Peter Jebson

Continuous Fick cardiac output compared to thermodilution cardiac output.

A system has been developed to monitor continuously the components of the oxygen Fick equation: oxygen consumption by a gas exchange analyzer and arterio-venous oxygen difference by pulse and fiberoptic oximetry. A computer-based system was developed which calculates cardiac output and other variables every 20 sec. Continuous Fick (CF) cardiac output was compared to thermodilution (TD) cardiac output in 21 ventilated post-cardiac surgery patients. A total of 237 simultaneous cardiac output measurements had a range between 2 and 11 L/min. The correlation between CF and TD cardiac outputs was r =.86, with an equation of TD cardiac output = 0.92 CF cardiac output + 1.16. There was a significant (p <.001) difference between the two methods of cardiac output estimation. The CF method was consistently lower than TD; this difference was greater at lower flows. CF cardiac output measurement is practical; it offers distinct advantages in viewing cardiac output together with oxygen demand and oxygen extraction.

Stable and reproducible porcine model of acute lung injury induced by oleic acid

Background and Methods.Previous studies on acute lung injury induced with oleic acid did not attempt to limit the influence of secondary changes on pulmonary circulation, and cardiopulmonary variable data were only collected and processed intermittently. Our study was designed to continuously monitor the following variables in five swine: systemic and pulmonary pressure; mixed venous oxygen saturation (Sao2) and arterial oxygen saturation (Sao2); minute oxygen consumption and CO2 production before, during, and for 4 hr after the infusion of oleic acid. A personal computer was programmed to produce 20-sec updates of deadspace ratio (VD/VT), venous admixture (Qsp/Qt), pulmonary (PVR) and systemic vascular resistance (SVR), and cardiac output (Qt) from these data. Results.During the oleic acid infusion, there were increases in PVR, SVR, heart rate (HR), mean pulmonary arterial pressure (MPAP), Qsp/Qt, and VD/VT, and a decrease in Qt, Sao2, and Svo2. Thirty minutes after the oleic acid infusion, there was a further increase in HR, Qsp/Qt, and VD/VT, while MPAP, PVR, and SVR gradually decreased to pre-oleic acid infusion levels. No further decrease in Sao2, Svo2, and Qt was observed during that time. After the 30-min period, there was no further change in the cardiopulmonary variables.Conclusion: Our method of continuous monitoring was able to demonstrate in swine both the dynamic changes during, and stability after, the oleic acid infusion. (Crit Care Med 1991; 19:405)

Continuous Fick Cardiac Output Compared to Continuous Pulmonary Artery Electromagnetic Flow Measurement in Pigs

A system for continuous Fick cardiac output measurement (CFCO) is described and compared to continuous electromagnetic pulmonary artery flow (EMCO) and intermittent thermodilution (TDCO) measurements. Oxygen consumption was determined from continuous respiratory gas exchange analysis and arterio-venous oxygen difference from fiberoptic oximetry. A computer calculated cardiac output and other variables every 20 s. Seven pigs were monitored for a total of 10 h, during which cardiac output was manipulated by obstructing venous return or infusing epinephrine. 1748 pairs of EMCO and CFCO values were compared. The best correlation was obtained when CFCO was advanced 20 s with respect to EMCO (R = .89, CFCO = .99 EMCO + .16). TDCO was compared to EMCO during periods of steady state (R = .85, TDCO = .89 EMCO + 1.25, N = 139). TDCO was also compared with simultaneous CFCO (R = .87, TDCO = .89 CFCO + 1.01, N = 251). CFCO is recommended as a reliable standard of continuous cardiac output measurement. It is not a real time measurement; the technique has a time lag of approximately 20 s which is the result of the time constant of the VO2 measurement. Sources for error are discussed with suggestions for improving quality control.

Swine model of early adult respiratory distress syndrome induced by intravenous ethchlorvynol

Although ethchlorvynol (ECV) has been used to induce pulmonary damage in animals, changes after injection of this drug have not been studied, nor has the stability of the animal been assessed after injection. Continuously monitored hemodynamic and respiratory changes were followed during and after iv injection of 55 mg/kg ECV in ethanol into anesthetized, paralyzed, and ventilated swine (n = 5) and compared to changes in a control group given ethanol alone (n = 5). Arterial and mixed venous saturations were measured by fiberoptic vascular catheters and oxygen exchange by a gas monitor. Twelve direct and derived variables were monitored every 20 sec using a computer data acquisition system. Arterial oxygen saturation was kept at 90 +/- 2% by adjustment of FIO2. Ethanol produced only transitory changes during infusion. Significant elevations in pulmonary vascular resistance (PVR), shunt (Qsp/Qt) and deadspace (VD/VT) were observed during and after ECV. These were unaccompanied by changes in cardiac output or arterial pressure. PVR increased by 137%, Qsp/Qt by 67%, and VD/VT by 28% over 30 min. These changes were then sustained in the postinfusion period, producing a stable model of early adult respiratory distress syndrome for 3.5 h.

Reduced venous admixture in hemorrhagic hypovolemia: maintenance of arterial oxygenation by selective pulmonary vascular collapse

In nine anesthetized and ventilated swine, a microcomputer calculated cardiac output, venous admixture (Qsp/Qt) and physiologic deadspace (VD/VT) every 20 sec, utilizing dual oximetry and a gas exchange analyzer. After lung injury with ethchlorvynol (ECV), animals were bled 40% blood volume over 40 min. Mean cardiac output decreased 7.0 to 2.2 L/min (p < .05) accompanied by a decrease in mean Qsp/Qt from 0.28 to 0.14 (p < .05) and an increase in mean VD/VT from 0.39 to 0.54 (p < .05). Arterial Hgb saturation (Sao2) increased from 88 ± 7% to 90 ± 6%. On regression of all data points for each variable, Qsp/Qt had a positive correlation with cardiac output (r = .90), mean arterial pressure (MAP, r = .87), mean pulmonary artery pressure (MPAP, r = .86), and mixed venous Hgb saturation (Svo2, r = .89, p < .001). VD/VT had an inverse correlation with cardiac output (r = −.90), MAP (r = −.82), Qsp/Qt (r = −.83), MPAP (r = −.77), and Svo2 (r = −.92, p < .001). The decreasing Qsp/Qt and increasing VD/VT, with decreasing pulmonary perfusion pressures, were attributed to selective loss of perfusion to alveoli with low ventilation/perfusion ratios. (Crit Care Med 1990; 18:208)