Quantitative Assessment of Pulmonary Edema

Levine, O. Robert; Mellins, Robert B.; Fishman, Alfred P.

doi:10.1161/01.res.17.5.414

Cited by 68 publications

(31 citation statements)

References 14 publications

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“…Larger doses produce cardiac failure (31,32), and so the possibility exists that a rise in pulmonary venous pressure had produced increased filling of the pulmonary capillary bed (33). However, the lungs were not wet at postmortem examination immediately afterwards, and the lung weight: body weight ratio of the anesthetized animals which were bled was not different from that of the conscious group, and so it may be deduced that the pulmonary venous pressure was not raised to that level necessary to cause the accumulation of edema fluid (34)(35)(36).…”

Section: Discussionmentioning

confidence: 99%

Indicator dilution measurements of extravascular water in the lungs

Goresky¹,

Cronin²,

wangel³

1969

J. Clin. Invest.

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A B S T R A C T Multiple indicator dilution studies of the pulmonary circulation were carried out in conscious, resting and exercising, and anesthetized dogs under conditions where there was no pulmonary edema. Labeled red cells, water, and albumin were injected together into the pulmonary artery, and effluent dilution patterns were obtained from the descending thoracic aorta. The product of the mean transit time differences between labeled water and red cells, and the pulmonary water flow was used to estimate extravascular parenchymatous water; and this was expressed as a proportion of the water content of the blood-drained lung at postmortem examination. These estimates of the proportional water content were found to increase with flow, and to approach an asymptotic value. Reconsideration of the flow patterns in capillaries, however, led to the postulate that extravascular water should be calculated, utilizing as the appropriate vascular reference a substance that uniformly labels the water in red cells and plasma, and which is confined to the circulation, rather than a tracer that only labels red cells. The mean transit time of this substance is approximated by the sum of the mean transit times of labeled red cells and albumin, each weighted according to the proportion of the water content of blood present in that phase. The values for lung water content so computed also increased with flow, and appeared to approach an asymptote that corresponded to approximately two-thirds of the wet lung weight. The estimated values for the water space after pentobarbital anesthesia corresponded to the lower values obtained in the resting conscious animals. When the anesthetized animals were also bled, the estimated water space was disproportionately large, in relation to the previous values. These experimental results support the hypothesis that dilutional This work was presented in part at the 51st Annual

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Section: Discussionmentioning

confidence: 99%

Indicator dilution measurements of extravascular water in the lungs

Goresky¹,

Cronin²,

wangel³

1969

J. Clin. Invest.

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“…This involved the combination of pulmonary venous hypertension and hemodilution (5). Partial pulmonary venous obstruction was produced by passing a double-lumen, end-hole balloon catheter retrogradely, under fluoroscopic control, through the aortic and mitral valves, and inflating the balloon in the left atrium with 3.5 ml of radiopaque material.…”

Section: Introductionmentioning

confidence: 99%

“…Left atrial pressure was measured through the hole in the end of the balloon catheter. Other catheters were also placed under fluoroscopic control for the measurement of pulmonary arterial, aortic arch, and right atrial pressures (5 (14). The areas under the corrected simultaneous curves were compared 10 times in 5 dogs under control conditions, and 10 times in 5 dogs with pulmonary edema; they agreed within 10% in all instances.…”

Section: Introductionmentioning

confidence: 99%

The Application of Starling's Law of Capillary Exchange to the Lungs*

Levine¹,

Mellins²,

Senior³

et al. 1967

J. Clin. Invest.

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124

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Summary. 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 (PLA) and plasma colloid osmotic pressures (7rp1) 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 PLA -7rpl, 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 PLA -7rpl the average rate of accumulation was 0.22 g per g per hour per mm Hg AP; 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.

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“…Intrapulmonary shunt rises with acute pulmonary edema 18 and compliance falls with pulmonary engorgement and edema. 19 At autopsy, the fraction of lung water (0.81) was normal.…”

Section: Discussionmentioning

confidence: 95%

Lymph and pulmonary response to isobaric reduction in plasma oncotic pressure in baboons.

Zarins¹,

Rice²,

Peters³

et al. 1978

Circulation Research

126

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LYMPH RESPONSE TO REDUCED ONCOTIC PRESSURE/Zanns et al. 925sodium concentration on calcium fluxes in isolated guinea pig auricles. J Physiol (Lond) 209: 1970 27. Benninger C, Einwachter HM, Haas HG, Kern R: Calciumsodium antagonism on the frog's heart: A voltage-clamp study. J Physiol (Lond) 259: 617-645, 1976 28. Chapman RA, Niedergerke R: Interaction between heart rate and calcium concentration in the control of contractile strength of the frog heart. J Physiol (Lond) 211: 1970 Thoracic duct lymph flow increased 6-fold and pulmonary lymph flow 7-fold. Thoracic duct lymph had a lower colloid osmotic pressure (2.0 ± 0.7 mm Hg) than plasma (4.7 ± 1.5 mm Hg), whereas the colloid osmotic pressure of pulmonary lymph (4.7 ± 0.7 mm Hg) was the same as that of plasma. The lymphplasma ratio for albumin fell in thoracic duct lymph but remained unchanged in pulmonary lymph. The difference between plasma colloid osmotic pressure and pulmonary artery wedge pressure decreased from 15.3 ± 1.9 to -0.7 ± 2.9 mm Hg. Despite this increase in filtration force, the lungs were protected from edema formation by a decrease of 11 mm Hg in pulmonary interstitial colloid osmotic pressure and a 7-fold increase in lymph flow.FLUID movement across capillary membranes is governed by a precise balance between hydrostatic and osmotic forces across the capillary wall and by the permeability characteristics of the capillary membrane. The Starling equation 1 describes this balance and is of central importance in the regulation of tissue fluid volume. Increased capillary hydrostatic pressure, decreased plasma colloid osmotic pressure, increased interstitial fluid osmotic pressure, and decreased lymphatic flow all tend to promote edema formation. The systemic lymphatics can compensate for conditions causing increased interstitial fluid by great increases in flow.2 A similar increase in lymph flow occurs in the lung when microvascular pressure is elevated 3 "5 and occurs at a lower microvascular pressure when combined with a decreased colloid osmotic pressure.6 However, reduced colloid osmotic pressure alone rarely causes pulmonary edema despite the fact that marked peripheral edema and ascites may be present.7 ' 8 To determine the effects of isobaric reduction Received November 15, 1977; accepted for publication June 26, 1978. in plasma colloid osmotic pressure on edema formation, we studies systemic and pulmonary lymphatic flow in baboons. Methods Five healthy male baboons (Papio anubis)weighing 21-28 kg were sedated with phencyclidine hydrochloride (Sernylan, 1 mg/kg). Under local 1% lidocaine anesthesia, catheters were introduced through the femoral vessels and positioned under fluoroscopic control in the descending aorta, right atrium, and pulmonary artery. The pulmonary artery catheter was a 7F flow-directed, balloon-tipped catheter (Edwards Laboratories) which allowed measurement of pulmonary artery wedge pressure.Additional phencyclidine was given (0.5-1 mg/kg), and the baboons were paralyzed with pancuronium bromide (Pavulon, 0....

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Quantitative Assessment of Pulmonary Edema

Cited by 68 publications

References 14 publications

Indicator dilution measurements of extravascular water in the lungs

Indicator dilution measurements of extravascular water in the lungs

The Application of Starling's Law of Capillary Exchange to the Lungs*

Lymph and pulmonary response to isobaric reduction in plasma oncotic pressure in baboons.

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