CO 2 anesthesia

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Classification according to ICD-10
T59 Toxic effect of other gases, vapors or other smoke
T59.7 carbon dioxide
ICD-10 online (WHO version 2019)

The medical term CO 2 anesthesia ( Coma hyperkapnicum ) describes unconsciousness as a result of an increased blood concentration of carbon dioxide (CO 2 ). This can result from internal processes as well as from external CO 2 effects.

physiology

Carbon dioxide is a product of metabolism of the body, which is formed in the cells and dissolved in the blood to the lungs is transported, where the air in the alveoli is discharged (alveoli) and exhaled by the exhaled air. Depending on the level of activity and metabolism, there is a lot or little CO 2 in the body; breathing must be adapted to the CO 2 attack. In healthy people, this happens primarily through the CO 2 content of the blood. An increase in the CO 2 - partial pressure leads (in healthy people) to increased respiratory drive and thus to increased respiratory activity, which in turn makes the CO 2 sink partial pressure. The normal range for the CO 2 partial pressure of the blood is 4.6 to 5.9  kPa (35 to 45  mmHg ; corresponds to 4.5 to 5.8 percent by volume at normal pressure ). Approximately from a CO 2 - partial pressure be expected from 7.8 to 9.1 kPa (60 to 70 mmHg and 7.7% to 9.0%) has a consciousness to unconsciousness, patients with chronic CO 2 -Increase can sometimes also tolerate significantly higher values.

Endogenous CO 2 anesthesia

In the medical field, endogenous CO 2 anesthesia also occur, in which the carbon dioxide comes from the body's own respiratory metabolism. Inadequate breathing movement ( hypoventilation ), measured against current needs , leads to the accumulation of carbon dioxide in the blood ( hypercapnia ), which in severe cases can lead to clouding of consciousness, unconsciousness ( coma ) and ultimately death. Causes of such reduced ventilation can be:

  • Poisoning or overdosing of medication or drugs that affect breathing
  • Traumatic causes, for example after severe chest injuries with impaired breathing
  • If CO 2 anesthesia occurs in connection with respiratory failure in the case of severe obesity , it is also known as Pickwick syndrome .

Modern concepts that view the exhaustion of the breathing pump as the cause of an increase in the partial pressure of CO 2 and attribute daytime sleepiness to disturbed sleep at night due to poor breathing have recently pushed the role of CO 2 anesthesia as a cause of sleepiness into the background. Terminal hypercapnia with respiratory arrest is seen here more as a sign of total exhaustion of the breathing pump. According to this, the respiratory arrest does not come about through hypercapnia, but is indicated by the increasing hypercapnia. According to these concepts, ventilation therapy does not primarily serve to normalize the CO 2 , but rather, when used intermittently , should contribute to the recovery of the breathing pump. With a recovered breathing pump, the patient can then exhale more CO 2 in the ventilator-free interval , which means that the CO 2 partial pressure can be reduced. The administration of oxygen here is even often useful and necessary because such a patient with a respiratory pump problem can further relieve his respiratory pump without the risk of further oxygen drop what he by a setpoint adjustment for the CO 2 - partial pressure indicates.

The drowsiness in Pickwick syndrome , which is also known today as obesity hypoventilation syndrome, is due to the accompanying sleep-related breathing disorder.

Oxygen therapy-related CO 2 anesthesia

The danger of CO 2 anesthesia plays a special role in patients with chronically increased CO 2 partial pressure, mostly as a result of chronic lung disease. In such patients, an uncontrolled supply of additional oxygen can lead to an increase in CO 2 in the blood. The reasons for this are as follows:

Disruption of blood flow in the lungs

Poorly ventilated (poorly ventilated) sections of the lungs are excluded from the blood flow ( perfusion ) by the body ( Euler-Liljestrand mechanism ), whereby the blood is diverted to better-ventilated sections. This mechanism is controlled by the oxygen concentration in the alveoli and is also called hypoxic pulmonary vasoconstriction. The uncontrolled supply of additional oxygen also causes high concentrations of oxygen to reach poorly ventilated sections of the lungs, which are then supplied with more blood again. This misdirection of blood in the lungs (shunting) means that less CO 2 can be exhaled and the CO 2 in the blood increases.

Disruption of CO 2 transport in hemoglobin

5–10% of the CO 2 in the blood is bound to hemoglobin and transported. Deoxygenated hemoglobin can transport more CO 2 than oxygenated hemoglobin ( Haldane effect ). Due to the uncontrolled supply of oxygen and increasing oxygen saturation, less CO 2 can be transported. Up to 25% of the CO 2 increase in the above Patients can be explained by the Haldane effect.

Questionable disorder of respiratory drive

Contrary to what is often suggested, the respiratory drive in the above-mentioned Oxygen supply does not significantly decrease patients. Several studies showed no relevant influence of oxygen administration on minute ventilation. Respiratory arrest is unthinkable this way. Rather, the two causes mentioned first lead to an increase in CO 2 , which can lead to CO 2 anesthesia, which then causes respiratory arrest in the end stage.

Exogenous CO 2 anesthesia

CO 2 anesthesia due to external causes (excessive CO 2 content in the ambient air) usually occurs as an accident. Well-known examples are deaths in fermentation cellars, in agricultural silos and in wells. Often thoughtless helpers who want to rescue a person at the scene of the accident also become victims of the anesthesia themselves due to the odorless and therefore imperceptible CO 2 .

In addition to the use of electric shock and bolt- firing methods, CO 2 anesthesia is used on a large scale to stunning animals before slaughter .

See also

Individual evidence

  1. ^ Wilson F Abdo, Leo MA Heunks: Oxygen-induced hypercapnia in COPD . In: Critical Care . 16, No. 5, 2012. doi : 10.1186 / cc11475 .
  2. ^ Matthew Cross: Physics, pharmacology, and physiology for anesthetists: key concepts for the FRCA . Cambridge University Press, Cambridge NY 2014, ISBN 978-1-107-61588-5 .