Estimation of resistance and elastance of the lungs in the presence of alinearities. A model study.
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Biomedical subjects
Publications and source records attributed to H Bobbaers.
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Pulmonary resistance, determined near zero flow by means of the isovolume technique, increases with the total amplitude of flow. This variation observed in healthy subjects at two frequencies, and documented also by other investigators, was stimulated in a model study. The main factor responsible for the amplitude dependence of pulmonary or airway resistance appears to be the asymmetrical elastic characteristics of the airways.
The dynamic elastance (E) and viscous resistance (R) of the canine intrathoracic trachea were determined by submitting excised tracheal segments to periodic variations of pressure at frequencies between 0.5 and 9 Hz, and by relating simultaneous transmural pressure and volume variations. Mean values of E and R are, respectively, 17.3 cmH2O.cm-1 and 0.16 cmH2O.cm-1.s, or, expressed in volume changes per cm length of the trachea, 53.5 cmH2O.ml-1 and 0.49 cmH2O.ml-1.s. E and R increase at higher longitudinal tension of the trachea and under the influence of acetylcholine.
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The frequency dependence of effective compliance, Ceff, and resistance, Reff, are reproduced by means of a two- or four-compartment linear mathematical model with pleural pressure as a sinusoidal input. The model simulates the mechanical properties of lung parenchyma, alveolar gas, bronchial wall, and cheeks, as well as the distribution of gaseous resistances and inertances within the airways. Values, representative for a young healthy adult, are assigned to these various parametersmit appears from this study: 1) that the gas inertance produces a very marked increase of Ceff, noticeable already below 1 cycle/smto obtain a frequency independence of Ceff between 0 and 2 cycles/s, it is necessary to introduce a marked inhomogeneity in the model. 2) Such an inhomogeneity is realized by simulating a pleural pressure difference of 6 cmH2O between the compartments of the bialveolar model. It can be shown that this corresponds to a total pleural pressure difference of about 9 cmH2O in a model consisting of an infinite number of compartments. 3) The influence of the compressibility of alveolar gas and of mechanical properties of the bronchial wall and of the cheeks on Ceff and Reff is small or negligible.
Horizontal gradients in the distribution of ventilation and of regional vital capacities, as well as a reversed vertical, esophageal pressure gradient, were observed in a patient with a unilateral painful chest wall lesion. The distribution abnormalities disappeared after surgical treatment. These findings suggest that the interdependency between chest wall and lungs, and within the latter, between lobes, is an important factor determining the regional distribution of ventilation and the pleural pressure gradient in man.
OBJECTIVE: The purpose of the study was to provide psychometric evaluation of the Dutch version of the Critical Care Family Needs Inventory. SETTING: The study took place in an intensive care unit of a university hospital. PARTICIPANTS: The participant group included 200 adult family members visiting a patient within the 72-hour interval after admission to the intensive care unit. RESULTS: Principal factor analysis with varimax rotation resulted in a 5-factor solution distinguishing 5 need types: need for information, need for comfort, need for support, need for assurance and anxiety reduction, and need for proximity and accessibility. The internal consistency of the resulting subscales ranged from 0.80 to 0.62, and all factors were significantly related to each other. The Critical Care Family Needs Inventory subscales were found to be clearly related to the demographic variables age, sex, and education level. CONCLUSION: The reliability and validity of the Dutch-language Critical Care Family Needs Inventory as a diagnostic tool in family needs assessment are supported.
Rapidly fatal pulmonary tumour embolism is a rare complication of malignancy, and often presents as progressive dyspnea without obvious cause. We describe two cases presenting with a dramatic clinical picture of lactic acidosis and cardiopulmonary arrest soon after admission on ICU. The first patient was a 29-year old woman with a breast cancer seeming in remission who was admitted with rapidly increasing dyspnea since two weeks. The second patient was a 46-year old woman with HIV and no history of malignancy, who developed dyspnea and lactic acidosis over the course of a few days while she was investigated for an occipital brain lesion. Both patients died soon after admission and massive tumour emboli were found on autopsy. Breast cancer was the origin of the emboli in both cases. Symptoms were out of proportion to the initial physical cardiopulmonary findings and radiographic features. Clinical signs of pulmonary tumour embolism are non-specific and subacute. Prognosis is poor and definite diagnosis is usually made post-mortem. Solid malignancies such as breast cancer account for most of the cases. Pulmonary tumour embolism should be considered in critically ill patients with unexplained hypoxemia and lactic acidosis, mild or no radiological abnormalities and fast clinical deterioration. It may occur in young patients and in patients without history of malignancy.
Lung volumes, maximal expiratory flows, pulmonary resistance and static recoil pressure-volume curves were measured before and after inhalation of isoprenaline in four groups of subjects: heqlthy patients with mild and severe chronic bronchitis and asthmatics. The observed changes were qualitatively similar in the four groups. Whereas total lung capacity and dynamic compliance were not influenced, there was an increase in vital capacity (not in healthy subjects and mild bronchitics), in FEV1, in maximal expiratory flows and a decrease in pulmonary resistance. The static recoil pressure-volume relationship was shifted to the left over its ascending part. The effect of isoprenaline tended to be larger in patients. Among the latter, the increase of vital capacity was especially pronounced in the severe bronchitics, whereas the maximal flows increased most in asthmatics. We suggest that the influence of isoprenaline on maximal flows results from a bronchodilation, associated with an increased collapsibility of the central intrathoracic airways, whereas the influence of VC might reflect a delayed onset of small airway closure.
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