DEVELOPMENT OF A FIVE-VA/Q COMPARTMENT LUNG COMPUTER MODEL
P.H. Breen, D.H. Chien, Joy L. Johnson · Anesthesia & Analgesia · 1999
S409 INTRODUCTION: We have developed a 5-compartment computer model of alveolar ventilation/perfusion (VA/Q) heterogeneity in the lung during steady-state conditions. This model can test mechanisms of CO2 and O2 gas kinetics during cardio-pulmonary perturbations in anesthesia or critical care medicine, such as causes of hypercarbia in trauma patients. METHODS: Physiologically and therapeutically, the lung is divided into 5 VA/Q compartments: shunt, low VA/Q unit, normal lung, high VA/Q unit, and alveolar dead space (VDalv) (see Figure 1). VA and Q are independently chosen to the 4 outlying compartments, which are subtracted from the central normal compartment to reduce the degrees of freedom. Other input variables ("Global Inputs" tab) included inspired gas fractions (FIO2 =0.5), hemoglobin, acid-base balance, etc. The model was solved in 2 steps: Step 1: For a chosen mixed venous point, for each compartment, PACO2 and PAO2 were found where the blood R and gas R lines intersect [1]. Step 2: The mixed venous point was adjusted (repeating Step 1 after each change) until pulmonary CO2 and O2 transfer equaled the values of tissue metabolism (VCO2 =240 ml/min, VO2 =300 ml/min). We tested potential mechanisms of hypercarbia in trauma victims under anesthesia. In addition to global hypoventilation and significant wasted ventilation, we examined a decrease in QT (CO2 retention in the peripheral tissue compartment) and severe pulmonary shunt (e.g. high right atrial pressure and probe-patent foramen ovale; CO2 in venous return bypasses the lung).Figure 1RESULTS: Figure 1 displays the normal lung, with most ventilation and perfusion delivered equally to the central compartment (unit C, VA/Q=1). Mixed venous PCO2 (PvCO2) was 50.2 mm Hg, PaCO2 was 43.0 mm Hg, and end-tidal PCO2 (PETCO2, actually average alveolar expired PCO2) [2] was 41.4 mm Hg. Further data is displayed in the scrollable lower output window. The model finds a solution in 5-15 sec, even with all 5 compartments activated. We then examined hypercarbia in trauma anesthesia. When global QT decreased from 5 to 2.5 L/min, PVCO2 increased from 50 to 57 mm Hg but PaCO (2) basically did not change. A 40% shunt mildly increased PVCO2 (50 to 55 mm Hg) and PaCO2 (43 to 49 mm Hg). However, a 40% decrease in global ventilation or addition of 40% VDalv vigorously increased PVCO2 (50 to 81 mm Hg) and PaCO2 (50 to 72 mm Hg). DISCUSSION: The use of 5 VA/Q compartments in the lung model allows pathophysiological and clinical correlates over the range of gas kinetics aberrations found in clinical anesthesia, while limiting the degrees of freedom to permit a solution with input of typically measured cardiopulmonary variables. The exploration of hypercarbia in trauma anesthesia demonstrates the utility of the model. A decrease in global QT caused only a mild redistribution of CO2 to the tissue compartment. Pulmonary shunting caused only mild venous and arterial hypercarbia because the remaining lung, that received all of the perfusion, was relatively hyperventilated. Thus, global hypoventilation (decreased VA) or wasted ventilation (VDalv or high VA/Q regions) must be present if severe hypercarbia develops during trauma anesthesia. Supported by: NIH grant HL-42637.