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In this investigation we have studied the effect of increments of pulmonary edema on pulmonary hemodynamics, and physiological and hemodynamic shunt in an isolated lung preparation. Hemodynamic shunt was defined by the slope of the relationship between pulmonary arterial and airway pressures; when the slope decreases, there is a greater degree of shunt. Cardiovascular changes were analyzed using a Starling resistor model of the pulmonary circulation where the effective downstream pressure to flow as seen from the pulmonary artery exceeds the pulmonary venous outflow pressure. This effective downstream pressure is referred to as the critical pressure (Pc), and at low lung inflation the locus of this critical pressure is in extra-alveolar vessels. With 3-4 h of progressive edema to an average of 185% initial lobe weight we found a progressive rise in pulmonary arterial pressure (Ppa) from 12.1 to 21.5 cmH2O. About one-third of this increase in Ppa resulted from an increased Pc and the remainder resulted from an increased resistance upstream from the locus of Pc. These results are consistent with the hypothesis that the interstitial accumulation of fluid creates enough of an increase in interstitial pressure to compress extra-alveolar vessels. There was no significant correlation between the amount of edema and the measured physiologic shunt, but the hemodynamic shunt showed a highly significant correlation. The hemodynamic shunt theoretically measures the extent of obstructed airways and may be a useful index of the degree of pulmonary edema.

To examine whether hypoxia causes constriction of alveolar or extra-alveolar vessels, we determined the relationships among transpulmonary pressure, pulmonary arterial pressure (Ppa), blood flow (Q), and transvascular fluid filtration rate (W) during normoxia (PO2 = 200 Torr) and hypoxia (PO2 = 50 Torr) in isolated pig lungs perfused with autologous blood. Left atrial pressures were always subatmospheric. The effects of lung inflation and hypoxic vasoconstriction on the Ppa-Q relationship were similar; when transpulmonary pressure was greater than 5 Torr, both shifted the curve to higher pressures in a parallel fashion. When transpulmonary pressure was 0–5 Torr, however, inflation had no effect on the Ppa-Q relationship during either normoxia or hypoxia. During normoxia at a transpulmonary pressure of 3.5 Torr, the relationship between fluid filtration rate and flow was characterized by a W of zero at Q less than 1.5 l/min and a rapid increase in W with Q above this value. Both hypoxia and inflation shifted this relationship to higher filtration rates in a parallel fashion. Furthermore, the combined effects of hypoxia and inflation on filtration rate were additive. These results suggest that hypoxia caused constriction of both alveolar and extra-alveolar vessels, resulting in increased intraluminal pressure and filtration of fluid in vessels upstream from the sites of constriction.

We describe simple high-frequency oscillation systems that incorporate a CO2 absorber and supply O2 on a need basis. These systems have the advantage of easy control of mean airway pressure and airway hydration and negligible loss of oscillatory tidal volume. Experiments done at constant tidal volume showed that as frequency (and hence total ventilation) increased, arterial CO2 tension (PaCO2) decreased. The fall in PaCO2 occurred until frequency reached approximately 20 Hz; above 20 Hz further increases in frequency had little or no effect on PaCO2. Because of their practical advantages the techniques described here may be quite useful in a clinical setting where an oscillator, rather than jet-type high-frequency, ventilation system is desired.

The confluent sinus pressure was measured in eight mongrel dogs in the head-up position to compare the effectiveness of positive end-expiratory pressure (PEEP) and jugular venous compression in increasing cerebral venous pressure. When the head was elevated 30 cm above the heart, confluent sinus pressure decreased from 9.6 +/- 1.8 (mean +/- SEM) to -5.3 +/- 0.5 mmHg. At constant arterial carbon dioxide tension (PaCO2 = 28 +/- 2 mmHg), PEEP (20 cmH2O) did not increase cerebral venous pressure. However, when the jugular veins were compressed with a neck tourniquet with pressures of 20-140 mmHg, cerebral venous pressure increased rapidly. When neck tourniquet pressure was maintained at 40 mmHg, confluent sinus pressure in all dogs was increased and sustained at 2.4 +/- 0.8 mmHg. Carotid artery pressure measured distal to the tourniquet was not altered. The efficacy of extrathoracic venous pressure elevation (neck tourniquet) is greater than intrathoracic (PEEP), and this may relate to the Starling resistor effects of neck veins and the presence of jugular venous valves. We conclude that prophylactic use of PEEP in the prevention of air embolism during the sitting position may not be as effective as jugular venous compression.