Extravascular Lung Thermal Volume Research Articles

Effects of increased left atrial pressure, endotoxemia and pulmonary air embolism on the measurement of extravascular lung thermal volume

Effects of increased left atrial pressure, endotoxemia and pulmonary air embolism on the measurement of extravascular lung thermal volume

Usefulness of sodium chloride as a nondiffusible indicator in the measurement of extravascular lung thermal volume in dogs.

The authors examined the usefulness of sodium chloride as a nondiffusible indicator during the first passage through dogs' lungs, before and after increased-permeability pulmonary oedema produced by an intravenous injection of alloxan. With an injection of a mixture of ice-cold 3 per cent sodium chloride and indocyanine green dye (a nondiffusible reference indicator), the authors simultaneously recorded three dilution curves from the aortic root: dye dilution, thermal and blood electrical conductivity dilution curves in six dogs. The mean transit time of sodium chloride in the conductivity dilution curve was significantly different from, but fairly equal to, that of indocyanine green dye (6.2 +/- 1.4 s (mean +/- SD) against 6.5 +/- 1.4 s (p < 0.01) in the baseline period, and 7.6 +/- 1.9 s against 8.4 +/- 2.1 s (p < 0.01) in the oedema period, respectively). The calculated extravascular lung thermal volume with the thermal and conductivity dilution method (Y, ml kg-1) correlated well with the gravimetrically determined extravascular lung mass in a total of 12 dogs, including six other dogs without intervention (x, g kg-1) (y = 0.72 x +3.03, r = 0.96). The authors conclude that sodium chloride is useful as a nondiffusible indicator in the first passage through the lungs, and that the thermal and conductivity dilution method is also useful for measuring extravascular lung water mass.

Effects of milrinone on lung water content in dogs with acute pulmonary hypertension

To evaluate the effects of milrinone (MIL) on hemodynamics and lung water content, we used 10 mongrel dogs with pulmonary hypertension (PH). To induce pulmonary hypertension, we administered two injections of glass beads stirred in saline to dogs. Mean pulmonary arterial pressure (PAP) and pulmonary vascular resistance significantly increased following induction. Milrinone, which inhibits cyclic AMP phosphodiesterase-(PDE) demonstrated pulmonary vasodilation, indicated a reduction in these two parameters. To clarify the drug mechanism, we measured lung water content as extravascular lung thermal volume (ETV L.) using a thermo/sodium double-indicator dilution method. The induction of pulmonary hypertension produced a transient reduction in extravascular lung thermal volume. The parameter remained constant following milrinone administration, whereas the control showed a gradual increase. Of the 10 dogs, five were killed to measure gravimetrically the volume of lung water content as a comparison with extravascular lung thermal volume. We concluded that milrinone produced pulmonary vasodilation which induced a reduction in the transmural capillary pressure gradient according to Starling's hypothesis. This study suggests that the reduction in the transmural pressure gradient induced by milrinone may also prevent the re-elevation in extravascular lung thermal volume. Milrinone increases the cyclic AMP level in the endothelium and in the platelet which may affect either directly or indirectly the permeability of capillary endothelium.

Reliability of extravascular lung thermal volume measurements by thermal conductivity technique in sheep.

We tested the accuracy, sensitivity, and reproducibility of a new lung water computer, based on the thermal conductivity technique, in 22 anesthetized closed-chest ventilated sheep with different treatments: 1) controls (n = 8), 2) 0.05 ml/kg of oleic acid + 100 ml/kg of lactated Ringer solution (n = 6), and 3) airway instillation of saline [3.1 +/- 1.3 (SD) g/kg, n = 8]. After 4 h, we determined the extravascular lung water gravimetrically. We found a significant overall correlation between the final extravascular lung thermal volume and the gravimetric extravascular lung mass (P < 0.001). Although the average ratio of extravascular lung thermal volume to extravascular lung mass was 0.97 +/- 0.25 ml/g for all groups, the computer overestimated extravascular lung mass in controls by 10% (17 g) and underestimated it in sheep with oleic acid by 15% (95 g) and in sheep with airway instillation by 8% (37 g). The computer also underestimated the small quantities of saline placed via the airway in the alveolar space by 75% (61 g). Reproducibility of three consecutive measurements was 4.3% (SE). We conclude that the thermal conductivity technique has an ability to detect the baseline extravascular lung mass but has a poor ability to detect an accurate increment of the extravascular lung water under poor tissue perfusion in anesthetized ventilated sheep.

Relationship between electron microscopic changes in alveolar septa and extravascular lung water volume

Lung water accumulates partly in the alveolar septa. However, morphological changes in alveolar septa have never been analyzed quantitatively nor correlated with lung water volume changes. We aimed to delineate these unsolved questions.Twenty-four mongrel dogs were studied under general anesthesia and spontaneous breathing. Extravascular lung thermal volume was measured with double indicator dilution technique using heat and Indocyanine green. Experimental groups were as follows: Group C; 6 control dogs, Group D-30; 100 ml/kg of dextran-70 over 30 min in 6 dogs, Group D-90; 100 ml/kg of dextran-70 over 30 min and waiting for another 60 min in 6 dogs, Group A; 100 mg/kg of alloxan. After final measurement of extravascular lung thermal volume, we immediately killed the dogs with the lungs inflated and we removed the lungs for lung water measurement with direct destructive method. Samples for electron microscopic examination were obtained by excising tissues from the surface of right lower lobe where edema appeared severe. Twenty electron micrographs were prepared from each dog without prior knowledge of the experimental intervention.

Effect of superior vena caval hypertension on alloxan-induced lung injury in dogs

To investigate how fast and to what extent superior vena caval hypertension (SVCH) increases lung water in acute increased-permeability state, we studied the time course of lung water accumulation for 3 h in anesthetized dogs under different treatments: 1) controls without intervention (5 dogs), 2) SVCH alone (5 dogs), 3) mild lung microvascular injury induced by low-dose alloxan (75 mg/kg) alone (5 dogs), and 4) SVCH coupled with low-dose alloxan (5 dogs). Neither low-dose alloxan alone nor SVCH alone [superior vena caval pressure (Psvc) = 11.0 +/- 3.1 (SD) mmHg] increased lung water significantly. The SVCH coupled with low-dose alloxan (Psvc = 11.3 +/- 2.7 mmHg) doubled extravascular lung thermal volume measured by the thermal-dye dilution technique within 1 h (5.3 +/- 0.9 ml/kg at base line and 10.9 +/- 4.7 ml/kg at 1 h), then remained unchanged (12.5 +/- 5.7 ml/kg at 3 h). This increase in lung water was confirmed by gravimetric method (5.69 +/- 1.71 g/g blood-free dry wt). We conclude that SVCH is one of the factors that may promote lung water accumulation in increased-permeability state.

Cardiac output measurement using femoral artery thermodilution in patients

This study was performed to assess thermal indicator loss between the pulmonary artery and the abdominal aorta after a single bolus injection in the right atrium, in order to validate cardiac output measurements from dilution curves recorded in an arterial vessel after central venous indicator injection. Thermal indicator dilution curves were simultaneously recorded in the pulmonary artery and the femoral artery after central venous injection of a 10 mL ice cold indocyanine-green dye solution. Cardiac outputs were determined on-line by identical cardiac output computers connected with thermistor catheters in the pulmonary artery catheter (CO PA) and the femoral artery (CO FA). Extravascular lung thermal volume was measured simultaneously. Paired dilution curves were measured on 804 occasions in 48 patients. The cardiac outputs correlate well (r = .94) with a least-square regression equation for the following data: CO FA = 0.97 CO PA ± 0.59 L/min. Mean femoral artery cardiac output was 7% greater than mean pulmonary artery cardiac output ( P < .001). We interpret this as being due to thermal indicator loss in passing through the lungs, left heart, and aorta. Thermal indicator loss is negatively correlated with cardiac output and extravascular lung thermal volume. We conclude that thermodilution measurements in a peripheral artery yield valid estimates of cardiac output with a 7% systematic overestimation due to thermal indicator loss.

Exponential increases in pulmonary intravascular and extravascular fluid volumes by overperfusion with dextran 70 in anesthetized dogs.

In the lung overperfused by dextran 70, it is not known how intravascular blood volume and extravascular water volume increase as a function of pulmonary microvascular pressure. To determine their characteristics, we produced an overperfusion state (high pressure and high blood flow) by infusing dextran 70 (100 ml/kg over 30 min) into 15 anesthetized dogs. Using the thermal and dye dilution technique, we simultaneously estimated the pulmonary blood volume (PBV) and the extravascular lung thermal volume (EVLTV), and correlated mathematically these variables with pulmonary artery end-diastolic pressure (PAEDP). Here, we defined PAEDP as the pulmonary microvascular pressure. From the values determined before, during and after dextran 70 infusion, we obtained the following exponential relations. PBV(ml/kg) = 30[1-0.902(e-0.021PAEDP(mmHg)) EVLTV(ml/kg) = 5.15(e0.027PAEDP (mmHg)) From these mathematical relations, we conclude that: (1) the pulmonary blood volume increases rapidly at low pressure and slowly at high pressure; and (2) the pulmonary extravascular water volume increases slowly at low pressure and then increases rapidly at high pressure. In addition, this equation indicates that the critical pressure from which the pulmonary extravascular water volume exceeds the upper limit of its normal volume is about 17 mmHg in PAEDP. Infusion of dextran 70 increased plasma macromolecular osmotic pressure from 20.8 +/- 0.6 (mean +/- SD) mmHg before infusion to 43.7 +/- 1.4 mmHg after infusion. Therefore, dextran 70 does not change the critical microvascular pressure against pulmonary edema.

FLUID VOLUME BALANCE BETWEEN PULMONARY INTRAVASCULAR SPACE AND EXTRAVASCULAR SPACE IN DOGS

We aimed to study the agreement of estimates of the pulmonary blood volume by the double indicator dilution method and the direct destructive method and the fluid volume balance between the pulmonary intravascular and extravascular spaces. We employed the double indicator dilution method using heat and indocyanine green, with a single injection (into the right atrium) and double sampling technique, that is from the pulmonary artery trunk (PAT) and the aortic root (Ao). With this method, we simultaneously determined the pulmonary extravascular water volume (PEWV), defined as the extravascular lung thermal volume estimated in Ao (LTVAo), and the pulmonary blood volume (PBV) from PAT to the left atrium (LA) (PBVPAT-LA). Dogs were divided into groups: a group without intervention (n = 16), a group loaded with dextran (n = 12) and a group loaded with alloxan (n = 7). When all groups were included, PBVPAT-LA (ml/kg) = 1.02 X PBVdirect(g/kg) + 0.96, n = 35, r = 0.83 where PBVdirect means the blood contents from the pulmonary artery bifurcation to the pulmonary vein measured by the direct destructive method. We substantiated the validity of the use of the double indicator dilution method. In studying the fluid volume balance, based on the results of the direct destructive method, the pulmonary intravascular-extravascular fluid volume ratio (intra/extra) was 1.3 +/- 0.3 (mean +/- SD) in the control state, implying that the interstitium in the lung is relatively "dry". As overt pulmonary edema developed by dextran infusion, the ratio exponentially decreased to 1.0 +/- 0.1 (p less than 0.01). The behavior of the fluid volume balance in question (intra/extra), studied with the double indicator dilution method, was essentially similar to that analyzed by the direct destructive method.

Pulmonary blood volume and pulmonary extravascular water volume in men.

In order to estimate the pulmonary blood volume between the pulmonary artery trunk and the left atrium (PBV PAT-LA), simultaneously with the pulmonary extravascular water volume (PEWV) in the chronically stable cardiac patients, we employed the double indicator dilution method using heat as a diffusible indicator and indocyanine green as a non-diffusible indicator. The PEWV was obtained as the extravascular lung thermal volume estimated in the aortic root (LTVAo). In the group of hemodynamically normal patients, in spite of ischemic heart disease (G-N, n = 22), the mean pulmonary artery wedge (PAW) pressure was 9.3 +/- 3.9 mmHg (mean +/- SD), PBVPAT-LA was 8.95 +/- 1.71 ml/kg, LTVAo was 5.71 +/- 1.37 ml/kg and PBVPAT-LA/LTVAo ratio was 1.64 +/- 0.44. In the group of hemodynamically slightly compromised patients with mitral stenosis (G-MS, n = 13), the mean PAW pressure was 14.2 +/- 2.6 mmHg, PBVPAT-LA was 11.12 +/- 2.86 ml/kg, LTVAo was 5.68 +/- 1.41 ml/kg and PBVPAT-LA/LTVAo ratio was 2.02 +/- 0.58. Between the two groups, LTVAo was not statistically significant, whereas the mean PAW pressure, PBVPAT-LA and PBVPAT-LA/LTVAo ratio were all significantly increased in G-MS (p less than 0.05). Neither PBVPAT-LA nor LTVAo correlated with the mean PAW pressure in both groups. From PBVPAT-LA/LTVAo ratio, fluid volume in the intravascular space was greater than that in the extravascular space in both groups. From LTVAo, PEWV in G-MS was identical with that in G-N, in spite of the elevated mean PAW pressure. Therefore, even in the patients with mitral stenosis, the interstitium in the lung is kept "dry" under conditions of the mean PAW pressure below 20 mmHg. The safety factors that prevent pulmonary edema, as evidenced in animal studies, seem to operate effectively in man.

Reappraisal of extravascular lung thermal volume as a measure of pulmonary edema.

Previous papers have evaluated extravascular thermal volume of the lung (ETVL) as a measure of lung water by using median transit time (tmed) rather than the correct mean transit time (tmean). Calculation of ETVL using tmean (ETVLmean) and tmed (ETVLmed) gave an excellent relationship, ETVLmean = 1.48 ETVLmed - 0.74 (r = 0.99). This allowed us to calculate a new ratio of ETVLmean to PETW = 1.55 +/- 0.17, WHERE PETW is the postmortem value of pulmonary extravascular tissue weight. Thermistors were placed in dogs to determine the contribution of chest wall, pleural and pericardial fluid, left heart, bronchi, and lung gas to the ETVL measurement. We found ETVLmean greater than PETW because of thermal distributioninto left heart (18 +/- 2% of ETVL), bronchi (estimate 7% of ETVL), pulmonary arteries and veins (estimate 7% of ETVL), and perhaps a small portion of chest wall. We could not detect any portion of lung gas or pleural or pericardial effusions as a part of the ETVL measurement. When the distribution into left heart, bronchi, pulmonary arteries, and veins is removed ETVLmean/PETW = 1.07.