Richard V. Ebert

The mechanics of pulmonary ventilation in normal subjects and in patients with emphysema

Abstract 1.1. The intrathoracic pressure exclusive of the pressure required to overcome the retractive force of the lung was measured and shown to be functionally related to the rate of respiratory flow in both normal and emphysematous subjects. This pressure increment at any given level of flow represents the pressure required to overcome both the resistance to air flow through the bronchopulmonary passages and the frictional resistance of the intrathoracic tissues to deformation. The resistance to gas flow is composed of resistance to laminar gas flow and resistance to turbulent gas flow. 2.2. Pressure-flow curves were obtained from normal subjects and from patients with pulmonary emphysema. Studies were made with subjects breathing air and breathing argon-oxygen. Comparison of the pressure-flow relationships obtained with these two gases demonstrated that tissue friction was negligible both in normal and emphysematous subjects. 3.3. The resistance to gas flow was evaluated in normal subjects and patients with pulmonary emphysema. The resistance was markedly increased in the patients with emphysema. 4.4. The resistance to both laminar gas flow and the resistance caused by eddying turbulence are important in normal subjects and patients with emphysema. As the rate of flow is increased, the resistance caused by eddying turbulence becomes progressively greater. 5.5. A change in the pressure-flow relationship with change in the amount of lung inflation was demonstrated. This was observed particularly during expiration. More pressure was required to produce a given flow at lesser degrees of lung inflation. This was marked in emphysematous subjects. The three variables, pressure, flow and lung inflation, were expressed on a three-dimensional graph. 6.6. During expiration in emphysematous subjects the pressure-flow curve bends rapidly to approach an asymptote of flow. This accounts for the inability of patients with emphysema to exceed a certain flow regardless of the pressure exerted. In emphysema there is an increase in resistance to air flow in the bronchioles and a decrease in the elastic force of the lung for a given degree of inflation of the lung. As a result, collapse of the unsupported bronchioles tends to occur when the pressure drop between the alveoli and the cartilaginously supported end of the bronchiole exceeds the elastic pressure of the lung.

Initial myocardial infarction among 503 Veterans: Five-year survival

Abstract 1.1. An analysis and follow up of 503 cases of initial transmural myocardial infarction is presented. 2.2. Advanced age of the patient, a history of hypertension, a definite history of angina pectoris, thromboembolic complications, shock, congestive failure, serious arrhythmias, high prolonged fever and marked leukocytosis were found to have an adverse effect upon the immediate mortality rate. 3.3. Except for atrioventricular block, marked leukocytosis, shock and thromboembolic complications, the same factors had an adverse effect upon the five-year mortality rate of recovered patients. 4.4. The marked variation in immediate mortality rates reported in various studies is discussed. 5.5. There is a remarkable agreement in long term mortality rates of survivors reported in recent studies. 6.6. In this study the mortality rate stabilized at about 4 per cent per annum for patients under fifty years of age who survived to the first anniversary of their attack. The mortality rate stabilized at about 9 per cent per annum for patients over fifty years of age who lived to the seventh month following onset of their first transmural myocardial infarction. 7.7. The excess mortality rate per annum observed in recovered patients varied from 3.4 per cent for patients thirty to thirty-nine years of age, to 5.2 per cent for patients fifty to fifty-nine years of age.

The Collagen and Elastin Content of the Lung in Emphysema

Excerpt Connective tissue fibers maintain the normal arrangement of lung structure. These are scleroprotein fibers: collagen, elastin, and reticulin. They are characterized by their insolubility, t...

Fibrous Network of the Lung and its Change with Age

The remarkable elastic behaviour of the lung entails both continuous tissue stress and a cyclic stress produced by the fluctuating difference between intrathoracic and intra-alveolar pressures throughout the entire span of life. In spite of these potentially disruptive forces, lung structure is preserved by the fibrous connective-tissue proteinscollagen, elastin, and reticulin. These extracellular proteins are characterized by their insolubility, resistance to destruction, and high tensile strength. Collagen and elastin both exhibit elastic behaviour, but great extensibility is a property only of elastin. The most reasonable assumption is that the elastic fibres, therefore, are principally responsible for the elastic behaviour of the lung tissue, but sure proof is lacking. Recently, Carton, Dainauskas, Tews, and Hass (1960) and Wright (1961) have described the nature of the network of elastic tissue in the lung. We sought to describe more fully the roles of collagenous and elastic fibres in the terminal air spaces of the lung, and thus their respective contributions to tissue elasticity and the general elastic performance of the lung. As the study developed, it seemed important to measure the amounts of collagen and elastin in the lung parenchyma and pleura. These findings have been correlated with the age of the subjects and interpreted according to knowledge about tissue elasticity.

The mechanics of pulmonary ventilation in patients with heart disease

Abstract 1.1. Using intraesophageal pressure as a measure of intrathoracic pressure, the elastic forces of the lung were studied in patients with heart disease. Pressure-volume diagrams were constructed by plotting the degree of lung inflation against the static intrathoracic pressure. An alteration in the elastic forces in the lungs of these patients was shown by the finding of an increase in the pressure required to produce a 100 cc. change in lung volume as compared with normal subjects. 2.2. A high correlation was demonstrated between the reciprocal of the vital capacity and the pressure change per 100 cc. change in lung volume both in normal subjects and patients with heart disease. The lung elasticity curves for normal subjects and patients with heart disease were identical when the level of lung inflation was expressed in terms of per cent of the vital capacity. 3.3. Pressure-flow curves were obtained from patients with heart disease. Comparison of the pressure-flow relationships obtained in these patients when breathing air and argon-oxygen demonstrated that tissue friction was a negligible factor and that the resistance to movement of the lungs was caused by resistance to gas flow. 4.4. Resistance to air flow was evaluated in patients with heart disease. It was found to be increased in certain patients with heart failure and normal in other patients. No correlation was found between resistance to air flow and reduction of vital capacity in these patients. 5.5. There may be no increase of resistance to air flow in patients with cardiac disease and exertional dyspnea. For this reason it appears that exertional dyspnea is most closely related to the reduction in vital capacity and altered elastic properties of the lung. On the other hand, it is likely that increased resistance to air flow plays an important role in the dyspnea of cardiac asthma.

Pulmonary hypertension in chronic pulmonary emphysema

Abstract 1.1. A significant elevation of pulmonary arterial diastolic pressure was found in twenty-four patients with chronic pulmonary emphysema. Systolic pressure was also elevated in the majority of these patients. Evidence is presented which indicates that pulmonary hypertension in emphysema is related to an increased vascular resistance in the lungs. 2.2. Marked respiratory variation is the outstanding characteristic of intravascular and intracardiac pressure records in patients with emphysema. This depends upon abnormally wide fluctuations in intrathoracic pressure. 3.3. There is no correlation between the degree of pulmonary hypertension and severity of the emphysema as estimated by the altered ratio of residual air to total lung volume. 4.4. Eight of the twenty-four patients with emphysema had definite evidence of right heart failure prior to study. The pulmonary arterial pressure was significantly higher and the oxygen saturation of the arterial blood was significantly lower in this group than in the group of sixteen patients with emphysema uncomplicated by right heart failure. 5.5. The mean arteriovenous oxygen difference in twenty-three patients with pulmonary emphysema was similar to that reported for normal subjects. No evidence was found to indicate that oxygen unsaturation of the arterial blood in emphysema induces an increase in the output of the heart.

The barrel deformity of the chest, the senile lung and obstructive pulmonary emphysema.

Abstract 1.1. A study has been made of the physiological basis of senile emphysema. 2.2. Measurements of the chest and physiological studies of lung function were carried out in a group of aged subjects who had a marked barrel deformity of the chest. Similar studies were performed in a group of subjects with obstructive pulmonary emphysema, in an unselected group of aged subjects and in a group of healthy young subjects. 3.3. Comparison of the mean values for total lung capacity, functional residual capacity, residual volume, intrapulmonary distribution of inspired gas, maximum breathing capacity, arterial hemoglobin oxygen saturation and arterial carbon dioxide tension failed to reveal any significant difference between the group of aged subjects with a marked barrel deformity of the chest and the unselected aged subjects. Additional studies were discussed which also have failed to disclose changes characteristic of those subjects with the barrel deformity of the chest. 4.4. It was concluded that physiological evidence for any condition such as senile, postural or non-obstructive emphysema is lacking.

MICROELECTROPHORESIS OF BLOOD PLATELETS AND THE EFFECTS OF DEXTRAN

The intravenous administration of dextran has previously been shown to produce a bleeding tendency in laboratory animals and in humans. Extensive studies concerning the hemostatic defect have yielded much useful information. Carbone, Furth, Scott and Crosby (1) found that the major abnormality consisted of a prolongation of the bleeding time. In seven of 11 patients given 1,500 to 6,500 ml. of dextran intravenously over a five day period the bleeding time was prolonged over 30 minutes. The concentration of platelets, clotting time, fibrinogen level, clot retraction time and prothrombin consumption test were not significantly affected by dextran. The prothrombin time was slightly abnormal. It appears unlikely that this finding explains the hemostatic defect because of the inconstancy and mild degree of the change. Adelson, Crosby and Roeder (2) found that smaller amounts of dextran were required to produce a prolonged bleeding time in dogs made thrombocytopenic by irradiation than in normal dogs. Comparable volumes of gelatin in the thrombocytopenic dogs did not prolong the

THE EFFECTS OF DEXTRAN IN NORMOVOLEMIC AND OLIGEMIC SUBJECTS

Dextran, a macromolecular plasma volume expander, was first used in 1943. Since that time, many clinical reports have appeared in the Scandinavian and English literature. In 1942 the Blood Substitute Committee of the National Research Council listed 11 requirements for a satisfactory plasma volume extender. These are: maintenance of satisfactory colloid osmotic pressure, constant composition, suitable viscosity, stability with temperature change, stability in storage, ease of sterilization, freedom from pyrogens, absence of immediate adverse effects, absence of immediate or delayed organic derangement, absence of antigenicity, and reasonable price (1). Dextran seems to fulfill all of these requirements except for the possible possession of antigenic properties. In addition, it has been suggested that a satisfactory extender should remain in the circulatory system, maintain increased plasma volume, and keep blood circulatory levels up to 50 per cent of the amount infused for at least 12 hours (1). Although it is of paramount importance that effects of any plasma volume expander upon plasma volume and plasma protein restitution be investigated, there has been a paucity of such reports in the literature.

Training of the Internist as a Primary Physician

Abstract The internist in the United States has traditionally served as a primary physician for his patients. The rapid and continuing decline in the number of general practitioners has made it imp...