breathing,premature heart beats, muscle twitches, and hand flaps (asterixis). The risk of dangerousirregularities of the heart beat is increased.[6][7] Hypercapnia also occurs when the breathing gas is contaminated with carbon dioxide, or respiratory gas exchange cannot keep up with the metabolic production of carbon dioxide, which can occur when gas density limits ventilation at high ambient pressures.[3]
In severe hypercapnia (generally greater than 10kPa or 75mmHg), symptomatology progresses to disorientation,panic,hyperventilation,convulsions,unconsciousness, and eventuallydeath.[8][9]
Carbon dioxide is a normal metabolic product but it accumulates in the body if it is produced faster than it is cleared. During strenuous exercise the production rate of carbon dioxide can increase more than tenfold over the production rate during rest. Carbon dioxide is dissolved in the blood and elimination is by gas exchange in the lungs during breathing.[10] Hypercapnia is generally caused byhypoventilation,lung disease, or diminishedconsciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide, such as from volcanic or geothermal activity, or byrebreathing exhaledcarbon dioxide. In this situation the hypercapnia can also be accompanied byrespiratory acidosis.[11]
Acute hypercapnic respiratory failure may occur in acute illness caused bychronic obstructive pulmonary disease (COPD), chest wall deformity, some forms ofneuromuscular disease (such asmyasthenia gravis), andobesity hypoventilation syndrome.[12] AHRF may also develop in any form of respiratory failure where the breathing muscles become exhausted, such as severepneumonia andacute severe asthma. It can also be a consequence of profound suppression of consciousness such asopioid overdose.[citation needed]
Normal respiration in divers results inalveolarhypoventilation resulting in inadequate CO2 elimination or hypercapnia. Lanphier's work at theUS Navy Experimental Diving Unit answered the question, "Why don't divers breathe enough?":[13]
A variety of reasons exist for carbon dioxide not being expelled completely when the diver exhales:
Skip breathing is a controversial technique to conservebreathing gas when usingopen-circuit scuba, which consists of briefly holding one's breath between inhalation and exhalation (i.e., "skipping" a breath). It can lead to CO2 not being exhaled efficiently.[19] The risk of burst lung (pulmonary barotrauma of ascent) is increased if the breath is held while ascending. It is particularly counterproductive with arebreather, 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-circuitrebreather diving, exhaled carbon dioxide must be removed from the breathing system, usually by ascrubber containing a solid chemical compound with a high affinity for CO2, such assoda lime. If not removed from the system, it may be reinhaled, causing an increase in the inhaled concentration.[20]
Under hyperbaric conditions, hypercapnia contributes tonitrogen narcosis andoxygen toxicity by causing cerebral vasodilation which increases the dosage of oxygen to the brain.[18]
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Hypercapnia normally triggers a reflex which increases breathing and access tooxygen (O2), such as arousal and turning the head during sleep. A failure of this reflex can be fatal, for example as a contributory factor insudden infant death syndrome.[21]
Hypercapnia can induce increased cardiac output, an elevation in arterial blood pressure (higher levels of carbon dioxide stimulate aortic and carotidchemoreceptors with afferents -CN IX and X- to medulla oblongata with followingchrono- andino-tropic effects),[clarification needed] and a propensity towardcardiac arrhythmias. Hypercapnia may increase pulmonary capillary resistance.[citation needed]
A high arterial partial pressure of carbon dioxide () causes changes in brain activity that adversely affect both fine muscular control and reasoning.EEG changes denoting minor narcotic effects can be detected for expired gasend tidal partial pressure of carbon dioxide () increase from 40 torrs (0.053 atm) to approximately 50 torrs (0.066 atm). The diver does not necessarily notice these effects.[10]
Higher levels of have a stronger narcotic effect: Confusion and irrational behaviour may occur around 72 torrs (0.095 atm), and loss of consciousness around 90 torrs (0.12 atm). Hightriggers the fight or flight response, affects hormone levels and can cause anxiety, irritability and inappropriate or panic responses, which can be beyond the control of the subject, sometimes with little or no warning. 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 of 50 torrs (0.066 atm), Intracranial pressure may rise, with a throbbing headache. If associated with a high the high delivery of oxygen to the brain may increase the risk of CNS oxygen toxicity at partial pressures usually considered acceptable.[10]
In many people a high causes a feeling of shortness of breath, but the lack of this symptom is no guarantee that the other effects are not occurring. A significant percentage of rebreather deaths have been associated with CO2 retention. The effects of high can take several minutes to hours to resolve once the cause has been removed.[10]
| This sectionneeds expansion with: from Drechsler M, Morris J. Carbon Dioxide Narcosis. [Updated 2023 Jan 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from:https://www.ncbi.nlm.nih.gov/books/NBK551620/. You can help byadding to it.(March 2023) |
Blood gas tests may be performed, typically byradial artery puncture, in the setting of acute breathing problems or other acute medical illness. Hypercapnia is generally defined as an arterial blood carbon dioxide level over 45 mmHg (6 kPa). Since carbon dioxide is in equilibrium withcarbonic 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,.[citation needed]
| %CO2 in inspired air | Expected tolerance for useful activity on continued exposure to elevated CO2 | |
|---|---|---|
| Duration | Major limitation | |
| 0.03 | lifetime | atmosphere, year 1780[22] |
| 0.04 | lifetime | current atmosphere |
| 0.5 | lifetime | no detectable limitations (Note: refer to modern research inCarbon dioxide#Below 1% which shows measurable effects below 1%.) |
| 1.0 | lifetime | |
| 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 |
Tests performed onmongrel dogs showed the physiological effect of carbon dioxide on the body of the animal: after inhalation of a 50% CO2 and 50% air mixture, respiratory movement increased for about 2 minutes, and then, it decreased for 30 to 90 minutes. Hill and Flack showed that CO2 concentrations up to 35% have an exciting effect upon both circulation and respiration, but those beyond 35% are depressant upon them.[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. The heart rate slowed slightly just after the gas mixture inhalation. It is believed that the initial BP depression with the decreased heart rate is due to the direct depressant effect of CO2 upon the heart and that the return of blood pressure to its original level was due to the rapid rise of. 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.
At higher concentrations of CO2, unconsciousness occurred almost instantaneously and respiratory movement ceased in 1 minute. After a few minutes of apnea, circulatory arrest was seen. These findings imply that the cause of death in breathing high concentrations of CO2 is not the hypoxia but the intoxication of carbon dioxide.[23]
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 toinvasive mechanical ventilation.[12] In the past, the drugdoxapram (a respiratory stimulant), was used for hypercapnia inacute 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.[12]
Very severe respiratory failure, in which hypercapnia may also be present, is often treated withextracorporeal membrane oxygenation (ECMO), in which oxygen is added to and carbon dioxide removed directly from the blood.[25]
A relatively novel modality isextracorporeal 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.[25][26]
Hypercapnia is the opposite ofhypocapnia, 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
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