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

The Venoarterial CO2 Gradient

The magnitude of the accumulation of CO₂ within the tissues can be masked in the patient unless both arterial and venous blood gases are measured at the same time. In a real life example, an arterial blood gas, 7.31 / 48 / 375 (pH / pCO₂ / pO₂), is diagnosed as a mild respiratory acidosis. This interpretation would normally prompt an increase in the ventilator rate and/or airway pressure which tends to impair cardiac function. A venous blood gas drawn at the same time was 6.90 / 106 / 26. The venoarterial CO₂ gradient was shown to be a colossal 58 mmHg. An elevated venoarterial CO₂ gradient is associated with sub-optimal cardiac function and poor perfused capillary density. Increasing the ventilator rate or airway pressure in an ill conceived attempt to reduce the paCO₂ would further impair cardiac function and hasten this patient’s demise. This particular patient died from a large brain hemorrhage within 24 hours of being placed on ECMO. Contrary to the interpretation from the arterial blood gas, this patient did not have respiratory acidosis in the true sense that CO₂ was being retained at the pulmonary level. In fact, the lungs were working extremely well to reduce the pCO₂ from 106 to 48 mmHg and to increase the pO₂ from 27 to 375 mmHg. What was diagnosed as arterial hypercapnea was in reality ‘CO₂ breakthrough’ to the arterial blood due to the overwhelming inflow of CO₂ into the lungs by the venous blood. This indicates severe cardiac dysfunction and poor perfused capillary density resulting in a lethal intracellular acidosis caused by CO₂ accumulating in the tissues.
A second example illustrates how the arterial blood gas may appear hypocapnic while the venous blood gas is hypercapnic simultaneously. The arterial blood gas is 7.35 / 32 / 154 which can be interpreted as a mild metabolic acidosis with respiratory compensation. However, the venous blood gas is 7.29 / 57 / 37. There is no ‘CO₂ breakthrough’ yet, even though the venous CO₂ is elevated. But the venoarterial CO₂ gradient is 25 mmHg, much higher than the normal 7 mmHg. So if only the arterial blood gases were examined, there would be no laboratory confirmation that the patient’s cardiac function is sub-optimal and that tissue acidosis is critical. This patient also died of a large brain hemorrhage.
According to the Krogh model, the venoarterial CO₂ gradient can be used to assess the global degree of intracellular trapping of CO₂. The mortality rate will increase as the venoarterial CO₂ gradient increases until a point is reached beyond which no patient can survive.