Monitoring in the Intensive Care

Figure 2

Venoarterial PCO₂ gradient: relationship to cardiac output and capillary hypoperfusion. (a) Schematic representation of the circulation (arterial in red, venous in blue, R.A: right atrium, L.A: left atrium, R.V: right ventricle, L.V: left ventricle, I: intestine, L: liver) and a generic capillary bed. (b) Schematic representation of both a hypoperfused capillaries (dashed lines) and normally perfused capillaries (continuous lines) receiving increased perfusion redistributed from the hypoperfused capillary. CO₂ builds up in the tissue adjacent to hypoperfused capillaries (gray cylinders). Due to its highly diffusible nature, accumulated CO₂ from hypoperfused tissue diffuses to tissue adjacent to perfused capillaries which successfully “washout” this increased amount of CO₂ leading to higher venous PCO₂ than normal and therefore a venoarterial PCO₂ gradient, P(v-a)CO₂, higher than the upper norm of 6 mmHg. (c) Relationship between P(v-a)CO₂ and cardiac output (CO). P(v-a)CO₂ decreases along an isopleth for a given metabolic production of CO₂ (VCO₂). For “normal” cardiac outputs over 4 L/min and normal VCO₂ (green area), P(v-a)CO₂ remains under the upper threshold of 6 mmHg. Decreased cardiac output below 4 L/min leads to increased P(v-a)CO₂ due to insufficient “washout” regardless of capillary perfusion. P(v-a)CO₂ increases over 6 mmHg in conditions of adequate cardiac output, and normal VCO₂ is pathological and reflects capillary hypoperfusion (off-isopleth orange area).