The forces governing the movement of water across the pulmonary capillaries were studied in 39 intact, spontaneously breathing dogs. A situation favoring the net movement of water out of the pulmonary capillaries was created by means of partial pulmonary venous obstruction (left atrial balloon catheter) followed by rapid saline hemodilution. A predetermined difference between pulmonary capillary and plasma colloid osmotic pressures was maintained for periods of 1 to 2 hours. Left atrial (P(LA)) and plasma colloid osmotic pressures (pi(pl)) were measured directly. The water content of the lungs was measured serially by an indicator-dilution technique, and at autopsy by drying the lungs. The rate of accumulation of lung water was measured in four groups of animals: in three of the groups, the capillary hydrostatic and colloid osmotic pressures were varied; in the fourth group, the right lymphatic duct was obstructed in addition. The average rate of water accumulation in the lungs varied in a nonlinear way with the level of the capillary hydrostatic-plasma colloid osmotic pressure difference and was unaffected by the level of the capillary hydrostatic pressure. At low levels of P(LA) - pi(pl), water accumulated in the lung at an average rate of 0.09 g per g dry lung per hour per mm Hg pressure difference. At higher levels of P(LA) - pi(pl) the average rate of accumulation was 0.22 g per g per hour per mm Hg DeltaP; in most of the experiments in this group water accumulated in the lungs slowly during the first 30 minutes of the test period and more rapidly as the period was extended. Obstruction of right lymphatic duct outflow did not alter the rate of water accumulation. Based on the control data of the present experiments, the pericapillary pressure in normal lungs is estimated to be of the order of - 9 mm Hg in the normal dog lung. The filtration coefficient for the pulmonary capillaries is estimated to be of the order of one-tenth to one-twentieth of that for canine muscle capillaries. The data of the present study indicate that edema formation in lung tissue cannot be defined solely in terms of intravascular forces, but may be governed to a significant degree by changes in pericapillary forces in the pulmonary interstitium.

Animals↗

PubMedDate not supplied

Disturbances of rhythm in chronic lung disease.

Patients with chronic obstructive lung disease have a high incidence and wide variety of cardiac arrhythmias. These arrhythmias are often clinically significant and may be life threatening. Although they occur particularly in the context of acute respiratory failure, arrhythmias are not infrequent in clinically stable patients. The relatively high incidence of sudden arrhythmias seen in acute respiratory failure are associated with a very poor prognosis, in particular, ventricular premature beats and multifocal atrial tachycardia. Long-term electrocardiographic monitoring is valuable in increasing the detection of these arrhythmias and in assessing their clinical significance and response to therapy. The mechanisms producing these arrhythmias are poorly understood and probably multiple. However, disturbances of blood gases, blood pH, and electrolytes or the presence of cor pulmonale or associated coronary artery disease is probably important. The therapy of these arrhythmias must include efforts to improve the patient's ventilatory status as well as careful use of standard antiarrhythmic drugs. Further investigation is needed to define the mechanisms, determine the prognosis, and improve the therapy of the arrhythmias found in chronic obstructive lung disease.

Arrhythmias, Cardiac↗