Adrian Versprille
Leiden University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Adrian Versprille.
Anesthesiology | 1996
Jos R. C. Jansen; Jan J. Schreuder; Jos J. Settels; Lilian Kornet; Olaf C. K. M. Penn; Paul G. H. Mulder; Adrian Versprille; Karel H. Wesseling
Background Application of the Stewart-Hamilton equation in the thermodilution technique requires flow to be constant. In patients in whom ventilation of the lungs is controlled, flow modulations may occur leading to large errors in the estimation of mean cardiac output. Methods To eliminate these errors, a modified equation was developed. The resulting flow-corrected equation needs an additional measure of the relative changes of blood flow during the period of the dilution curve. Relative flow was computed from the pulmonary artery pressure with use of the pulse contour method. Measurements were obtained in 16 patients undergoing elective coronary artery bypass surgery. In 11 patients (group A), pulmonary artery pressure was measured with a catheter tip transducer, in a partially overlapping group of 11 patients (group B), it was measured with a fluid-filled system. For reference cardiac output we used the proven method of four uncorrected thermodilution estimates equally spread over the ventilatory cycle. Results A total of 208 cardiac output estimates was obtained in group A, and 228 in group B. In group B, 48 estimates could not be corrected because of insufficient pulmonary artery pressure waveform quality from the fluid-filled system. Individual uncorrected Stewart-Hamilton estimates showed a large variability with respect to their mean. In group A, mean cardiac output was 5.01 l/min with a standard deviation of 0.53 l/min, or 10.6%. After flow correction, this scatter decreased to 5.0% (P < 0.0001). With no bias, the corresponding limits of agreement decreased from plus/minus 1.06 to plus/minus 0.5 l/min after flow correction. In group B, the scatter decreased similarly and the limits of agreement also became plus/minus 0.5 l/min after flow correction. Conclusion It was concluded that a single thermodilution cardiac output estimate using the flow-corrected equation is clinically feasible. This is obtained at the cost of a more complex computation and an extra pressure measurement, which often is already available. With this technique it is possible to reduce the fluid load to the patient considerably.
Critical Care Medicine | 1991
Rainer Assmann; Carl F. Heidelmeyer; Hans-J. Trampisch; Khosrow Mottaghy; Adrian Versprille; Wilhelm Sandmann; Konrad J. Falke
ObjectivesTo 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 repro-ducibility with reference values obtained during long-term apnea. DesignCrossover trial in patients; reference values from apneic animals. SettingUniversity ICU and physiology laboratory. PatientsSix consecutive male ICU patients (48 to 70 yrs) after major abdominal vascular surgery. Animals: two adult female sheep. InterventionsThree 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. MeasurementsMeasurements 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 ResultsAt 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 sees 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). ConclusionsAt 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.
Developmental Brain Research | 1982
Karel J. de Neef; J. R. C. Jansen; Adrian Versprille
The morphological and physiological features of the rabbit vagus nerve were studied at different ages after birth. The total fibre count is about 37,500 of which at birth 1-2% and in the adult animal approximately 10% are myelinated. In the postnatal period the cross-sectional area of the vagus grows to 5 times its perinatal size due to an increase of endoneural collagen, fibre growth and myelinization. The myelinization is most pronounced in the first 2 weeks after birth, axonal growth is predominant thereafter. The available data suggest that the begin of myelinization as well as the subsequent development of the myelin sheath are not dependent on axonal size. There seems to be no fundamental difference between the morphological development of the vagus and other peripheral nerves, e.g. the sciatic nerve of the rat. At birth the vagus nerve contains 2 fibre groups as can be measured from the compound action potential with conduction velocities of 11.4 and 0.9 m.s-1 respectively. Upon subsequent development the conduction velocity of these fibres increases to 31.9 and 1.2 m.s-1 in full-grown animals. THe compound action potential of the adult nerve implies 2 additional fibre groups with conduction velocities of 12.3 and 4.6 m.s-1 respectively. These two fibre populations develop gradually from 1 to 2 weeks after birth and arise probably from the slowest conducting, non-myelinated or C-fibres. It is concluded that the functional innervation of the sinoauricular node may be operational at birth as far as the cervical vagus nerve is concerned.
Archive | 1982
Adrian Versprille; Jos R. C. Jansen; Jan J. Schreuder
Two types of changes in airway pressure influence flow and pressure in the systemic and pulmonary circulation. Firstly, there is a static level, which is zero under normal breathing, but which is increased either in continuous positive airway pressure breathing (CPAP) or in artificial ventilation with positive end-expiratory pressure (PEEP). Secondly, there is the phasic or cyclic fluctuation of airway pressure during artificial ventilation, being either intermittent positive pressure ventilation (IPPV) when the end-expiratory pressure is zero (ZEEP) or continuously positive pressure ventilation (CPPV) when PEEP is applied.
Archive | 1998
Adrian Versprille; Jos R. C. Jansen
Independent ventilation of each lung was performed in 1972 by Seed and Sykes1 using a tracheal divider. They called this technique differential ventilation (DV). Subsequently, DV has been used to apply different ventilatory patterns to each lung in patients with predominantly unilateral lung disease (references before 1983,2 later3-5). DV, applied either synchronously (SV) or non-synchronously,6,7 did not decrease cardiac output when compared to conventional, common ventilation of both lungs. Alternating ventilation, in which one lung is inflated while the other is being deflated, was applied by Muneyuki et al. in 1983 in mongrel dogs.8 They observed no changes in cardiac output between synchronous and alternating ventilation (AV) in spite of a significant decrease in oesophageal pressure, as a substitute for intrathoracic pressure. We reasoned that during AV, volume expansion of one lung by inflation would cause an expiration of the opposite lung below its end-expiratory volume as existing during SV, due to compression. Consequently, its mean volume and therefore mean thoracic expansion (and intrathoracic pressure) would be less during AV than during SV, causing a lower central venous pressure.
Archive | 1987
W. van Rooyen; Adrian Versprille
Many patients suffering from chronic obstructive pulmonary disease (COPD), especially severe emphysema, perform their expiratory effort through pursed lips. As an elevated expiratory flow resistance is one of the main problems in COPD, it does seem conflicting to further increase airway resistance during expiration by pursed lips breathing, but the expiratory obstruction is caused mainly by a collapse of the small airways due to a loss of pulmonary elasticity. Pursed lips breathing may prevent this phenomenon of collapse by causing an extra-obstruction downstream from the bronchial level, resulting in a decreased expiratory flow and therefore an increase of the intraluminal airway pressure, thus reducing the effective transbronchial pressure difference [1]. Expiratory flow depends on the pressure gradient along the airways from alveoli to ambient air. By pursed lips breathing this pressure gradient will be decreased when airway resistance is extended with an extra-external barrier and driving force is kept constant. This mechanism is explained in Figure 1. So, pursed lips breathing results in a slow expiration and may thus cause a more uniform emptying of different parts of the lung [2]. Improvement of gas exchange has been attributed to a more effective ventilation through a shift of ventilatory air to the slow spaces, which represent the more poorly ventilated areas of the lungs, giving rise to an improvement of ventilation to perfusion relationships in different parts of the lungs. A higher arterial oxygen pressure (PaCO2) and a lower arterial carbon dioxide pressure (PaCO2) will result [2, 3].
Journal of Applied Physiology | 1981
Jos R. C. Jansen; J. J. Schreuder; J. M. Bogaard; W. van Rooyen; Adrian Versprille
Critical Care Medicine | 1981
A. Zwart; Jos R. C. Jansen; Adrian Versprille
American Journal of Physiology-heart and Circulatory Physiology | 1998
Lilian Kornet; Jos R. C. Jansen; F. C. A. M. Nijenhuis; G.J. Langewouters; Adrian Versprille
Critical Care Medicine | 1981
Jan J. Schreuder; Jos R. C. Jansen; Adrian Versprille