Small and large airways narrow in LVF and the term cardiac asthma is often used. However, current usage of this term is inconsistent and its meaning is therefore ambiguous. The term is better avoided despite several emerging similarities with bronchial asthma. Airway narrowing may be precipitated by acute elevation of pulmonary or bronchial vascular pressures. This appears to be mainly due to reflex bronchoconstriction. The afferents of this reflex are C-fibers with their endings in the lung parenchyma, bronchi, and pulmonary blood vessels and RAR in the larger airways, and they run in the vagus nerves, as do the efferent bronchoconstrictor fibers. Chronic elevation of pulmonary vascular pressures, as in mitral stenosis, are also associated with airway narrowing. Pulmonary edema (in the absence of vascular hypertension) also causes reflex bronchoconstriction. Bronchial responsiveness to bronchoconstrictor drugs is increased in LVF, partly, at least, due to reflex mechanisms. Bronchial mucosal swelling may also contribute. Narrowing by nonreflex mechanisms definitely occurs and there is direct evidence that decreased lung volume caused by pulmonary edema may cause this. There is little evidence for bronchial narrowing due to the mechanical effect of peribronchial edema, or by swelling of the bronchial mucosa. However, edema foam may terminally cause grave obstruction. Patients with LVF are commonly treated with bronchodilator drugs, but the basis for this approach needs further clarification.

The increased sensitivity of asthmatics to inhaled isoprenaline suggests that they may also be more sensitive to their endogenous adrenaline, which may thus dilate and stabilize their airways. Taken with enhanced antagonism by propranolol, this provides insight into the aggravation of asthma by beta-blocking drugs.

We have examined the inhibitory effect of atropine and sodium cromoglycate (SCG) on the bronchial response to sulphur dioxide (SO2) in groups of normal and asthmatic subjects. Eleven normal subjects were premedicated with propranolol (100 mg orally) one laboratory workers (table 1) in all of whom we studied the blocking effects of atropine and sodium cromoglycate. In four of these subjects we studied the reproducibility of the SO2 response in addition.We also examined the blocking effect of atropine and sodium cromoglycate in four asthmatics (table 1). Three of these were atopic with symptoms beginning in childhood, positive family history and positive cutaneous sensitivity tests to several allergens. The other asthmatic developed symptoms of asthma in his fifth decade, had no known allergies, negative family history, and negative skin tests. Symptoms in the atopic subjects were mild; one subject was asymptomatic apart from exercise-induced wheezing, while the other two had intermittent mild wheezing attacks, usually at night, relieved by inhaled salbutamol, and they were also taking sodium cromoglycate regularly. Both salbutamol and sodium cromoglycate were discontinued 24 hours before the experiments. The non-allergic asthmatic had severe symptoms requiring continuous treatment with prednisolone and corticotrophin, and intermittent salbutamol inhalation.

We have compared extravascular lung water after extracellular fluid volume expansion with that predicted from lung sucrose space measured in control dogs. In control lungs mean extravascular water:dry weight ratio was 3.81 +/- 0.16 (SD) (n = 5) and extravascular sucrose space/dry weight was 1.79 +/- 0.45 (n = 4). After acute expansion of extracellular fluid volume by 10% of body weight mean extravascular water:dry lung weight was 4.17 +/- 0.27 (m = 5), less than half the predicted increase to 4.63 +/- 0.19, suggesting some degree of protection. After 20% (n = 4), 30% (n = 2), and 40% (n = 1) expansion, no protection was demonstrated and there was considerable scatter of lung water at each infusion volume. When volume expansion increased pulmonary capillary intravascular forces (due to decreased protein osmotic pressure and increased hydrostatic pressure) by more than 20 cmH2O there was a linear increase in extravascular lung water with increasing intravascular forces. Three dogs did not conform to this relationship and had disproportionately large increases in lung water, possibly due to alveolar flooding.

We have induced acute pulmonary oedema in upright anaesthetized dogs by increasing pulmonary microvascular permeability or by extracellular fluid volume overload in order to determine the sensitivity and specificity of the radiograph to the presence of abnormal lung water. Radiographs were taken before and after development of oedema. At the end of the experiment we removed the inflated lungs and froze them in liquid nitrogen and subsequently examined them macroscopically in the frozen state. The extravascular water/dry lung weight ratio was measured gravimetrically on seven portions of each lung. Finally without the base-line films for comparison. We directly measured the change in opacity of the films with a radiographic densitometer. When a dog's mean extravascular water/g dry lung was increased by more than 35% it was invariably recognized, in one or more zones, as definite oedema. Control dogs were reliably recognized as normal when base-line films were used but the distinction between normal and minor degrees of oedema could not be made without the base-line films. There was a positive correlation between radiological grade and lung water, but a great deal of overlap between grades. Densitometry was not a sensitive or reliable method for diagnosing or quantifying oedema. Oedema was usually associated with a decrease in volume of the lower lung zones.