Exacerbation of hypercapnia and acidosis of central venous blood and tissue following administration of sodium bicarbonate during cardiopulmonary resuscitation.

Administration of sodium bicarbonate during cardiopulmonary resuscitation (CPR) is controversial, and our aim was to elucidate whether or not its administration is beneficial by analyzing the acid-base status and the level of carbon dioxide in central venous blood during CPR, and their changes following administration of sodium bicarbonate. Six patients were studied. They had all been admitted to the intensive care unit (ICU), had already had pulmonary arterial or central venous catheters inserted, and had acute episodes of circulatory collapse during their stay in the ICU. The following phenomena were observed: 1) hypercapnia and acidosis of central venous blood were prominent during both cardiogenic shock and CPR, although arterial hypocapnia was maintained by hyperventilation; 2) administration of sodium bicarbonate during cardiogenic shock and CPR induced exacerbation of hypercapnia and acidosis of central venous blood; 3) when arterial hypercapnia was present due to disturbed ventilation, administration of sodium bicarbonate exacerbated hypercapnia and acidosis of both arterial and central venous blood; 4) administration of sodium bicarbonate did not induce hypercapnia of central venous blood in a septic shock patient in whom the septic hyperdynamic state was prevalent in spite of low systemic perfusion pressure. It was concluded that hypercapnia and acidosis of the central venous blood and tissues were exacerbated by administration of sodium bicarbonate during CPR, and that such an effect might be dependent on the severity of the decrease in tissue perfusion.