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Biomedical subjects

K E Finucane

Publications and source records attributed to K E Finucane.

At least 37 records · Page 2Linked to original sources
PubMed1987

A model of the respiratory pump.

The interaction of forces that produce chest wall motion and lung volume change is complex and incompletely understood. To aid understanding we have developed a simple model that allows prediction of the effect on chest wall motion of changes in applied forces. The model is a lever system on which the forces generated actively by the respiratory muscles and passively by impedances of rib cage, lungs, abdomen, and diaphragm act at fixed sites. A change in forces results in translational and/or rotational motion of the lever; motion represents volume change. The distribution and magnitude of passive relative to active forces determine the locus and degree of rotation and therefore the effect of an applied force on motion of the chest wall, allowing the interaction of diaphragm, rib cage, and abdomen to be modeled. Analysis of moments allow equations to be derived that express the effect on chest wall motion of the active component in terms of the passive components. These equations may be used to test the model by comparing predicted with empirical behavior. The model is simple, appears valid for a variety of respiratory maneuvers, is useful in interpreting relative motion of rib cage and abdomen and may be useful in quantifying the effective forces acting on the rib cage.

Animals↗
PubMed1986

The pattern of breathing in acute severe asthma.

The pattern of breathing was studied in 8 patients with acute severe asthma on admission to hospital and during recovery to determine how chest wall motion varied with the degree of air-flow obstruction (AO), the relationship between degree of AO and respiratory timing and ventilation, and whether the pattern suggested respiratory muscle fatigue when asthma was most severe. Pattern was assessed by simultaneous measurement of respired volumes (pneumotachygraph) and anteroposterior (AP) motion of lower rib cage and abdomen (magnetometers). There was a phase lag of AP rib cage relative to AP abdominal motion that was greatest in those with lowest FEV1 and progressively decreased during recovery. Fractional inspiratory time was decreased in severe asthma. Mean inspiratory flow was increased in moderately severe asthma but decreased when FEV1 was less than 25% predicted. Breathing pattern was no more variable during severe asthma than during recovery. We conclude that during severe AO the magnitude of phase lag of AP rib cage relative to AP abdominal motion reflects severity of asthma; respiratory drive is increased but is not associated with increased ventilation below an FEV1 of 25% predicted, and analysis of the breathing pattern provides no clear evidence of respiratory muscle fatigue.

Abdominal Muscles↗
PubMed1985

Irreversible airflow obstruction. Evolution in asthma.

To determine whether asthma can cause irreversible airflow obstruction (IAO) 89 subjects with uncomplicated asthma received intensive treatment for four weeks. FEV1 was measured at 0, two and four weeks; pulmonary elasticity and flow resistance was measured in 46 of the subjects at four weeks. Severity of asthma and cigarette consumption were ascertained by a questionnaire. The mean difference between the predicted and highest FEV1 during treatment was 0.29 L (P less than 0.001). The highest FEV1% predicted correlated (P less than 0.001) with the duration and severity of asthma in the entire group, in the 51 nonsmokers, and in the 47 subjects with the adult onset of asthma. Pulmonary resistance, but not elastic recoil, correlated with the duration and severity of asthma (P less than 0.01). The results show that chronic asthma can cause narrowed airways and IAO, and suggest that this may be prevented by improved control of asthma.

Adrenal Cortex Hormones↗
PubMed1985

Continuous positive airway pressure: a breathing system to minimize respiratory work.

During continuous positive airway pressure (CPAP) the work of breathing is least when there is no change of airway pressure measured at the mouth (delta Paw) during respiration. In this study we consider the physical properties of CPAP circuits which determine the magnitude of delta Paw, and apply this information to the design of a simple, reliable CPAP system that minimizes delta Paw and incorporates the additional advantages of low-flow rates and the use of commonly available proven components. Using a weighted reservoir bag and threshold CPAP valve to maintain pressure, we found that delta Paw may be reduced to less than 1.0 cm H2O during quiet breathing, at a tidal volume of 700 ml and maximum inspiratory flow of 1.35 L/sec. delta Paw was dependent on both the resistance and the reactance of the circuit components; it was increased when resistance or flow rates were high, and when delivery pressure depended on the elastic tension in the wall of the reservoir bag or on compression of the bag with springs or elastic bands.

Equipment Design↗
PubMed1984

Asthma and irreversible airflow obstruction.

To determine whether asthma alone can cause irreversible airflow obstruction 42 men and 47 women with chronic asthma (mean duration 22 (SD 13) years) without evidence of other disease likely to cause irreversible airflow obstruction were treated with theophylline orally and a beta agonist both orally and by inhalation for four weeks. After two weeks of treatment the FEV1 was less than 85% of the predicted normal value (%P) in 48 patients and these individuals then received prednisolone 0.6 mg/kg/day for two weeks. Duration and severity of asthma and smoking history were quantified by questionnaire; 38 patients were current smokers or ex-smokers. FEV1 was measured at 0, 2, and 4 weeks. The mean difference between the best FEV1 during the study and the predicted normal value was 0.29 l (p less than 0.001); FEV1 %P decreased with age (r = -0.30, p less than 0.01) and with the duration (r = -0.47, p less than 0.001) and severity (r = -0.55, p less than 0.001) of asthma. Similar findings were noted when the results for non-smokers and those whose asthma started in adult life were analysed separately. We conclude that asthma alone can cause irreversible airflow obstruction and that the degree of obstruction is a function of the duration and severity of previous asthma. The results suggest the possibility that irreversible airflow obstruction in asthma may be preventable by minimising the degree of persistent asthma.

Adult↗
PubMed1984

Lung function in diffuse interstitial lung disease of unknown cause.

To examine the role of lung function tests in diagnosis and management of patients with diffuse interstitial lung disease (DILD) we measured total lung capacity (TLC), gas transfer (Tl), lung distensibility and arterial saturation (SaO2) and ventilation during progressive exercise in 24 patients with DILD including 18 with biopsy confirmation. Tl was decreased in all patients, in 21/24 there was progressive hypoxia with exercise, in 12/24 TLC was greater than 80% predicted and in 6/18 lung distensibility was normal. Tl and the change of SaO2 with work output during exercise were highly correlated (r = -0.65, p less than 0.001). In serial studies, the change of SaO2 with work output altered most with clinical improvement or deterioration. The clinical course and response to treatment was not related to a particular pattern of abnormal function. These results and those of previous studies indicate that in DILD the most sensitive index of abnormal parenchymal function is Tl, that lung volumes and distensibility may be normal so that the term "restrictive lung disease" can be misleading, that the fall of SaO2 with work output and Tl are the most sensitive parameters for assessing severity and following the course of the disease and that lung function alone does not predict outcome.

Adult↗
PubMed1984

Mechanical properties of the lung in diffuse interstitial lung disease.

To define the mechanical properties of the lungs in diffuse interstitial lung disease (DILD) the static deflation volume-pressure (VP) and maximum expiratory flow-volume characteristics were measured in 18 patients with DILD including 14 with biopsy confirmation. Elastic recoil, defined by the position of the VP curve, was increased in 12, normal in four and decreased in two patients. The distensibility of inflatable lung, defined by the constant K of a single exponential fitted to the VP data, was decreased in 10 of the 12 with increased recoil and increased in the two with decreased recoil. Those with a normal or increased pulmonary distensibility smoked more than those with decreased distensibility (p less than 0.05). Maximum expiratory flow rates (MEFR) were decreased at any elastic recoil pressure in 12 patients; when corrected for lung size MEFR were decreased in seven patients, six of whom were smokers. These results show that in DILD a decreased pulmonary distensibility is common but not invariable, that an increased elastic recoil reflects both loss of lung units and decreased distensibility of inflatable units and that an increased flow resistance is common. Co-existent emphysema could explain a normal or increased pulmonary distensibility in DILD. The increased flow resistance is due in part to fibrosis and loss of lung units with functional loss of the attendant airways. Decreased MEFR, despite correction for lung size, in seven subjects suggests that structural narrowing of airways, due to cigarette smoking and/or bronchiolar involvement by the disease, also contributes to an increased flow resistance in some patients with DILD.

Airway Resistance↗
PubMed1984

Spirometry.

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Female↗
PubMed1983

The effect of hyperinflation on lung elasticity in healthy subjects.

In acute severe asthma, lung distensibility may increase. To determine whether hyperinflation alone can increase lung distensibility acutely total lung capacity (TLC) and static volume-pressure (VP) properties were measured in six healthy subjects after quiet breathing, and two periods of hyperinflation of 20-60 min, with negative pressure assistance at the chest wall (NPA) in one period and positive airways pressure assistance (PPA) in the other. In five subjects there was no change with NPA; with PPA lung volume at a static transpulmonary pressure of 10 cm H2O (VL 10) increased by 0.3 L (P less than 0.01) and K, the shape constant of an exponential function fitted to the deflation VP curve, increased (P less than 0.001) without a change in TLC. In Subject 6, with both NPA and PPA, VL 10 increased by 1.3 L (P less than 0.001). K increased (P less than 0.001 with NPA; P less than 0.05 with PPA) and TLC increased (P less than 0.001 with NPA; P less than 0.01 with PPA); volume hysteresis was unchanged. The small increase of lung distensibility in five subjects after PPA we attribute to decreased pulmonary blood volume; in Subject 6 the changes with hyperinflation suggest decreased tissue forces. We conclude that hyperinflation can cause an acute increase in lung distensibility in some individuals. The variable response between subjects parallels that seen in asthma.

Adult↗
PubMed1975

Resistance of intrathoracic airways of healthy subjects during periodic flow.

The resistance and reactance of lower airways were measured as functions of the frequency and amplitude of periodic flow in three healthy subjects by relating flow, produced with a piston pump, to the difference between lateral tracheal and alveolar pressure, estimated plethysmorgraphically. Resistance consistently increased with frequency; reactance was small never exceeding resistance. This result cannot be explained by distortion of velocity profiles by inertia because, in long pipes, resistance increases only when inertial forces are large and reactance exceeds resistance. Theoretical analyses of airway resistance suggested that the results reflected inhomogeneity. In lung models which considered airway wall distensibility and inertial reactance of airways, resistance increased with frequency and inertial reactance was small. These results imply that in health, as in lung disease, resistance is determined by the distribution of resistance and reactance within the lung and is not simply the total resistance of the individual airways. As flow amplitude increased at constant frequency, flow-pressure relationships became distorted and resistance increased, due probably to motion of airway walls and further distortion of velocity profiles

Adult↗
PubMed1975

Estimation of alveolar pressure during forced oscillation of the respiratory system.

A method for obtaining a continuous estimate of alveolar pressure (PAlv) during periodic flow is described; it was developed to improve the precision of measurements of airway and respiratory tissue impedance using the improved resolution of relatively high-frequency (approximately 5 Hz) singlas. The respiratory system was modulated with a piston pump, and lung volume and the volume change due to compression and expansion of alveolar gas were measured plethysmorgraphically; these signals and an analog divider were used to obtain a continuous solution of Boyle's law during flow. The plethysmorgraph was of the "flow" type; with it volume changes at frequencies up to 10 Hz and with rates of change up to 6 l/s were measured without amplitude or phase distortion. The method permits control of frequency and flow amplitude during PAlv measurement and calibration of PAlv in the absence of an active chest wall. However, it is technically complex.

Airway Resistance↗