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Biomedical subjects

A Versprille

Publications and source records attributed to A Versprille.

At least 37 records · Page 2Linked to original sources

Transfer of carbon monoxide during an inspiratory pause procedure in mechanically ventilated pigs.

We studied the effect of forced inflation at different alveolar volumes (VA) on carbon monoxide diffusing capacity (DLCO) in anaesthetized, paralysed and mechanically ventilated healthy pigs. An inspiratory pause procedure (equivalent of the single-breath technique) consisting of a pause between an inflation and expiration, both at a constant flow rate, was used. The procedure was computer-controlled and could easily be standardized. In five pigs, VA was varied at constant inflation volume by increasing positive end-expiratory pressure (PEEP) from 2 to 10 cmH2O. Inspiratory pause time was varied from 1 to 8 s to verify whether the decay of CO was exponential. In nine pigs, DLCO was estimated at four different VA values by inflating with 15-30 ml kg-1 at 2 cmH2O PEEP. An exponential decay of CO was always obtained. With increasing VA by either an increase in PEEP or inflation volume, DLCO remained constant. Since the diffusing capacity of the pulmonary membrane is expected to increase with increasing VA, the constant DLCO may be attributed to a decrease in capillary blood volume.

Animals↗

Rate of uptake of CO by hemoglobin in pig erythrocytes as a function of PO2.

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.

Animals↗

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.

Animals↗

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.

Humans↗

Systemic filling pressure in intact circulation determined on basis of aortic vs. central venous pressure relationships.

In the intact circulation, mean systemic filling pressure (Psf) is determined by applying a series of inspiratory pause procedures (IPPs) and using Guyton's equation of venous return (Qv) and central venous pressure (Pcv): Qv = a - b x Pcv. During an IPP series, different tidal volumes are applied to set Pcv at different values. From the linear regression between Qv and Pcv, Psf can be calculated as Psf = a/b. Guyton's equation can also be written as Qv = (Psf - Pcv)/Rsd, where Rsd is the flow resistance downstream of the places where blood pressure is equal to Psf. During an IPP, a steady state is observed. Therefore, we can also formulate the following equation for flow: Qs = (Pao - Psf)/Rsu, where Qs is systemic flow, Rsu is the systemic flow resistance upstream to Psf, and Pao is aortic pressure. Because both flows (Qs and Qv) are equal, it follows that Pao = Psf(1 + Rsu/Rsd) - Rsu/Rsd x Pcv. This equation implies a method to determine mean systemic filling pressure on the basis of Pao measurements instead of flow determinations. Using 22 IPPs in 10 piglets, we determined the mean systemic filling pressure, and we compared the values obtained from the flow curves with those obtained from the aortic pressure curves. The mean difference between the two methods was 0.03 +/- 1.16 mmHg. With the use of Pao measurements, the Psf can be estimated as accurately as in using flow determinations. The advantage of the new method is that estimation of cardiac output is not required.

Animals↗

Diffusing capacity dependent on lung volume and age in normal subjects.

In this study we determined reference values of total diffusing capacity of carbon monoxide (DLCO) and DLCO per liter alveolar volume (DLCO/VA) at total lung capacity (TLC) and at lung volumes below TLC in sitting position. In 55 healthy nonsmoking volunteers (20-85 yr old), we determined reference values at TLC level in which age was the only parameter. In a subgroup (n = 16) these references did not change by correction for normal variability in hemoglobin concentration. In all volunteers DLCO decreased and DLCO/VA increased with decreasing VA. The increase in DLCO/VA was linear and less in older subjects. We derived equations to calculate reference values of DLCO/VA for lung volumes at and below TLC with two methods: 1) "random coefficients linear" model, which calculates the reference values directly, and 2) a conversion method, which calculates DLCO/VA for lower VA levels from reference values at TLC. An advantage of the conversion method is the suitability of DLCO/VA reference values at TLC of other populations. A disadvantage is the greater standard deviation of these reference values compared with those obtained by the random coefficients linear method. DLCO can be found by multiplying DLCO/VA with VA.

Adult↗

Basic mechanisms and clinical consequences of cyclic changes in pulmonary blood flow and blood volume during mechanical ventilation.

One of the main functions of the pulmonary circulation is its capacity function, including its function as a reservoir of blood. Changes in pulmonary blood volume occur if the input (right ventricular output) and the output (left ventricular output) of the pulmonary circulation are different. Transient differences between the input and the output occur during each ventilatory cycle of mechanical ventilation due to changes in intrathoracic pressure and consequent changes in central venous pressure. The haemodynamic effects of these transient changes in input and output and their dependence on the volaemic condition have been reduced to basic physiological mechanisms. The consequences have been extrapolated to clinical conditions.

Blood Volume↗

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.

Animals↗

Pulmonary vasoconstriction in oleic acid induced lung injury. A morphometric study.

Distribution and severity of active vasoconstriction of muscular pulmonary arteries were morphometrically assessed in anaesthetized, paralysed and mechanically ventilated pigs with respiratory distress, induced by oleic acid. Vasoconstriction was deduced from the medial thickness which was measured and expressed as a percentage of external diameter. Six pigs received oleic acid (0.12 +/- 0.07 ml/kg), dissolved 1:1 in 96% alcohol, in multiple injections of 0.1 ml. Six pigs were used as controls. After the oleic acid injections a stable hypoxaemia (PaO2 = 57 +/- 8 mmHg, at an inspiratory oxygen fraction of 0.6) and pulmonary hypertension (mean Ppa = 36 +/- 2 mmHg) were obtained for several hours. Electron microscopy revealed swelling of endothelial cells with signs of degeneration. Medial thickness was far greater in the oleic acid group than in the control group; overall mean values were 8.1 +/- 3.2 and 3.8 +/- 1.7% respectively (P < 0.001). Arteries with prominent vasoconstriction were lying in clusters. This pattern was the same in dependent and non-dependent regions. We concluded that in oleic acid induced respiratory distress active vasoconstriction of muscular pulmonary arteries is an important factor in the development of pulmonary hypertension. Besides vasoconstriction, endothelial swelling and intravascular clotting may contribute to the development of pulmonary hypertension.

Animals↗

Effects of local nerve cooling on conduction in vagal fibres shed light upon respiratory reflexes in the rabbit.

In ten vagus nerves the effect of local cooling on the compound action potential was studied in the temperature range of 34 to 0 degrees C in spontaneously breathing, anaesthetized rabbits. The mean temperature at which the myelinated (A) fibres were completely blocked, was 10.2 +/- 2.4 degrees C (mean +/- S.D.). In nine nerves, local vagus cooling to 0 degrees C failed to block all non-myelinated (C) fibres. In one nerve, total blocking occurred at 2.0 degrees C. We conclude that in the rabbit, the earlier found increase in tonic activity of the diaphragm following lung inflation or deflation during bilateral local vagus cooling to a temperature between 8 and 0 degrees C is due to afferent impulses in vagal C fibres.

Action Potentials↗

Serial lung model for simulation and parameter estimation in body plethysmography.

A serial lung model with a compressible segment has been implemented to simulate different types of lung and airway disorders such as asthma, emphysema, fibrosis and upper airway obstruction. The model described can be used during normal breathing, and moreover the compliant segment is structured according to more recent physiological data. A parameter estimation technique was applied and its reliability and uniqueness were tested by means of sine wave input signals. The characteristics of the alveolar pressure/flow patterns simulated with the model agree to a great extent with those found in the literature. In the case of absence of noise the parameter estimation routine produced unique solutions for different simulated pathologic classes. The sensitivity of the different parameters depended on the values belonging to each class of pathology. Some more simplified models are presented and their advantages over the complex model in special types of pathology are demonstrated. Noise added to the simulated flow appeared to have no influence on the estimated parameters, in contradiction to the effects with noise added to the pressure signal. In that case effective resistance was accurately estimated. Where parameters had no influence, as for instance upper airway resistance in emphysema or peripheral airway resistance in upper airway obstruction, the measurement accuracy was less. In all other cases, a satisfactory accuracy could be obtained.

Humans↗

A lung function information system.

A lung function information system (LFIS) was developed for the data analysis of pulmonary function tests at different locations. This system was connected to the hospital information system (HIS) for the retrieval of patient data and the storage of the lung function variables of patients to generate follow-up reports and to support financial and administrative management. The application programs were developed in such a way that high flexibility was obtained with respect to the patient-computer-technician interaction. The sampled data are stored on a disc to correct earlier decisions, perform recalculations and reanalyse the data for research purposes. When the measurements performed on a patient are authorized, the sampled data are deleted, except for when they are needed for future research. A distributed computer system was chosen to combine the benefits of a centralized system with those of several stand-alone systems. The main tasks of the central unit are to store collected data and computer programs, generate a final lung function report on laser printer and provide a connection to the HIS. In the satellite computers, which are located close to the lung function equipment, the signals and raw data are processed. Furthermore, the satellite computers were in use for program development and several research projects, and for the offline data processing of the lung function measurements from two other hospitals by means of a modem connection. The LFIS improved the quantity and quality of data acquisition. It resulted in an increased capacity of about 50% concerning spirometry, and facilitated time-consuming complex analyses. It also avoided miscalculations and mistakes in reports previously experienced with hand calculations.

Computer Systems↗

Right ventricular function assessed by thermodilution technique during apnea and mechanical ventilation.

OBJECTIVES: To evaluate strategies for thermodilution-based measurement of cardiac output and right ventricular (RV) ejection fraction and to assess the effects of controlled mechanical ventilation in patients. Furthermore, to compare strategy-associated reproducibility with reference values obtained during long-term apnea. DESIGN: Crossover trial in patients; reference values from apneic animals. SETTING: University ICU and physiology laboratory. PATIENTS: Six consecutive male ICU patients (48 to 70 yrs) after major abdominal vascular surgery. ANIMALS: two adult female sheep. INTERVENTIONS: Three ventilatory rates (8, 16, and 24 cycles/min) and 15-sec periods of apnea were selected for measurements in patients. In animals, continuous apnea was achieved with extracorporeal CO2 removal and apneic oxygenation. MEASUREMENTS: Measurements were performed using an appropriate pulmonary artery catheter and an ejection fraction/cardiac output computer prototype. The thermal indicator was injected automatically at four defined points of the ventilatory cycle, but triggered manually during apnea. MAIN RESULTS: At 8 cycles/min, there was a wide mean range of cyclic variable modulation, with a coefficient of variation of 11.6% and 23.2% for cardiac output and RV ejection fraction, respectively. Allowing for ventilatory phase or changing from 8 to 16 cycles/min reduced errors by half. Combining both procedures resulted in a coefficient of variation of 4.7% and 6.6% for cardiac output and RV ejection fraction, respectively. The best coefficient of variation values obtained during 15 secs of apnea in patients approached those variations in experimental apnea (coefficient of variation of 2.1% and 4.5% for cardiac output and RV ejection fraction, respectively). CONCLUSIONS: At low ventilatory rates, best results are achieved by averaging four phase-selected measurements. One-point measurements were less accurate and random point measurements less reproducible.

Aged↗

Effect of lung volume and positional changes on pulmonary diffusing capacity and its components.

Normal subjects have a larger diffusing capacity normalized per liter alveolar volume (DL/VA) in the supine than in the sitting position. Body position changes total lung diffusing capacity (DL), DL/VA, membrane conductance (Dm), and effective pulmonary capillary blood volume (Qc) as a function of alveolar volume (VA). These functions were studied in 37 healthy volunteers. DL/VA vs. VA yields a linear relationship in sitting as well as in supine position. Both have a negative slope but usually do not run parallel. In normal subjects up to 50 yr old DL/VA and DL increased significantly when subjects moved from a sitting to a supine posture at volumes between 50 and 100% of total lung capacity (TLC). In subjects greater than 50 yr old the responses of DL/VA and DL to change in body position were not significant at TLC. Functional residual capacity (FRC) decreases and DL/VA increases in all normal subjects when they change position from sitting to supine. When DL/VA increases more than predicted from the DL/VA vs. VA relationship in a sitting position, we may infer an increase in effective Qc in the supine position. In 56% of the volunteers, supine DL was smaller than sitting DL despite a higher DL/VA at FRC in the supine position because of the relatively larger decrease in FRC. When the positional response at TLC is studied, an estimation obtained accidentally at a volume lower than TLC may influence results. Above 80% of TLC, Dm decreased significantly from sitting to supine. Below this lung volume the decrease was not significant. The relationship between Qc and VA was best described by a second-order polynomial characterized by a maximum Qc at a VA greater than 60% of TLC. Qc was significantly higher in the supine position than in the sitting position, but the difference became smaller with increasing age. In observing the sitting and supine positions, we saw a decrease in maximum Qc normalized per square meter of body surface area with age.

Adolescent↗

Alveolar pressure during high-frequency jet ventilation.

We studied the influence of ventilatory frequency (1-5 Hz), tidal volume, lung volume and body position on the end-expiratory alveolar-to-tracheal pressure difference during high-frequency jet ventilation (HFJV) in Yorkshire piglets. The animals were anesthetized and paralysed. Alveolar pressure was estimated with the clamp off method, which was performed by a computer controlled ventilator and which had been extensively tested on its feasibility. The alveolar-to-tracheal pressure difference increased with increasing frequency and with increasing tidal volume, the common determinant appearing to be the mean expiratory flow. The effects in prone and in supine position were similar. Increasing thoracic volume decreased the alveolar-to-tracheal pressure difference indicating a dependence of this pressure difference on airway resistance. We concluded that the main factors determining the alveolar-to-tracheal pressure difference (delta P) during HFJV are expiratory flow (V'E) and airway resistance (R), delta P congruent to V'E x R.

Airway Resistance↗

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.

Aged↗