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Hypercapnia (from the Greek hyper, "above" or "too much" and kapnos, "smoke"), also known as hypercarbia and CO 2 retention, is a condition of abnormally elevated carbon dioxide (CO 2) levels in the blood. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs.
Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia ; a rise in arterial carbon dioxide levels is called hypercapnia .
Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction ...
Hypocapnia (from the Greek words ὑπό meaning below normal and καπνός kapnós meaning smoke), also known as hypocarbia, sometimes incorrectly called acapnia, is a state of reduced carbon dioxide in the blood. [1] Hypocapnia usually results from deep or rapid breathing, known as hyperventilation. Hypocapnia is the opposite of hypercapnia.
Meaning Origin language and etymology Example(s) a-, an-not, without (alpha privative) Greek ἀ-/ἀν-(a-/an-), not, without analgesic, apathy, anencephaly: ab-from; away from Latin abduction, abdomen: abdomin-of or relating to the abdomen: Latin abdōmen, abdomen, fat around the belly abdomen, abdominal -ac: pertaining to; one afflicted with
As a side effect of medicines or recreational drugs, hypoventilation may become potentially life-threatening.Many different central nervous system (CNS) depressant drugs such as ethanol, benzodiazepines, barbiturates, GHB, sedatives, and opioids produce respiratory depression when taken in large or excessive doses, or mixed with other depressants.
Causes may include heart failure, kidney failure, narcotic poisoning, intracranial pressure, and hypoperfusion of the brain (particularly of the respiratory center). The pathophysiology of Cheyne–Stokes breathing can be summarized as apnea leading to increased CO 2 which causes excessive compensatory hyperventilation, in turn causing decreased CO 2 which causes apnea, restarting the cycle.
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