Continuous Negative External Chest Pressure Decreases Transvascular Lung Water Transport in Sheep after Pseudomonas Bacteremia

Abstract

A B S T R A C T We studied the effects of continuous negative external chest pressure (CNECP) produced by a cuirass appliance on lung water and protein transport in sheep with chronic lung lymphatic fistulas. We compared data obtained during periods of mechanical ventilation (base line) to period of CNECP, using identical ventilatory support. Three groups were studied: six sheep were studied before and after application of CNECP for 1 h (control) and again after induction of a pulmonary vascular permeability defect (PVPD) by infusing live Pseudomonas bacteria (group I); another six sheep were studied under control conditions before and after prolonged application of CNECP for over 4 h (group II); 10 sheep were studied 24 h after a Pseudomonas infusion (PVPD), before and after 4 h of CNECP (group III).Compared to base-line data, CNECP produced significant increases in functional residual capacity and decreases in pulmonary blood volume, pulmonary artery pressure, and left atrial pressure in all groups. Lung lymph flow (QL) was unchanged during the 1st h of CNECP and therefore was not significantly different from base line in group I, but after prolonged CNECP a steady-state decrease in QL as well as a decrease in lung albumin transport was found in groups II and III (P < 0.05 by paired t test). We postulate that decreased pleural pressure during CNECP produces decreased hydrostatic filtration pressures, thereby decreasing QL. Reduction of both convective forces as well as microvascular surface area available for solute exchange account for decreases in lung albumin transport. Histologic examination and gravimetric studies on four sheep failed to demonstrate increase in lung water accumulation after 4 h of CNECP. We conclude that CNECP mechanically reversed the PVPD in our group III sheep. These physiologic effects of CNECP may be of benefit in the management of patients with adult respiratory distress syndrome.

Continuous external negative pressure improves oxygenation and respiratory mechanics in Experimental Lung Injury in Pigs – A pilot proof-of-concept trial

“…Also, abdominal CENP may more effectively dislocate the diaphragm [10], resulting in more pronounced effects on pleural pressures. The dislocation of the diaphragm increased end-expiratory lung volume (EELV) in a bacterial infection model in sheep [26]. Although EELV was not assessed in our study, the results of the gas exchange suggest an increase EELV comparable to that resulting from PEEP alone.…”

“…In fact, the application of external negative pressure on the abdomen CENP decreased the ventro-dorsal pleural pressure gradient in another experimental study [25]. The vertical gradient of transpulmonary pressure, which is associated with lung collapse in dependent lung regions, is induced by gravitational forces [26]. One hypothesis of applying local negative pressure externally to the thorax is to decrease or even invert this vertical gradient to reduce derecruitment and shift the ventilation towards dependent lung regions.…”

Continuous negative extrathoracic pressure combined with high-frequency oscillation improves oxygenation with less impact on blood pressure than high-frequency oscillation alone in a rabbit model of surfactant depletion

“…CNEP has favorable effects on permeability and hydrostatic pulmonary edema [ 6 , 7 ]. In a sheep model inoculated with Pseudomonas bacteria, CNEP decreased hydrostatic filtration pressure and lung lymph flow [ 13 ]. In dogs with pulmonary edema induced by oleic acid, CNEP increased extravascular lung water volume, but did not change central blood volume [ 14 ].…”

Pulmonary Hemodynamics

“…However, CNECP has been shown to have an advantage in improving cardiac output compared to PEEP with identical increases in FRC. CNECP has also been shown to decrease pulmonary blood volume, pulmonary arterial pressure, and hydrostatic filtration pressures, thereby decreasing lung lymph flow (Krumpe and Gorin, 1981). However, the more negative pleural and interstitial pressures during CNECP might result in increased filtration of fluid into the lung interstitium, thereby causing pulmonary edema.…”

“…It has been suggested that a significant increase in alveolar surface tension can induce pulmonary edema, even when the capillary oncotic and hydrostatic pressures are normal (Culver and Butler, 1980;Krumpe and Gorin, 1981;Pain and West, 1966). The presence of such edema can, in turn, alter the relationship between the pulmonary arterial and alveolar pressures.…”