Session 2: Viability Index Scoring For Critical Cardiopulmonary and Extracorporeal Support Patients

Venoarterial CO2 Gradient & Survival

A p[v-a]CO₂ increase is related to the reduction in cardiac output. This suggests a state of shock in the form of poor capillary perfusion, whatever the cause. Because capillary transit time slows down as the cardiac output declines, there is a larger than normal accumulation of CO₂ per unit of venous blood. The capillaries are further overloaded as perfused capillary density declines. This results in fewer open capillaries to remove CO₂ from the tissues. These factors generate hypercapnea in the venous blood. The relationship is not linear because a change of cardiac output will result in the greatest increase in p[v-a]CO₂ (aka DPCO₂) in the lowest range of cardiac output. However a simple formula can be used clinically to estimate the cardiac index. In adults the formula is: Cardiac Index = 12.9 / p[v-a]CO₂. In infants the formula is: Cardiac Index = 18 / p[v-a]CO₂. Infants use a larger constant because of their greater production of CO₂/kg.
This figure illustrates the lethality of a larger than normal p[v-a]CO₂ in 454 ECMO patients. Those patients with an average p[v-a]CO₂ over time of less than 10 mmHg have the lowest mortality rate (15%). The mortality rate progressively increases until the average p[v-a]CO₂ exceeds 20 mmHg correlating to 100% lethality. Even though these patients are being supported by cardiopulmonary bypass in the form of ECMO, the accumulation of CO₂ in the tissues causes lethal complications often independent of the primary diagnosis. For example, a patient with a large p[v-a]CO₂ who is suffering from pulmonary hypertension may have an intracranial hemorrhage, renal failure, multiple organ failure or just simply failure to improve.