Abstract
During cardiac arrest and cardio-pulmonary resuscitation (CPR) only limited blood flow and consequently organ perfusion can be maintained by chest compression. Cardiac output during CPR averages only 25 to 35% of normal and thus severely reduces oxygen delivery to the tissues. The metabolism therefore turns to its energetic emergency pathway resulting in the production of anaerobic metabolites. The buildup of lactic acid is slow, while the CO2 concentration rapidly increases during CPR. After onset of cardiac arrest intramyocardial CO2 progressively increases to levels exceeding 400 mmHg. These increases in CO2 can only be reversed by improving coronary blood flow and its associated oxygen delivery.
With support of the Swiss National Science Foundation.
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© 1990 Springer-Verlag Berlin Heidelberg
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von Planta, M. (1990). Acidosis in CPR: Pathophysiology and Treatment. In: Vincent, J.L. (eds) Update 1990. Update in Intensive Care and Emergency Medicine, vol 10. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84125-5_61
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DOI: https://doi.org/10.1007/978-3-642-84125-5_61
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