45 research outputs found
Kennen en kunnen
REDE uitgesproken bij de aanvaarding van het ambt van gewoon lector in de beademingsleer en het longfunktieonderzoek aan de Erasmus Universiteit te Rotterdam op woensdag 8 september 197
Tidal variation of pulmonary blood flow and blood volume in piglets during mechanical ventilation during hyper-, normo- and hypovolaemia
Effects of changes in blood volume on changes in pulmonary blood flow and pulmonary blood volume during the ventilatory cycle during mechanical ventilation with a positive end-expiratory pressure of 2 cm H2O were determined in six pentobarbital anaesthetized, curarized pigs weighing about 10 kg. Haemodynamic variables were analysed for each cardiac cycle in eight ventilatory cycles in four consecutive series under hyper-, normo- and hypovolaemic conditions. Cardiac output was highest in hypervolaemia. Compared with normo- and hypovolaemia, it decreased less during inflation, due to a smaller rise in central venous pressure and presumably a larger filling state of the venous system. The smaller decrease in right ventricular output in hypervolaemia coincided with a larger fall in transmural central venous pressure (right ventricular filling pressure), due to right ventricular action at a higher, less steep part of its function curve. The difference between right ventricular-output (electromagnetic flow measurement) and left ventricular-output (pulse contour) indicated changes in pulmonary blood volume. In hypervolaemia less blood shifted from the pulmonary circulation into the systemic system during inflation than in normo- and hypovolaemia. This difference can be explained by two mechanisms namely, the smaller fall in input into the pulmonary vascular beds and a smaller pulmonary vascular volume decrease as a result of transmural pressure fall at a steeper part of the pressure-volume curve
Effects of endotoxin infusion on mean systemic filling pressure and flow resistance to venous return
Mean systemic filling pressure (Psf) is an indicator of the filling state of the systemic circulation. Cardiac output (Q′) is related linearly to the difference between Psf and central venous pressure (Pcv), according to:Q′ = (Psf -Pcv)/Rsf, where Rsf is the flow resistance downstream from the sites where blood pressure is equal to Psf In 16 anaesthetized pigs we evaluated Psf, Rsf and Q′ during baseline conditions, continuous endotoxin infusion and after subsequent fluid loading. Psf and Rsf were determined from simultaneous measurements of Q′ and Pcv at seven levels of lung inflation. The following results were obtained. Psf was 8.1 ±1.8 mm Hg (mean ± SD) during baseline conditions, increased after endotoxin infusion to 9.9 ± 3.2 mm Hg (P = 0.04) and remained the same after infusion of 18 ml · kg-1 of Ringer's lactate. Rsf increased from 0.34 ± 0.07 to 0.80 ± 0.34 mm Hg · ml-1 · s by endotoxin and decreased after fluid infusion to 0.58 ± 0.14. Q′ changed inversely proportional to Rsf (P = 0.001). Rsf changes were highly correlated with the changes in total systemic flow resistance (RS) (P < 0.001). Endotoxin caused haemoconcentration and a decrease in plasma volume. The stability of Psf during endotoxin infusion and after volume loading indicate that the stressed volume was well maintained and changes in blood volume are compensated by changes in nonstressed volume. The increase in Rsf can be attributed to arteriolar vasoconstriction, venous vasoconstriction and haemoconcentration
Alternating versus synchronous ventilation of left and right lungs in piglets
Objective: We tested whether alternating ventilation (AV) of each lung (i.e. with a phase difference of half a ventilatory cycle) would decrease central venous pressure and so increase cardiac output when compared with simultaneous ventilation (SV) of both lungs. Theory: If, during AV, the inflated lung expands partly via compression of the opposite lung, mean lung volume will be smaller during AV than SV. As a consequence, mean intrathoracic pressure (as cited in the literature), and therefore, central venous pressure will be smaller. Design: The experiments were performed in seven anaesthetized and paralyzed piglets using a double-piston ventilator. Minute ventilation was the same during AV and SV. Starting at SV, we alternated three times between AV and SV for periods of 10 min. Results: During AV, central venous pressure was decreased by 0.7 mmHg and cardiac output was increased by 10±4.4% (mean, ±SD) compared with SV. AV also resulted in increased arterial pressure. During one-sided inflation with closed outlet of the opposite lung, a pressure rise occurred in the opposite lung, indicating compression. Conclusion: The higher cardiac output during AV than SV can be explained by the fact that central venous pressure is lower during AV. This lower central venous pressure is very probably due to the lower mean intrathoracic pressure caused by compression of the opposite lung during unilateral inflation
Computer-controlled mechanical lung model for application in pulmonary function studies
A computer controlled mechanical lung model has been developed for testing lung function equipment, validation of computer programs and simulation of impaired pulmonary mechanics. The construction, function and some applications are described. The physical model is constructed from two bellows and a pipe system representing the alveolar lung compartments of both lungs and airways, respectively. The bellows are surrounded by water simulating pleural and interstitial space. Volume changes of the bellows are accomplished via the fluid by a piston. The piston is driven by a servo-controlled electrical motor whose input is generated by a microcomputer. A wide range of breathing patterns can be simulated. The pipe system representing the trachea connects both bellows to the ambient air and is provided with exchangeable parts with known resistance. A compressible element (CE) can be inserted into the pipe system. The fluid-filled space around the CE is connected with the water compartment around the bellows; The CE is made from a stretched Penrose drain. The outlet of the pipe system can be interrupted at the command of an external microcomputer system. An automatic sequence of measurements can be programmed and is executed without the interaction of a technician
Determination of the mean cross-sectional area of the thoracic aorta using a double indicator dilution technique
A double indicator dilution technique for determining the mean cross-sectional area (CSA) of a blood vessel in vivo is presented. Analogous to the thermodilution method, dilution of hypertonic saline was measured by an electrical conductance technique. Because the change in conductance rather than absolute conductance was used to calculate CSA, pulsatile changes in shear rate of blood and conductance of surrounding tissues had no effect on the data. To calculate CSA from an ion mass balance, cardiac output was needed and estimated from the thermodilution curve using the same 'cold' (hypertonic) saline injection. The mean CSA, obtained from this double indicator dilution method (CSA(GD)), was compared with the CSA obtained from the intravascular ultrasound method (IVUS) in 44 paired observations in six piglets. The regression line is close to the line of identity (CSA(GD) = -1.83 + 1.06 · CSA(IVUS), r = 0.96). The difference between both CSAs was independent of the diameter of the vessel, on average -0.99 mm2 ± 2.64 mm2 (mean CSA(GD) = 46.84 ± 8.21 mm2, mean CSA(IVUS) = 47.82 ± 9.08 mm2) and not significant. The results show that the double indicator dilution method is a reliable technique for estimating the CSA of blood vessels in vivo
An adequate strategy for the thermodilution technique in patients during mechanical ventilation
The application of the thermodilution method in conditions associated with variations in blood flow implies a misuse of the Stewart Hamilton equation. Therefore, we studied the reliability of the thermodilution method for the estimation of mean cardiac output (CO) during mechanical ventilation in patients (n=9). Variation of the injection moment in the ventilatory cycle elicited a cyclic variation of CO estimates. This variation was not the same for all patients neither in phase nor in amplitude. Therefore, no specific phase in the ventilatory cycle could be selected for an accurate estimation of mean CO. Averaging CO estimates randomly distributed in the ventilatory cycle led to an improvement of accuracy with the square root of the number of observations. The averaging of CO estimates spread equally over the ventilatory cycle led to a much better result, e.g., the variation in the average of two estimates equally spread in the ventilatory cycle was similar to the variation in the average of four random estimates. We conclude that averaging of 3 or 4 estimates spread equally over the ventilatory cycle is an adequate strategy to estimate mean cardiac output in patients reliably