Pulmonary flow can be derived from a pulmonary arterial pressure curve for patients for which this pressure is routinely determined, such as patients who are undergoing intensive care, cardio-thoracic surgery or a catheterization for diagnostic reasons, without the use of a flow probe. To compute the pulmonary blood flow beat-to-beat for a specific haemodynamic condition from the arterial pressure curve a windkessel model should be used. To do so, the dynamic compliance of the pulmonary artery under the specified haemodynamic condition must first be known. Dynamic compliance is the change in cross-sectional area (CSA) related to the change in pulmonary arterial pressure (Ppa) during a heart beat. Static compliance is the change in mean CSA related to the change in mean Ppa. We define static compliance measured in vivo as pseudo-static compliance, because the pressure and CSA fluctuate cyclically during one heart beat.

This study was initiated to obtain data on the rate of carbon monoxide (CO) uptake (theta CO) by hemoglobin in pig erythrocytes to derive, in a later study, the pulmonary capillary blood volume (Qc) in pigs from the Roughton-Forster relationship. Blood from five different female pigs was used. The theta CO, the milliliters of CO taken up by 1 ml of whole blood per minute per Torr CO tension, was determined on each blood sample with a continuous-flow rapid-mixing apparatus and double-beam spectrophotometry at 37 degrees C and pH 7.4 at four or five different PO2 values. Because the individual regression lines of theta CO vs. PO2 were not significantly different, a common regression equation was calculated: 1/theta CO = 0.0084 PO2 + 0.63. The slope of this regression line is significantly steeper than the reported slopes of regression lines for human and dog erythrocytes measured under the same conditions. Our results revealed that calculation of Qc in pigs by using theta CO values for human or dog erythrocytes would result in an underestimation of 51 and 50%, respectively.

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To determine how much myocardial O2 consumption (VO2) would increase during an additional load on the heart in shunt as compared with control lambs, we studied 12 7-wk-old lambs with an aortopulmonary left-to-right shunt (59 +/- 3% of left ventricular output, mean +/- SE) and 11 control lambs during exercise at 80% of their predetermined peak VO2 (VO2peak), at 12 +/- 1 days after surgery. During exercise, systolic aortic pressure increased by 25% in the two groups. Left atrial pressure and left ventricular stroke volume did not change significantly and remained considerably higher in shunt than in control lambs. Heart rate, however, increased less in shunt than in control lambs (163 +/- 8 to 235 +/- 8 vs. 107 +/- 7 to 230 +/- 8 beats/min). The same was true for left ventricular myocardial blood flow (245 +/- 19 to 391 +/- 27 vs. 128 +/- 10 to 320 +/- 45 ml.min-1 x 100 g-1) and myocardial VO2 (847 +/- 101 to 1,692 +/- 136 vs. 528 +/- 58 to 1,579 +/- 178 mumol O2 x min-1 x 100 g-1). We conclude that, despite the volume load, myocardial VO2 of shunt lambs does not increase to a greater extent than in control lambs during a considerable additional load on the heart.

We studied the effect of increasing alveolar volume on pulmonary carbon monoxide transfer (DLCO) and its components, i.e. membrane diffusing capacity (DM) and capillary blood volume (Qc), during mechanical ventilation in eight anaesthetized and paralysed healthy pigs (mean weight 11.2 kg). We used an inspiratory pause procedure for simulation of the single-breath technique, and inflated 15, 20, 25 and 30 ml kg-1 in random order. DM and Qc were derived using the Roughton-Forster equation. Per litre BTPS increase in effective VA, DLCO (inspiratory oxygen fraction 0.30) decreased on average by 11.8 mumol s-1 kPa-1, DM slightly increased by 2.7 mumol s-1 kPa-1 and Qc decreased by 241 ml. The increase in DM was much smaller than might be expected from the increase in VA, which we ascribe to a loss of the alveolar capillary membrane for gas transfer because of the concomitant decrease in Qc. The decrease in Qc may be explained by a squeezing effect of the intrapulmonary pressure rise on the alveolar wall and by stretching of lung tissue.